pmid title sentence year journal region virus mutation mutation_start mutation_end gene gene_start gene_end disease disease_start disease_end 10534722 A novel hepatitis B virus variant S 129 (Gln-->Leu): lack of correlation between antigenicity and immunogenicity. A novel hepatitis B virus variant S 129 (Gln-->Leu): lack of correlation between antigenicity and immunogenicity. 1999 Journal of medical virology Title HBV Q129L 36 50 S 34 35 10760047 Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L-FMAU, DAPD, penciclovir and lobucavir. Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L-FMAU, DAPD, penciclovir and lobucavir. 2000 Journal of viral hepatitis Title HBV M550V 52 57 P 41 51 10775637 A frequent, naturally occurring mutation (P130T) of human hepatitis B virus core antigen is compensatory for immature secretion phenotype of another frequent variant (I97L). A frequent, naturally occurring mutation (P130T) of human hepatitis B virus core antigen is compensatory for immature secretion phenotype of another frequent variant (I97L). 2000 Journal of virology Title HBV P130T;I97L 42;167 47;171 C 76 80 10982356 Low-level secretion of human hepatitis B virus virions caused by two independent, naturally occurring mutations (P5T and L60V) in the capsid protein. Low-level secretion of human hepatitis B virus virions caused by two independent, naturally occurring mutations (P5T and L60V) in the capsid protein. 2000 Journal of virology Title HBV P5T;L60V 113;121 116;125 Capsid 134 140 11092260 De novo acute hepatitis B infection in a previously vaccinated liver transplant recipient due to a strain of HBV with a Met 133 Thr mutation in the "a" determinant. De novo acute hepatitis B infection in a previously vaccinated liver transplant recipient due to a strain of HBV with a Met 133 Thr mutation in the "a" determinant. 2000 Liver Title HBV M133T 120 131 Acute Hepatitis B 8 35 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. 2000 The Journal of infection Title HBV G145R 95 100 S 72 79 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. 2001 The Journal of clinical investigation Title HBV L528M 15 20 P 4 14 11208474 Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene. Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene. 2000 Medical science monitor Title HBV E129D;G145A 85;103 98;116 S;S 12;124 15;131 12185284 Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis. Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis. 2002 The Journal of general virology Title HBV G1862T 32 38 Fulminant Hepatitis B 93 112 12210428 Core promoter mutations (A(1762)T and G(1764)A) and viral genotype in chronic hepatitis B and hepatocellular carcinoma in Guangxi, China. Core promoter mutations (A(1762)T and G(1764)A) and viral genotype in chronic hepatitis B and hepatocellular carcinoma in Guangxi, China. 2002 Journal of medical virology Title HBV A1762T;G1764A 24;38 34;47 Core promoter 0 13 Chronic Hepatitis B;Hepatocellular carcinoma 70;94 89;118 12414948 Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. 2002 Journal of virology Title HBV I97L 123 127 Capsid 106 112 12457969 Presence of hepatitis B surface antigen mutant G145R DNA in the peripheral blood leukocytes of the family members of an asymptomatic carrier and evidence of its horizontal transmission. Presence of hepatitis B surface antigen mutant G145R DNA in the peripheral blood leukocytes of the family members of an asymptomatic carrier and evidence of its horizontal transmission. 2002 Virus research Title HBV G145R 47 52 S 24 31 12500185 Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro. Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro. 2003 Hepatology (Baltimore, Md.) Title HBV G1896A 14 20 Precore 21 28 12759982 [A mutation specific polymerase chain reaction for detecting hepatitis B virus genome with A-to-C mutation at nt585]. [A mutation specific polymerase chain reaction for detecting hepatitis B virus genome with A-to-C mutation at nt585]. 1999 Zhonghua shi yan he lin chuang bing du xue za zhi Title HBV A585C 91 115 12805468 Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion. Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion. 2003 Journal of virology Title HBV I97L;P5T 57;49 61;52 C 84 88 12931030 Low HBeAg serum levels correlate with the presence of the double A1762T/G1764A core promoter mutation and a positive response to interferon in patients with chronic hepatitis B virus infection. Low HBeAg serum levels correlate with the presence of the double A1762T/G1764A core promoter mutation and a positive response to interferon in patients with chronic hepatitis B virus infection. 2003 Intervirology Title HBV G1764A;A1762T 72;65 78;71 Core promoter;C 79;4 92;9 Chronic HBV infection 157 192 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. 2003 Journal of virology Title HBV V173L 44 49 RT;P 42;22 44;32 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. 2003 Hepatology (Baltimore, Md.) Title HBV G145R 101 106 15308745 Hepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L. Hepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L. 2004 Journal of virology Title HBV F97L 78 82 Capsid 18 24 15634980 Development of a molecular-beacon assay to detect the G1896A precore mutation in hepatitis B virus-infected individuals. Development of a molecular-beacon assay to detect the G1896A precore mutation in hepatitis B virus-infected individuals. 2005 Journal of clinical microbiology Title HBV G1896A 54 60 Precore 61 68 HBV infections 81 107 15778957 Transmission of G145R mutant of HBV to an unrelated contact. Transmission of G145R mutant of HBV to an unrelated contact. 2005 Journal of medical virology Title HBV G145R 16 21 15858045 Failure of the lamivudine-resistant rtM204I hepatitis B virus mutants to efficiently support hepatitis delta virus secretion. Failure of the lamivudine-resistant rtM204I hepatitis B virus mutants to efficiently support hepatitis delta virus secretion. 2005 Journal of virology Title HBV M204I 38 43 RT 36 38 15872296 Prevalence, incidence, and clinical relevance of the reverse transcriptase V207I mutation outside the YMDD motif of the hepatitis B virus polymerase during lamivudine therapy. Prevalence, incidence, and clinical relevance of the reverse transcriptase V207I mutation outside the YMDD motif of the hepatitis B virus polymerase during lamivudine therapy. 2005 Journal of clinical microbiology Title HBV V207I 75 80 P;RT;P 138;53;102 148;74;106 15973769 Character of HBV (hepatitis B virus) polymerase gene rtM204V/I and rtL180M mutation in patients with lamivudine resistance. Character of HBV (hepatitis B virus) polymerase gene rtM204V/I and rtL180M mutation in patients with lamivudine resistance. 2005 Journal of Zhejiang University. Science. B Title HBV M204V;M204I;L180M 55;55;69 62;62;74 RT;RT;P 53;67;37 55;69;47 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. 2005 Virology journal Title HBV M130K;V131I 4;14 9;19 X 0 3 16637866 Hepatitis B virus genotypes and G1896A precore mutation in 486 Spanish patients with acute and chronic HBV infection. Hepatitis B virus genotypes and G1896A precore mutation in 486 Spanish patients with acute and chronic HBV infection. 2006 Journal of viral hepatitis Title HBV G1896A 32 38 Precore 39 46 16757589 Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). 2006 Journal of clinical microbiology Title HBV N236T;A181V;A181T 15;27;27 20;34;34 RT;RT 13;25 15;27 Chronic HBV infection 124 159 16963200 A unique amino acid substitution, T126I, in human genotype C of hepatitis B virus S gene and its possible influence on antigenic structural change. A unique amino acid substitution, T126I, in human genotype C of hepatitis B virus S gene and its possible influence on antigenic structural change. 2006 Gene Title HBV T126I 34 39 S 82 83 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. 2007 Intervirology Title HBV G1862T 0 6 HBV infections 22 48 17302381 Unusual selection of rtA181V HBV mutants cross-resistant to adefovir following prolonged lamivudine monotherapy: report of two cases. Unusual selection of rtA181V HBV mutants cross-resistant to adefovir following prolonged lamivudine monotherapy: report of two cases. 2006 Antiviral therapy Title HBV A181V 23 28 RT 21 23 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. 2007 Antimicrobial agents and chemotherapy Title HBV L80I 4 8 P;RT 83;29 93;50 17763322 Replicative competence of the T131I, K141E, and G145R surface variants of hepatitis B Virus. Replicative competence of the T131I, K141E, and G145R surface variants of hepatitis B Virus. 2007 The Journal of infectious diseases Title HBV T131I;K141E;G145R 30;37;48 35;42;53 S 54 61 18008227 Hepatitis B virus containing the I233V mutation in the polymerase reverse-transcriptase domain remains sensitive to inhibition by adefovir. Hepatitis B virus containing the I233V mutation in the polymerase reverse-transcriptase domain remains sensitive to inhibition by adefovir. 2007 The Journal of infectious diseases Title HBV I233V 33 38 P;RT 55;66 65;87 18331765 Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. 2008 Journal of hepatology Title HBV A181V;A181T 30;30 37;37 RT 28 30 18434744 A unique amino acid substitution, L215Q, in the hepatitis B virus small envelope protein of a genotype F isolate that inhibits secretion of hepatitis B virus subviral particles. A unique amino acid substitution, L215Q, in the hepatitis B virus small envelope protein of a genotype F isolate that inhibits secretion of hepatitis B virus subviral particles. 2008 Intervirology Title HBV L215Q 34 39 S 66 80 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. 2008 Hepatology (Baltimore, Md.) Title HBV W172X;A181T 54;48 60;53 RT;S 46;54 48;55 18675784 A1762T/G1764A mutations of hepatitis B virus, associated with the increased risk of hepatocellular carcinoma, reduce basal core promoter activities. A1762T/G1764A mutations of hepatitis B virus, associated with the increased risk of hepatocellular carcinoma, reduce basal core promoter activities. 2008 Biochemical and biophysical research communications Title HBV G1764A;A1762T 7;0 13;6 BCP 117 136 Hepatocellular carcinoma 84 108 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. 2008 The American journal of gastroenterology Title HBV A1762T;G1764A 4;12 10;18 S 87 92 Hepatocellular carcinoma 128 152 19043921 The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. 2008 Antiviral therapy Title HBV A181T 47 52 RT;S 45;54 47;61 19070921 The association of HBV core promoter double mutations (A1762T and G1764A) with viral load differs between HBeAg positive and anti-HBe positive individuals: a longitudinal analysis. The association of HBV core promoter double mutations (A1762T and G1764A) with viral load differs between HBeAg positive and anti-HBe positive individuals: a longitudinal analysis. 2009 Journal of hepatology Title HBV A1762T;G1764A 55;66 61;72 Core promoter;C;C 23;130;106 36;133;111 19178836 [A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding]. [A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding]. 2008 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Title HBV G1896A 71 77 Precore 55 63 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. 2009 Hepatology (Baltimore, Md.) Title HBV A194T 6 11 C;C;RT;P 105;140;4;12 114;149;6;22 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. 2009 Liver international Title HBV L80V;L80I 29;29 35;35 RT 27 29 19420079 Genetic characterization of hepatitis B virus in peripheral blood leukocytes: evidence for selection and compartmentalization of viral variants with the immune escape G145R mutation. Genetic characterization of hepatitis B virus in peripheral blood leukocytes: evidence for selection and compartmentalization of viral variants with the immune escape G145R mutation. 2009 Journal of virology Title HBV G145R 167 172 19553583 Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. 2009 Journal of clinical microbiology Title HBV M204V 30 35 19651117 Detection of the rtA181V/T and rtN236T mutations associated with resistance to adefovir dipivoxil using a ligase detection reaction assay. Detection of the rtA181V/T and rtN236T mutations associated with resistance to adefovir dipivoxil using a ligase detection reaction assay. 2009 Clinica chimica acta; international journal of clinical chemistry Title HBV A181V;A181T;N236T 19;19;33 26;26;38 RT;RT 17;31 19;33 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. 2009 Viral immunology Title HBV G1896A 44 50 Precore 51 59 Chronic HBV infection 72 107 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2010 Journal of virology Title HBV G145R;P120T 47;57 52;62 C 124 133 20007398 Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. 2010 Journal of clinical microbiology Title HBV I233V 40 45 RT 38 40 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. 2010 Journal of Korean medical science Title HBV A181T;A181V 97;97 104;104 P;S 105;18 115;25 20337225 T3098C and T53C mutations of HBV genotype C is associated with HBV infection progress. T3098C and T53C mutations of HBV genotype C is associated with HBV infection progress. 2009 Biomedical and environmental sciences Title HBV T3098C;T53C 0;11 6;15 HBV infections 63 76 20374224 Main mutations in the hepatitis B virus basic core promoter (A1762T/G1764A) before HBeAg loss are markers that identify patients who will require long-term treatment. Main mutations in the hepatitis B virus basic core promoter (A1762T/G1764A) before HBeAg loss are markers that identify patients who will require long-term treatment. 2010 Alimentary pharmacology & therapeutics Title HBV G1764A;A1762T 68;61 74;67 BCP;C 40;83 59;88 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. 2010 Journal of viral hepatitis Title HBV E218G 2 7 RT 0 2 Chronic Hepatitis B 99 118 20814897 Hepatitis B virus-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma. Hepatitis B virus-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma. 2010 Hepatology (Baltimore, Md.) Title HBV G1764A;A1762T 59;52 65;58 BCP 32 51 Hepatocellular carcinoma 139 163 20843617 [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors]. [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors]. 2011 Pathologie-biologie Title HBV G1896A 120 126 Precore 127 134 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. 2011 Journal of virology Title HBV F141L 6 11 PreS2 12 18 Hepatocellular carcinoma;Chronic HBV infection 71;113 95;142 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Title HBV G1764A;A1762T 45;38 51;44 BCP 34 37 Liver disease 85 115 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. 2011 Hepatitis research and treatment Title HBV Y100C 59 64 S 32 39 21562108 Ultrasensitive quantification of hepatitis B virus A1762T/G1764A mutant by a SimpleProbe PCR using a wild-type-selective PCR blocker and a primer-blocker-probe partial-overlap approach. Ultrasensitive quantification of hepatitis B virus A1762T/G1764A mutant by a SimpleProbe PCR using a wild-type-selective PCR blocker and a primer-blocker-probe partial-overlap approach. 2011 Journal of clinical microbiology Title HBV G1764A;A1762T 58;51 64;57 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. 2011 Virology journal Title HBV T337C;A336C;A336T 12;0;0 17;7;7 C;C 36;74 40;83 Chronic Hepatitis B 92 111 21686872 Polymorphism rtQ215H in primary resistance to adefovir dipivoxil in hepatitis B virus infection: a case report. Polymorphism rtQ215H in primary resistance to adefovir dipivoxil in hepatitis B virus infection: a case report. 2009 BMJ case reports Title HBV Q215H 15 20 RT 13 15 21739444 Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. 2011 Journal of medical virology Title HBV G1764A;A1762T;G1896A 52;45;34 58;51;40 Acute on chronic liver failure 108 138 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. 2012 Journal of gastroenterology and hepatology Title HBV L180M 2 7 RT 0 2 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. 2011 PloS one Title HBV G1613A 4 10 Core promoter;C 101;46 114;51 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. 2011 Antiviral chemistry & chemotherapy Title HBV A194T 15 20 BCP;RT;Precore;YMDD 124;13;112;4 143;15;119;8 21865669 Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. 2012 Intervirology Title HBV G1764A;A1762T 41;34 47;40 PreS 15 19 Hepatocellular carcinoma 113 116 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. 2011 BMC cancer Title HBV W172X;A181T 25;19 31;24 RT;S 17;25 19;26 Hepatocellular carcinoma 61 69 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. 2012 The Journal of antimicrobial chemotherapy Title HBV S117F;M204I 38;90 43;95 RT;RT 36;88 38;90 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. 2011 BMC cancer Title HBV G1613A;C1653T 42;53 48;59 Core promoter 18 31 Hepatocellular carcinoma;HBV infections 94;133 118;145 22037043 Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France. Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France. 2012 Clinics and research in hepatology and gastroenterology Title HBV G1896A 58 64 Precore 65 72 22052677 Phenotypic assay of a hepatitis B virus strain carrying an rtS246T variant using a new strategy. Phenotypic assay of a hepatitis B virus strain carrying an rtS246T variant using a new strategy. 2012 Journal of medical virology Title HBV S246T 61 66 RT 59 61 22053371 [Identification the relationship between mutation patterns of rtM204I/V in the polymerase gene and genotypes of hepatitis B virus]. [Identification the relationship between mutation patterns of rtM204I/V in the polymerase gene and genotypes of hepatitis B virus]. 2011 Zhonghua gan zang bing za zhi Title HBV M204I;M204V 64;64 71;71 P;RT 79;62 89;64 22100339 The effect of the G1888A mutation of subgenotype A1 of hepatitis B virus on the translation of the core protein. The effect of the G1888A mutation of subgenotype A1 of hepatitis B virus on the translation of the core protein. 2012 Virus research Title HBV G1888A 18 24 C 99 103 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. 2012 Antiviral research Title HBV N238H 79 84 P;RT 85;77 95;79 Chronic Hepatitis B 137 156 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. 2012 Antiviral research Title HBV G1764A;A1762T 55;48 61;54 BCP;S;C 18;109;145 37;114;150 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. 2012 Virology journal Title HBV W172X;A181T 42;36 48;41 RT;S 34;42 36;43 23261845 The amino acid substitutions rtP177G and rtF249A in the reverse transcriptase domain of hepatitis B virus polymerase reduce the susceptibility to tenofovir. The amino acid substitutions rtP177G and rtF249A in the reverse transcriptase domain of hepatitis B virus polymerase reduce the susceptibility to tenofovir. 2013 Antiviral research Title HBV P177G;F249A 31;43 36;48 RT;RT;P;RT 29;41;106;56 31;43;116;77 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. 2013 Journal of viral hepatitis Title HBV N236T 34 39 RT 32 34 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. 2012 Iranian journal of public health Title HBV G1764A;A1762T 37;30 43;36 Hepatocellular carcinoma;Liver cirrhosis 72;102 96;111 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. 2013 Bioinformation Title HBV I233V 12 17 P;RT 48;10 58;12 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. 2013 Iranian journal of microbiology Title HBV N236T 15 20 RT;P 13;114 15;118 23547448 [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Title HBV C1799G;C1673T 48;41 54;47 Core promoter 62 72 23621183 Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. 2013 Asian Pacific journal of cancer prevention Title HBV C1653T 23 29 Hepatocellular carcinoma 56 80 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. 2013 Journal of virology Title HBV L60V 4 8 C 40 44 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. 2013 The Journal of infection Title HBV M204V;M204I 34;34 41;41 RT 32 34 23967738 [Clinical efficacy of various antiviral-based strategies to treat chronic hepatitis patients with positivity for hepatitis B e antigen and rtN236T mutation]. [Clinical efficacy of various antiviral-based strategies to treat chronic hepatitis patients with positivity for hepatitis B e antigen and rtN236T mutation]. 2013 Zhonghua gan zang bing za zhi Title HBV N236T 141 146 C;RT 125;139 134;141 Chronic Hepatitis B 66 83 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. 2013 Journal of clinical microbiology Title HBV W4P;W4R 14;14 19;19 PreS1 36 42 Liver disease 110 124 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. 2009 Brazilian journal of microbiology Title HBV G1896A 26 32 C;Precore;PreS1 67;18;138 76;25;144 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. 2013 Hepatitis monthly Title HBV A1846T;C1913A;C1913G 46;57;57 52;65;65 Acute on chronic liver failure 71 101 24389280 Detection of hepatitis B virus A1762T/G1764A mutant by amplification refractory mutation system. Detection of hepatitis B virus A1762T/G1764A mutant by amplification refractory mutation system. 2014 The Brazilian journal of infectious diseases Title HBV G1764A;A1762T 38;31 44;37 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. 2014 PloS one Title HBV M204Q 2 7 RT 0 2 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. 2014 Biochimica et biophysica acta Title HBV W182X 129 135 S;S 129;116 130;123 24693312 The Effect of HBV Genotype C on the Development of HCC Differs Between Wild-Type Viruses and Those With BCP Double Mutations (T(1762)A(1764)). The Effect of HBV Genotype C on the Development of HCC Differs Between Wild-Type Viruses and Those With BCP Double Mutations (T(1762)A(1764)). 2014 Hepatitis monthly Title HBV T1762A 126 133 BCP 104 107 Hepatocellular carcinoma 51 54 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. 2014 Journal of virology Title HBV A181T 49 54 RT;P;S 47;36;149 49;46;156 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. 2014 Antiviral therapy Title HBV N236V 93 98 RT 91 93 HBV infections 130 142 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. 2014 Journal of hepatology Title HBV G1896A 112 118 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. 2014 Journal of medical virology Title HBV M204V;M204I 67;67 74;74 RT 65 67 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. 2014 The Journal of general virology Title HBV I187V 16 21 RT;P 14;22 16;32 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. 2015 Journal of viral hepatitis Title HBV A181S 6 11 RT 4 6 25567052 Hepatitis B Virus Core Promoter A1762T/G1764A (TA)/T1753A/T1768A Mutations Contribute to Hepatocarcinogenesis by Deregulating Skp2 and P53. Hepatitis B Virus Core Promoter A1762T/G1764A (TA)/T1753A/T1768A Mutations Contribute to Hepatocarcinogenesis by Deregulating Skp2 and P53. 2015 Digestive diseases and sciences Title HBV G1764A;A1762T;T1753A;T1768A 39;32;51;58 45;38;57;64 Core promoter 18 31 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. 2015 Molecular cancer Title HBV W4P 62 65 S 32 45 25654280 [Relationship between hepatitis B virus polymerase gene mutation patterns of rtM204I/V and pre-core/basal core promoter mutations]. [Relationship between hepatitis B virus polymerase gene mutation patterns of rtM204I/V and pre-core/basal core promoter mutations]. 2014 Zhonghua gan zang bing za zhi Title HBV M204I;M204V 79;79 86;86 BCP;P;Precore;RT 100;40;91;77 119;50;99;79 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. 2015 Zhonghua gan zang bing za zhi Title HBV A181T 69 74 RT 67 69 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. 2015 Jundishapur journal of microbiology Title HBV G1896A 32 38 C;Precore 61;39 66;46 Chronic Hepatitis B 70 81 25842192 Reactivation of resolved infection with the hepatitis B virus immune escape mutant G145R during dasatinib treatment for chronic myeloid leukemia. Reactivation of resolved infection with the hepatitis B virus immune escape mutant G145R during dasatinib treatment for chronic myeloid leukemia. 2015 International journal of hematology Title HBV G145R 83 88 Chronic myeloid leukemia 120 144 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. 2016 Journal of clinical laboratory analysis Title HBV G1896A 40 46 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. 2016 Antiviral therapy Title HBV I233V 33 38 RT 31 33 26165271 Biological characteristics of the A1762T/G1764A mutant strain of hepatitis B virus in vivo. Biological characteristics of the A1762T/G1764A mutant strain of hepatitis B virus in vivo. 2015 Molecular medicine reports Title HBV G1764A;A1762T 41;34 47;40 26260331 HBsAg sT123N mutation induces stronger antibody responses to HBsAg and HBcAg and accelerates in vivo HBsAg clearance. HBsAg sT123N mutation induces stronger antibody responses to HBsAg and HBcAg and accelerates in vivo HBsAg clearance. 2015 Virus research Title HBV T123N 6 12 C;S;S;S;S 71;0;61;101;6 76;5;66;106;7 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. 2015 Acta crystallographica. Section F, Structural biology communications Title HBV Q151M 45 50 P;RT;RT 201;23;107 211;44;128 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. 2016 Japanese journal of infectious diseases Title HBV W172X 62 68 S 62 63 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. 2015 Hepatitis monthly Title HBV G1896A 0 6 C;Precore 45;7 50;14 Chronic Hepatitis B 105 124 26715821 Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. 2015 World journal of gastroenterology Title HBV V5M 154 157 X 145 146 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. 2016 Saudi journal of gastroenterology Title HBV A181V;A181T 87;87 94;94 RT 85 87 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. 2016 Oncotarget Title HBV G1764A;A1762T 47;40 53;46 BCP 20 39 Hepatocellular carcinoma 90 126 27133305 Discordant diagnostic results due to a hepatitis B virus T123A HBsAg mutant. Discordant diagnostic results due to a hepatitis B virus T123A HBsAg mutant. 2016 Diagnostic microbiology and infectious disease Title HBV T123A 57 62 S 63 68 27165167 Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations. Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations. 2016 Clinical journal of gastroenterology Title HBV T1768A;C1766T 96;89 102;95 Core promoter 103 116 Fulminant Hepatitis B 6 25 27303803 Hepatitis B Virus Core Promoter Double Mutations (A1762T, G1764A) Are Associated with Lower Levels of Serum Dihydrolipoyl Dehydrogenase. Hepatitis B Virus Core Promoter Double Mutations (A1762T, G1764A) Are Associated with Lower Levels of Serum Dihydrolipoyl Dehydrogenase. 2016 Intervirology Title HBV A1762T;G1764A 50;58 56;64 Core promoter 18 31 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. 2016 Experimental and therapeutic medicine Title HBV L180M;M204I;M204V 23;35;35 28;42;42 RT;RT 21;33 23;35 27473751 Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. 2016 The Journal of general virology Title HBV C1766T;T1768A 127;138 133;144 Precore 43 50 Fulminant Hepatitis B 171 190 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. 2016 Hepatitis monthly Title HBV G145R 15 20 S 91 98 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. 2016 PloS one Title HBV G145R 18 23 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. 2016 Oncogenesis Title HBV W172X 89 95 PreS;S;S 67;73;89 72;74;90 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. 2016 Scientific reports Title HBV A181T 47 52 RT;S 45;91 47;96 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. 2017 Clinical microbiology and infection Title HBV I97L;P79Q 5;39 9;43 C;S 0;90 4;93 Chronic Hepatitis B 129 148 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. 2017 Emerging microbes & infections Title HBV G145R 108 113 28339094 F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. 2017 Molecular medicine reports Title HBV F221Y 0 5 RT 36 57 Hepatocellular carcinoma 77 101 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. 2017 Virology journal Title HBV A181V;A181T 56;56 63;63 RT 54 56 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. 2017 Journal of hepatology Title HBV S78T 72 76 RT;P 70;81 72;91 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. 2018 Antiviral therapy Title HBV H55R;M204I;M204V 17;73;73 21;80;80 RT;RT;P 15;71;22 17;73;32 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. 2017 Sensors (Basel, Switzerland) Title HBV M204I 31 36 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. 2017 The Brazilian journal of infectious diseases Title HBV G1764A;A1762T 43;36 49;42 28654219 A comparative study of hepatitis B virus X protein mutants K130M, V131I and KV130/131MI to investigate their roles in fibrosis, cirrhosis and hepatocellular carcinoma. A comparative study of hepatitis B virus X protein mutants K130M, V131I and KV130/131MI to investigate their roles in fibrosis, cirrhosis and hepatocellular carcinoma. 2017 Journal of viral hepatitis Title HBV K130M;V131I 59;66 64;71 X 41 42 Liver cirrhosis;Hepatocellular carcinoma 128;142 137;166 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. 2017 The Journal of general virology Title HBV G1862T 27 33 C 41 44 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. 2017 Scientific reports Title HBV C1485T 16 22 X 39 42 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. 2018 Antiviral research Title HBV W28X 25 29 Precore 17 24 HBV-HIV coinfections 79 119 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. 2018 Scandinavian journal of gastroenterology Title HBV A1846T;C1913A;C1913G 41;52;52 47;60;60 Liver disease 109 123 29424069 Development of a fibrosis index including hepatitis B virus basal core promoter A1762T mutation for pretherapeutic evaluation. Development of a fibrosis index including hepatitis B virus basal core promoter A1762T mutation for pretherapeutic evaluation. 2018 Journal of gastroenterology and hepatology Title HBV A1762T 80 86 BCP 60 79 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. 2018 World journal of gastroenterology Title HBV W4P 126 129 PreS1 146 151 Liver disease 46 58 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. 2018 Antiviral research Title HBV W172X;A181T;A181T 143;20;137 149;25;142 RT;S;RT;S 18;26;135;143 20;27;137;144 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. 2018 Journal of viral hepatitis Title HBV G1896A 8 14 S;Precore 60;0 65;7 HBV-HIV coinfections 91 124 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. 2017 Voprosy virusologii Title HBV G145R 98 103 S 80 83 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. 2018 Pharmacology Title HBV W4P 78 81 S 48 61 Hepatocellular carcinoma 109 133 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. 2018 Virus research Title HBV M133T;Q129N;T131N 41;25;35 46;30;40 S;S;S 79;141;62 84;146;69 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. 2018 Hepatology communications Title HBV A181C 83 88 RT 61 82 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. 2019 Clinical microbiology and infection Title HBV F30V 23 27 X;X 10;167 13;170 Hepatocellular carcinoma 44 68 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. 2018 Saudi journal of biological sciences Title HBV G1896A 26 32 C;Precore 81;18 86;25 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. 2019 Journal of viral hepatitis Title HBV T1719G 4 10 Enh II;X 59;70 65;73 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. 2019 Antiviral research Title HBV A186T 59 64 RT 57 59 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. 2019 Emerging microbes & infections Title HBV L180M;A181C;M204V 37;43;49 42;48;54 RT 35 37 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. 2019 Molecular cancer research Title HBV V131I;K130M 10;4 15;9 X 0 3 Hepatocellular carcinoma 25 37 3118876 Site-directed mutagenesis of hepatitis B surface antigen sequence at codon 160 from arginine to lysine for conversion of subtypic determinant from r to w. Site-directed mutagenesis of hepatitis B surface antigen sequence at codon 160 from arginine to lysine for conversion of subtypic determinant from r to w. 1987 Biochemical and biophysical research communications Title HBV R160K 75 102 S 41 48 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The Effect of the Hepatitis B Virus Surface Protein Truncated sC69* Mutation on Viral Infectivity and the Host Innate Immune Response. 2019 Frontiers in microbiology Title HBV C69X 62 67 S;S 62;36 63;43 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. 2019 Antiviral research Title HBV C69X;S78T 48;43 53;47 RT;S 41;48 43;49 HBV infections 92 104 31442597 The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. 2019 Infection, genetics and evolution Title HBV I126T 33 39 S;S;S 98;33;18 99;34;23 31498528 Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance. Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance. 2020 Liver international Title HBV T184L;M204V;L180M;A200V 39;45;33;67 44;50;38;72 RT;RT 31;65 33;67 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. 2019 World journal of gastroenterology Title HBV M204I 118 123 RT 116 118 Chronic Hepatitis B 58 77 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. 2020 Antiviral research Title HBV A181S;T184I;M204I 37;43;49 42;48;54 RT 35 37 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. 2020 Frontiers in microbiology Title HBV G1764A;G1896A;A1762T 167;128;160 173;134;166 BCP;Precore 139;118 158;126 32763811 The sK122R mutation of hepatitis B virus (HBV) is associated with occult HBV infection: Analysis of a large cohort of Chinese patients. The sK122R mutation of hepatitis B virus (HBV) is associated with occult HBV infection: Analysis of a large cohort of Chinese patients. 2020 Journal of clinical virology Title HBV K122R 4 10 S 4 5 HBV infections 73 86 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. 2020 International journal of molecular sciences Title HBV W196X;M204I 51;45 57;50 PreS;S;RT;S 18;23;43;51 22;24;45;52 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. 2021 Journal of viral hepatitis Title HBV A194T 59 64 P 38 48 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. 2021 Infection and drug resistance Title HBV A194T 20 25 RT 18 20 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. 2021 Journal of infection and public health Title HBV G1896A 37 43 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. 2021 Journal of clinical and translational hepatology Title HBV M204V 31 36 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. 2021 Journal of virology Title HBV M204V;L180M 101;95 106;100 P 79 89 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. 2021 Viruses Title HBV Q129H 13 18 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. 2022 Vaccines Title HBV G145R 43 48 S 12 17 35293188 [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. 2022 Voprosy virusologii Title HBV S143L;G145R 56;66 61;71 8834756 A new immune escape mutant of hepatitis B virus with an Asp to Ala substitution in aa144 of the envelope major protein. A new immune escape mutant of hepatitis B virus with an Asp to Ala substitution in aa144 of the envelope major protein. 1995 Research in virology Title HBV D144A 56 88 S 96 104 9472623 Wild-type levels of pregenomic RNA and replication but reduced pre-C RNA and e-antigen synthesis of hepatitis B virus with C(1653) --> T, A(1762) --> T and G(1764) --> A mutations in the core promoter. Wild-type levels of pregenomic RNA and replication but reduced pre-C RNA and e-antigen synthesis of hepatitis B virus with C(1653) --> T, A(1762) --> T and G(1764) --> A mutations in the core promoter. 1998 The Journal of general virology Title HBV C1653T;A1762T;G1764A 122;137;155 136;152;170 Core promoter;C;Precore 187;77;63 200;86;68 9687422 The M539V polymerase variant of human hepatitis B virus demonstrates resistance to 2'-deoxy-3'-thiacytidine and a reduced ability to synthesize viral DNA. The M539V polymerase variant of human hepatitis B virus demonstrates resistance to 2'-deoxy-3'-thiacytidine and a reduced ability to synthesize viral DNA. 1998 Antimicrobial agents and chemotherapy Title HBV M539V 4 9 P 10 20 9875378 The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. 1998 Antiviral chemistry & chemotherapy Title HBV M539V 22 27 P 28 38 10089043 Detection of mutations in the enhancer 2/core promoter region of hepatitis B virus in patients with chronic hepatitis B virus infection: comparison with mutations in precore and core regions in relation to clinical status. The most frequent substitutions from A to T at nucleotide 1764 and from G to A at nucleotide 1766 were seen in none of the 10 asymptomatic carriers and in 14 (70%) of the 20 chronic liver disease patients. 1999 Journal of medical virology Abstract HBV A1764T;G1766A 37;72 62;97 10091998 Functional analysis of mutations conferring lamivudine resistance on hepatitis B virus. The combination of the L515M and M539V mutations gave an intermediate level of replication competence, compared with either mutation alone, and increased resistance to lamivudine. 1999 The Journal of general virology Abstract HBV L515M;M539V 23;33 28;38 10091998 Functional analysis of mutations conferring lamivudine resistance on hepatitis B virus. The L515M and M539V mutations provided only partial resistance while the M539I mutation conferred a high degree of lamivudine resistance. 1999 The Journal of general virology Abstract HBV L515M;M539V;M539I 4;14;73 9;19;78 10091998 Functional analysis of mutations conferring lamivudine resistance on hepatitis B virus. The M539I mutation reduced replication competence. 1999 The Journal of general virology Abstract HBV M539I 4 9 10091998 Functional analysis of mutations conferring lamivudine resistance on hepatitis B virus. The M539I substitution in the conserved YMDD motif occurs independently of other changes, whereas the M539V substitution is associated with an additional upstream change (L515M). 1999 The Journal of general virology Abstract HBV M539I;M539V;L515M 4;102;171 9;107;176 P 40 44 10211946 Detection of hepatitis B surface antigen mutants and their integration in human hepatocellular carcinoma. Southern blot analysis indicated that the HBsAg mutant with the Glycine to Arginine change at position 145 was integrated in HCC, whereas those with a Threonine at position 133 instead of a Methionine were identified in the serum of aggressive HCC. 1999 Cancer letters Abstract HBV G145R;T133M 64;151 106;200 S 42 47 Hepatocellular carcinoma;Hepatocellular carcinoma 125;244 128;247 10320044 Hepatitis B virus variants with lamivudine-related mutations in the DNA polymerase and the 'a' epitope of the surface antigen are sensitive to ganciclovir. Both the wild type HBV and lamivudine-related mutants with the Gly145-->Arg145 HBsAg mutation were suppressed following ganciclovir treatment, indicating a beneficial additive effect of both drugs against different forms of HBV mutants. 1999 Antiviral research Abstract HBV G145R 63 78 S 79 84 10320044 Hepatitis B virus variants with lamivudine-related mutations in the DNA polymerase and the 'a' epitope of the surface antigen are sensitive to ganciclovir. Here we report the identification of a novel type of lamivudine-related mutations located in both the polymerase (YM552DD-->Y1552DD) and the 'a' epitope of HBsAg (Gly130-->Asp130). 1999 Antiviral research Abstract HBV G130D 163 178 S;P 156;102 161;112 10320044 Hepatitis B virus variants with lamivudine-related mutations in the DNA polymerase and the 'a' epitope of the surface antigen are sensitive to ganciclovir. The same virus carried a HBsAg Gly145-->Arg145 mutation prior to therapy. 1999 Antiviral research Abstract HBV G145R 31 46 S 25 30 10353255 Sensitivity of L-(-)2,3-dideoxythiacytidine resistant hepatitis B virus to other antiviral nucleoside analogues. It was found that the L526M mutation alone caused greater resistance to penciclovir (PCV) than did the V553I mutation alone. 1999 Biochemical pharmacology Abstract HBV L526M;V553I 22;103 27;108 10353255 Sensitivity of L-(-)2,3-dideoxythiacytidine resistant hepatitis B virus to other antiviral nucleoside analogues. The A546V mutation had no impact on the sensitivity to L(-)SddC, L-FMAU, and PCV. 1999 Biochemical pharmacology Abstract HBV A546V 4 9 10353255 Sensitivity of L-(-)2,3-dideoxythiacytidine resistant hepatitis B virus to other antiviral nucleoside analogues. When these single mutations were coupled with the M550V/I mutation, all the double mutants were resistant to those drugs. 1999 Biochemical pharmacology Abstract HBV M550V;M550I 50;50 57;57 10364324 The mechanism of an immature secretion phenotype of a highly frequent naturally occurring missense mutation at codon 97 of human hepatitis B virus core antigen. We have dissected further the relationship between the intracellular and extracellular phenotypes of mutant F97L. 1999 Journal of virology Abstract HBV F97L 108 112 10377169 Susceptibility of lamivudine-resistant hepatitis B virus to other reverse transcriptase inhibitors. In this study, susceptibility of wild-type and lamivudine-resistant HBV M552I, M552V, and L528M/M552V mutants to other reverse transcriptase inhibitors was investigated by transient transfection of full-length HBV DNA into human hepatoma cells. 1999 The Journal of clinical investigation Abstract HBV M552V;L528M;M552I;M552V 96;90;72;79 101;95;77;84 RT 119 140 Hepatocellular carcinoma 229 237 10385663 Mutational pattern of hepatitis B virus on sequential therapy with famciclovir and lamivudine in patients with hepatitis B virus reinfection occurring under HBIg immunoglobulin after liver transplantation. However, 7 patients developed a breakthrough within 12, 29 (n = 2), 32, 37, 54, and 145 weeks under treatment with LAM associated with the methionine-to-valine signature mutation (M552V) in the YMDD motif in all. 1999 Hepatology (Baltimore, Md.) Abstract HBV M552V 180 185 P 194 198 10385663 Mutational pattern of hepatitis B virus on sequential therapy with famciclovir and lamivudine in patients with hepatitis B virus reinfection occurring under HBIg immunoglobulin after liver transplantation. Our results indicate that the L528M mutation is a risk factor for LAM breakthrough, because breakthrough during LAM occurred earlier in patients with this mutation (50 +/- 10 weeks vs. 1999 Hepatology (Baltimore, Md.) Abstract HBV L528M 30 35 10385663 Mutational pattern of hepatitis B virus on sequential therapy with famciclovir and lamivudine in patients with hepatitis B virus reinfection occurring under HBIg immunoglobulin after liver transplantation. With FCV, no unique, but a dominant, resistance pattern with the L528M mutation was identified for patients with breakthrough under FCV. 1999 Hepatology (Baltimore, Md.) Abstract HBV L528M 65 70 10418752 Perspectives for the treatment of hepatitis B virus infections. L528M and M552V/I) in the HBV DNA polymerase upon long-term treatment. 1999 International journal of antimicrobial agents Abstract HBV L528M;M552V;M552I 0;10;10 5;17;17 P 34 44 10430358 Liver graft infection by HBV S-gene mutants in transplant patients receiving long-term HBIg prophylaxis. A HBV S-gene mutant containing a G to A nucleotide mutation at position 587, converting Glycine to Arginine (G145A), was identified in all three patients as the dominant population at reinfection but not pre-transplantation. 1999 Hepato-gastroenterology Abstract HBV G145A 109 114 S 6 7 10430358 Liver graft infection by HBV S-gene mutants in transplant patients receiving long-term HBIg prophylaxis. CONCLUSIONS: These data demonstrate that long-term polyclonal anti-HBs immunoprophylaxis selected the most commonly described G145R S-gene escape HBV variant which became the dominant virus population and was responsible for graft infection. 1999 Hepato-gastroenterology Abstract HBV G145R 126 131 S;S 132;67 133;70 10430358 Liver graft infection by HBV S-gene mutants in transplant patients receiving long-term HBIg prophylaxis. Therefore, immunoglobulins with high affinity for the G145R HBs variant should be included in HBIg to prevent recurrent HBV infection in transplant patients. 1999 Hepato-gastroenterology Abstract HBV G145R 54 59 S 60 63 HBV infections 120 133 10449493 Hepatitis B virus (HBV) mutations associated with resistance to lamivudine in patients coinfected with HBV and human immunodeficiency virus. In seven of these nine patients, Met(550), belonging to the highly conserved YMDD motif, was mutated to Val and was associated with a substitution of Met for Leu(526) in each case. 1999 Journal of clinical microbiology Abstract HBV L526M 150 166 P 77 81 10449493 Hepatitis B virus (HBV) mutations associated with resistance to lamivudine in patients coinfected with HBV and human immunodeficiency virus. In the two remaining patients, we found a Met(550)-to-Ile change that was associated in only one case with a Leu(526)-to-Met mutation. 1999 Journal of clinical microbiology Abstract HBV M550I;L526M 41;108 58;125 10485623 Analysis of the precore and core promoter DNA sequence in liver tissues from patients with hepatocellular carcinoma. Among 20 tumorous and nontumorous tissues, HBV with a C to T mutation at nucleotide (nt) 1846 was detected in six and eight, respectively, and was associated with the virus carrying a mutation (1896 or 1899) except in two tumorous tissues. 1999 Journal of Korean medical science Abstract HBV C1846T 53 94 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. A substitution of methionine for leucine at residue 526 (L526M) has also been identified. 1999 Journal of medical virology Abstract HBV L526M;L526M 57;18 62;55 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. In four patients, a substitution of valine or isoleucine for leucine at residue 426, which has not been reported previously, emerged in combination with M550I. 1999 Journal of medical virology Abstract HBV M550I;L426I 153;46 158;83 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. In the remaining patient, an alteration of leucine to methionine at residue 428 co-occurred with M550V. 1999 Journal of medical virology Abstract HBV M550V;L428M 97;43 102;79 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. Lamivudine resistance has been attributed mainly to a substitution of isoleucine or valine for methionine at residue 550 (M550I or M550V) in the catalytic site of the virus polymerase. 1999 Journal of medical virology Abstract HBV M550I;M550V;M550V 122;131;84 127;136;120 P 173 183 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. One also harbored L526M. 1999 Journal of medical virology Abstract HBV L526M 18 23 10502255 Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B. Our results indicate that occurrence of HBV polymerase mutations at residue 426 in combination with M550I is frequent in Japanese or genotype C virus-in- fected patients who develop resistance to lamivudine. 1999 Journal of medical virology Abstract HBV M550I 100 105 P 44 54 10514111 Diversity of core promoter mutations in immune clearance phase of chronic HBV infection. While mutations at nucleotide 1762 (A-->T) and 1764(G-->A) were not found in ASC, mutations at the same positions were found in all the cases of CH group (40 clones) (P=0.003). 1999 European journal of gastroenterology & hepatology Abstract HBV A1762T;G1764A 30;47 42;58 Chronic Hepatitis B 145 147 10533799 T1762/A1764 variants of the basal core promoter of hepatitis B virus; serological and clinical correlations in Chinese patients. BACKGROUND: A double variant in the basal core promoter, converting nucleotide 1762 from A to T (T1762) and nucleotide 1764 from G to A (A[764), has been described in patients with chronic hepatitis B infection. 1999 Liver Abstract HBV T1762T;G1764A 68;119 95;135 BCP 36 55 Chronic HBV infection 181 210 10534721 Hepatitis B virus core promoter mutations in children with multiple anti-HBe/HBeAg reactivations result in enhanced promoter activity. In both patients, rare mutations were found in the BCP at nucleotides 1764(G-->T)/1766(C-->G) and 1766(C-->T)/1768(T-->A) in case 1 and 2, respectively. 1999 Journal of medical virology Abstract HBV C1766G;T1768A;G1764T;C1766T 82;110;70;98 93;121;81;109 BCP 51 54 10534722 A novel hepatitis B virus variant S 129 (Gln-->Leu): lack of correlation between antigenicity and immunogenicity. This A-to-T point mutation at nucleotide 540 resulted in a glutamine-to-leucine substitution at amino acid residue 129 (129L). 1999 Journal of medical virology Abstract HBV A540T;Q129L 5;59 44;118 10554127 Age at time of hepatitis Be antibody seroconversion in childhood chronic hepatitis B infection and mutant viral strain detection rates. Specifically, a mutant strain showing a G-to-A substitution at nucleotide 83 in the pre-C region, or a mutant strain showing an A-to-T substitution at nucleotide 1762 and a G-to-A substitution at nucleotide 1764, was detected in only two of eight cases (25%) from the HBeAb-positive carriers with documented seroconversion before age 6. 1999 Journal of pediatric gastroenterology and nutrition Abstract HBV G83A;A1762T;G1764A 40;128;173 76;166;211 Precore 84 89 10559327 Subtype-independent immature secretion and subtype-dependent replication deficiency of a highly frequent, naturally occurring mutation of human hepatitis B virus core antigen. Despite its immature secretion phenotype, the adr variant I97L replicates as well as its parental adr wild-type I97I, supporting the conclusion that the extracellular phenotype of immature secretion is not a consequence of the intracellular HBV DNA replication defect. 1999 Journal of virology Abstract HBV I97L;I97I 58;112 62;116 10559327 Subtype-independent immature secretion and subtype-dependent replication deficiency of a highly frequent, naturally occurring mutation of human hepatitis B virus core antigen. Recently, a phenylalanine (F)-to-leucine (L) mutation at this position (mutant F97L) in HBV surface antigen subtype ayw has been shown to result in an immature secretion phenotype, which is characterized by the nonselective export of an excessive amount of virions containing minus-strand, single-stranded HBV DNA. 1999 Journal of virology Abstract HBV F97L 79 83 S 92 99 10559327 Subtype-independent immature secretion and subtype-dependent replication deficiency of a highly frequent, naturally occurring mutation of human hepatitis B virus core antigen. We report here that the immature secretion phenotype indeed can be found in an HBV strain (subtype adr) prevalent in Asia, changing from an isoleucine (I) to a leucine (mutant I97L). 1999 Journal of virology Abstract HBV I97L 176 180 10559327 Subtype-independent immature secretion and subtype-dependent replication deficiency of a highly frequent, naturally occurring mutation of human hepatitis B virus core antigen. While subtype ayw mutant F97L has been found in Europe, the major reservoir of HBV resides in Asia and Africa. 1999 Journal of virology Abstract HBV F97L 25 29 10573159 Hepatitis B virus maturation is affected by the incorporation of core proteins having a C-terminal substitution of arginine or lysine stretches. Additionally, triple-plasmid transfection experiments showed that nucleocapsids containing various amounts of C144Arg and wild-type core proteins exhibited a bias in selecting a shorter pregenome for encapsidation and DNA replication. 1999 The Journal of general virology Abstract HBV C144R 110 117 C 132 136 10573159 Hepatitis B virus maturation is affected by the incorporation of core proteins having a C-terminal substitution of arginine or lysine stretches. In this study, two hepatitis B virus (HBV) core mutants (C144Arg and C144Lys) in which the C-terminal SPRRR (Ser-Pro-Arg-Arg-Arg) motif was replaced by a stretch of arginine or lysine residues were generated to test their role in pregenome encapsidation and virus maturation. 1999 The Journal of general virology Abstract HBV C144R;C144K 57;69 64;76 C 43 47 10573159 Hepatitis B virus maturation is affected by the incorporation of core proteins having a C-terminal substitution of arginine or lysine stretches. Nucleocapsids formed by C144Arg and C144Lys, however, lost the endogenous polymerase activity to repair HBV DNA. 1999 The Journal of general virology Abstract HBV C144R;C144K 24;36 31;43 P 74 84 10596008 Effect of variation in the common "a" determinant on the antigenicity of hepatitis B surface antigen. The results suggest that amino acid substitution of T131I, K141E and G145R and insertion of 3 amino acids between residues 123 and 124 markedly affect the antigenic structure of HBsAg. 2000 Journal of medical virology Abstract HBV T131I;K141E;G145R 52;59;69 57;64;74 S 178 183 10607231 Hepatitis B envelope protein mutants in human hepatocellular carcinoma tissues. The mutation Gly145Arg, which has been reported to be associated with immunoevasion, was found in seven of the 18 HCC tissues. 1999 Journal of viral hepatitis Abstract HBV G145R 13 22 Hepatocellular carcinoma 114 117 10607259 The core promoter of hepatitis B virus. The most frequently described mutations within this region are an A to T transversion at position 1762 together with a G to A transition at position 1764. 1999 Journal of viral hepatitis Abstract HBV A1762T;G1764A 66;119 102;153 10613749 In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance. In in vitro enzymatic assays, the V555I mutation displayed the most resistance (with K(i) increased by 6.2-fold) to PCVTP. 2000 Hepatology (Baltimore, Md.) Abstract HBV V555I 34 39 10613749 In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance. Several mutations (V521L, P525L, L528M, T532S, and V555I) in the gene for hepatitis B virus (HBV) polymerase have been identified in HBV isolated from patients that displayed break-through viremia during famciclovir treatment. 2000 Hepatology (Baltimore, Md.) Abstract HBV V521L;P525L;L528M;T532S;V555I 19;26;33;40;51 24;31;38;45;56 P 98 108 10613749 In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance. The lamivudine-resistant mutations M552I, M552V, and L528M+M552V, which were previously shown to display 8- to 25-fold resistance to LAMTP, were less resistant (< or = 3.1-fold) to PCVTP. 2000 Hepatology (Baltimore, Md.) Abstract HBV M552I;M552V;L528M;M552V 35;42;53;59 40;47;58;64 10613749 In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance. The V521L and L528M mutations showed moderately decreased sensitivity to PCVTP (K(i) increased by >3-fold). 2000 Hepatology (Baltimore, Md.) Abstract HBV V521L;L528M 4;14 9;19 10613749 In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance. The V521L, L528M, and T532S mutations were also sensitive to lamivudine triphosphate (LAMTP); however, the P525L and V555I mutations displayed moderately decreased sensitivity to LAMTP in enzymatic assays (3.6-fold decreased sensitivity). 2000 Hepatology (Baltimore, Md.) Abstract HBV V521L;L528M;T532S;P525L;V555I 4;11;22;107;117 9;16;27;112;122 10624597 Polymorphism of precore region of hepatitis B virus DNA among patients with chronic HBV infection in Turkey. Seven of 47 HBeAg-positive patients (15%) and 29 of 34 HBeAg-negative patients (85%) had precore stop codon mutations (G to A change at nucleotide 1896). 1999 Infection Abstract HBV G1896A 119 151 C;C;Precore 12;55;89 17;60;96 10628774 Fulminant hepatic failure resulting from lamivudine-resistant hepatitis B virus in a renal transplant recipient: durable response after orthotopic liver transplantation on adefovir dipivoxil and hepatitis B immune globulin. Sequencing of HBV polymerase gene from preliver transplantation sera did not detect the usual lamivudine resistance mutations in the YMDD motif but instead two other mutations (F514-->L, L528-->M). 1999 Transplantation Abstract HBV F514L;L528M 177;187 185;195 P;P 18;133 28;137 10630955 Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role. In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promoter. 2000 Journal of medical virology Abstract HBV G1896A 32 59 Precore;Precore 67;133 71;137 10630955 Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role. Patients who are chronic carriers of the HBV and who have a G to A mutation at nucleotide 1896 in the precore region may develop more severe liver disease, possibly because of rapid selection and enhanced replication ability of the mutant strain. 2000 Journal of medical virology Abstract HBV G1896A 60 94 Precore 102 109 Liver disease 141 154 10655370 Line probe assay for monitoring drug resistance in hepatitis B virus-infected patients during antiviral therapy. A set of 38 highly specific oligonucleotide probes covering three different codon positions, L528M, M552V/I, and V/L/M555I, were selected. 2000 Journal of clinical microbiology Abstract HBV L528M;M552V;M552I;V555I;L555I;M555I 93;100;100;113;113;113 98;107;107;122;122;122 10669360 Selection of multiresistant hepatitis B virus during sequential nucleoside-analogue therapy. Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. 2000 The Journal of infectious diseases Abstract HBV M550V;L526M;M550I 151;162;181 156;167;186 P 102 112 10682123 Analysis of hepatitis B virus quasispecies changes during emergence and reversion of lamivudine resistance in liver transplantation. Lamivudine resistance was found to be associated with L526M and M550V changes in two patients and M550I change in three patients. 1999 Antiviral therapy Abstract HBV L526M;M550V;M550I 54;64;98 59;69;103 10682123 Analysis of hepatitis B virus quasispecies changes during emergence and reversion of lamivudine resistance in liver transplantation. Other changes associated with lamivudine resistance in some patients were V509I, A546V, S565A and A568T. 1999 Antiviral therapy Abstract HBV V509I;A546V;S565A;A568T 74;81;88;98 79;86;93;103 10745228 Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis. Of note as negative data, the mutations C1653T and T1753M of the enhancer II (Enh II) and A1762T and G1764A of the precore/core promoter regions, once reported to be relevant to severe or fulminant hepatitis, were not found in the present cases. 2000 Journal of medical virology Abstract HBV C1653T;T1753M;A1762T;G1764A 40;51;90;101 46;57;96;107 Core promoter;Enh II;Enh II;Precore 123;78;65;115 136;84;76;122 Fulminant Hepatitis B 188 207 10745228 Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis. Remarkably, the nonsense mutation at precore codon 28 (Trp82Stop) was found in four of the five patients with fulminant hepatitis, while all the acute hepatitis patients harbored wild type (one had a mixture of wild and mutant types). 2000 Journal of medical virology Abstract HBV W82X 55 64 Precore 37 44 Fulminant Hepatitis B;Acute Hepatitis B 110;145 129;160 10745228 Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis. The missense mutations within the core region, Ile97Leu and Pro130Ile/Thr/Ser, were also remarkable in fulminant hepatitis. 2000 Journal of medical virology Abstract HBV I97L;P130I;P130T;P130S 47;60;60;60 55;77;77;77 C 34 38 Fulminant Hepatitis B 103 122 10745228 Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis. The results with the Vietnamese cases of fulminant hepatitis corroborated results of previous studies with respect to the mutations Trp28Stop of precore and Ile97Leu and Pro130Ile/Thr/Ser of core, but not for the mutations within Enh II and precore/core promoter region. 2000 Journal of medical virology Abstract HBV W28X;I97L;P130I;P130T;P130S 132;157;170;170;170 141;165;187;187;187 C;Core promoter;Enh II;Precore;Precore 191;249;230;145;241 195;262;236;152;248 Fulminant Hepatitis B 41 60 10745228 Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis. Whether the Ser41Pro mutation in the X region of genotype B HBV is Vietnam-specific or disease-specific deserves further investigation. 2000 Journal of medical virology Abstract HBV S41P 12 20 X 37 38 10760047 Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L-FMAU, DAPD, penciclovir and lobucavir. As expected, lamivudine was much less ( approximately 200-fold) effective at inhibiting replication of the M550V mutant virus than the wild-type virus. 2000 Journal of viral hepatitis Abstract HBV M550V 107 112 10760047 Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L-FMAU, DAPD, penciclovir and lobucavir. Several nucleoside analogues (penciclovir, lobucavir, dioxalane guanine [DXG], 1-beta-2,6-diaminopurine dioxalane [DAPD], L-FMAU, lamivudine) and acyclic nucleoside phosphonate analogues (adefovir, tenofovir) that are in clinical use, in clinical trials or under preclinical development for the treatment of hepatitis B virus (HBV) infections, were evaluated for their inhibitory effect on the replication of a la- mivudine-resistant HBV variant containing the methionine --> valine substitution (M550V) in the polymerase nucleoside-binding domain. 2000 Journal of viral hepatitis Abstract HBV M550V 497 502 P 511 521 10760047 Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L-FMAU, DAPD, penciclovir and lobucavir. The antiviral activity was determined in the tetracycline-responsive HepAD38 and HepAD79 cells, which are stably transfected with either a cDNA copy of the wild-type pregenomic RNA or with cDNA containing the M550V mutation. 2000 Journal of viral hepatitis Abstract HBV M550V 209 214 10762559 Evolution of hepatitis B virus polymerase gene sequence during famciclovir therapy for chronic hepatitis B. No mutation in the YMDD motif was observed, whereas an L528M mutation was clearly selected by famciclovir treatment in 2 patients, as well as 14 novel mutations in 7 patients. 2000 The Journal of infectious diseases Abstract HBV L528M 55 60 P 19 23 10775637 A frequent, naturally occurring mutation (P130T) of human hepatitis B virus core antigen is compensatory for immature secretion phenotype of another frequent variant (I97L). Our current study demonstrates that this abnormality can be efficiently offset by another frequent core mutation, P130T. 2000 Journal of virology Abstract HBV P130T 114 119 C 99 103 10804824 [Hepatitis B virus gene mutations in the sera of three patients with coexisting hepatitis B surface antigen and anti-surface antibody]. Case 1 possessed a point mutation, T to C at nucleotide position 1753, in the region overlapping the coding region of the X gene and the CCAAT/enhancer binding protein(C/EBP) binding region within the core promoter region. 2000 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV T1753C 35 69 Core promoter;X 201;122 214;123 10827158 Clearance of the original hepatitis B virus YMDD-motif mutants with emergence of distinct lamivudine-resistant mutants during prolonged lamivudine therapy. Of the 23 patients included, 13 harbored either one or a mixture of the two common YMDD-motif mutants (methionine 552-to-isoleucine [M552I] and leucine 528-to-methionine/methionine 552-to-valine [L528M/M552V]) throughout the course, whereas in the remaining 10 patients, distinct mutants became dominant over the original mutants to cause continuing chronic hepatitis. 2000 Hepatology (Baltimore, Md.) Abstract HBV M552V;M552V;L528M;M552I;M552I;L528M 202;170;144;103;133;196 207;194;169;139;138;201 P 83 87 Chronic Hepatitis B 350 367 10827158 Clearance of the original hepatitis B virus YMDD-motif mutants with emergence of distinct lamivudine-resistant mutants during prolonged lamivudine therapy. Of them, 3 developed an alanine 529-to-threonine (A529T) mutant, 6 developed a leucine 528-to-methionine/methionine 552-to-isoleucine (L528M/M552I) mutant, and 1 developed these two mutants sequentially. 2000 Hepatology (Baltimore, Md.) Abstract HBV M552I;A529T;A529T;M552I;L528M;L528M 141;24;50;105;79;135 146;48;55;133;104;140 10827158 Clearance of the original hepatitis B virus YMDD-motif mutants with emergence of distinct lamivudine-resistant mutants during prolonged lamivudine therapy. The nucleotide substitution in the A529T mutant concomitantly generated a stop codon at the surface gene, leading to impaired secretion of HBsAg. 2000 Hepatology (Baltimore, Md.) Abstract HBV A529T 35 40 S;S 139;92 144;99 10949955 Detection of hepatitis B virus surface antigen mutants in paraffin-embedded hepatocellular carcinoma tissues. Mutations on the "a" determinant (Thr126Ser, Gly145Arg, a double mutant Thr126Ser/Gln129Asn, Met 133Leu and Thr140Ile) were identified in 5 samples while the wild type sequence was found in 2 others. 2000 Virus genes Abstract HBV Q129N;T126Q;T126N;T126S;G145R;T126S;T140I;M133L 82;72;72;34;45;72;108;93 91;81;81;43;54;81;117;103 10996115 In vivo dynamics and pathogenicity of wild-type and resistant Hepatitis B virus during long-term lamivudine monotherapy - a clinical note. Nineteen weeks later, the virus exhibited additional resistance-associated mutations (L528M and I552V). 2000 Journal of clinical virology Abstract HBV L528M;I552V 86;96 91;101 10996115 In vivo dynamics and pathogenicity of wild-type and resistant Hepatitis B virus during long-term lamivudine monotherapy - a clinical note. Significant genotypic resistance was detectable after 68 weeks, indicated by a substitution of isoleucine for methionine at residue 552 (M552I). 2000 Journal of clinical virology Abstract HBV M552I;M552I 137;95 142;135 11002246 Hepatitis B virus X gene variability in French-born patients with chronic hepatitis and hepatocellular carcinoma. The changes K130M and V131I, considered as "hot spot mutations," were found in strains of HCC patients carrying an ayw subtype of the HBV genome but not in the ones of chronically infected patients. 2000 Journal of medical virology Abstract HBV K130M;V131I 12;22 17;27 Hepatocellular carcinoma 90 93 11020004 Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance. Breakthrough viremia was not associated with the single L528M mutation. 2000 Journal of hepatology Abstract HBV L528M 56 61 11020004 Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance. CONCLUSION: Our observations show that the virus populations conferring resistance to lamivudine can evolve from single to double mutations at amino acid 552 and 528 of the HBV polymerase, and that M552I/ L528M or M552V/L528M seem to be the predominant mutations arising during long-term antiviral therapy with lamivudine. 2000 Journal of hepatology Abstract HBV L528M;M552I;L528M;M552V 220;198;205;214 225;204;210;219 P 177 187 11020004 Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance. In the majority of lamivudine-resistant isolates the mutations have been reported to occur within the YMDD motif of the viral polymerase, either as a single mutation M552I or as M552V concomitant with L528M. 2000 Journal of hepatology Abstract HBV L528M;M552I;M552V 201;166;178 206;171;183 P;P 126;102 136;106 11020004 Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance. RESULTS: Genotypic succession of the virus populations was observed to occur from M552I to M552I/L528M (n=2) and from L528M to M552V/L528M (n=1). 2000 Journal of hepatology Abstract HBV L528M;L528M;M552I;M552I;L528M;M552V 97;133;82;91;118;127 102;138;87;96;123;132 11020004 Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance. The double mutations M552I/L528M (n=4) or M552V/L528M (n=2) were found in six out of seven patients, and represented the stable virus populations throughout the follow-up period. 2000 Journal of hepatology Abstract HBV L528M;L528M;M552I;M552V 27;48;21;42 32;53;26;47 11050059 Early detection of viral resistance by determination of hepatitis B virus polymerase mutations in patients treated by lamivudine for chronic hepatitis B. Determination of viral genotype, precore mutants, and polymerase gene mutants (L528M, M552V, M552I) was performed using the research version of Lipa-HBV. 2000 Hepatology (Baltimore, Md.) Abstract HBV L528M;M552V;M552I 79;86;93 84;91;98 P;Precore 54;33 64;40 11076934 A novel chromosome region maintenance 1-independent nuclear export signal of the large form of hepatitis delta antigen that is required for the viral assembly. An HDAg-L mutant with a substitution of Pro-205 to alanine could neither form HDV-like particles nor shift the subcellular localization in the presence of HBsAg. 2001 The Journal of biological chemistry Abstract HBV P205A 40 58 S 155 160 11083647 Characterization of novel human hepatoma cell lines with stable hepatitis B virus secretion for evaluating new compounds against lamivudine- and penciclovir-resistant virus. In this report, three cell lines HepG2-WT10, HepG2-SM1, and HepG2-DM2 are presented; these cell lines were established by transfection of HepG2 cells with unique fully functional 1.1x hepatitis B virus (HBV) genomes: wild-type HBV-adr and its L526M and L526MM550V variants, respectively. 2000 Antimicrobial agents and chemotherapy Abstract HBV L526M 243 248 11092260 De novo acute hepatitis B infection in a previously vaccinated liver transplant recipient due to a strain of HBV with a Met 133 Thr mutation in the "a" determinant. Subsequent analysis of the predominant HBV strain revealed mutations in the "a" determinant: Met 133 Thr (codon change ATG to ACG) and Asn 131 Thr. 2000 Liver Abstract HBV M133T;N131T 93;135 104;146 11115057 Sequence variations of precore/core and precore promoter regions of hepatitis B virus in patients with or without viral reactivation during cytotoxic chemotherapy. A G-to-A mutation at nt 1896 in the preC/C region (HBeAg negative/ anti-HBe positive) has been associated with more severe liver disease than that caused by wild type virus. 2000 Journal of viral hepatitis Abstract HBV G1896A 2 28 C;C;Precore;C 72;51;36;41 75;56;40;42 Liver disease 123 136 11115057 Sequence variations of precore/core and precore promoter regions of hepatitis B virus in patients with or without viral reactivation during cytotoxic chemotherapy. With respect to the preC promoter region, the two commonest mutations detected were at nt 1762 (A to T) and nt 1764 (G to A). 2000 Journal of viral hepatitis Abstract HBV A1762T;G1764A 90;111 103;124 Precore 20 24 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. CONCLUSIONS: The G145R mutant could be transmitted horizontally among family members, and this could occur in the presence of high levels of anti-HBs. 2000 The Journal of infection Abstract HBV G145R 17 22 S 146 149 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. Improvement of detection system for the G145R and other HBsAg mutant will be needed for their effective control. 2000 The Journal of infection Abstract HBV G145R 40 45 S 56 61 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. In addition, liver damage was seen in one G145R carrier infant. 2000 The Journal of infection Abstract HBV G145R 42 47 Liver disease 13 25 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. In families 2 and 3, the G145R mutant detected previously in child 1 was detected in the father. 2000 The Journal of infection Abstract HBV G145R 25 30 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. METHODS: Serum samples from family members of 10 vaccinated infants who carried this G145R mutant were collected. 2000 The Journal of infection Abstract HBV G145R 85 90 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. OBJECTIVES: To provide intra-familial evidence on the horizontal transmission of hepatitis B virus surface antigen (HBsAg) mutant G145R. 2000 The Journal of infection Abstract HBV G145R 130 135 S;S 116;99 121;106 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. RESULTS: The G145R mutant was identified in family members of three of the 10 infants. 2000 The Journal of infection Abstract HBV G145R 13 18 11120616 Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R. The G145R mutant was found in samples with high levels of neutralizing antibody against HBV (anti-HBs). 2000 The Journal of infection Abstract HBV G145R 4 9 S 98 101 11124839 A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C. Japan HBV Genotype Research Group. The double mutation in the basic core promoter (A-to-T at nt 1762 and G-to-A at nt 1764), however, was significantly more frequent in genotype C than B patients (58% vs. 2001 Hepatology (Baltimore, Md.) Abstract HBV A1762T;G1764A 48;70 65;87 BCP 27 46 11124839 A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C. Japan HBV Genotype Research Group. The predominance of mutants with G-to-A mutation at nucleotide (nt) 1896 in the precore region (A1896) over the wild-type was comparable between genotype B and C patients (60% and 62%, respectively), and it correlated with anti-HBe. 2001 Hepatology (Baltimore, Md.) Abstract HBV G1896A 32 73 C;Precore 228;80 231;87 11161275 Vaccination of chronic hepatitis B virus carriers with preS2/S envelope protein is not associated with the emergence of envelope escape mutants. Two mutations (T140S and P127L) diverged from subtype variations. 2001 The Journal of general virology Abstract HBV T140S;P127L 15;25 20;30 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. After receiving lamivudine for 3 years to treat chronic hepatitis B, 67-75% of patients develop B-domain L528M, C-domain M552I, or M552V mutations in the HBV polymerase that render hepatitis B virus (HBV) drug-resistant. 2001 The Journal of clinical investigation Abstract HBV M552I;M552V;L528M 121;131;105 126;136;110 P 158 168 Chronic Hepatitis B 48 67 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. However, addition of the B-domain mutation L528M restored replication competence. 2001 The Journal of clinical investigation Abstract HBV L528M 43 48 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. The B-domain mutation (L528M) of HBV polymerase not only restores the replication competence of C-domain mutants, but also increases resistance to nucleoside analogues. 2001 The Journal of clinical investigation Abstract HBV L528M 23 28 P 37 47 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. The replication competency of the single C-domain mutants M552I and M552V was markedly decreased compared with that of wild-type HBV. 2001 The Journal of clinical investigation Abstract HBV M552I;M552V 58;68 63;73 11181644 The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance. We investigated the replication fitness and susceptibility of the wild-type and five mutant HBVs (L528M, M552I, M552V, L528M/M552I, and L528M/M552V) to 11 compounds [lamivudine, adefovir, entecavir (BMS-200475) (+)-BCH-189 (+/-)-FTC (racivir) (-)-FTC (emtricitabine) (+)-FTC, L-D4FC, L-FMAU (clevudine), D-DAPD, and (-)-carbovir] by transfecting HBV DNA into hepatoma cells and monitoring viral products by Southern blotting. 2001 The Journal of clinical investigation Abstract HBV M552I;M552V;M552I;M552V;L528M;L528M;L528M 125;142;105;112;119;136;98 130;147;110;117;124;141;103 Hepatocellular carcinoma 359 367 11208474 Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene. Also, HBV variant with substitution at position 145 (Gly to Ala) has been recently reported to be antigenically altered and to show impaired recognition by polyclonal hepatitis B hyperimmune globulin in vitro. 2000 Medical science monitor Abstract HBV G145A 48 64 11208474 Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene. However, the substitution of substitution glycine to alanine at position 129 introduce a putative glycosylation site (Asn-Gly-Thr), which may interfere with the antigenicity of HbsAg. 2000 Medical science monitor Abstract HBV G129A 42 76 S 177 182 11208474 Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene. Rare substitution was identified both at positions 129 (glutamine to asparagine) and at position 145 (glycine to alanine) in the 'a' determinant region, which is considered to be within a larger antigenic area known as the major hydrophilic region (MHR). 2000 Medical science monitor Abstract HBV Q129N;G145A 51;97 80;121 S 130 144 11230757 Nomenclature for antiviral-resistant human hepatitis B virus mutations in the polymerase region. In this proposal, the HBV rt domain starts with the highly conserved EDWGPCDEHG motif, contains 344 amino acids, and the lamivudine-related resistance mutations are found at amino acid rtL180M (previously amino acid 528, 526, 515, or 525) and rtM204V/I (previously 552, 550, 539, or 549). 2001 Hepatology (Baltimore, Md.) Abstract HBV L180M;M204V;M204I 187;245;245 192;252;252 RT;RT;RT 26;185;243 28;187;245 11264736 Hepatitis B surface antigen variants in vaccinees, blood donors and an interferon-treated patient. One child had a double mutation (P142S and G145R) and the other a G145A substitution. 2001 Journal of viral hepatitis Abstract HBV P142S;G145R;G145A 33;43;66 38;48;71 11264736 Hepatitis B surface antigen variants in vaccinees, blood donors and an interferon-treated patient. Three of seven anti-HBc positive Chinese blood donors had a T131I substitution, whilst the interferon-treated patient had a treble amino acid substitution (P142S, G145R and N146D). 2001 Journal of viral hepatitis Abstract HBV T131I;P142S;G145R;N146D 60;156;163;173 65;161;168;178 C 20 23 11312349 Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC). Specifically, steric conflict between the Cgamma2-methyl group of Ile or Val at position 552 in HBV polymerase and the sulfur atom in the oxathiolane ring (common to both beta-L-nucleoside analogs lamivudine and emtricitabine) is proposed to account for the resistance observed upon Met552Ile/Val mutation. 2001 Journal of virology Abstract HBV M552I;M552V 283;283 296;296 P 100 110 11312349 Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC). The effects of Leu528Met, Met552Ile, and Met552Val mutations on the binding of HBV polymerase inhibitors and the natural substrate dCTP were evaluated using an in vitro HBV polymerase assay. 2001 Journal of virology Abstract HBV L528M;M552V;M552I 15;41;26 24;50;35 P 83 93 11312349 Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC). The effects of the Leu528Met mutation, which also occurs near the HBV polymerase active site, appeared to be less direct, potentially involving rearrangement of the deoxynucleoside triphosphate-binding pocket residues. 2001 Journal of virology Abstract HBV L528M 19 28 P 70 80 11312349 Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC). The predominant lamivudine resistance mutations in HBV-infected patients are Met552IIe and Met552Val (Met552Ile/Val), frequently in association with a second mutation, Leu528Met. 2001 Journal of virology Abstract HBV M552V;M552I;M552V;L528M 91;102;102;168 100;115;115;177 HBV infections 51 63 11312349 Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC). The results from the in vitro studies were as follows: (i) dCTP substrate binding was largely unaffected by the mutations, with Km changing moderately, only in a range of 0.6 to 2.6-fold; (ii) K(i)s for 3TCTP and FTCTP against Met552Ile/Val mutant HBV polymerases were increased 8- to 30-fold; and (iii) the Leu528Met mutation had a modest effect on direct binding of these beta-L-oxathiolane ring-containing nucleotide analogs. 2001 Journal of virology Abstract HBV M552I;M552V;L528M 227;227;308 240;240;317 P 252 263 11353615 Cross-resistance testing of antihepadnaviral compounds using novel recombinant baculoviruses which encode drug-resistant strains of hepatitis B virus. For these studies, novel recombinant HBV baculoviruses which encoded the L526M, M550I, and L526M M550V drug resistance mutations were generated and used to examine the effects of these substitutions on viral sensitivity to lamivudine, penciclovir (the active form of famciclovir), and adefovir, three compounds of clinical importance. 2001 Antimicrobial agents and chemotherapy Abstract HBV L526M;L526M;M550V;M550I 73;91;97;80 78;96;102;85 11353615 Cross-resistance testing of antihepadnaviral compounds using novel recombinant baculoviruses which encode drug-resistant strains of hepatitis B virus. The following observations were made: (i) the L526M mutation confers resistance to penciclovir and partial resistance to lamivudine, (ii) the YMDD mutations M550I and L526M M550V confer high levels of resistance to lamivudine and penciclovir, and (iii) adefovir is active against each of these mutants. 2001 Antimicrobial agents and chemotherapy Abstract HBV M550V;L526M;M550I;L526M 173;46;157;167 178;51;162;172 P 142 146 11385295 Vaccine- and hepatitis B immune globulin-induced escape mutations of hepatitis B virus surface antigen. Notably, HBsAg with an arginine replacement for glycine at amino acid 145 is considered the quintessential immune escape mutant because it has been isolated consistently in clinical samples of HBIg-treated individuals and vaccinated infants of chronically infected mothers. 2001 Journal of biomedical science Abstract HBV G145R 23 73 S 9 14 11395201 Anti-HBs after hepatitis B immunization with plasma-derived and recombinant DNA-derived vaccines: binding to mutant HBsAg. Anti-HBs binding to synthetic peptids (25-mers, 7aa overlap) from the "a"-loop was significantly reduced by the G145R substitution and by changing the amino acid sequence from adw(2) into adr. 2001 Vaccine Abstract HBV G145R 112 117 S 5 8 11395201 Anti-HBs after hepatitis B immunization with plasma-derived and recombinant DNA-derived vaccines: binding to mutant HBsAg. In a previous study we found that plasma-derived and recombinant DNA-derived vaccine HBsAg reacted differently with monoclonal antibodies sensitive for the G145R change. 2001 Vaccine Abstract HBV G145R 156 161 S 85 90 11395201 Anti-HBs after hepatitis B immunization with plasma-derived and recombinant DNA-derived vaccines: binding to mutant HBsAg. The G145R mutant of the small S-protein is a major escape mutant of hepatitis B virus observed in natural infection, after immunization and HBIG therapy. 2001 Vaccine Abstract HBV G145R 4 9 S 24 31 11395201 Anti-HBs after hepatitis B immunization with plasma-derived and recombinant DNA-derived vaccines: binding to mutant HBsAg. With mutant G145R rHBsAg the inhibitory activity of vaccine anti-HBs was decreased compared to rHBsAg wild type. 2001 Vaccine Abstract HBV G145R 12 17 S;S;S 65;18;95 68;24;101 11397661 Detection of hepatitis B virus resistance to antivirals. Recent reports on larger series of patients pointed that other mutations residing outside of the C domain but mainly in the B domain of the viral polymerase (L528M) could be associated with these mutations in the YMDD motif. 2001 Journal of clinical virology Abstract HBV L528M 158 163 P;YMDD 146;213 156;217 11397661 Detection of hepatitis B virus resistance to antivirals. Sequence analysis of the reverse transcriptase domain of resistant viral strains, at the time of viral breakthrough, revealed the occurrence of mutations located in the YMDD motif within the C domain of the viral enzyme with a methionine to valine (M552V) or to isoleucine (M5521) change. 2001 Journal of clinical virology Abstract HBV M552V 249 254 RT;P 25;169 46;173 11397661 Detection of hepatitis B virus resistance to antivirals. The lamivudine resistant mutants, selected in vivo, can be classified in 2 main groups: group I with a double mutation L528M and M552V, and group II with a single mutation M5521. 2001 Journal of clinical virology Abstract HBV L528M;M552V 119;129 124;134 11410701 Emergence of vaccine-induced escape mutant of hepatitis B virus with multiple surface gene mutations in a Korean child. We present for the first time in Korea the independent emergence of an escape mutant with substitution of arginine for glycine at amino acid 145 and proline for glutamate at amino acid 120 in "a" determinant after immunization. 2001 Journal of Korean medical science Abstract HBV G145R;E120P 106;149 144;188 11424118 Full-length genomic analysis of hepatitis B virus isolates in a patient progressing from hepatitis to hepatocellular carcinoma. High frequency of mutations at nucleotides 1762(A-->T) and 1764(G-->A) in the core promoter region have been described in HCC. 2001 Journal of medical virology Abstract HBV A1762T;G1764A 43;59 54;70 Core promoter 78 91 11468748 Full-length genomic analysis of hepatitis B virus isolates in a patient progressing from hepatitis to hepatocellular carcinoma. High frequency of mutations at nucleotides 1762(A-->T) and 1764(G-->A) in the core promoter region have been described in HCC. 2001 Journal of medical virology Abstract HBV A1762T;G1764A 43;59 54;70 Core promoter 78 91 Hepatocellular carcinoma 122 125 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. BACKGROUND: Mutations in the core promoter and precore regions of the hepatitis B virus (HBV) genome, notably the double substitution (AGG to TGA) at nt positions 1762-1764 in the core promoter, and the precore stop codon mutation G to A at nt 1896, can often explain the anti-HBe phenotype in chronic carriers. 2001 BMC microbiology Abstract HBV G1896A 231 248 Core promoter;Core promoter;C;Precore;Precore 29;180;277;47;203 42;193;280;54;210 11480792 Efficacy and tolerability of long-term therapy using high lamivudine doses for the treatment of chronic hepatitis B. The YMDD mutation was detected in 12 nonresponder patients (9 YVDD, 2 YIDD, and 1 mixed population Y(V/I)DD), generally associated with the L528M mutation. 2001 Journal of gastroenterology Abstract HBV L528M 140 145 P;P;P 70;4;62 74;8;66 11481624 A dominant hepatitis B virus population defective in virus secretion because of several S-gene mutations from a patient with fulminant hepatitis. This was caused by a combination of amino acid changes in the S-protein including the mutation G145R frequently emerging after hyperimmunoglobulin treatment. 2001 Hepatology (Baltimore, Md.) Abstract HBV G145R 95 100 S 62 63 11502520 In vitro susceptibilities of wild-type or drug-resistant hepatitis B virus to (-)-beta-D-2,6-diaminopurine dioxolane and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil. The L526M substitution, which is associated with famciclovir resistance, conferred cross-resistance to L-FMAU but not to adefovir or DAPD. 2001 Antimicrobial agents and chemotherapy Abstract HBV L526M 4 9 11502520 In vitro susceptibilities of wild-type or drug-resistant hepatitis B virus to (-)-beta-D-2,6-diaminopurine dioxolane and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil. The M550V substitution in isolation conferred a similar phenotype to M550I, except that it did not confer significant resistance to L-FMAU. 2001 Antimicrobial agents and chemotherapy Abstract HBV M550V;M550I 4;69 9;74 11502520 In vitro susceptibilities of wild-type or drug-resistant hepatitis B virus to (-)-beta-D-2,6-diaminopurine dioxolane and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil. We found that the M550I and M550V plus L526M substitutions, which confer lamivudine resistance, did not confer cross-resistance to adefovir or DAPD, but conferred cross-resistance to L-FMAU. 2001 Antimicrobial agents and chemotherapy Abstract HBV M550I;M550V;L526M 18;28;39 23;33;44 11509998 Effectiveness of hepatitis B vaccination in babies born to hepatitis B surface antigen-positive mothers in Italy. One carrier child had a double mutation, with substitution of proline-->serine at codons 120 (P120S) and 127 (P127S) within the a determinant of HBsAg. 2001 The Journal of infectious diseases Abstract HBV P120S;P127S 94;110 99;115 S;S 128;145 141;150 11526151 Phylogenetic origin of hepatitis B virus strains with precore C-1858 variant. The predominant mutation, the precore G-->A-1896 mutation, is restricted by the variability at position 1858 and is rare in strains with cytosine at nucleotide 1858. 2001 Journal of clinical microbiology Abstract HBV G1896A 38 48 Precore 30 37 11533157 Replication of the wild type and a natural hepatitis B virus nucleocapsid promoter variant is differentially regulated by nuclear hormone receptors in cell culture. A natural hepatitis B virus (HBV) variant associated with seroconversion from HBeAg to anti-HBe antibody contains two nucleotide substitutions (A1764T and G1766A) in the proximal nuclear hormone receptor binding site in the nucleocapsid promoter. 2001 Journal of virology Abstract HBV A1764T;G1766A 144;155 150;161 C;C 92;78 95;83 11536229 Localization of hepatitis B surface antigen epitopes present on variants and specifically recognised by anti-hepatitis B surface antigen monoclonal antibodies. In contrast, 2G2G10 reacted strongly with all tested variants including variant with the G145R mutation. 2001 Journal of medical virology Abstract HBV G145R 89 94 11536229 Localization of hepatitis B surface antigen epitopes present on variants and specifically recognised by anti-hepatitis B surface antigen monoclonal antibodies. Whereas 6H6B6 did not detect mutations T123N, S143L, D144A and G145R, 27E7F10 binding was affected by mutations P120T and G145R. 2001 Journal of medical virology Abstract HBV T123N;S143L;D144A;G145R;P120T;G145R 39;46;53;63;112;122 44;51;58;68;117;127 11559794 Frequency of spontaneous mutations in an avian hepadnavirus infection. In this study, we measured the frequency of revertants of a cytopathic strain of the duck hepatitis B virus that bears a single nucleotide substitution in the pre-S envelope protein open reading frame, resulting in the amino acid substitution G133E. 2001 Journal of virology Abstract HBV G133E 243 248 S;PreS 165;159 173;164 11559794 Frequency of spontaneous mutations in an avian hepadnavirus infection. Spontaneous revertants were found to be present at frequencies of 1 x 10(-5) to 6 x 10(-5) per G133E genome inoculated. 2001 Journal of virology Abstract HBV G133E 95 100 11559794 Frequency of spontaneous mutations in an avian hepadnavirus infection. Virus outgrowth was accompanied by a coselection of wild-type and spontaneous revertants during recovery of the ducklings from the acute liver injury caused by death of the G133E-infected cells. 2001 Journal of virology Abstract HBV G133E 173 178 11578069 Reactivation of latently infected hepatitis B virus in a leukemia patient with antibodies to hepatitis B core antigen. Mutation-specific assay based on competitive polymerase chain reaction (PCR) and sequencing analyses revealed the predominant reactivation of an HBV strain with missence mutation (point mutation G-to-A at nucleotide 1896) in the precore regions, as well as point mutations in the core promoter regions. 2001 Journal of gastroenterology Abstract HBV G1896A 195 220 Core promoter;Precore 280;229 293;236 11584376 Factors associated with hepatitis B virus DNA breakthrough in patients receiving prolonged lamivudine therapy. Patients with HBV DNA breakthroughs had higher percentages of YMDD variants without the presence of wild-type YMDD compared with patients without HBV DNA breakthrough (25.6% vs. 9%, P =.007 for single M552I variant; 20.9% vs. 8.1%, P =.026 for single M552V variant; 30.2% vs. 9.9%, P =.004 for M552I/M552V variants). Patients with HBV DNA levels of more than 10(3) copies/mL after 6 months of lamivudine therapy had a 63.2% chance of subsequently developing YMDD variants. 2001 Hepatology (Baltimore, Md.) Abstract HBV M552V;M552I;M552I;M552V 300;201;294;251 305;206;299;256 P;P;P 62;110;458 66;114;462 11584376 Factors associated with hepatitis B virus DNA breakthrough in patients receiving prolonged lamivudine therapy. There was no increase in the rate of development of YMDD variants or L528M mutation in patients receiving lamivudine 25 mg daily or famciclovir 500 mg 3 times a day before being given lamivudine 100 mg daily. 2001 Hepatology (Baltimore, Md.) Abstract HBV L528M 69 74 YMDD 52 56 11595588 Hepatitis B virus harboring nucleotide deletions in the core promoter region and genotype B correlate with low viral replication activity in anti-HBe positive carriers. RESULTS: Various mutations were detected including C to T point mutation at nt 1653, A to T and G to A contiguous point mutations at nt 1762 and 1764 in the core promoter region, and G to A point mutation at nt 1896 in the precore region, but no common mutations were detected that were directly related to the virus titer from earlier reported mutations. 2001 Journal of clinical virology Abstract HBV C1653T;A1762T;A1762G;A1762A;G1896A 51;85;85;85;183 83;140;140;140;215 Core promoter;Precore 157;223 170;230 11596083 Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B. A relatively large number of mutations were present in the middle region of the core gene in those isolates without G1896A or A1762T, G1764A mutations, although the pattern was not consistent with those in published studies. 2001 Journal of medical virology Abstract HBV G1896A;A1762T;G1764A 116;126;134 122;132;140 C 80 84 11596083 Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B. G1896A was, however, present in the one genotype D isolate. 2001 Journal of medical virology Abstract HBV G1896A 0 6 11596083 Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B. The mutation most often reported in patients with fulminant hepatitis B, the G1896A precore stop-codon substitution, was, as expected, not present in the genotype A isolates with the exception of one in which it was accompanied by a compensatory C1858T substitution. 2001 Journal of medical virology Abstract HBV G1896A;C1858T 77;246 83;252 Precore 84 91 Fulminant Hepatitis B 50 69 11596083 Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B. The other mutation commonly found in patients with fulminant hepatitis B, the paired A1762T, G1764A substitution in the basic core promoter, was present in only one patient and G1764A in one other. 2001 Journal of medical virology Abstract HBV A1762T;G1764A;G1764A 85;93;177 91;99;183 BCP 120 139 Fulminant Hepatitis B 51 70 11596084 Residual hepatitis B virus particles in liver transplant recipients receiving lamivudine: PCR quantitation of HBV DNA and ELISA of preS1 antigen. Among the three patients who did not respond to lamivudine, one had pol mutations (L450P and S550C) that had not been described previously, in addition to the common mutations within the YMDD locus and B domain. 2001 Journal of medical virology Abstract HBV L450P;S550C 83;93 88;98 P;P 68;187 71;191 11679975 Prevalence of naturally occurring surface gene variants of hepatitis B virus in nonimmunized surface antigen-negative Chinese carriers. These changes involved 11 positions inside and 5 outside of the historical first and second loops of the "a" determinant, and included the following: Q101K, T115A, K122N, T123A, T126N, Q129N, G130R, T131I, M133T, F134L, C138Y, K141E, P142S, G145R, N146S, and C147F/R. 2001 Hepatology (Baltimore, Md.) Abstract HBV Q101K;T115A;K122N;T123A;T126N;Q129N;G130R;T131I;M133T;F134L;C138Y;K141E;P142S;G145R;N146S;C147F;C147R 150;157;164;171;178;185;192;199;206;213;220;227;234;241;248;259;259 155;162;169;176;183;190;197;204;211;218;225;232;239;246;253;266;266 11680583 Hepatitis B virus genomes of chronic hepatitis patients do not contain specific mutations related to acute exacerbation. A 1896 precore stop codon mutant (G to A at nt 1896) coexisting with the wild sequence was found in both patients prior to seroconversion from HBeAg to anti-HBe. 2001 Digestive diseases and sciences Abstract HBV G1896A 34 51 C;C;Precore 157;143;7 160;148;14 11680583 Hepatitis B virus genomes of chronic hepatitis patients do not contain specific mutations related to acute exacerbation. Core promoter mutations at nucleotide positions 1762 (A to T) and 1764 (G to A) were found in both patients throughout the observation period. 2001 Digestive diseases and sciences Abstract HBV A1762T;G1764A 48;66 61;79 Core promoter 0 13 11689047 Transcription and replication of a natural hepatitis B virus nucleocapsid promoter variant is regulated in vivo by peroxisome proliferators. A hepatitis B virus (HBV) transgenic mouse containing a naturally occurring mutation in the nucleocapsid promoter (A1764T plus G1766A) that inhibits the retinoid X receptor alpha (RXRalpha) plus peroxisome proliferator-activated receptor alpha (PPARalpha) heterodimer from binding to the proximal nuclear hormone receptor recognition sequence has been generated. 2001 Virology Abstract HBV A1764T;G1766A 115;127 121;133 X 162 163 11696228 Characterization of a novel hepatitis B virus mutant: demonstration of mutation-induced hepatitis B virus surface antigen group specific "a" determinant conformation change and its application in diagnostic assays. Interestingly, none of the mutations was found within the group-specific "a" determinant region (124-147) and, specifically, two of the five mutations, T118K and P120Q, were located only a few amino acids adjacent to the 124-147 region. 2001 Transfusion medicine (Oxford, England) Abstract HBV T118K;P120Q 152;162 157;167 11745929 Prevalence of HBV core promoter/precore/core mutations in Gambian chronic carriers. The two point mutations, from A to T and G to A at nt positions 1762 and 1764 in the basic core promoter region, were found in only 7/99 (7%) of the samples where this region was sequenced. 2001 Journal of medical virology Abstract HBV A1762T;A1762G;A1762A 30;30;30 68;68;68 BCP 85 104 11753968 Reactivation of precore mutant hepatitis B virus in chemotherapy-treated patients. A point mutation from G to A at nt 1896 was detected in five of these six patients. 2001 Cancer Abstract HBV G1896A 22 39 11753968 Reactivation of precore mutant hepatitis B virus in chemotherapy-treated patients. BACKGROUND: A point mutation from G to A at nucleotide (nt) 1896 of the precore region of hepatitis B virus (HBV) DNA has been shown to be associated with fulminant and severe hepatitis. 2001 Cancer Abstract HBV G1896A 33 65 Precore 72 79 Hepatitis 176 185 11753968 Reactivation of precore mutant hepatitis B virus in chemotherapy-treated patients. Prophylactic use of lamivudine is strongly recommended for patients who carry mutant HBV at precore region, especially at nt 1896 (G to A), before and during chemotherapy. 2001 Cancer Abstract HBV G1896A 125 138 Precore 92 99 11778699 Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations. In the third patient, a G1899A substitution was seen which compensated the impaired U at position 1855. 2001 Virus genes Abstract HBV G1899A 24 30 11778699 Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations. One patient showed an additional G1897A substitution, presenting as a novel precore stop codon mutation (UGG-->UAA), followed by a compensatory mutation at position 1857. 2001 Virus genes Abstract HBV G1897A 33 39 Precore 76 83 11778699 Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations. The destabilized C : G base-pairing in the lower stem of epsilon-hairpin due to G1896A substitution is reportedly compensated by a second C1858T mutation and suggested to play an important role in enhanced selection of the HBe negative variant. 2001 Virus genes Abstract HBV G1896A;C1858T 80;138 86;144 C 223 226 11778699 Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations. The HBe negative phenotype, a natural precore mutant (G1896A/G1897A) of HBV with aborted HBeAg expression is known to cause chronic hepatitis. 2001 Virus genes Abstract HBV G1897A;G1896A 61;54 67;60 C;C;Precore 4;89;38 7;94;45 Chronic Hepatitis B 124 141 11778699 Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations. Three of the 5 HBe negative patients had classical G1896A mutation having a second compensatory mutation at nt. 2001 Virus genes Abstract HBV G1896A 51 57 C 15 18 11792065 Comparing the immunogenicity of hepatitis B virus S gene variants by DNA immunization. Computer modeling showed that a change from glutamine to leucine at 129 residue led to higher hydrophobicity and could result in decreased immunogenicity. 2001 Viral immunology Abstract HBV Q129L 44 71 11792996 Efficacy of famciclovir in the treatment of lamivudine resistance related to an atypical hepatitis B virus mutant. The severe hepatitic flare consequent to the lamivudine resistance in this patient was successfully treated with famciclovir, indicating that both M550V and M550I mutants with preserved wild-type sequence at position 526 of HBV reverse transcriptase are susceptible to famciclovir. 2002 Transplantation Abstract HBV M550V;M550I 147;157 152;162 RT 228 249 11792996 Efficacy of famciclovir in the treatment of lamivudine resistance related to an atypical hepatitis B virus mutant. Treatment with famciclovir has not been effective in the majority of patients who developed lamivudine resistance due to methionine-to-valine mutation at position 550, because this mutation has been uniformly associated with leucine-to-methionine mutation at position 526, a mutation that is associated with resistance to famciclovir. 2002 Transplantation Abstract HBV M550V;L526M 121;225 166;271 11851835 Prevalence of vaccine-induced escape mutants of hepatitis B virus in the adult population in China: a prospective study in 176 restaurant employees. Four out of these six cases had a point mutation within the 'a' determinant; they were Gly-145-Ala, and Ile/Thr-126-Asn/Ser. 2001 Journal of gastroenterology and hepatology Abstract HBV I126N;I126S;T126N;T126S;G145A 104;104;104;104;87 123;123;123;123;98 S 61 75 11886250 Reduced antigenicity of the hepatitis B virus HBsAg protein arising as a consequence of sequence changes in the overlapping polymerase gene that are selected by lamivudine therapy. HBsAg mutants including E164D, W196S, I195M, M198I, and E164D/I195M (corresponding to the polymerase protein changes of V519L, M550I, L526M/M550V V553I, and V519L/L526M/M550V) selected during lamivudine treatment also demonstrated reduced binding to anti-HBs antibody. 2002 Virology Abstract HBV I195M;M550V;L526M;M550V;W196S;I195M;M198I;E164D;M550I;V519L;E164D;V519L;V553I;L526M 62;140;163;169;31;38;45;56;127;157;24;120;146;134 67;145;168;174;36;43;50;61;132;162;29;125;151;139 S;S;P 255;0;90 258;5;100 11886250 Reduced antigenicity of the hepatitis B virus HBsAg protein arising as a consequence of sequence changes in the overlapping polymerase gene that are selected by lamivudine therapy. HBsAg proteins containing the vaccine escape mutations G145R and D144E/G145R demonstrated markedly reduced binding to anti-HBs antibody. 2002 Virology Abstract HBV G145R;G145R;D144E 71;55;65 76;60;70 S;S 0;123 5;126 11891535 Transactivation of human alpha-fetoprotein gene by X-gene product of hepatitis B virus in human hepatoma cells. In addition, a G-->A substitution at nucleotide -119 in the AFP promoter sequence abrogated the stimulatory effect of HBX on the AFP promoter in HepG2 cells. 2002 International journal of molecular medicine Abstract HBV G119A 15 52 X 118 121 11907436 Seroconversion after the addition of famciclovir therapy in a child with hepatitis B virus infection after liver transplantation who developed lamivudine resistance. Sixteen months later, lamivudine resistance developed; a mutation (M552I) was confirmed by sequencing through the YMDD locus of the HBV polymerase gene. 2002 Transplantation Abstract HBV M552I 67 72 P;P 136;114 146;118 11916202 Fatal hepatic failure after emergence of the hepatitis B virus mutant during lamivudine therapy in a patient with liver cirrhosis. Emergence of the HBV mutant with substitution of isoleucine for leucine at residue 426 (L4261) in combination with isoleucine for methionine at residue 550 (M5501) was observed at 10 and 13 months of treatment. 2002 Scandinavian journal of gastroenterology Abstract HBV L426I;M550I 49;115 86;155 11938042 Lamivudine therapy of chronic hepatitis B in three groups of patients: non transplanted patients, liver recipients, and kidney recipients. After the development of lamivudine resistance, mutations rtM204V and rtL180M were detected in all studied patients, mutation rtM207I in one, with similar results from traditional nucleotide sequencing and a commercial line probe assay. 2002 Gastroenterologie clinique et biologique Abstract HBV M204V;L180M;M207I 60;72;128 65;77;133 RT;RT;RT 58;70;126 60;72;128 11953207 [A novel stop codon mutation in S gene: the molecular basis of a patient with cryptogenic cirrhosis]. An uncommon point mutation at nucleotide 336 (C to A) in S gene was found, resulting in the change of the 61st codon into a novel stop codon and failure of synthesis of HbsAg. 2002 Zhonghua yi xue za zhi Abstract HBV C336A 41 53 S;S 169;57 174;58 11981772 Characterization of two hepatitis B virus populations isolated from a hepatitis B surface antigen-negative patient. Both genomes possess the common A1762T-G1764A double mutation of the basal core promoter (BCP), and the genotype D virus is also mutated in the << TATA box >> of the large surface antigen promoter. 2002 Hepatology (Baltimore, Md.) Abstract HBV A1762T;G1764A 32;39 38;45 BCP;BCP;S 69;90;166 88;93;179 11993512 Hepatitis B genotypes and precore/basal core promoter mutants in HBeAg-negative chronic hepatitis B. BACKGROUND: Mutations in the precore stop codon (G1896A) and the basal core promoter (A1762T and G1764A) are frequently found in hepatitis B envelope antigen (HBeAg)-negative chronic hepatitis B. 2002 Journal of gastroenterology Abstract HBV G1896A;A1762T;G1764A 49;86;97 55;92;103 BCP;Envelope;C;Precore 65;141;159;29 84;149;164;36 Chronic Hepatitis B 175 194 12010505 Sequential analysis of hepatitis B virus core promoter and precore regions in cancer survivor patients with chronic hepatitis B before, during and after interferon treatment. Five of the six (83%) responders displayed the double CP mutation A1762T/G1764A always in association with a T1753C change. 2002 Journal of viral hepatitis Abstract HBV G1764A;A1762T;T1753C 73;66;109 79;72;115 Core promoter 54 56 12010505 Sequential analysis of hepatitis B virus core promoter and precore regions in cancer survivor patients with chronic hepatitis B before, during and after interferon treatment. The G1896A change creating the PC stop codon mutation was never detected in any of the patients. 2002 Journal of viral hepatitis Abstract HBV G1896A 4 10 Precore 31 33 12014730 Occult HBV infection in cryptogenic liver cirrhosis in an area with high prevalence of HBV infection. a determinant mutations were detected in two patients in group I (K122N and G145R, C125A) and one patient in group II (1126N). 2002 The American journal of gastroenterology Abstract HBV K122N;G145R;C125A 68;78;85 73;83;90 12033768 In vivo suppression of precore mRNA synthesis is associated with mutations in the hepatitis B virus core promoter. Our in vivo study shows therefore that the double A1762T/G1764A mutation is associated with the specific suppression of precore mRNA synthesis directed by the HBV core promoter. 2002 Virology Abstract HBV G1764A;A1762T 57;50 63;56 Core promoter;Precore 163;120 176;127 12033768 In vivo suppression of precore mRNA synthesis is associated with mutations in the hepatitis B virus core promoter. Precore mRNA synthesis was suppressed by the A1762T/G1764A mutation regardless of the presence of the precore stop codon mutation G1896A, suggesting that in addition to downregulating an immunomodulatory protein this double basic core promoter mutation may also confer a replication advantage to the virus. 2002 Virology Abstract HBV G1764A;A1762T;G1896A 52;45;130 58;51;136 BCP;Precore;Precore 224;0;102 243;7;109 12033768 In vivo suppression of precore mRNA synthesis is associated with mutations in the hepatitis B virus core promoter. The double A1762T/G1764A mutation in the basic core promoter was detected in 11 cases. 2002 Virology Abstract HBV G1764A;A1762T 18;11 24;17 BCP 41 60 12050364 Influence of a putative intermolecular interaction between core and the pre-S1 domain of the large envelope protein on hepatitis B virus secretion. Here, we further demonstrated that a pre-S1 envelope mutation at position 119, changing an alanine (A) to a phenylalanine (F), can offset the immature secretion phenotype of the mutant I97L (isoleucine to leucine) and successfully restore the wild-type-like selective export of the mature genome of the double mutant pre-S1-A119F/core-I97L. 2002 Journal of virology Abstract HBV I97L;A119F;I97L 185;324;335 189;329;339 C;PreS1;PreS1 330;317;37 334;323;52 12050364 Influence of a putative intermolecular interaction between core and the pre-S1 domain of the large envelope protein on hepatitis B virus secretion. In addition, the secretion kinetics of the mature genomes are comparable between the wild-type HBV and the mutant F97L. 2002 Journal of virology Abstract HBV F97L 114 118 12050364 Influence of a putative intermolecular interaction between core and the pre-S1 domain of the large envelope protein on hepatitis B virus secretion. In this study, our kinetic analysis of virion secretion of the mutant F97L (phenylalanine to leucine) indicates that the secretion of its immature genome does not occur earlier than that of its mature genome. 2002 Journal of virology Abstract HBV F97L 70 74 12050364 Influence of a putative intermolecular interaction between core and the pre-S1 domain of the large envelope protein on hepatitis B virus secretion. Therefore, the immature secretion phenomenon of mutant F97L is not caused by premature secretion or more efficient secretion. 2002 Journal of virology Abstract HBV F97L 55 59 12076712 Clinical features and viral sequences of various genotypes of hepatitis B virus compared among patients with acute hepatitis B. Two of seven patients with thymidine at 1858 also had a G to A mutation at 1896. 2002 Hepatology research Abstract HBV G1896A 56 79 12076758 Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. In contrast, A566T mutant was approximately 10-fold more resistant to 3TC, replicated intracellularly as well as wild type, but produced 10-fold lower levels of virions than wild type. 2002 Antiviral research Abstract HBV A566T 13 18 12076758 Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. In transfected Huh7 cells, WHV containing the M589V mutation conferred at least 100-fold increased resistance to 3TC, but replicated approximately 5-fold less efficiently than wild-type virus as judged by both extracellular virus production and intracellular DNA replicative forms. 2002 Antiviral research Abstract HBV M589V 46 51 12076758 Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. The appearance of the A566T mutation was temporally associated with viral recrudescence. 2002 Antiviral research Abstract HBV A566T 22 27 12076758 Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. These findings are consistent with the observation that the A566T mutation alters the overlapping WHV surface antigen reading frame. 2002 Antiviral research Abstract HBV A566T 60 65 S 102 109 12076758 Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. Three WHV molecular infectious clones were constructed to study this mutation in greater detail in vitro: A566T, analogous to A181T in HBV; M589V, analogous to the M204V in HBV; and the double mutant A566T/M589V, analogous to A181T/M204V in HBV. 2002 Antiviral research Abstract HBV M589V;M204V;A566T;A181T;A181T;A566T;M589V;M204V 206;232;200;226;126;106;140;164 211;237;205;231;131;111;145;169 12089278 Sensitive detection of HBsAg mutants by a gap ligase chain reaction assay. Detection of the G145R mutant in clinical specimens was evaluated by testing 56 suspect serum specimens. 2002 Journal of clinical microbiology Abstract HBV G145R 17 22 12089278 Sensitive detection of HBsAg mutants by a gap ligase chain reaction assay. The G145R mutation was most frequently observed in specimens producing a diagnostic anomaly or from transplant patients but was also observed in specimens from vaccinated individuals and specimens in which HBsAg diagnostic escape was suspected. 2002 Journal of clinical microbiology Abstract HBV G145R 4 9 S 206 211 12089278 Sensitive detection of HBsAg mutants by a gap ligase chain reaction assay. The G145R mutation was observed in 18 of 28 HBV-DNA-positive samples. 2002 Journal of clinical microbiology Abstract HBV G145R 4 9 12089278 Sensitive detection of HBsAg mutants by a gap ligase chain reaction assay. The most common mutation observed in these variants is a glycine-to-arginine substitution at amino acid 145 (G145R). 2002 Journal of clinical microbiology Abstract HBV G145R;G145R 109;57 114;107 12089278 Sensitive detection of HBsAg mutants by a gap ligase chain reaction assay. Therefore, the gLCR assay is a sensitive and specific method for detection of G145R mutants, which could be modified to include the detection of other HBV mutants. 2002 Journal of clinical microbiology Abstract HBV G145R 78 83 12121939 Novel nucleoside analogue MCC-478 (LY582563) is effective against wild-type or lamivudine-resistant hepatitis B virus. The emergence of resistant hepatitis B virus (HBV) with the L528M mutation and/or the M552V and M552I mutations in the polymerase gene following long-term lamivudine treatment is becoming an important clinical problem. 2002 Antimicrobial agents and chemotherapy Abstract HBV L528M;M552V;M552I 60;86;96 65;91;101 P 119 129 12121939 Novel nucleoside analogue MCC-478 (LY582563) is effective against wild-type or lamivudine-resistant hepatitis B virus. The MCC-478 EC(50)s were 0.027 microM for wild-type HBV (about 20 times more efficient than lamivudine), 2.6 microM for M552I, 3.3 microM for M552V, and 2.0 microM for L528M/M552V. 2002 Antimicrobial agents and chemotherapy Abstract HBV M552V;L528M;M552I;M552V 174;168;120;142 179;173;125;147 12121939 Novel nucleoside analogue MCC-478 (LY582563) is effective against wild-type or lamivudine-resistant hepatitis B virus. The susceptibility of wild-type HBV and lamivudine-resistant mutants (M552I, M552V, and L528M/M552V) to MCC-478 was examined by transient transfection of full-length HBV DNA into human hepatoma cells. 2002 Antimicrobial agents and chemotherapy Abstract HBV M552V;L528M;M552I;M552V 94;88;70;77 99;93;75;82 Hepatocellular carcinoma 185 193 12135788 'Hbe minus' mutants of hepatitis B virus. Molecular characterization and its relation to viral genotypes. Precore mutations, mainly M1 (G1896A, stop at codon 28) were similarly found among viral genotypes A and D: seven cases (58%) and six cases (55%), respectively. 2002 Virus research Abstract HBV G1896A 30 36 Precore 0 7 12167344 Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the "fingers" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene. In contrast, the HBV a determinant HBIg/vaccine escape mutants sP120T, sT123N, sG145R, and sD144E/G145R (that produce rtT128N, Q130P, rtW153Q, and rtG153E respectively) yielded as much virus as wild-type HBV while the sM133L (rtY141S) mutant was replication impaired. 2002 Virology Abstract HBV G145R;T128N;W153Q;G153E;Y141S;D144E;Q130P;P120T;T123N;G145R;M133L 98;120;136;149;228;91;127;63;71;79;218 103;125;141;154;233;97;132;69;77;85;224 S;RT;RT;RT;RT;S;S;S;S;S 21;118;134;147;226;63;71;79;91;218 34;120;136;149;228;64;72;80;92;219 12167344 Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the "fingers" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene. The LMV-resistant HBV mutants rtM204I and rtL180M/M204V produced substantially weaker HBV DNA replicative intermediate signals by Southern blot analysis and less total intracellular HBV DNA by real-time PCR compared to wild-type virus. 2002 Virology Abstract HBV M204V;M204I;L180M 50;32;44 55;37;49 RT;RT 30;42 32;44 12167344 Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the "fingers" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene. The two most common LMV-resistant mutants produce changes in the viral polymerase protein (rt) of rtM204I and rtL180M/M204V (previously rtM550I and rtL526M/M550V). 2002 Virology Abstract HBV M204V;M550V;M204I;M550I;L180M;L526M 118;156;100;138;112;150 123;161;105;143;117;155 RT;RT;RT;RT;RT;P 91;98;110;136;148;71 93;100;112;138;150;81 12167344 Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the "fingers" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene. Two of these mutants, rtT128N and rtW153Q, when introduced into a replication-competent HBV vector containing the rtL180M/M204V polymerase mutation restored the replication phenotype of this LMV-resistant mutant. 2002 Virology Abstract HBV M204V;T128N;W153Q;L180M 122;24;36;116 127;29;41;121 P;RT;RT;RT 128;22;34;114 138;24;36;116 12171302 Identification of a new variant in the YMDD motif of the hepatitis B virus polymerase gene selected during lamivudine therapy. A new hepatitis B virus variant selected during lamivudine treatment was detected, in which the methionine (rtM204) in the so-called YMDD motif in the C domain of the catalytic site of the polymerase gene was replaced by a serine (rtM204S). 2002 Journal of medical microbiology Abstract HBV M204S 233 238 P;RT;RT;P 189;108;231;133 199;110;233;137 12171302 Identification of a new variant in the YMDD motif of the hepatitis B virus polymerase gene selected during lamivudine therapy. The mutation was followed by a leucine to methionine change at position 180 (rtL180M). 2002 Journal of medical microbiology Abstract HBV L180M;L180M 79;31 84;75 RT 77 79 12171302 Identification of a new variant in the YMDD motif of the hepatitis B virus polymerase gene selected during lamivudine therapy. This change simultaneously resulted in a tyrosine-195 into valine variant (sY195V) in the surface protein HBsAg. 2002 Journal of medical microbiology Abstract HBV Y195V;Y195V 41;75 65;81 S;S;S 75;106;90 76;111;97 12185284 Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis. The G-->T substitution at position 1862 leads to an amino acid change in codon 17 of the precore protein of the virus, which is part of a signal peptidase recognition motif. 2002 The Journal of general virology Abstract HBV G1862T 4 39 Precore 89 96 12185284 Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis. The prevalence of a G1862T variant of hepatitis B virus (HBV) has been investigated in patients with fulminant hepatitis and chronic liver disease, using primer mismatch amplification, followed by restriction fragment length polymorphism analysis. 2002 The Journal of general virology Abstract HBV G1862T 20 26 Fulminant Hepatitis B 101 120 12210410 Sequence analysis of pre-S/surface and pre-core/core promoter genes of hepatitis B virus in chronic hepatitis C patients with occult HBV infection. In addition, a novel core promoter mutant (a dinucleotide substitution: T-to-C at nucleotide 1,802 and T-to-G at nucleotide 1,803, T1802C/T1803G) was found frequently in patients with occult HBV infection as compared to sex- and age-matched HBsAg-positive patients. 2002 Journal of medical virology Abstract HBV T1802C;T1803G;T1802C;T1803G 72;103;131;138 98;129;137;144 Core promoter;S 21;241 34;246 HBV infections 191 204 12210427 Genotypes and S-gene variability of Mexican hepatitis B virus strains. One genotype F strain from an HBsAg positive chronic carrier had a T to A mutation at position 647, forming a translational stop at codon 216. 2002 Journal of medical virology Abstract HBV T647A 67 98 S 30 35 12210427 Genotypes and S-gene variability of Mexican hepatitis B virus strains. Two genotype F strains from HBsAg negative chronic carriers had a Val180 instead of an Ala found in the other genotype F strains. 2002 Journal of medical virology Abstract HBV V180A 66 90 S 28 33 12210428 Core promoter mutations (A(1762)T and G(1764)A) and viral genotype in chronic hepatitis B and hepatocellular carcinoma in Guangxi, China. Hepatitis B viruses (HBV) with core promoter mutations (A(1762)T, G(1764)A) were found in a previous study to be highly prevalent in patients from Guangxi, China with hepatocellular carcinoma (HCC). 2002 Journal of medical virology Abstract HBV A1762T;G1764A 56;66 64;75 Core promoter 31 44 Hepatocellular carcinoma;Hepatocellular carcinoma 167;193 191;196 12232637 A Hepatitis B Virus Variant with an Ile to Ser Mutation at aa126 of HBsAg. As aa126 is located in the first loop of the two-looped conformational structure of the determinant, and the Ile to Ser at aa 126 is a drastic change, it is suggested that the antigenicity of the HBsAg might be altered and the immune failure in patient No.19 was probably related to the mutation. 1996 Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica Abstract HBV I126S 109 129 S 196 201 12232637 A Hepatitis B Virus Variant with an Ile to Ser Mutation at aa126 of HBsAg. There was a G at nt 531 instead of T, leading to a change of Ile to Ser at aa126 of the major HBsAg. 1996 Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica Abstract HBV I126S 61 80 S 94 99 12358268 Core promoter mutations 3 years after anti-hepatitis B e seroconversion in patients with chronic hepatitis B or hepatitis B and C infection and cancer remission. The G1896A precore stop codon mutation was never observed. 2002 The American journal of gastroenterology Abstract HBV G1896A 4 10 Precore 11 18 12368144 [Evaluation of a quantitative HBV-DNA PCR assay in lamivudine treated hepatitis B-infected patients]. In 6 of these patients, was found a M184V mutation in the VIH polymerase. 2002 Annales de biologie clinique Abstract HBV M184V 36 41 P 62 72 12368144 [Evaluation of a quantitative HBV-DNA PCR assay in lamivudine treated hepatitis B-infected patients]. Mutations in the YMDD motif of the DNA polymerase gene were identified in 11 patients (3 with M550V/I mutation; 7 with M550V/I and L256M mutations; 1 with M550V/I, L526M and V519L mutations). 2002 Annales de biologie clinique Abstract HBV M550V;M550I;M550V;M550I;L256M;M550V;M550I;L526M;V519L 94;94;119;119;131;155;155;164;174 101;101;126;126;136;162;162;169;179 P;P 39;17 49;21 12414948 Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. In addition, the level of encapsidated RNA pregenome in mutant I97L was about 5.7-fold higher than that of the wild-type HBV in Huh7 cells. 2002 Journal of virology Abstract HBV I97L 63 67 12414948 Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. In our systematic study of virus-host interactions, we have examined the replication efficiency of a site-directed mutant, I97L, and its parental wild-type HBV in several different hepatoma cell lines. 2002 Journal of virology Abstract HBV I97L 123 127 Hepatocellular carcinoma 181 189 12414948 Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. This finding of a profound replication advantage for mutant I97L in Huh7 and J3 cells but not in HepG2 cells may have important implications for the emergence of this mutant in chronic HBV carriers. 2002 Journal of virology Abstract HBV I97L 60 64 Chronic Hepatitis B 177 188 12414948 Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus. Unlike Huh7 cells, no significant difference in viral DNA replication between the same I97L mutant and its parental wild-type HBV was observed in HepG2, a human hepatoblastoma cell line. 2002 Journal of virology Abstract HBV I97L 87 91 Hepatocellular carcinoma 161 175 12436473 Hepatitis B virus S gene mutants in a patient with chronic active hepatitis with circulating Anti-HBs antibodies. Other mutations were Q129R, C138R, C139R, and S140T (one clone each). 2003 Journal of medical virology Abstract HBV Q129R;C138R;C139R;S140T 21;28;35;46 26;33;40;51 12436473 Hepatitis B virus S gene mutants in a patient with chronic active hepatitis with circulating Anti-HBs antibodies. Within this region, two clones showed either C124R or C124Y mutations. 2003 Journal of medical virology Abstract HBV C124R;C124Y 45;54 50;59 12445424 Mutations of polymerase, precore and core promoter gene in hepatitis B virus during 5-year lamivudine therapy. Mutations in L526M, M550V and M550I in polymerase were found in seven, six and six patients, respectively. 2002 Journal of hepatology Abstract HBV M550V;L526M;M550I 20;13;30 25;18;35 P 39 49 12445424 Mutations of polymerase, precore and core promoter gene in hepatitis B virus during 5-year lamivudine therapy. The L526M mutant was found at the time or after detection of M550V/I mutant in six of seven patients. 2002 Journal of hepatology Abstract HBV M550I;L526M;M550V 61;4;61 68;9;68 12448687 Hepatitis B virus resistance to lamivudine and its clinical implications. These mutations are found at codon (or AA) rtL180M and rtM204V/I in the reverse transcriptase (RT) domain of the HBV polymerase for all genotypes according to a new standardized RT domain numbering system. 2002 Antiviral chemistry & chemotherapy Abstract HBV L180M;M204V;M204I 45;57;57 50;64;64 P;RT;RT;RT;RT;RT 117;72;43;55;95;178 127;93;45;57;97;180 12457969 Presence of hepatitis B surface antigen mutant G145R DNA in the peripheral blood leukocytes of the family members of an asymptomatic carrier and evidence of its horizontal transmission. As all of them were seronegative for HBsAg/antiHBc, the presence of G145R mutant in the PBL signaled possibility of spread of the vaccine escape mutant virus by blood transfusion, unsafe injection practices or through sexual root. 2002 Virus research Abstract HBV G145R 68 73 S 37 42 12457969 Presence of hepatitis B surface antigen mutant G145R DNA in the peripheral blood leukocytes of the family members of an asymptomatic carrier and evidence of its horizontal transmission. The study not only establishes the persistence of surface mutant G145R HBV DNA, within the PBL of HBsAg negative individuals from the non-vaccinated random population, but also suggests possible horizontal transmission of the mutant among the family members although none of the family members has received immunoprophylaxis against HBV or had clinically apparent disease or any other known risk factors of HBV infection. 2002 Virus research Abstract HBV G145R 65 70 S;S 98;50 103;57 HBV infections 407 420 12457969 Presence of hepatitis B surface antigen mutant G145R DNA in the peripheral blood leukocytes of the family members of an asymptomatic carrier and evidence of its horizontal transmission. This indicates the presence of established vaccine escape mutant of the virus (G145R) and suggests two different sources of infection within the family. 2002 Virus research Abstract HBV G145R 79 84 12500185 Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro. HBV baculoviruses encoding the G1896A PC stop codon mutation were generated in wild-type (WT) and lamivudine-resistant (rtM204I and rtL180M + rtM204V) backgrounds, resulting in a panel of 6 related recombinant baculoviruses. 2003 Hepatology (Baltimore, Md.) Abstract HBV M204I;L180M;M204V;G1896A 122;134;144;31 127;139;149;37 Precore;RT;RT;RT 38;120;132;142 40;122;134;144 12500185 Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro. Hepatitis B e antigen (HBeAg) negative chronic hepatitis B (CHB) is frequently caused by a mutation (G1896A) in the hepatitis B virus (HBV) precore (PC) reading frame that creates a stop codon, causing premature termination of the PC protein. 2003 Hepatology (Baltimore, Md.) Abstract HBV G1896A 101 107 C;C;Precore;Precore;Precore 12;23;149;231;140 21;28;151;233;147 Chronic Hepatitis B;Chronic Hepatitis B 39;60 58;63 12526951 Genotypic and phenotypic resistance: longitudinal and sequential analysis of hepatitis B virus polymerase mutations in patients with lamivudine resistance after liver transplantation. METHODS: Sequential serum samples from 10 consecutive patients with lamivudine resistance after liver transplantation were analyzed for viral genotype, precore mutants, and viral polymerase gene mutants (L528M, M552V, M552I) using restriction fragment length polymorphism. 2003 The American journal of gastroenterology Abstract HBV L528M;M552V;M552I 204;211;218 209;216;223 P;Precore 179;152 189;159 12526951 Genotypic and phenotypic resistance: longitudinal and sequential analysis of hepatitis B virus polymerase mutations in patients with lamivudine resistance after liver transplantation. The M552I pure viral population was found mainly in these patients, and all retained stable graft function (median follow-up 33 months). 2003 The American journal of gastroenterology Abstract HBV M552I 4 9 12532452 Targeted ribonuclease can inhibit replication of hepatitis B virus. Control plasmids, including p/hEDN, p/HBVc, and p/TNmut in which a Lys113-Arg mutation was introduced by sequential PCR to eliminate the ribonuclease activity of hEDN, were also constructed. 2003 World journal of gastroenterology Abstract HBV K113R 67 77 12558915 Targeted destruction of the polymerized human serum albumin binding site within the preS2 region of the HBV surface antigen while retaining full immunogenicity for this epitope. In this regard, the preS2(120-145/Y140S) sequence may be an HBV vaccine where epitopes, with intrinsic properties have been deleted without affecting the immunogenicity of the epitope itself. 2003 Journal of viral hepatitis Abstract HBV Y140S 34 39 PreS2 20 25 12558915 Targeted destruction of the polymerized human serum albumin binding site within the preS2 region of the HBV surface antigen while retaining full immunogenicity for this epitope. To overcome these limitations, a novel single a.a substitute of the preS2 region was designed that corresponds to a tyrosine to serine exchange at position 140 of preS2. 2003 Journal of viral hepatitis Abstract HBV Y140S 116 159 PreS2;PreS2 68;163 73;168 12657823 [Natural YMDD motif mutations of HBV polymerase in the chronic hepatitis B virus infected patients]. To detect YMDD mutants, YVDD (M552V), and YIDD (M552I), we used direct sequencing and the restriction fragment length polymorphism (RFLP) method. 2003 Taehan Kan Hakhoe chi Abstract HBV M552V;M552I 30;48 35;53 P;P;P 42;10;24 46;14;28 12659834 The influence of glycosylation on secretion, stability, and immunogenicity of recombinant HBV pre-S antigen synthesized in Saccharomyces cerevisiae. Three types of recombinant pre-S antigens (i.e., pre-S1S2) of hepatitis B virus (HBV) were synthesized in Saccharomyces cerevisiae and secreted into extracellular medium: wild type (pre-S1S2) and two mutant antigens, pre-S1 degrees S2 (Asn15Gln) and pre-S1 degrees S2 degrees (Asn15Gln and Asn123Gln). 2003 Biochemical and biophysical research communications Abstract HBV N15Q;N15Q;N123Q 236;277;290 244;285;299 PreS;PreS1;PreS1;PreS1;PreS1 27;49;182;217;250 32;55;188;223;256 12665929 [Pre-Core mutation of HBV among 26 families with history of chronic HBV infection in Shenyang]. CONCLUSIONS: The G to A mutation at nucleotide 1896 in the pre C gene of HBV DNA could be associated with persistent HBV infection. 2002 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1896A 17 51 Precore 59 64 HBV infections 117 130 12665929 [Pre-Core mutation of HBV among 26 families with history of chronic HBV infection in Shenyang]. METHODS: The G to A mutation at nucleotide 1896 in the pre C gene of HBV DNA was detected by PCR-RFLP. 2002 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1896A 13 47 Precore 55 60 12665929 [Pre-Core mutation of HBV among 26 families with history of chronic HBV infection in Shenyang]. RESULTS: The results showed that the mutation rate of G to A mutation at nucleotide 1896 in the pre C gene of HBV DNA was much higher in patients (56.3%) and their family members (40.5%) than in their spouses (25.0%). 2002 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1896A 54 88 Precore 96 101 12667359 [The prevalence of hepatitis B virus precore mutant isolated from asymptomatic carriers in Guangxi]. Among samples with stopped mutation, 4 samples had mutation at nt1846 (A-->T), 2 samples at nt1862 (G-->T). 2002 Zhonghua liu xing bing xue za zhi Abstract HBV A1846T;G1862T 65;94 77;106 12667359 [The prevalence of hepatitis B virus precore mutant isolated from asymptomatic carriers in Guangxi]. Both mutation at nt1856 (C-->T) and nt1858 (T-->C) could be seen in sample 734. 2002 Zhonghua liu xing bing xue za zhi Abstract HBV C1856T;T1858C 19;38 31;50 12667359 [The prevalence of hepatitis B virus precore mutant isolated from asymptomatic carriers in Guangxi]. The common mutation in the southern part was seen T-->C at nt1858 while nt1896 stop mutation was discovered in one sample only, which was accompanied by point mutation at nt1837 (A-->G). 2002 Zhonghua liu xing bing xue za zhi Abstract HBV A1837G;T1858C 173;50 185;83 12673447 Molecular analysis of antigenicity and immunogenicity of a vaccine-induced escape mutant of hepatitis B virus. METHODS: Mutation from glycine to arginine at aa145 was introduced into replication-competent DNA of HBV. 2003 Journal of gastroenterology Abstract HBV G145R 23 51 12716526 [Quasispecies and mutation of hepatitis B virus polymerase gene in lamivudine- treated patients]. By sequencing the predominant clones, there were 2 patients with M550V/L528M mutation, 3 patients with M550I mutation and 1 patient with wild type after lamivudine therapy. 2003 Zhonghua gan zang bing za zhi Abstract HBV L528M;M550V;M550I 71;65;103 76;70;108 12727536 Lamivudine and Famciclovir resistant hepatitis B virus associated with fatal hepatic failure. Subsequent to the instigation of antiviral therapy, the dominant drug resistant HBV which caused virological breakthrough and was associated with hepatic failure displayed a series of unique mutations particularly in the BCP (A1762T and G1764A) and in the polymerase (rtL180M, rtM204V, rtA222T and rtL336V), core (cP5T, cS26A, cV85I and cP135A), surface (sI195M and sM213I) and X (xK95Q, xN118T, xK130M and xV131I) proteins. 2003 Journal of clinical virology Abstract HBV L180M;M204V;A222T;L336V;P5T;S26A;V85I;P135A;I195M;M213I;K95Q;N118T;K130M;V131I;A1762T;G1764A 270;279;288;300;314;320;327;337;355;366;381;388;396;407;226;237 275;284;293;305;318;325;332;343;361;372;386;394;402;413;232;243 BCP;C;C;C;C;C;P;RT;RT;RT;RT;S;S;S;X;X;X;X;X 221;314;320;327;337;308;256;268;277;286;298;355;366;346;378;381;388;396;407 224;315;321;328;338;312;266;270;279;288;300;356;367;353;379;382;389;397;408 Liver disease 146 161 12740387 Central role of a serine phosphorylation site within duck hepatitis B virus core protein for capsid trafficking and genome release. Finally, wild-type and S245D but not S245N virions were infectious in primary duck hepatocytes. 2003 The Journal of biological chemistry Abstract HBV S245D;S245N 23;37 28;42 12740387 Central role of a serine phosphorylation site within duck hepatitis B virus core protein for capsid trafficking and genome release. The potential key phosphorylation site at serine 245 within the core protein, the building block of DHBV capsids, was substituted by alanine (S245A), aspartic acid (S245D) and asparagine (S245N), respectively. 2003 The Journal of biological chemistry Abstract HBV S245A;S245D;S245N 142;165;188 147;170;193 Capsid;C 105;64 112;68 12740387 Central role of a serine phosphorylation site within duck hepatitis B virus core protein for capsid trafficking and genome release. Wild-type and S245N but not S245A and S245D fully protected capsid-associated mature viral DNA from nuclease action. 2003 The Journal of biological chemistry Abstract HBV S245N;S245A;S245D 14;28;38 19;33;43 Capsid 60 66 12747252 Development of peptide nucleic acid mediated polymerase chain reaction clamping (PMPC)--direct sequencing method for detecting lamivudine-resistant hepatitis B virus (HBV) variants with high sensitivity and specificity. Before treatment, all 4 patients showed HBV with rtM204I encoded by ATA. 2003 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV M204I 51 56 RT 49 51 12747252 Development of peptide nucleic acid mediated polymerase chain reaction clamping (PMPC)--direct sequencing method for detecting lamivudine-resistant hepatitis B virus (HBV) variants with high sensitivity and specificity. During treatment, HBV with the rtM204I(ATT) emerged in the 2 breakthrough patients more than 3 months before the breakthrough, whereas this and other known lamivudine-resistant viruses did not appear in the 2 non-breakthrough patients. 2003 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV M204I 33 38 RT 31 33 12747252 Development of peptide nucleic acid mediated polymerase chain reaction clamping (PMPC)--direct sequencing method for detecting lamivudine-resistant hepatitis B virus (HBV) variants with high sensitivity and specificity. Two of these exhibited a break-through of the HBV mutant with rtM204I(ATT), while the other 2 did not. 2003 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV M204I 64 69 RT 62 64 12747252 Development of peptide nucleic acid mediated polymerase chain reaction clamping (PMPC)--direct sequencing method for detecting lamivudine-resistant hepatitis B virus (HBV) variants with high sensitivity and specificity. We first tested this method for its sensitivity and specificity in detecting a mutant on HBV DNA standards consisting of serial copy number ratios of a known lamivudine-resistant, mutant clone with rtM204I(ATT) to a wild-type clone with rtM204(ATG). 2003 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV M204I 200 205 RT;RT 198;237 200;239 12759956 [Dynamic changes of basal core promoter and pre-core mutants of hepatitis B virus in patients with chronic hepatitis B virus infection]. Using two mis-matched primers to amplify BCP and pre-c gene fragments, in combination with restricted fragment length polymorphism assay, we studied the presence of these two mutants(nt 1762A-->T, 1764G-->A and nt1896G-->A) in 105 serum samples. 1999 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A1762T;G1764A;G1896A 186;197;213 195;206;222 BCP;Precore 41;49 44;54 12759982 [A mutation specific polymerase chain reaction for detecting hepatitis B virus genome with A-to-C mutation at nt585]. It was shown that HBV mutants with A-to-C mutation at nt585 could be confirmed. 1999 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A585C 35 59 12759982 [A mutation specific polymerase chain reaction for detecting hepatitis B virus genome with A-to-C mutation at nt585]. METHODS: A mutation specific polymerase chain reaction (msPCR) was established for amplifying HBV DNAs with A-to-C mutation at nt585. 1999 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A585C 108 132 12760870 Generation of stable cell lines expressing Lamivudine-resistant hepatitis B virus for antiviral-compound screening. HBV produced by these cell lines was shown to have a marked decrease in sensitivity to lamivudine, with 450- and 3,000-fold shifts in the 50% inhibitory concentrations for the rtM204I and rtL180M/M204V viruses, respectively, compared to that for the wild-type virus. 2003 Antimicrobial agents and chemotherapy Abstract HBV M204V;M204I;L180M 196;178;190 201;183;195 RT;RT 176;188 178;190 12760870 Generation of stable cell lines expressing Lamivudine-resistant hepatitis B virus for antiviral-compound screening. Replication-competent HBV constructs containing the reverse transcriptase domain L180M/M204V and M204I (rtL180M/M204V and rtM204I) mutations associated with lamivudine resistance were used to produce stable cell lines that express the resistant virus. 2003 Antimicrobial agents and chemotherapy Abstract HBV M204V;M204V;L180M;L180M;M204I;M204I 87;112;81;106;124;97 92;117;86;111;129;102 RT;RT;RT 52;104;122 73;106;124 12767980 Genome replication, virion secretion, and e antigen expression of naturally occurring hepatitis B virus core promoter mutants. A much higher replication capacity was reported for a naturally occurring core promoter mutant implicated in the outbreak of fulminant hepatitis, which was caused by the neighboring C1766T/T1768A mutations instead. 2003 Journal of virology Abstract HBV T1768A;C1766T 189;182 195;188 Core promoter 74 87 Fulminant Hepatitis B 125 144 12767980 Genome replication, virion secretion, and e antigen expression of naturally occurring hepatitis B virus core promoter mutants. All had 1762/1764 mutations and an additional substitution at position 1753 (T to C), at position 1766 (C to T), or both. 2003 Journal of virology Abstract HBV T1753C;C1766T 71;98 84;111 12767980 Genome replication, virion secretion, and e antigen expression of naturally occurring hepatitis B virus core promoter mutants. The core promoter mutants of hepatitis B virus (HBV) emerge as the dominant viral population at the late HBeAg and the anti-HBe stages of HBV infection, with the A1762T/G1764A substitutions as the hotspot mutations. 2003 Journal of virology Abstract HBV G1764A;A1762T 169;162 175;168 Core promoter;C;C 4;124;105 17;127;110 HBV infections 138 151 12780567 Characterization of hepatitis B virus surface antigen and polymerase mutations in liver transplant recipients pre- and post-transplant. All three patients with hepatitis B immune globulin (HBIG) treatment failure followed by nucleoside analogue treatment failure were infected with HBV genotype C; a pre-existing HBV S antigen (HBsAg) mutation (sD144A) was identified in one patient pretransplant, while sG145R mutations emerged in the other two patients post-transplant. 2003 American journal of transplantation Abstract HBV D144A;G145R 209;268 215;274 S;S;S;S 192;181;209;268 197;182;210;269 12780567 Characterization of hepatitis B virus surface antigen and polymerase mutations in liver transplant recipients pre- and post-transplant. Significant viral polymerase mutations (rtL180M and rtM204I/V) also emerged in all of these patients following treatment with lamivudine and/or famciclovir. 2003 American journal of transplantation Abstract HBV L180M;M204I;M204V 42;54;54 47;61;61 RT;RT;P 40;52;18 42;54;28 12794713 Molecular epidemiology and transmission of hepatitis B virus in close family contacts of HBV-related chronic liver disease patients. G1896A mutation was found in 7 of 11 (64%) specimens changing amino acid tryptophane (W) to stop codon. 2003 Journal of medical virology Abstract HBV G1896A 0 6 12794713 Molecular epidemiology and transmission of hepatitis B virus in close family contacts of HBV-related chronic liver disease patients. T143M and G145R mutations in the second loop of the "a" determinant were found in 9% of the specimens. 2003 Journal of medical virology Abstract HBV T143M;G145R 0;10 5;15 12794713 Molecular epidemiology and transmission of hepatitis B virus in close family contacts of HBV-related chronic liver disease patients. The commonest S-gene mutations were T118V and A128V, present in 44 and 38% specimens, respectively. 2003 Journal of medical virology Abstract HBV T118V;A128V 36;46 41;51 S 14 15 12794713 Molecular epidemiology and transmission of hepatitis B virus in close family contacts of HBV-related chronic liver disease patients. The results of the study, demonstrate (1) clustering of Pre-C and S-gene mutations in the families, (2) horizontal mode of transmission and a common source infection appears to be frequent as evidenced by sequence homology and detailed history, (3) T118V and A128V were the commonest mutations in the S-gene region, while (4) M2 (G1896A) was the commonest pre-C gene mutation, and (5) long-term follow-up evaluation of these mutations suggested. 2003 Journal of medical virology Abstract HBV T118V;A128V;G1896A 249;259;330 254;264;336 Precore;Precore;S;S 56;356;66;301 61;361;67;302 12805468 Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion. Core mutations P5T and I97L were found to be mutually compensatory in offsetting their respective distinct effects on virion secretion. 2003 Journal of virology Abstract HBV I97L;P5T 23;15 27;18 C 0 4 12805468 Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion. Unlike a Tokyo isolate of hepatitis B virus variants, we found a Shanghai isolate that secretes few virions with an immature genome despite its core I97L mutation. 2003 Journal of virology Abstract HBV I97L 149 153 C 144 148 1281839 Loss of the common "A" determinant of hepatitis B surface antigen by a vaccine-induced escape mutant. A substitution of arginine for glycine at amino acid 145 in HBsAg was observed. 1992 The Journal of clinical investigation Abstract HBV G145R 18 56 S 60 65 12823591 YSDD: a novel mutation in HBV DNA polymerase confers clinical resistance to lamivudine. In addition, this new variant had the rtL180M mutation and a 12 base pair deletion in the pre-S1 region between nucleotides 43-54. 2003 Journal of viral hepatitis Abstract HBV L180M 40 45 PreS1;RT 90;38 96;40 12823591 YSDD: a novel mutation in HBV DNA polymerase confers clinical resistance to lamivudine. In conclusion, the results indicate that, in addition to a Met --> Val and Met --> Ile change in YMDD, a Met --> Ser change at rt204 (YMDD --> YSDD) associated with the rtL180M change can also emerge during lamivudine treatment, which confers lamivudine resistance in vivo and in vitro, leading to virological breakthrough and ALT increases. 2003 Journal of viral hepatitis Abstract HBV L180M 171 176 RT;RT;P;P;P 127;169;97;134;143 129;171;101;138;147 12823591 YSDD: a novel mutation in HBV DNA polymerase confers clinical resistance to lamivudine. Of the seven patients, six were HBeAg positive at baseline, and four had a double mutation consisting of rtM204V and rtL180M, while two had an rtM204I change. 2003 Journal of viral hepatitis Abstract HBV M204V;L180M;M204I 107;119;145 112;124;150 C;RT;RT;RT 32;105;117;143 37;107;119;145 12823594 Analysis of clinical, biochemical and viral factors associated with early relapse after lamivudine treatment for hepatitis B e antigen-negative chronic hepatitis B patients in Taiwan. G1896A was predominant in genotype B infected patients (95.2%vs 63.6%, P = 0.037). 2003 Journal of viral hepatitis Abstract HBV G1896A 0 6 12823594 Analysis of clinical, biochemical and viral factors associated with early relapse after lamivudine treatment for hepatitis B e antigen-negative chronic hepatitis B patients in Taiwan. Precore (G1896A) and basic core promoter (BCP, A1762T & G1764A) mutations were determined by PCR and direct sequencing. 2003 Journal of viral hepatitis Abstract HBV G1896A;A1762T;G1764A 9;47;56 15;53;62 BCP;BCP;Precore 21;42;0 40;45;7 12829991 Week 48 resistance surveillance in two phase 3 clinical studies of adefovir dipivoxil for chronic hepatitis B. Four substitutions (rtS119A, rtH133L, rtV214A, and rtH234Q) developed once each at conserved sites in HBV polymerase in 4 ADV-treated patients. 2003 Hepatology (Baltimore, Md.) Abstract HBV S119A;H133L;V214A;H234Q 22;31;40;53 27;36;45;58 P;RT;RT;RT;RT 106;20;29;38;51 116;22;31;40;53 12837218 [Clinical study of oligonucleotide microarray on monitoring the lamivudine-resistance mutations in hepatitis B virus]. The most common mutated type was M539V+L515M and next M539I. 2003 Zhonghua gan zang bing za zhi Abstract HBV M539V;L515M;M539I 33;39;54 38;44;59 12853747 Prevalence and characterization of lamivudine-resistant hepatitis B virus mutations in HIV-HBV co-infected individuals. Unique mutations were detected in HBV polymerase, including rtV173L plus rtL180M plus rtM204V, which occurred in three patients. 2003 AIDS (London, England) Abstract HBV V173L;L180M;M204V 62;75;88 67;80;93 P;RT;RT;RT 38;60;73;86 48;62;75;88 12854154 A novel stop codon mutation in HBsAg gene identified in a hepatitis B virus strain associated with cryptogenic cirrhosis. Sequencing of the HBsAg gene clones revealed a unique point mutation at nucleotide 336 (C to A), which resulted in a novel stop codon at aa 61. 2003 World journal of gastroenterology Abstract HBV C336A 83 95 S 18 23 12858404 Mutations within the hepatitis B virus genome among chronic hepatitis B patients with hepatocellular carcinoma. A high proportion (69%) also had mutations at position 1762 (A --> T) and/or 1764 (G --> A) in the core promoter region, but the proportion of core promoter mutations was no different from what was found in a control group of HBV carriers without HCC (68%). 2003 Journal of medical virology Abstract HBV A1762T;G1764A 55;77 69;91 Core promoter;Core promoter 99;143 112;156 Hepatocellular carcinoma 247 250 12867638 The T(1858) variant predisposing to the precore stop mutation correlates with one of two major genotype F hepatitis B virus clades. The precore mutation G(1896)-->A occurs frequently in anti-HBe-positive carriers of HBsAg with T(1858) in the stem of the encapsidation signal. 2003 The Journal of general virology Abstract HBV G1896A 20 33 C;S;Precore 59;84;4 62;89;11 12870011 [Analysis of three lamivudine-resistant HBV mutants with the method of restriction enzyme digestion and its application]. Six of them were infected with M5501 mutant; five were infected with M550V mutant (one of them had both M550V and L526M mutations). 2003 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV M550V;M550V;L526M 69;104;114 74;109;119 12885906 Endocytosis of hepatitis B immune globulin into hepatocytes inhibits the secretion of hepatitis B virus surface antigen and virions. The specificity of intracellular HBsAg- anti-HBs interaction was further investigated in cells transfected with HBV genomes expressing wild-type HBsAg or immune escape HBsAg (with a G145R mutation). 2003 Journal of virology Abstract HBV G145R 182 187 S;S;S;S 45;33;145;168 48;38;150;173 12891527 Resistance to adefovir dipivoxil therapy associated with the selection of a novel mutation in the HBV polymerase. In vitro testing of a laboratory strain encoding the rtN236T mutation and testing of patient-derived virus confirmed that the rtN236T substitution caused a marked reduction in susceptibility to adefovir. 2003 Gastroenterology Abstract HBV N236T;N236T 55;128 60;133 RT;RT 53;126 55;128 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. CD-PCR could detect one copy of G1896A variant among 10-100 copies of wild-type plasmid DNA. 2003 World journal of gastroenterology Abstract HBV G1896A 32 38 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. CD-PCR was evaluated by detecting G1896A variant of hepatitis B virus (HBV) in form of recombinant plasmids and in sera from patients with hepatitis B, and compared with allele-specific PCR (AS-PCR) and competitive AS-PCR. 2003 World journal of gastroenterology Abstract HBV G1896A 34 40 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. HBV G1896A or other more important mutations have to be routinely detected in patients with a detectable level of viremia after HBeAg/antibody conversion in clinical practice. 2003 World journal of gastroenterology Abstract HBV G1896A 4 10 C 128 133 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. HBV G1896A variant was more often found in HBeAg (-) patients with a lower level of detectable viremia than that with a higher level of detectable viremia (P=0.0192). 2003 World journal of gastroenterology Abstract HBV G1896A 4 10 C 43 48 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. It could clearly distinguish wild-type and mutant-type plasmid DNA of G1896A variant when the amount of plasmid DNA was between 10(2)-10(8)copies/reaction, while for AS-PCR and competitive AS-PCR, the DNA amount was between 10(2)-10(4)copies/reaction. 2003 World journal of gastroenterology Abstract HBV G1896A 70 76 12918112 Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus. The specificity of CD-PCR was higher than those of AS-PCR and competitive AS-PCR in the detection of HBV G1896A variant in sera from patients with hepatitis B. 2003 World journal of gastroenterology Abstract HBV G1896A 105 111 12931030 Low HBeAg serum levels correlate with the presence of the double A1762T/G1764A core promoter mutation and a positive response to interferon in patients with chronic hepatitis B virus infection. Five of 6 responders (83%) and none of the nonresponders had the A1762T/G1764A CP mutations (0/8, p < 0.003). 2003 Intervirology Abstract HBV G1764A;A1762T 72;65 78;71 Core promoter 79 81 12939180 [Core promoter mutations of HBV isolated from patients with chronic hepatitis B in Guangxi]. A --> G at nt1752 (resulting in isoleucine to valine) was seen in 37.1% (13/35) of the HBV DNA positive patients, and T --> C at nt1753 was seen in 20% (7/35). 2003 Zhonghua gan zang bing za zhi Abstract HBV T1753C 118 135 12939180 [Core promoter mutations of HBV isolated from patients with chronic hepatitis B in Guangxi]. The next was C --> G at nt1799, counting for 54.4% (19/35), but this was no function. 2003 Zhonghua gan zang bing za zhi Abstract HBV C1799G 13 30 12939588 Prevalence of HBV precore/core promoter variants in the United States. Variants in the precore (G(1896)A) and core promoter (A(1762)T, G(1764)A) regions of hepatitis B virus (HBV) may be related to serum HBV DNA levels and severity of liver disease. 2003 Hepatology (Baltimore, Md.) Abstract HBV G1896A;A1762T;G1764A 25;54;64 34;61;73 Core promoter;Precore 39;16 52;23 Liver disease 164 177 12962435 Frequency of infection by hepatitis B virus and its surface mutants in a northern Indian population. None had the G587A mutation, which is known to be associated with loss of the 'a' determinant of HBsAg. 2003 Indian journal of gastroenterology Abstract HBV G587A 13 18 S;S 79;97 93;102 12966541 Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy. Our study suggests that mutations in the HBsAg (D144E) and the polymerase (L426I/L526M/M550I) of HBV genome may be responsible for viral breakthrough despite HBIG prophylaxis and lamivudine therapy. 2003 Journal of medical virology Abstract HBV L526M;M550I;L426I;D144E 81;87;75;48 86;92;80;53 S;P 41;63 46;73 12966541 Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy. Sequence analysis of full-length viral genome before transplantation revealed many point mutations as compared with a wild-type genotype C sequence, including the T1753G/A1762T/G1764A triple mutation in the basal core promoter and the G1896A nonsense mutation in the precore region. 2003 Journal of medical virology Abstract HBV A1762T;G1764A;T1753G;G1896A 170;177;163;235 176;183;169;241 BCP;Precore 207;267 226;274 12966541 Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy. These mutations caused L426I/L526M/M550I triple mutation (equivalent to L428I/L528M/M552I in previous reports) in the polymerase, and D144E mutation in the "a" determinant of HBsAg. 2003 Journal of medical virology Abstract HBV L526M;M550I;L528M;M552I;L428I;L426I;D144E 29;35;78;84;72;23;134 34;40;83;89;77;28;139 S;P 175;118 180;128 12966541 Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy. Transfection experiments revealed that the D144E mutation reduced HBsAg affinity to anti-HBs, confirming its active role for immune escape. 2003 Journal of medical virology Abstract HBV D144E 43 48 S;S 89;66 92;71 12974898 Identification of a novel pre-S2 mutation in a subgroup of chronic carriers with spontaneous clearance of hepatitis B virus surface antigen. RESULTS: A novel pre-S2 mutation, G149R, was found in nine (group I) but not in 17 (group II) patients carrying HBV DNA with intact pre-S/S reading frames. 2003 Journal of gastroenterology and hepatology Abstract HBV G149R 34 39 PreS;S;PreS2 132;138;17 137;139;23 12974898 Identification of a novel pre-S2 mutation in a subgroup of chronic carriers with spontaneous clearance of hepatitis B virus surface antigen. Site-directed mutagenesis experiments showed that secretion of HBsAg was not defective in the pre-S2 G149R mutant. 2003 Journal of gastroenterology and hepatology Abstract HBV G149R 101 106 S;PreS2 63;94 68;100 1309904 Naturally occurring point mutation in the C terminus of the polymerase gene prevents duck hepatitis B virus RNA packaging. Using genetic approaches, it was determined that a change of cysteine to tyrosine in position 711 in the polymerase (P) gene C terminus led to this RNA-packaging defect. 1992 Journal of virology Abstract HBV C711Y 61 97 P;P 117;105 118;115 14552712 [Relationship between the HBV core gene mutation and the cellular immunity in host]. OBJECTIVES: To study the relationship between the mutation of Leu60Val in HBV core region and the cellular immunity in patients with chronic hepatitis B (CHB). 2003 Zhonghua gan zang bing za zhi Abstract HBV L60V 62 70 C 78 82 Chronic Hepatitis B;Chronic Hepatitis B 133;154 152;157 14552712 [Relationship between the HBV core gene mutation and the cellular immunity in host]. RESULTS: The mutation of Leu60Val was found in 19 out of the 91 CHB patients. 2003 Zhonghua gan zang bing za zhi Abstract HBV L60V 25 33 Chronic Hepatitis B 64 67 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. A second mutation, rtL180M, was previously reported to partially restore replication fitness as well as to augment drug resistance in vitro. 2003 Journal of virology Abstract HBV L180M 21 26 RT 19 21 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. Genotypic changes in the YMDD motif (reverse transcriptase [rt] mutations rtM204V/I) conferred resistance to lamivudine as well as reducing the in vitro replication efficiency of HBV. 2003 Journal of virology Abstract HBV M204V;M204I 76;76 83;83 RT;RT;RT;YMDD 60;74;37;25 62;76;58;29 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. Here we report the functional characterization of a third polymerase mutation (rtV173L) associated with resistance to lamivudine and famciclovir. 2003 Journal of virology Abstract HBV V173L 81 86 RT;P 79;58 81;68 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. In these patients, rtV173L was invariably found as a third mutation in conjunction with rtL180M and rtM204V. 2003 Journal of virology Abstract HBV V173L;L180M;M204V 21;90;102 26;95;107 RT;RT;RT 19;88;100 21;90;102 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. In vitro analyses indicated that rtV173L did not alter the sensitivity of wild-type or lamivudine-resistant HBV to lamivudine, penciclovir, or adefovir but instead enhanced viral replication efficiency. 2003 Journal of virology Abstract HBV V173L 35 40 RT 33 35 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. rtV173L was observed at baseline in 9 to 22% of patients who entered clinical trials of adefovir dipivoxil for the treatment of lamivudine-resistant HBV. 2003 Journal of virology Abstract HBV V173L 2 7 RT 0 2 14557667 The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. Together, these results suggest that rtV173L is a compensatory mutation that is selected in lamivudine-resistant patients due to an enhanced replication phenotype. 2003 Journal of virology Abstract HBV V173L 39 44 RT 37 39 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. Furthermore, cotransfection studies were performed with the G145R variant and a Wt virus S-protein expressing construct and vice versa. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 60 65 S 89 90 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. Hepatitis B virus with a G145R mutation in the small surface protein is considered the quintessential immune escape mutant because it frequently is found in vaccinated individuals with breakthrough infections and liver transplant recipients under anti-hepatitis B surface antigen (HBsAg) immunoglobulin prophylaxis. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 25 30 Small S;S;S 47;281;264 60;286;271 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. However, because spread of a virus depends not only on immune pressure but also on the viral phenotype, we investigated the biologic properties of the G145R variant. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 151 156 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. In conclusion, the significant defect of the G145R mutant for secretion of infectious virions and the diminished stability of mutant virions may limit global spread of the mutant. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 45 50 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. Only 20% of virions were found in the medium of G145R variant-transfected cells compared with Wt virus. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 48 53 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. Production and stability of viral messenger RNAs (mRNAs), DNA, and proteins were not affected by the G145R mutation. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 101 106 14578867 Deficiency in virion secretion and decreased stability of the hepatitis B virus immune escape mutant G145R. The G145R mutation was introduced into wild-type (Wt) virus genome by in vitro mutagenesis. 2003 Hepatology (Baltimore, Md.) Abstract HBV G145R 4 9 14614604 An outbreak of fulminant hepatitis B in immunocompromised hemodialysis patients. RESULTS: All five patients had hepatitis B surface antigen (HBsAg) genotype C, a G-to-A stop codon mutation at nucleotide (nt) 1896 in the precore region, an A-to-T mutation at nt 1762 and an G-to-A mutation at nt 1764 in the basal core promoter. 2003 Journal of gastroenterology Abstract HBV G1896A;A1762T;G1764A 80;158;192 132;184;218 BCP;S;Precore;S 226;60;139;43 245;65;146;50 14618083 The 113th and 117th charged amino acids in the 5th alpha-helix of the HBV core protein are necessary for pgRNA encapsidation. First, endogenous polymerase activity (EPA) was assayed and activity was not detected only in the two mutants, E113K and E117K. 2003 Virus genes Abstract HBV E113K;E117K 111;121 116;126 14638401 Mutations of the surface protein of hepatitis B virus. The G145R mutant is replication competent and is stable, and it appears to be the most common variant. 2003 Antiviral research Abstract HBV G145R 4 9 14642631 Selection of a hepatitis B virus strain resistant to adefovir in a liver transplantation patient. RESULTS: Sequence analyses of the HBV polymerase gene revealed a sequential selection of lamivudine resistance mutations L180M+M204V, followed by a reversion to wild-type, and subsequently the selection of a novel adefovir resistance mutation N236T. 2003 Journal of hepatology Abstract HBV L180M;M204V;N236T 121;127;243 126;132;248 P 38 48 14642631 Selection of a hepatitis B virus strain resistant to adefovir in a liver transplantation patient. The selection of the N236T polymerase mutant was associated with resistance to ADV but remained sensitive to lamivudine in vitro and in vivo. 2003 Journal of hepatology Abstract HBV N236T 21 26 P 27 37 14645551 Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins. Instead of displaying the wild-type selective export of virions containing mature genomes, human hepatitis B virus (HBV) mutant I97L, changing from an isoleucine to a leucine at amino acid 97 of HBV core antigen (HBcAg), lost the high stringency of selectivity in genome maturity during virion export. 2003 Journal of virology Abstract HBV I97L;I97L 128;151 132;191 C;C 199;213 203;218 14645551 Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins. No difference in the ratio between T=3 (78%) and T=4 particles (20.3%) are found between wild-type HBV and mutant I97L in the context of HBcAg1-140. 2003 Journal of virology Abstract HBV I97L 114 118 C 137 142 14645551 Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins. To understand the structural basis of this so-called "immature secretion" phenomenon, we compared the stability and morphology of self-assembled capsid particles from the wild-type and mutant I97L HBV, in either full-length (HBcAg1-183) or truncated core protein contexts (HBcAg1-149 and HBcAg1-140). 2003 Journal of virology Abstract HBV I97L 192 196 Capsid;C;C;C;C 145;250;225;273;288 151;254;230;278;293 14645551 Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins. We found no significant differences in capsid stability between wild-type and mutant I97L particles under denaturing pH and temperature in either full-length or truncated core protein contexts. 2003 Journal of virology Abstract HBV I97L 85 89 C;Capsid 171;39 175;45 14654974 Early response to interferon alpha treatment and long-term clinical outcome in Japanese patients with chronic HBV genotype C infection. 92%) and a higher frequency of core promoter mutation (A1762T/G1764A). 2004 International journal of molecular medicine Abstract HBV G1764A;A1762T 62;55 68;61 Core promoter 31 44 14654974 Early response to interferon alpha treatment and long-term clinical outcome in Japanese patients with chronic HBV genotype C infection. Although not significant, responders tended to have younger age, a higher serum transaminase level, a lower frequency of precore mutation (G1896A) (67% vs. 2004 International journal of molecular medicine Abstract HBV G1896A 139 145 Precore 121 128 14675262 Evolution of wild type and mutants of the YMDD motif of hepatitis B virus polymerase during lamivudine therapy. M552I was detected before therapy in one patient but M552V became the domain strain after therapy. 2003 Journal of gastroenterology and hepatology Abstract HBV M552I;M552V 0;53 5;58 14675262 Evolution of wild type and mutants of the YMDD motif of hepatitis B virus polymerase during lamivudine therapy. The replication ability of the M552V mutant strain might be stronger than that of the M552I mutant strain. 2003 Journal of gastroenterology and hepatology Abstract HBV M552V;M552I 31;86 36;91 14688448 Classifying hepatitis B virus genotypes. The mutation for a stop codon in the precore region (G1896A) for aborting the translation of hepatitis B e antigen (HBeAg) is prohibited in HBV genomes of genotype A, as well as some of genotypes C and F, because they possess C at position 1858 that makes a Watson-Crick pair with G at position 1896. 2003 Intervirology Abstract HBV G1896A 53 59 C;C;Precore 105;116;37 114;121;44 14688451 Subclones of drug-resistant hepatitis B virus mutants and the outcome of breakthrough hepatitis in patients treated with lamivudine. Major HBV mutants during breakthrough hepatitis were those with M552I in the YMDD motif of viral DNA polymerase/reverse transcriptase in 7 patients (54%), M552I/L528M in 4 patients (31%) and M552V/L528M in 2 patients (15%). 2003 Intervirology Abstract HBV L528M;L528M;M552I;M552V;M552I 161;197;64;191;155 166;202;69;196;160 P;RT;P 101;112;77 111;133;81 Fulminant Hepatitis B 25 47 14712514 [Sequence detection of HBV-DNA P and C region in HIV/HBV superinfection subjects with drug resistance to HAART]. It's HBV-DNA C region sequence had mutation on 2 sites (nt 2412 T/C; nt 2413 T/C) and 1 mutation P region (nt 741 A/G, also YMDD/YVDD) compared with HBV international Genbak reference sequence. 2003 Zhejiang da xue xue bao. Yi xue ban Abstract HBV T2412C;T2413C;A741G 59;72;110 67;80;117 P;P;P 97;124;129 98;128;133 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. Because HBV DNA synthesis occurs in the nucleocapsid, we examined the kinetics of the reverse transcriptase activity from wild-type (wt) and mutated DPs with the wt or G1896A-mutated RNA template in the nucleocapsid. 2004 Molecular pharmacology Abstract HBV G1896A 168 174 RT 86 107 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The additional L526M mutation increased the efficiency of the M550V-mutated DP but no more than that of the L526M-mutated DP. 2004 Molecular pharmacology Abstract HBV L526M;M550V;L526M 15;62;108 20;67;113 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The e antigen-negative variant of HBV associated with the G1896A mutation in the precore region has a high prevalence. 2004 Molecular pharmacology Abstract HBV G1896A 58 64 Precore;C 81;4 88;13 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The G1896A mutation had impacts on the interactions between different DPs and deoxy-NTPs, except dCTP. 2004 Molecular pharmacology Abstract HBV G1896A 4 10 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The L526M and M550V mutations caused a greater decrease in the Vmax using the wt RNA template compared with the G1896A-mutated template. 2004 Molecular pharmacology Abstract HBV L526M;M550V;G1896A 4;14;112 9;19;117 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The L526M, M550V, and L526M/M550V mutations caused varying degrees of resistance to the different M-nucleoside triphosphates. 2004 Molecular pharmacology Abstract HBV M550V;L526M;L526M;M550V 28;22;4;11 33;27;9;16 14742682 Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates. The use of L(-)SddC [beta-L-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC)] for the treatment of Herpes B virus (HBV) infection is hindered by the emergence of drug-resistance associated with the L526M, L550V, and L526M/M550V mutations of the viral DNA polymerase (DP). 2004 Molecular pharmacology Abstract HBV M550V;L526M;L550V;L526M 221;215;204;197 226;220;209;202 P 254 264 HBV infections 98 128 14748061 Clade analysis and surface antigen polymorphism of hepatitis B virus American genotypes. One isolate obtained from a blood donor could not be classified in any clade and harbored amino acid substitutions characteristic of a vaccine escape mutant (G145R) and a stop codon in the surface antigen. 2004 Journal of medical virology Abstract HBV G145R 158 163 S 189 196 14752824 Identification of HBV DNA sequences that are predictive of response to lamivudine therapy. Reversions of precore mutations A1762T/G1764A and G1896A were observed in 29% and 25% of patients, respectively, but none became HBeAg-positive. 2004 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;G1896A 39;32;50 45;38;56 C;Precore 129;14 134;21 14756274 Efficacy of combined lamivudine and adefovir dipivoxil treatment for severe HBV graft reinfection after living donor liver transplantation. Hepatitis B virus sequence analysis revealed several mutations in the polymerase gene (L528M, M552I, M552V) as well as in the surface gene region encoding the immunogenic major hydrophilic loop of the small surface protein (G130N, M133T, D144G). 2003 Clinical transplantation Abstract HBV L528M;M552I;M552V;G130N;M133T;D144G 87;94;101;224;231;238 92;99;106;229;236;243 P;S;S 70;201;126 80;214;133 14760897 Monitoring the emergence of hepatitis B virus polymerase gene variants during lamivudine therapy in human immunodeficiency virus coinfected patients: performance of CLIP sequencing and line probe assay. Interestingly, TRUGENE sequencing identified on late samples from three patients a variant carrying rtV173L plus rtL180M plus M204V mutations, having the in vitro characteristics of 'vaccine escape' mutants. 2003 Antiviral therapy Abstract HBV V173L;L180M;M204V 102;115;126 107;120;131 RT;RT 100;113 102;115 14968937 Mechanism of antiviral activities of 3'-substituted L-nucleosides against 3TC-resistant HBV polymerase: a molecular modelling approach. Analysis of the minimized structure of rtM204V HBV polymerase/3TCTP complex shows that, instead of the steric stress produced by rtV204, a loss of the van der Waals contact around the oxathiolane sugar moiety of 3TCTP caused by the mutation results in the disruption of the active site. 2003 Antiviral chemistry & chemotherapy Abstract HBV M204V 41 46 P;RT;RT 51;39;129 61;41;131 14968937 Mechanism of antiviral activities of 3'-substituted L-nucleosides against 3TC-resistant HBV polymerase: a molecular modelling approach. As an example, our study shows that the 3'-fluorine atom contributes to the antiviral activity of L-3'-Fd4CTP against rtM204V HBV polymerase by readily compensating for the loss of the van der Waals interaction around the 2',3'-double bond through a formation of a hydrogen bond to the amide backbone of rtD205. 2003 Antiviral chemistry & chemotherapy Abstract HBV M204V 120 125 P;RT;RT 130;118;304 140;120;306 14981758 Identification of rare polymerase variants of hepatitis B virus using a two-stage PCR with peptide nucleic acid clamping. This variant did not have the L528M mutation, which is often associated with YVDD variants, and lamivudine therapy in this patient suppressed HBV replication. 2004 Journal of medical virology Abstract HBV L528M 30 35 P 77 81 14987532 Detection of hepatitis B virus variants resistant to lamivudine and famciclovir among randomly selected chronic carriers from Spain. Wild-type strains together with either the rtM204I (M552I) or rtV207I (V555I) point mutation were found in two of these cases, and the rtV207I mutation alone was detected in the third. 2004 Enfermedades infecciosas y microbiologia clinica Abstract HBV M204I;V207I;V207I;M552I;V555I 45;64;137;52;71 50;69;142;57;76 RT;RT;RT 43;62;135 45;64;137 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. A T552C point mutation in the 4B genome was responsible for its enhanced virion secretion, whereas a G510A mutation in 3.4 and G660C in 4C impaired virus secretion. 2004 Journal of virology Abstract HBV T552C;G510A;G660C 2;101;127 7;106;132 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. However, its inhibitory effect was suppressed in the 4B genome by the T552C mutation, the enhancer of virion secretion. 2004 Journal of virology Abstract HBV T552C 70 75 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. Of the two mutations inhibitory of virion secretion, G510A greatly reduced small envelope protein (hepatitis B surface antigen [HBsAg]) levels both inside cells and in culture medium, whereas G660C specifically abolished HBsAg secretion. 2004 Journal of virology Abstract HBV G510A;G660C 53;192 58;197 S;S;S;S 128;221;75;111 133;226;89;118 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. Surprisingly, a T484G mutation in the 4B genome, generating an I110M substitution in the S domain, could also reduce HBsAg secretion and block virion secretion. 2004 Journal of virology Abstract HBV T484G;I110M 16;63 21;68 S;S 117;89 122;90 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. T552C can also override the inhibitory G510A mutation, but not the G660C mutation. 2004 Journal of virology Abstract HBV T552C;G510A;G660C 0;39;67 5;44;72 15016847 Modulation of hepatitis B virus secretion by naturally occurring mutations in the S gene. The three point mutations generate M133T, G119E, and R169P substitutions in the S domains of viral envelope proteins, respectively, without modifying the coding capacity of the overlapping polymerase gene. 2004 Journal of virology Abstract HBV M133T;G119E;R169P 35;42;53 40;47;58 S;P;S 99;189;80 107;199;81 15039524 Epidemiological and sequence differences between two subtypes (Ae and Aa) of hepatitis B virus genotype A. In the pregenome encapsidation (epsilon) signal, a point mutation from G to A or T at nt 1862 was detected in 16 of the 19 (84 %) HBV/Aa isolates but not in any of the 20 HBV/Ae isolates, which may affect virus replication and translation of hepatitis B e antigen. 2004 The Journal of general virology Abstract HBV G1862A;G1862T 71;71 93;93 C 254 263 15048802 Fibrosing cholestatic hepatitis secondary to precore/core promoter hepatitis B variant with lamivudine resistance: successful retransplantation with combination adefovir dipivoxil and hepatitis B immunoglobulin. Analysis of gene sequence variation by polymerase chain reaction (PCR) and direct sequencing showed that both had a core promoter variant A1762T/G1764A and 1 had a concomitant precore stop codon G1896A variant in prelamivudine and postrecurrence serum samples. 2004 Liver transplantation Abstract HBV G1764A;A1762T;G1896A 145;138;195 151;144;201 Core promoter;Precore 116;176 129;183 15048802 Fibrosing cholestatic hepatitis secondary to precore/core promoter hepatitis B variant with lamivudine resistance: successful retransplantation with combination adefovir dipivoxil and hepatitis B immunoglobulin. Comparison of the HBV polymerase gene in the 2 serum samples revealed a single mutation with methionine-to-isoleucine substitution at codon 552 (M552I) in both patients. 2004 Liver transplantation Abstract HBV M552I;M552I 93;145 143;150 P 22 32 15059411 [Emergence and clinical significance of YMDD and HBeAg-related mutations during lamivudine treatment]. 3 of the 8 patients had G1896A mutant, 2 had A1814C and the remaining had G1896A + A1814C, A1762T and G1764A, A1762T and G1764A + G1896A. 2004 Zhonghua nei ke za zhi Abstract HBV G1896A;A1814C;G1896A;A1814C;A1762T;G1764A;A1762T;G1764A;G1896A 24;45;74;83;91;102;110;121;130 30;51;80;89;97;108;116;127;136 15059411 [Emergence and clinical significance of YMDD and HBeAg-related mutations during lamivudine treatment]. METHODS: From sera of chronic hepatitis B patients with 9 - 30 months lamivudine therapy, signal-base mutations of YMDD motif, G1896A, A1814C, A1762T and G1764A were analyzed by gene chips technique. 2004 Zhonghua nei ke za zhi Abstract HBV G1896A;A1814C;A1762T;G1764A 127;135;143;154 133;141;149;160 P 115 119 Chronic Hepatitis B 22 41 15074469 Evaluation of sensitivity for wild type and mutant forms of hepatitis B surface antigen by four commercial HBsAg assays. It is noteworthy that the most frequently reported HBsAg mutation, G145 R, remained undetected in three of the assays tested. 2004 Clinical laboratory Abstract HBV G145R 67 73 S 51 56 15078472 Sequential combination therapy of HBe antigen-negative/virus-DNA-positive chronic hepatitis B with famciclovir or lamivudine and interferon-alpha-2a. CONCLUSION: Sequential combination therapy can induce sustained virologic response in a subgroup of CHBe-, but most with the G1896A precore mutant HBV relapse. 2004 Liver international Abstract HBV G1896A 125 131 Precore 132 139 15078472 Sequential combination therapy of HBe antigen-negative/virus-DNA-positive chronic hepatitis B with famciclovir or lamivudine and interferon-alpha-2a. Most patients (5/7) with the G1896A mutation relapsed within 4 months after therapy. 2004 Liver international Abstract HBV G1896A 29 35 15078472 Sequential combination therapy of HBe antigen-negative/virus-DNA-positive chronic hepatitis B with famciclovir or lamivudine and interferon-alpha-2a. Only two of them had been infected by HBV with the G1896A mutation. 2004 Liver international Abstract HBV G1896A 51 57 15134177 Comparisons of the HBV and HIV polymerase, and antiviral resistance mutations. Recently, resistance to adefovir has also been described in the D Domain at rtN236T. 2004 Antiviral therapy Abstract HBV N236T 78 83 RT 76 78 15134188 No benefit to continue lamivudine therapy after emergence of YMDD mutations. AIM: To evaluate whether continuing lamivudine therapy after emergence of rt M 204 I/V is appropriate. 2004 Antiviral therapy Abstract HBV M204I;M204V 77;77 86;86 RT 74 76 15134188 No benefit to continue lamivudine therapy after emergence of YMDD mutations. BACKGROUND: Mutations in the sequence of the conserved tyrosine-methionine-aspartate-aspartate (YMDD) locus of the HBV RNA-dependent DNA polymerase (rt M 204 I/V) may develop after 6-9 months of lamivudine therapy. 2004 Antiviral therapy Abstract HBV M204I;M204V 152;152 161;161 P;RT;P;P 137;149;55;96 147;151;94;100 15134188 No benefit to continue lamivudine therapy after emergence of YMDD mutations. CONCLUSION: These results suggest that there is no benefit to continued lamivudine therapy after emergence of rt M 204 I/V. 2004 Antiviral therapy Abstract HBV M204I;M204V 113;113 122;122 RT 110 112 15134188 No benefit to continue lamivudine therapy after emergence of YMDD mutations. In addition, experiments have shown that the defective replication competency of rt M 204 I/V restores upon addition of lamivudine. 2004 Antiviral therapy Abstract HBV M204I;M204V 84;84 93;93 RT 81 83 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. BACKGROUND/AIMS: Detection of hepatitis B virus (HBV) core-promoter A(1762)T-G(1764)A and pre-core G(1896)A mutants has relied on qualitative assays. 2004 Journal of hepatology Abstract HBV A1762T;G1896A;G1764A 67;98;76 78;108;86 Core promoter;Precore 54;90 67;98 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. CONCLUSIONS: The A(1762)T-G(1764)A and G(1896)A mutants existed in a high proportion of patients before and were unaffected after HbeAg seroconversion. 2004 Journal of hepatology Abstract HBV A1762T;G1896A;G1764A 16;38;25 27;48;35 C 130 135 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. Quantity of A(1762)T-G(1764)A mutants was positively correlated with alanine aminotransferase (ALT) (P<0.001) and HBV DNA (P<0.001) levels, both before and after HBeAg seroconversion. 2004 Journal of hepatology Abstract HBV A1762T;G1764A 11;20 22;30 C 162 167 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. Quantity of G(1896)A mutant was negatively correlated with ALT (P=0.044) and HBV DNA (P=0.007) levels. 2004 Journal of hepatology Abstract HBV G1896A 11 21 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. RESULTS: Significant quantities (>20%) of core-promoter A(1762)T-G(1764)A mutant existed in 65% of patients before and after HBeAg seroconversion, and were significantly changed (>20% increase/decrease) in 13% of patients after seroconversion. 2004 Journal of hepatology Abstract HBV A1762T;G1764A 55;64 66;74 Core promoter;C 42;125 55;130 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. Significant quantities of pre-core G(1896)A mutant existed in about 90% of patients before and after HBeAg seroconversion, and were changed in 16% of patients after seroconversion. 2004 Journal of hepatology Abstract HBV G1896A 34 44 C;Precore 101;26 106;34 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. The quantities of A(1762)T-G(1764)A mutant were positively and G(1896)A mutant negatively correlated with liver inflammation and viral replication. 2004 Journal of hepatology Abstract HBV A1762T;G1896A;G1764A 17;62;26 28;72;36 Liver inflammation 106 124 15158343 Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion. We tested the hypothesis that the quantity of A(1762)T-G(1764)A and G(1896)A mutants might have clinical impact, by quantifying these mutants before and after HBe antigen (HBeAg) seroconversion in 58 patients. 2004 Journal of hepatology Abstract HBV A1762T;G1896A;G1764A 45;67;54 56;77;64 C;C 159;172 162;177 15239096 Usefulness of dried blood samples for quantification and molecular characterization of HBV-DNA. The purpose of this study was to assess the use of dried blood spot (DBS) samples for hepatitis B virus (HBV) DNA quantification, HBV genotyping, and detection of G1896A precore mutants and variants in the YMDD polymerase motif. 2004 Hepatology (Baltimore, Md.) Abstract HBV G1896A 163 169 P;Precore;P 211;170;206 221;177;210 15240859 Longitudinal study on mutation profiles of core promoter and precore regions of the hepatitis B virus genome in children. Higher frequency of A1775G and G1799C mutation rates and lower frequency of A1752G mutation rate were found in the seroconverters. 2004 Pediatric research Abstract HBV A1775G;G1799C;A1752G 20;31;76 26;37;82 15256984 Polyarteritis nodosa associated with hepatitis B virus infection. The role of antiviral treatment and mutations in the hepatitis B virus genome. In one patient a stop codon in the pre-core region and a double mutation A1762T-G1764A were found during antiviral therapy. 2004 European journal of gastroenterology & hepatology Abstract HBV A1762T;G1764A 73;80 79;86 Precore 35 43 15259898 In vitro susceptibility of lamivudine-resistant hepatitis B virus to adefovir and tenofovir. Although all patients responded to ADV in this clinical study, the serum HBV reduction was lower in the seven patients with the triple mutation (median -3.3 log copies/ml) compared to the patients who had only the rtL180M/M204V mutations (median -4.1 log copies/ml) at week 48 (P=0.04, Mann-Whitney test). 2004 Antiviral therapy Abstract HBV M204V;L180M 222;216 227;221 RT 214 216 15259898 In vitro susceptibility of lamivudine-resistant hepatitis B virus to adefovir and tenofovir. At the ADV concentration of 0.1 microM, presence of the V173L mutation reduced the inhibition of HBsAg production from 50 to 30% (P<0.01) and the viral replication from 45 to 32% (P<0.01, Mann-Whitney). 2004 Antiviral therapy Abstract HBV V173L 56 61 S 97 102 15259898 In vitro susceptibility of lamivudine-resistant hepatitis B virus to adefovir and tenofovir. For ADV and TDF, comparison of wild-type and lamivudine-resistant HBV IC50 (rtL180M-M204V) showed, respectively, 2.85-fold (from 0.07 to 0.2 microM) and 3.3-fold (from 0.06 to 0.2 microM) increases, indicating a mild decrease of both drug activities, in vitro. 2004 Antiviral therapy Abstract HBV L180M;M204V 78;84 83;89 RT 76 78 15259898 In vitro susceptibility of lamivudine-resistant hepatitis B virus to adefovir and tenofovir. In a clinical study of ADV (Gilead 460i study), seven of the 35 patients carried HBV strains with the triple lamivudine resistance-associated amino-acid changes rtV173L/L180M/M204V at baseline. 2004 Antiviral therapy Abstract HBV L180M;M204V;V173L 169;175;163 174;180;168 RT 161 163 15259898 In vitro susceptibility of lamivudine-resistant hepatitis B virus to adefovir and tenofovir. In our in vitro system, lamivudine IC50 on lamivudine-resistant HBV carrying amino-acid substitutions rtL180M and rtM204V within the polymerase encoding region increased by more than 16,000-fold (from 6 nM to over 100 microM) when compared to wild-type HBV. 2004 Antiviral therapy Abstract HBV L180M;M204V 104;116 109;121 P;RT;RT 133;102;114 143;104;116 15261293 Molecular mechanisms of adefovir sensitivity and resistance in HBV polymerase mutants: a molecular dynamics study. In the case of rtN236T mutant, loss of two hydrogen bonds accompanied by significant decrease in electrostatic interactions is observed, which explains the observed decrease in drug sensitivity and binding affinity of adefovir diphosphate toward the rtN236T mutant HBV polymerase. 2004 Bioorganic & medicinal chemistry letters Abstract HBV N236T;N236T 17;252 22;257 P;RT;RT 269;15;250 279;17;252 15261293 Molecular mechanisms of adefovir sensitivity and resistance in HBV polymerase mutants: a molecular dynamics study. Molecular modeling studies of adefovir diphosphate with the wild type and the mutant HBV polymerase-DNA complex demonstrated that the increase in adefovir sensitivity toward HBV polymerase mutants (rtL180M, rtM204V/I, rtL180M-M204V/I) is a result of increased van der Waals interaction and is supplemented by the decreased affinity of natural substrate toward the mutant HBV polymerase. 2004 Bioorganic & medicinal chemistry letters Abstract HBV M204V;M204I;L180M;M204V;M204I;L180M 226;226;200;209;209;220 233;233;205;216;216;225 P;P;P;RT;RT;RT 89;178;375;198;207;218 99;188;385;200;209;220 15280461 Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants. Resistance to LMV (rtM204I/rtL180M+rtM204V) was accompanied by a reduced replication efficacy as evidenced by reduced pregenomic RNA, encapsidated progeny DNA, polymerase activity, and virion release. 2004 Journal of virology Abstract HBV M204I;M204V;L180M 21;37;29 26;42;34 P;RT;RT;RT 160;19;27;35 170;21;29;37 15280461 Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants. The PC mutation (G1896A+C1858T) creates a translational stop codon resulting in absent HBeAg expression, whereas BCP mutations (A1762T/G1764A) reduce HBeAg expression by transcriptional mechanisms. 2004 Journal of virology Abstract HBV G1764A;G1896A;A1762T;C1858T 135;17;128;24 141;23;134;30 BCP;C;C;Precore 113;87;150;4 116;92;155;6 15280461 Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants. Treatment of chronic HBV infection with lamivudine (LMV) often selects drug-resistant strains with single (rtM204I) or double (rtL180M+rtM204V) point mutations in the YMDD motif of HBV reverse transcriptase. 2004 Journal of virology Abstract HBV M204I;L180M;M204V 109;129;137 114;134;142 RT;RT;RT;RT;YMDD 107;127;135;185;167 109;129;137;206;171 Chronic HBV infection 13 34 15280461 Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants. We cloned replication-competent HBV vectors (genotype A, adw2) combining mutations in the core (wild type [wt], PC, and BCP) and polymerase gene (wt, rtM204I, and rtL180M/M204V) and analyzed virus replication and drug sensitivity in vitro. 2004 Journal of virology Abstract HBV M204V;M204I;L180M 171;152;165 176;157;170 BCP;C;Precore;P;RT;RT 120;90;112;129;150;163 123;94;114;139;152;165 15302140 Suppression of lamivudine-resistant B-domain mutants by adefovir dipivoxil in the woodchuck hepatitis virus model. In the group maintained on lamivudine monotherapy, A566T alone was present in one animal, another carried both A566T and L565V, and in the third, no B-domain mutations were detected. 2004 Antiviral research Abstract HBV A566T;A566T;L565V 51;111;121 56;116;126 15302140 Suppression of lamivudine-resistant B-domain mutants by adefovir dipivoxil in the woodchuck hepatitis virus model. In woodchucks treated with adefovir dipivoxil, two had the A566T mutation, and one had both A566T and L565V. 2004 Antiviral research Abstract HBV A566T;A566T;L565V 59;92;102 64;97;107 15302140 Suppression of lamivudine-resistant B-domain mutants by adefovir dipivoxil in the woodchuck hepatitis virus model. Mutations observed in the highly conserved FLLA motif of the B domain were L564V, L565M, and A566T, with A566T being the most frequently observed. 2004 Antiviral research Abstract HBV L564V;L565M;A566T;A566T 75;82;93;105 80;87;98;110 15308745 Hepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L. Since the structures of the mutant and wild-type capsids are essentially the same and the mutation is not involved in the contact between dimers, we suggest that the F97L mutation affects the dynamic behavior of dimer and capsid. 2004 Journal of virology Abstract HBV F97L 166 170 Capsid;Capsid 222;49 228;56 15308745 Hepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L. We examined in vitro assembly of empty HBV capsids from wild-type and F97L core protein assembly domains. 2004 Journal of virology Abstract HBV F97L 70 74 C;Capsid 75;43 79;50 15308845 Detection of YMDD motif mutants by oligonucleotide chips in lamivudine-untreated patients with chronic hepatitis B virus infection. M552I mutants were detected by the oligonucleotide chips in 7.5% (3/40) of chronic HBV infected patients (2 chronic hepatitis and 1 cirrhosis). 2004 Journal of Korean medical science Abstract HBV M552I 0 5 Chronic Hepatitis B;Liver cirrhosis;HBV infections 108;132;83 125;141;95 15308845 Detection of YMDD motif mutants by oligonucleotide chips in lamivudine-untreated patients with chronic hepatitis B virus infection. Serum samples were tested by the oligonucleotide chips designed for detection of wild-type YMDD motif, M552V and M552I. 2004 Journal of Korean medical science Abstract HBV M552V;M552I 103;113 108;118 P 91 95 15311721 Efficacy of alpha interferon therapy for lamivudine resistance in chronic hepatitis B. Genotypic analysis showed M552V, M552I and L528M mutations. 2004 International journal of clinical practice Abstract HBV M552V;M552I;L528M 26;33;43 31;38;48 15328117 Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine. For liver transplant patient B (AI463015-B), previous famciclovir, ganciclovir, foscarnet, and 3TC therapies had failed, and RT changes rtS78S/T, rtV173L, rtL180M, rtT184S, and rtM204V were present at study entry. 2004 Antimicrobial agents and chemotherapy Abstract HBV S78S;S78T;V173L;L180M;T184S;M204V 138;138;148;157;166;179 144;144;153;162;171;184 RT;RT;RT;RT;RT;RT 125;136;146;155;164;177 127;138;148;157;166;179 15328117 Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine. Reduced ETV susceptibility in vitro required the rtM250V substitution in addition to the 3TC(r) substitutions. 2004 Antimicrobial agents and chemotherapy Abstract HBV M250V 51 56 RT 49 51 15328117 Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine. Reduced susceptibility in vitro was highest when both the rtT184G and the rtS202I changes were combined with the 3TC(r) substitutions. 2004 Antimicrobial agents and chemotherapy Abstract HBV T184G;S202I 60;76 65;81 RT;RT 58;74 60;76 15328117 Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine. The 3TC(r) RT substitutions rtV173L, rtL180M, and rtM204V were present at study entry, and the additional substitutions rtI169T and rtM250V emerged during ETV-3TC combination treatment. 2004 Antimicrobial agents and chemotherapy Abstract HBV V173L;L180M;M204V;I169T;M250V 30;39;52;122;134 35;44;57;127;139 RT;RT;RT;RT;RT;RT 11;28;37;50;120;132 13;30;39;52;122;134 15328117 Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine. Viral rebound occurred after 76 weeks of therapy with ETV at 1.0 mg, with the emergence of rtT184G, rtI169T, and rtS202I substitutions within the preexisting 3TC(r) background. 2004 Antimicrobial agents and chemotherapy Abstract HBV T184G;I169T;S202I 93;102;115 98;107;120 RT;RT;RT 91;100;113 93;102;115 15338371 Prognostic indicators of breakthrough hepatitis during lamivudine monotherapy for chronic hepatitis B virus infection. Univariate statistical analyses showed that possible prognostic indicators for the occurrence of BTH were pre-S deletions ( P = 0.03) and L180M/M204L mutations ( P = 0.04). 2004 Journal of gastroenterology Abstract HBV M204L;L180M 144;138 149;143 PreS 106 111 Fulminant Hepatitis B 97 100 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. After reinstitution of lamivudine (2002), the predominant HBV population exhibited a rare triple mutation (V519L, L526M, M550V), which has previously been associated with an in vitro reduction of virus antigenicity (escape mutant). 2004 BMC infectious diseases Abstract HBV V519L;L526M;M550V 107;114;121 112;119;126 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. RESULTS: HBV isolate derived from a sample collected in 1999 during an antiretroviral treatment with lamivudine showed the lamivudine resistant double mutation (L526M, M550V). 2004 BMC infectious diseases Abstract HBV L526M;M550V 161;168 166;173 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. The M550V variation may be accompanied by L526M mutation, notably in HIV-HBV co-infected patients. 2004 BMC infectious diseases Abstract HBV M550V;L526M 4;42 9;47 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. The resistance occurs through M550V or M550I aminoacid replacements. 2004 BMC infectious diseases Abstract HBV M550V;M550I 30;39 35;44 15340520 [A study on detection method of lamivudine related mutations in hepatitis B virus polymerase gene]. Mutation in the tyrosine methionine aspartic aspartic acid (YMDD) motif of HBV polymerase gene was found in eight patients and mutations of YMDD motif associated with L526M were found in another three patients. 2004 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV L526M 167 172 P;P;P 79;60;140 89;64;144 15340547 [Detection and identification of emergence of HBV YMDD motif mutation during lamivudine treatment by hybridization to an oligonucleotide array]. By direct sequencing of the PCR products, 11 cases were found to have YVDD with adenine741 changed into cytidine resulted in methionine552 changed into valine in which 6 cases with adenine669 changed into cytidine and leucine changed into methionine, 10 cases had YIDD motif mutation with guanosine743 altered thymidine methionine552 changed into isoleucine, including 3 cases with thymidine281 changed into cytidine and leucine565 altered proline. 2003 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV M552V;M552I 125;320 158;357 P;P 264;70 268;74 15361503 Survey of hepatitis B surface variant infection in children 15 years after a nationwide vaccination programme in Taiwan. RESULTS: The prevalence of a determinant mutants in HBV-DNA positive children was 7.8% (8/103) in 1984, which significantly increased to 19.6% (10/51) in 1989, peaked at 28.1% (9/32) in 1994, and remained at 23.1% ((3/13) (T131I, G145R, G145R)) in 1999; it was higher in those fully vaccinated compared with those not vaccinated (15/46 v 15/153; p<0.001). 2004 Gut Abstract HBV T131I;G145R;G145R 223;230;237 228;235;242 S 27 40 15365009 Oligonucleotide chip for detection of Lamivudine-resistant hepatitis B virus. Among these, 17 contained rtM204V (YVDD), 24 contained rtM204I3 (YIDD3), 3 contained rtM204I2 (YIDD2), and 36 contained mixed types. 2004 Journal of clinical microbiology Abstract HBV M204V 28 33 RT;P;P;P 26;65;95;35 28;69;99;39 15457560 Replication and gene expression of mutant hepatitis B virus in a transgenic mouse containing the complete viral genome with mutant s gene. Founders with HBsAg in serum were named lineages G145R-15 and G145R-18. 2004 World journal of gastroenterology Abstract HBV G145R;G145R 49;62 54;67 S 14 19 15457560 Replication and gene expression of mutant hepatitis B virus in a transgenic mouse containing the complete viral genome with mutant s gene. Of the 16 F1 offsprings generated by G145R-15 founder, 12 were positive for HBV genome with PCR, 10 were positive for HBsAg and HBcAg with immunohistochemistry and 7 were positive for HBsAg and HBeAg with ELISA. 2004 World journal of gastroenterology Abstract HBV G145R 37 42 C;C;S;S 128;194;118;184 133;199;123;189 15457560 Replication and gene expression of mutant hepatitis B virus in a transgenic mouse containing the complete viral genome with mutant s gene. Only 1 of 8 F1 offsprings generated by G145R-18 founder was survived and it was detected positive for HBV genome, HBsAg, HBcAg and HBeAg. 2004 World journal of gastroenterology Abstract HBV G145R 39 44 C;C;S 121;131;114 126;136;119 15469692 Increased DNA polymerase fidelity of the Lamivudine resistant variants of human hepatitis B virus DNA polymerase. From the f(ins) value analysis, it is evident that M550I and M550V exhibit higher fidelity values than the wild-type HBV DNA polymerase, while M550A exhibits similar fidelity values. 2004 Journal of biochemistry and molecular biology Abstract HBV M550I;M550V;M550A 51;61;143 56;66;148 P 125 135 15469692 Increased DNA polymerase fidelity of the Lamivudine resistant variants of human hepatitis B virus DNA polymerase. It is therefore suggested that lamivudine resistance comes from the stringency to dNTP binding and the discrimination of dCTP and lamivudine in M550V and M550I. 2004 Journal of biochemistry and molecular biology Abstract HBV M550V;M550I 144;154 149;159 15469692 Increased DNA polymerase fidelity of the Lamivudine resistant variants of human hepatitis B virus DNA polymerase. The FLAG-tagged wild-type (FPolE) and Met550 variants (FPolE/M550A, M550V, and M550I) of HBV DNA polymerases were expressed in insect cells, then purified. 2004 Journal of biochemistry and molecular biology Abstract HBV M550A;M550V;M550I 55;68;79 66;73;84 P 97 108 15472342 Pyrosequencing for detection of lamivudine-resistant hepatitis B virus. Lamivudine-resistant HBV mutants display specific mutations in the YMDD (tyrosine, methionine, aspartate, aspartate) motif of the viral polymerase (reverse transcriptase [rt]), which is the catalytic site of the enzyme, i.e., methionine 204 to isoleucine (rtM204I) or valine (rtM204V). 2004 Journal of clinical microbiology Abstract HBV M204I;M204V;M204I 258;278;226 263;283;254 P;RT;RT;RT;RT;P 136;148;171;256;276;67 146;169;173;258;278;71 15472342 Pyrosequencing for detection of lamivudine-resistant hepatitis B virus. The latter mutation is often accompanied by a compensatory leucine-to-methionine change at codon 180 (rtL180M). 2004 Journal of clinical microbiology Abstract HBV L180M;L180M 104;59 109;100 RT 102 104 15486926 Occult hepatitis B virus infection in a North American adult hemodialysis patient population. Seven of the 9 (78%) were nt 587 mutation (sG145R mutant) positive. 2004 Hepatology (Baltimore, Md.) Abstract HBV G145R 43 49 S 43 44 15486926 Occult hepatitis B virus infection in a North American adult hemodialysis patient population. The majority of these infections are associated with low viral loads and a high prevalence of the sG145R mutant. 2004 Hepatology (Baltimore, Md.) Abstract HBV G145R 98 104 S 98 99 15518823 Mutant hepatitis B virus surface antigens (HBsAg) are immunogenic but may have a changed specificity. Based on this fact, we further investigated whether the mtHBsAg with the aa substitution G145R is able to induce mutant-specific antibody responses. 2004 Virology Abstract HBV G145R 89 94 15518823 Mutant hepatitis B virus surface antigens (HBsAg) are immunogenic but may have a changed specificity. One MAb recognized mtHBsAg with G145R but not wild type and other mtHBsAg. 2004 Virology Abstract HBV G145R 32 37 15518823 Mutant hepatitis B virus surface antigens (HBsAg) are immunogenic but may have a changed specificity. Strikingly, serum samples from mice immunized with mtHBsAg with G145R recognized plasma-derived mtHBsAg. 2004 Virology Abstract HBV G145R 64 69 15518823 Mutant hepatitis B virus surface antigens (HBsAg) are immunogenic but may have a changed specificity. The amino acid (aa) substitutions like G145R, F134S, and C147W affected the binding of anti-HBs antibodies to corresponding mtHBsAg to different extents. 2004 Virology Abstract HBV C147W;G145R;F134S 57;39;46 62;44;51 S 92 95 15518823 Mutant hepatitis B virus surface antigens (HBsAg) are immunogenic but may have a changed specificity. The impact of aa substitutions G145R and F134S on the immunogenicity was accessed by genetic immunization of mice with vectors expressing middle HBsAg with the corresponding mutations. 2004 Virology Abstract HBV G145R;F134S 31;41 36;46 S 145 150 15543574 Comparison of full length sequences of hepatitis B virus isolates in hepatocellular carcinoma patients and asymptomatic carriers of Korea. Third, mutations (I127T/N, K130M, and V131I) at three codons in the carboxy functional region of X protein were observed in isolates from all three HCC patients. 2005 Journal of medical virology Abstract HBV I127T;I127N;K130M;V131I 18;18;27;38 25;25;32;43 X 97 98 Hepatocellular carcinoma 148 151 15544736 [Determination of hepatitis B virus genotype and detection of lamivudine-resistance mutations]. Patients with genotype A showed the pattern M204I+WT in the first 12 months and those with genotype D showed the pattern L180M+M204V with or without WT at 18 months. 2004 Gastroenterologia y hepatologia Abstract HBV M204I;L180M;M204V 44;121;127 49;126;132 15564475 Nucleolar localization of human hepatitis B virus capsid protein. However, the recognition of this exposed epitope by an anti-HBc antibody appeared to be affected by the I97E mutation or by histidine tagging at the C terminus of mutant HBcAg, which is presumably in the capsid interior. 2004 Journal of virology Abstract HBV I97E 104 108 Capsid;C;C 204;60;170 210;63;175 15564475 Nucleolar localization of human hepatitis B virus capsid protein. In contrast, changing an isoleucine to a leucine at amino acid 97 (I97L) of the HBV core antigen (HBcAg) causes it to release immature genomes. 2004 Journal of virology Abstract HBV I97L;I97L 25;67 65;71 C;C 84;98 88;103 15564475 Nucleolar localization of human hepatitis B virus capsid protein. Surprisingly, the nuclear HBcAg of mutants I97E and I97W, produced from either a replicon or an expression vector, was found to be colocalized with nucleolin and B23 at a frequency of nearly 100% by confocal immunofluorescence microscopy. 2004 Journal of virology Abstract HBV I97E;I97W 43;52 47;56 C 26 31 15564475 Nucleolar localization of human hepatitis B virus capsid protein. The I97D mutant had a near lethal phenotype, the I97P mutant exhibited a significantly reduced level of virion secretion, and the I97G mutant lacked the full-length relaxed circular form of viral DNA. 2004 Journal of virology Abstract HBV I97D;I97P;I97G 4;49;130 8;53;134 15572007 The precore mutation is associated with severity of liver damage in Brazilian patients with chronic hepatitis B. BACKGROUND: The clinical relevance of the G1896A precore mutation in chronic hepatitis B is still poorly understood. 2005 Journal of clinical virology Abstract HBV G1896A 42 48 Precore 49 56 Chronic Hepatitis B 69 88 15572007 The precore mutation is associated with severity of liver damage in Brazilian patients with chronic hepatitis B. OBJECTIVES: To assess the frequency of G1896A precore mutation in Brazilian patients with chronic hepatitis B, as well as its relation to the viral genotype, serum HBV-DNA levels and liver damage. 2005 Journal of clinical virology Abstract HBV G1896A 39 45 Precore 46 53 Chronic Hepatitis B;Liver disease 90;183 109;195 15572007 The precore mutation is associated with severity of liver damage in Brazilian patients with chronic hepatitis B. There was no association between G1896A mutation and cytoplasmic expression of HBcAg. 2005 Journal of clinical virology Abstract HBV G1896A 33 39 C 79 84 15577546 Successful therapy of hepatitis B with tenofovir in HIV-infected patients failing previous adefovir and lamivudine treatment. In two isolates we identified hepatitis B virus DNA polymerase mutation L217R, in one case we found multiple frameshifts in the same region. 2004 AIDS (London, England) Abstract HBV L217R 72 77 P 52 62 15577546 Successful therapy of hepatitis B with tenofovir in HIV-infected patients failing previous adefovir and lamivudine treatment. Surprisingly, adefovir therapy failed, although none of the virus isolates displayed mutations known to be associated with adefovir resistance (A181V, N236T). 2004 AIDS (London, England) Abstract HBV A181V;N236T 144;151 149;156 15605678 Acute leukaemia in chronic hepatitis B patients with lamivudine therapy. D553N mutant hepatitis B virus was detected in granulocytes of her peripheral blood. 2004 International journal of clinical practice Abstract HBV D553N 0 5 15605678 Acute leukaemia in chronic hepatitis B patients with lamivudine therapy. The first case developed acute myeloid leukaemia, 1 year after stopping lamivudine therapy, when A529T mutant HBV-DNA was still detectable. 2004 International journal of clinical practice Abstract HBV A529T 97 102 Acute myeloid leukemia 25 48 15618847 Long-term therapy with lamivudine in renal transplant recipients with chronic hepatitis B. Analysis of HBV sequencing after breakthrough revealed specific resistance mutations in both the B and C domains of the polymerase (rtL180M/M204V, n = 5; rtM204I, n = 2). 2004 European journal of gastroenterology & hepatology Abstract HBV M204V;L180M;M204I 140;134;156 145;139;161 P;RT;RT 120;132;154 130;134;156 15619810 [In vitro expression of wild type and precore mutant woodchuck hepatitis virus]. Hepatitis B virus (HBV) precore 1896 and 1898 G-->A mutations are regarded as hot spots to study. 1997 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1898A 41 51 Precore 24 31 15640866 [Full-length sequence of hepatitis B virus isolated from high incidence hepatocellular carcinoma area-Longan county]. Six point mutations including the double mutations (nt 1762 A to T, 1764 G to A) were found in X gene leading to 4 amino acids change. 2004 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A 68 79 X 95 96 15648063 Clinical and virological characteristics of lamivudine resistance in chronic hepatitis B patients: a single center experience. Four kinds of new mutants were found in over two patients including rtL80I, rtG172E, rtG174C, and rtG172E/rtG174C. 2005 Journal of medical virology Abstract HBV L80I;G172E;G174C;G172E;G174C 70;78;87;100;108 74;83;92;105;113 RT;RT;RT;RT;RT 68;76;85;98;106 70;78;87;100;108 15648063 Clinical and virological characteristics of lamivudine resistance in chronic hepatitis B patients: a single center experience. In vitro transfection and real-time analysis showed that rtG172E, rtG174C, and rtG172E/rtG174C mutants had a decreased replication competence compared with wild type (33%, 27%, and 15% of the wild type HBV, respectively). 2005 Journal of medical virology Abstract HBV G172E;G174C;G172E;G174C 59;68;81;89 64;73;86;94 RT;RT;RT;RT 57;66;79;87 59;68;81;89 15655050 Activity of adefovir dipivoxil against all patterns of lamivudine-resistant hepatitis B viruses in patients. Four major patterns of lamivudine-resistant HBV were identified: rtL180M + rtM204V (60%), rtV173L + rtL180M + rtM204V (19%), rtM204I (9%) and rtL180M + rtM204I (9%). 2005 Journal of viral hepatitis Abstract HBV L180M;M204V;V173L;L180M;M204V;M204I;L180M;M204I 67;77;92;102;112;127;144;154 72;82;97;107;117;132;149;159 RT;RT;RT;RT;RT;RT;RT;RT 65;75;90;100;110;125;142;152 67;77;92;102;112;127;144;154 15655050 Activity of adefovir dipivoxil against all patterns of lamivudine-resistant hepatitis B viruses in patients. In addition to the rtM204V/I and the rtL180M mutations, the mutation rtV173L was identified in 19% of patients. 2005 Journal of viral hepatitis Abstract HBV M204V;M204I;L180M;V173L 21;21;39;71 28;28;44;76 RT;RT;RT 19;37;69 21;39;71 15664258 Sustained HBs seroconversion during lamivudine and adefovir dipivoxil combination therapy for lamivudine failure. Lamivudine resistance was associated with the selection of a L180M+M204V polymerase mutant. 2005 Journal of hepatology Abstract HBV L180M;M204V 61;67 66;72 P 73 83 15720529 Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? The biological implications of substitutions L60V and I97L in the core (c) gene of hepatitis B virus (HBV) were investigated in order to determine whether they could change the immunogenicity of HBcAg or influence the immune response in mice. 2005 Journal of viral hepatitis Abstract HBV L60V;I97L 135;144 139;148 C;C;C;C 162;40;156;285 163;44;160;290 15720529 Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? In conclusion, the L60V and I97L substitutions had no influence on humoral immune responses, but could downregulate T-cell responses to HBcAg, suggesting that L60V and I97L were immune escape mutants. 2005 Journal of viral hepatitis Abstract HBV L60V;I97L;L60V;I97L 19;28;159;168 23;32;163;172 C 136 141 15720529 Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? The biological implications of substitutions L60V and I97L in the core (c) gene of hepatitis B virus (HBV) were investigated in order to determine whether they could change the immunogenicity of HBcAg or influence the immune response in mice. 2005 Journal of viral hepatitis Abstract HBV L60V;I97L 45;54 49;58 C;C;C 72;66;195 73;70;200 15720529 Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? Three strains of recombinant adenoviruses--AdHBV-WT, AdHBV-L60V and AdHBV-I97L--containing wild-type or mutant HBV genomes were constructed using the AdEasy system and used to infect BALB/c mice intranasally. 2005 Journal of viral hepatitis Abstract HBV L60V;I97L 59;74 63;78 15720529 Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? We found that AdHBV-WT induced a stronger T-cell proliferation response than AdHBV-L60V and AdHBV-I97L. 2005 Journal of viral hepatitis Abstract HBV L60V;I97L 83;98 87;102 15720530 Long-term follow-up of chronic hepatitis B after the emergence of mutations in the hepatitis B virus polymerase region. In most cases, wild-type HBV was mutated with the substitution of only rtM204I at first, and rtL180M/M204I mutations and then rtL180M/M204V mutations subsequently appeared. 2005 Journal of viral hepatitis Abstract HBV M204I;M204V;M204I;L180M;L180M 101;134;73;95;128 106;139;78;100;133 RT;RT;RT 71;93;126 73;95;128 15720534 Three-phase sequential combined treatment with lamivudine and interferon in young patients with chronic hepatitis B. After IFN withdrawal, viraemia transiently increased to high levels in five of 11 (45%) patients who showed rt M204V/I lamivudine mutant resistant. 2005 Journal of viral hepatitis Abstract HBV M204V;M204I 111;111 118;118 RT 108 110 15720534 Three-phase sequential combined treatment with lamivudine and interferon in young patients with chronic hepatitis B. One patient presented core-promoter (A1762T/G1764A) and precore stop codon mutations. 2005 Journal of viral hepatitis Abstract HBV G1764A;A1762T 44;37 50;43 Core promoter;Precore 22;56 35;63 15720535 Clinical outcome and virological characteristics of hepatitis B-related acute liver failure in the United States. Prevalence of HBV genotypes, precore stop (G1896A) and core promoter dual (T1762A, A1764T) variants among patients with HBV-ALF were compared with a cohort of 530 patients with chronic HBV infection. 2005 Journal of viral hepatitis Abstract HBV G1896A;T1762A;A1764T 43;75;83 49;81;89 Core promoter;Precore 55;29 68;36 Chronic HBV infection;Liver disease 177;124 198;127 15778957 Transmission of G145R mutant of HBV to an unrelated contact. Mutant G145R along with T118V and T143M was identified in three subjects who included one 1 degrees, one 2 degrees, and one 3 degrees contact. 2005 Journal of medical virology Abstract HBV G145R;T118V;T143M 7;24;34 12;29;39 15778957 Transmission of G145R mutant of HBV to an unrelated contact. Mutation T118V was present in all the six subjects. 2005 Journal of medical virology Abstract HBV T118V 9 14 15778957 Transmission of G145R mutant of HBV to an unrelated contact. Of these three contacts with G145R mutation, only one 1 degrees contact was found to be HBsAg-ve. 2005 Journal of medical virology Abstract HBV G145R 29 34 S 88 93 15778957 Transmission of G145R mutant of HBV to an unrelated contact. Presence of T118V and T143M mutations along with G145R mutation in these subjects provides an indirect evidence for the possible horizontal transmission of G145R HBV variant to a 3 degrees unrelated contact. 2005 Journal of medical virology Abstract HBV T118V;T143M;G145R;G145R 12;22;49;156 17;27;54;161 15778957 Transmission of G145R mutant of HBV to an unrelated contact. The data also reaffirms the earlier finding of HBsAg positivity in presence of G145R mutation of the S-gene. 2005 Journal of medical virology Abstract HBV G145R 79 84 S;S 101;47 102;52 15778957 Transmission of G145R mutant of HBV to an unrelated contact. There is limited information on the horizontal transmission of Gly 145 Arg (G145R) mutant to related contacts. 2005 Journal of medical virology Abstract HBV G145R;G145R 63;76 74;81 15834874 Nucleotide mutations associated with hepatitis B e antigen negativity. Six mutations were found to be significantly more common in the former group than in the latter: G529A (3/4 vs. 0/5), C934A (4/4 vs. 1/5), A1053G (4/4 vs. 1/5), G1915T/A (4/4 vs. 0/5), T2005C/A (4/4 vs. 0/5), and C3026T (3/4 vs. 0/5). 2005 Journal of medical virology Abstract HBV C934A;T2005C;T2005A;A1053G;G1915T;G1915A;C3026T;G529A 118;185;185;139;161;161;213;97 123;193;193;145;169;169;219;102 15850475 HBsAg-negative hepatitis B virus infections in hepatitis C virus-associated hepatocellular carcinoma. HBV mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found in the majority of cases, mutations that have previously been reported in HBV that is integrated in HCC DNA. 2005 Journal of viral hepatitis Abstract HBV G1764A 50 60 Core promoter 68 81 Hepatocellular carcinoma 200 203 15850475 HBsAg-negative hepatitis B virus infections in hepatitis C virus-associated hepatocellular carcinoma. In 18 of 21 (86%) patients with detectable HBV core promoter sequences, mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found. 2005 Journal of viral hepatitis Abstract HBV G1764A 118 128 Core promoter;Core promoter 47;136 60;149 15858045 Failure of the lamivudine-resistant rtM204I hepatitis B virus mutants to efficiently support hepatitis delta virus secretion. The major HBV lamivudine (LMV)-resistant mutations in the polymerase gene within the reverse transcriptase (rt) region at rtM204V or rtM204I are associated with changes in the overlapping envelope gene products, in particular, the gene encoding small envelope protein (s) at sI195M or sW196L/S/Stop. 2005 Journal of virology Abstract HBV M204V;M204I;I195M;W196L;W196S;W196X 124;135;275;285;285;285 129;140;281;298;298;298 S;P;RT;RT;RT;RT;S;S;S;S 188;58;85;108;122;133;269;275;285;245 196;68;106;110;124;135;270;276;286;259 15858045 Failure of the lamivudine-resistant rtM204I hepatitis B virus mutants to efficiently support hepatitis delta virus secretion. We have demonstrated that the LMV resistance mutations corresponding to sW196L/S inhibited secretion of HDV particles, while changes corresponding to sI195M did not affect secretion. 2005 Journal of virology Abstract HBV W196L;W196S;I195M 72;72;150 80;80;156 S;S 72;150 73;151 15872296 Prevalence, incidence, and clinical relevance of the reverse transcriptase V207I mutation outside the YMDD motif of the hepatitis B virus polymerase during lamivudine therapy. The reverse transcriptase V207I mutation within the hepatitis B virus (HBV) polymerase is associated with resistance to lamivudine in vitro. 2005 Journal of clinical microbiology Abstract HBV V207I 26 31 P;RT 76;4 86;25 15893561 A novel accurate amplification created restriction site method for determination of the wild type and the precore mutant hepatitis B virus variants. It can be carried out for follow-up of G1896A precore mutant variant in hepatitis B virus infected subjects at routine molecular diagnostic laboratories. 2005 Journal of virological methods Abstract HBV G1896A 39 45 Precore 46 53 15893561 A novel accurate amplification created restriction site method for determination of the wild type and the precore mutant hepatitis B virus variants. The most commonly occurring hepatitis B virus (HBV) mutation is the G to A mutation at nucleotide 1896 in the precore region. 2005 Journal of virological methods Abstract HBV G1896A 68 102 Precore 110 117 15896869 Virus and transaminase levels determine the emergence of drug resistance during long-term lamivudine therapy in chronic hepatitis B. BACKGROUND/AIMS: The results of earlier studies on determinants for the emergence of tyrosine-methionine-aspartate-aspartate (YMDD) mutants (rtM204 I/V) were controversial. 2005 Journal of hepatology Abstract HBV M204I;M204V 143;143 151;151 RT;P;P 141;85;126 143;124;130 15896869 Virus and transaminase levels determine the emergence of drug resistance during long-term lamivudine therapy in chronic hepatitis B. RESULTS: rtM204 I/V emerged in 37 noncirrhotic and 36 cirrhotic patients. 2005 Journal of hepatology Abstract HBV M204I;M204V 11;11 19;19 RT 9 11 Liver cirrhosis 54 63 15896869 Virus and transaminase levels determine the emergence of drug resistance during long-term lamivudine therapy in chronic hepatitis B. Stepwise logistic regression analysis showed that baseline hepatitis B e antigen (HBeAg) status [odds ratio (OR), 7.728; 95% confidental interval (CI), 2.886-12.957; P=0.0026], HBV-DNA level (OR, 3.756; 95% CI, 1.058-5.089; P=0.0202), alanine transaminase (ALT) level (OR, 6.285; 95% CI, 1.057-11.990; P=0.00246) and treatment duration (OR, 19.88; 95% CI, 8.652-31.762; P<0.0004) were independent determinants for the emergence of rtM204 I/V. 2005 Journal of hepatology Abstract HBV M204I;M204V 433;433 441;441 C;C;RT 71;82;431 80;87;433 15896869 Virus and transaminase levels determine the emergence of drug resistance during long-term lamivudine therapy in chronic hepatitis B. The aim was to evaluate the impact of viral factors, host factors, host-viral interaction and drug factor on the emergence of rtM204 I/V. 2005 Journal of hepatology Abstract HBV M204I;M204V 128;128 136;136 RT 126 128 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. Considering the use of de novo or add-on 3TC+ADV bitherapy, we investigated the possibility of the emergence of an HBV strain harboring polymerase mutations conferring resistance to both 3TC (rtL180M+M204V) and ADV (rtN236T). 2005 Hepatology (Baltimore, Md.) Abstract HBV N236T;L180M;M204V 218;194;200 223;199;205 P;RT;RT 136;192;216 146;194;218 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. In conclusion, the combination of rtL180M+M204V and rtN236T mutations impairs HBV replication and confers resistance to both 3TC and ADV in vitro. 2005 Hepatology (Baltimore, Md.) Abstract HBV N236T;L180M;M204V 54;36;42 59;41;47 RT;RT 34;52 36;54 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. Interferon alfa inhibited equally the replication of wt and L180M+M204V+N236T HBV. 2005 Hepatology (Baltimore, Md.) Abstract HBV L180M;M204V;N236T 60;66;72 65;71;77 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. Phenotypic assays indicated that the L180M+M204V+N236T mutant is resistant to pyrimidine analogs (3TC, -FTC, beta-L-FD4C, L-FMAU). 2005 Hepatology (Baltimore, Md.) Abstract HBV L180M;M204V;N236T 37;43;49 42;48;54 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. The triple mutant replicates its genome in vitro, but less efficiently than either the wild-type (wt) HBV or L180M+M204V and N236T mutants. 2005 Hepatology (Baltimore, Md.) Abstract HBV L180M;M204V;N236T 109;115;125 114;120;130 15915463 Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. We constructed the L180M+M204V+N236T mutant and determined its replication capacity and its susceptibility to different nucleos(t)ide analogs in transiently transfected hepatoma cell lines. 2005 Hepatology (Baltimore, Md.) Abstract HBV L180M;M204V;N236T 19;25;31 24;30;36 Hepatocellular carcinoma 169 177 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. AIM: G1896A mutation in precore or A1762T/G1764A mutations in basal core promoter are suspected to be responsible for patients with detectable level of HBV DNA in serum after seroconversion from HBeAg to anti-HBe. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 42;35;5 48;41;11 BCP;C;C;Precore 62;195;209;24 81;200;212;31 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. Coexistence mutations were found in 77.1% (64/83) out of sera with A1762T/G1764A mutations, and in 50.0% (64/128) out of sera with G1896A mutation. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 74;67;131 80;73;137 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. Compared with variants with G1896A mutation only, the coexistence mutations were predominant in patients with high level of serum HBV DNA, and related to higher total bilirubin, lower serum albumin and progressive liver diseases. 2005 World journal of gastroenterology Abstract HBV G1896A 28 34 Liver disease 214 228 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. CONCLUSION: The coexistence of G1896A mutation and A1762T/G1764A mutations is very common, and responsible for the major cases with high level of HBV DNA in serum and progressive liver diseases after HBeAg-to-anti-HBe seroconversion. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 58;51;31 64;57;37 C;C 214;200 217;205 Liver disease 179 193 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. However, G1896A variant has impaired, while A1762T/G1764A variant may have intact replication ability. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 51;44;9 57;50;15 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. Mutations of G1896A and A1762T/G1764A among these serum samples were detected using competitively differentiated PCR. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 31;24;13 37;30;19 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. RESULTS: G1896A and/or A1762T/G1764A mutations were detected in 89.1% (147/165) out of patients with detectable HBV DNA in serum after HBeAg-to-anti-HBe seroconversion. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 30;23;9 36;29;15 C;C 135;149 140;152 15918203 High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter. The positive rate of G1896A variants was significantly higher than that of A1762T/G1764A mutations (77.6% vs 50.3%, chi2 = 26.61, P<0.01). 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A 82;75;21 88;81;27 15918335 Evaluation of methods for monitoring drug resistance in chronic hepatitis B patients during lamivudine therapy based on mass spectrometry and reverse hybridization. A total of 60 patient samples were analysed for the presence of mutations at rtL1 80M and rtM204I/V of HBV polymerase by the LiPA and RFMP assays. 2005 Antiviral therapy Abstract HBV M204I;M204V 92;92 99;99 RT;RT;P 77;90;107 79;92;117 15918335 Evaluation of methods for monitoring drug resistance in chronic hepatitis B patients during lamivudine therapy based on mass spectrometry and reverse hybridization. The ability to detect mutations at rtM204I/V was compared with defined mixtures of wild-type and mutant HBV cloned in plasmids at relative concentrations ranging from 1-25%. 2005 Antiviral therapy Abstract HBV M204I;M204V 37;37 44;44 RT 35 37 15932365 Changes in different regions of hepatitis B virus gene in hepatitis B 'e' antigen-negative patients with chronic hepatitis B: the effect of long-term lamivudine therapy. About 75% of the patients with M204V mutations were responders and none with M204I or mixed pattern sustained response. 2005 Alimentary pharmacology & therapeutics Abstract HBV M204V;M204I 31;77 36;82 15932365 Changes in different regions of hepatitis B virus gene in hepatitis B 'e' antigen-negative patients with chronic hepatitis B: the effect of long-term lamivudine therapy. Patients carrying M204V mutations are more likely to respond to therapy. 2005 Alimentary pharmacology & therapeutics Abstract HBV M204V 18 23 15932365 Changes in different regions of hepatitis B virus gene in hepatitis B 'e' antigen-negative patients with chronic hepatitis B: the effect of long-term lamivudine therapy. YMDD mutations were observed in nine cases and both, L180M and M204V/I mutations were simultaneously detected in six cases. 2005 Alimentary pharmacology & therapeutics Abstract HBV L180M;M204V;M204I 53;63;63 58;70;70 P 0 4 15946130 Precore stop codon mutation of hepatitis B virus is associated with low breakthrough rate following long-term lamivudine therapy. The purpose of the present study was to evaluate the effects of precore stop codon mutation (G to A mutation at nucleotide 1896; A(1896)) of hepatitis B virus (HBV) on the occurrence of viral breakthrough following lamivudine therapy. 2005 Journal of gastroenterology and hepatology Abstract HBV G1896A 93 127 Precore 64 71 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. Deletion of nucleotides 23 to 55 (amino acids 12 to 22) was identified in the pre-S2 region. 2005 Journal of Korean medical science Abstract HBV del 23-55;del 12_22 0;0 32;55 PreS2 78 84 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. Methionine of rtM204 in the P gene was substituted for isoleucine indicating YIDD mutation (rtM204I). 2005 Journal of Korean medical science Abstract HBV M204I 94 99 P;RT;RT;YIDD 28;14;92;77 29;16;94;81 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. Sequencing of the 'a' determinant revealed amino acid substitutions as I126S, T131N, M133T, and S136Y. 2005 Journal of Korean medical science Abstract HBV I126S;T131N;M133T;S136Y 71;78;85;96 76;83;90;101 S 19 33 15962285 Functional analysis of hepatitis B virus reactivating in hepatitis B surface antigen-negative individuals. Furthermore, nuclear run-on transcription showed that the G458A mutation acts at the posttranscriptional level. 2005 Hepatology (Baltimore, Md.) Abstract HBV G458A 58 63 15962285 Functional analysis of hepatitis B virus reactivating in hepatitis B surface antigen-negative individuals. The G458A mutation was also effective if the S gene was placed under control of a heterologous promoter. 2005 Hepatology (Baltimore, Md.) Abstract HBV G458A 4 9 S 45 46 15962387 Optimization of competitively differentiated polymerase chain reaction in detection of HBV basal core promoter mutation. A1762T/G1764A mutant was detected in 41.8% (51/122) of patients with HBV infection, but not detected in controls with negative HBsAg. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T 7;0 13;6 S 127 132 HBV infections 69 82 15962387 Optimization of competitively differentiated polymerase chain reaction in detection of HBV basal core promoter mutation. METHODS: Recombinant plasmid of double point mutation A1762T/G1764A in basal core promoter of HBV constructed by site-directed mutagenesis was used as mutant control. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T 61;54 67;60 BCP 71 90 15962387 Optimization of competitively differentiated polymerase chain reaction in detection of HBV basal core promoter mutation. Optimized CD-PCR was evaluated by detecting A1762T/G1764A mutation in recombinant plasmids and clinical sera from patients with HBV infection. 2005 World journal of gastroenterology Abstract HBV G1764A;A1762T 51;44 57;50 HBV infections 128 141 15973769 Character of HBV (hepatitis B virus) polymerase gene rtM204V/I and rtL180M mutation in patients with lamivudine resistance. Among them, 45 patients had rtL180M/M204V mutation (41.28%), 28 patients had rtL180M/M204I mutation (25.70%) and 36 patients had rtM204I mutation (33.02%). 2005 Journal of Zhejiang University. Science. B Abstract HBV M204V;M204I;M204I;L180M;L180M 36;85;131;30;79 41;90;136;35;84 RT;RT;RT 28;77;129 30;79;131 15973769 Character of HBV (hepatitis B virus) polymerase gene rtM204V/I and rtL180M mutation in patients with lamivudine resistance. There were 6 patients with rtL180M mutation in 32 lamivudine resistance patients. 2005 Journal of Zhejiang University. Science. B Abstract HBV L180M 29 34 RT 27 29 15977237 Complete genome sequence and phylogenetic analysis of hepatitis B virus isolated from Turkish patients with chronic HBV infection. There were two pre-core stop codons (G1896A) in two HBeAg negative and three core promoter dual mutations (T1762/A1764) in one HBeAg positive and two HBeAg negative patients' HBV genomes. 2005 Journal of medical virology Abstract HBV G1896A 37 43 Core promoter;C;C;C;Precore 77;52;127;150;15 90;57;132;155;23 15980328 Emergence of a novel mutation in the FLLA region of hepatitis B virus during lamivudine therapy. The major mechanism of resistance has been attributed to the alteration in the YMDD motif of the HBV polymerase due to an amino acid change of rtM204 to V/I and an accompanying rtL180M conversion. 2005 Antimicrobial agents and chemotherapy Abstract HBV L180M;M204V;M204I 179;145;145 184;156;156 RT;RT;P;YMDD 143;177;101;79 145;179;111;83 15980328 Emergence of a novel mutation in the FLLA region of hepatitis B virus during lamivudine therapy. The mutant had a rtL180C/M204I genotype and was detected after 2 years of therapy with lamivudine. 2005 Antimicrobial agents and chemotherapy Abstract HBV M204I;L180C 25;19 30;24 RT 17 19 15980328 Emergence of a novel mutation in the FLLA region of hepatitis B virus during lamivudine therapy. The resistance profile was comparable to that of the previously reported rtL180 M/M204I-containing virus. 2005 Antimicrobial agents and chemotherapy Abstract HBV M204I;L180M 82;75 87;81 RT 73 75 15980328 Emergence of a novel mutation in the FLLA region of hepatitis B virus during lamivudine therapy. Transient transfection studies in human hepatoma cells with HBV carrying the new mutant demonstrated that the rtL180C/M204I mutant was resistant to lamivudine up to 10 microM. 2005 Antimicrobial agents and chemotherapy Abstract HBV M204I;L180C 118;112 123;117 RT 110 112 Hepatocellular carcinoma 40 48 15985011 Response to long-term lamivudine treatment (up to 5 years) in patients with severe chronic hepatitis B, role of genotype and drug resistance. YMDD mutation at rtL180M and rtM204V/I measured by restriction digest of amplified products. 2005 Journal of viral hepatitis Abstract HBV L180M;M204V;M204I 19;31;31 24;38;38 RT;RT;YMDD 17;29;0 19;31;4 15987916 Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B. Resistance mutations rtN236T and rtA181V were identified in 5.9 percent of patients after 144 weeks. 2005 The New England journal of medicine Abstract HBV N236T;A181V 23;35 28;40 RT;RT 21;33 23;35 15993954 Validation and comparison of different PCR-based methods for detection of hepatitis B virus precore region mutants. Three PCR-based assays for quantitation of G1896A precore HBV mutants: two allele specific PCRs, single tube (single-AS-PCR) with enzymatic restriction or separate tubes (twin-AS-PCR) and one oligohybridization assay (OA) with three probes were developed and standardized. 2005 Journal of virological methods Abstract HBV G1896A 43 49 Precore 50 57 16004082 Inhibition of hepatitis B virus gene expression and replication by helioxanthin and its derivative. The lamivudine-resistant HBV, L526M/M550V double mutant strain, was also sensitive to helioxanthin and 5-4-2. 2005 Antiviral chemistry & chemotherapy Abstract HBV M550V;L526M 36;30 41;35 16024943 Nucleic acid sequence analysis of basal core promoter/precore/core region of hepatitis B virus isolated from chronic carriers of the virus from Kolkata, eastern India: low frequency of mutation in the precore region. CONCLUSION: The pattern of core promoter and precore mutation of HBV isolates in the present study is atypical and not in accordance with reports from other parts of the world, where genotype D and genotype C with T at codon 1858 are common. 2005 Intervirology Abstract HBV C1858T 207 229 Core promoter;Precore 27;45 40;52 16027776 [Influence of the mutants of hepatitis B surface antigen on the cell immunity]. But it should not be ignored that HBV T126S or M133T mutation may assert a potential impact on the cell immunity. 2005 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV T126S;M133T 38;47 43;52 16027776 [Influence of the mutants of hepatitis B surface antigen on the cell immunity]. It was deserved to point out that the HBsAg with T126S mutation could increase the expression of IFN-gamma in the culture medium while the HBsAg with M133T mutation induced more expression of IL-10. 2005 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV T126S;M133T 49;150 54;155 S;S 38;139 43;144 16027787 [SNaPshot technique for detection of single-nucleotide polymorphisms (SNPs) in HBV polymerase gene region of HBV gene]. RESULTS: Aside from mutation of YMDD, there were mutations of 514C-A, 523C-A, 562T-A, 667C-A. 2005 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV C523A;T562A;C667A 70;78;86 76;84;92 P 32 36 16027787 [SNaPshot technique for detection of single-nucleotide polymorphisms (SNPs) in HBV polymerase gene region of HBV gene]. Specific primers of SNaPshot were designed to detect 741A-G (YVDD), 743G-T (YIDD). 2005 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G743T 68 74 P;P 76;61 80;65 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. A change in the amino acid sequences at positions 130 and 131 in the HBV-X protein (M130K and V131I) produced by T-A point mutations at the nucleic acids level has been associated with severe liver damage and HCC in patients from China and Africa. 2005 Virology journal Abstract HBV M130K;V131I 84;94 89;99 X 73 74 Liver disease;Hepatocellular carcinoma 192;209 204;212 16094714 Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated. As compared to standard genotype C HBx, I127T mutant showed higher transactivation activity, while the other four types of mutants showed no differences. 2005 World journal of gastroenterology Abstract HBV I127T 40 45 X 35 38 16094714 Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated. METHODS: Five types of "hot-spot" mutations of genotype B or C HBV X genes, which sequentially lead to the amino acid substitutions of HBx as I127T, F132Y, K130M+V131I, I127T+K130M+V131I, or K130M+V131I+F132Y, respectively, were generated by means of site-directed mutagenesis. 2005 World journal of gastroenterology Abstract HBV K130M;I127T;K130M;I127T;F132Y;V131I;K130M;V131I;V131I;F132Y 156;169;191;142;149;162;175;181;197;203 161;174;196;147;154;167;180;186;202;208 X;X 135;67 138;68 16094714 Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated. RESULTS: As compared to standard genotype B HBx, mutants of I127T and I127T+K130M+V131I showed higher transactivation and anti-proliferative activities, while the mutants of F132Y, K130M+V131I, and K130M+V131I+F132Y showed lower activities. 2005 World journal of gastroenterology Abstract HBV I127T;K130M;K130M;I127T;K130M;V131I;F132Y;V131I;V131I;F132Y 70;181;198;60;76;82;174;187;204;210 75;186;203;65;81;87;179;192;209;215 X 44 47 16094714 Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated. With regard to anti-proliferative activity, compared to standard genotype C HBx, F132Y and K130M+ V131I mutants showed lower activities, and K130M+V131I +F132Y mutant, on the other hand, showed higher activity, while the mutants of I127T and I127T+K130M+V131I showed no differences. 2005 World journal of gastroenterology Abstract HBV K130M;I127T;F132Y;K130M;V131I;V131I;F132Y;I127T;K130M;V131I 141;242;81;91;98;147;154;232;248;254 146;247;86;96;103;152;159;237;253;259 X 76 79 16099111 [HBs antigen mutants: prevalence, clinical and diagnostic implications]. Changes I195 M and W196L, reflecting lamivudine resistance are present among 18 patients (33%). 2005 Pathologie-biologie Abstract HBV I195M;W196L 8;19 14;24 16099903 T1764G1766 core promoter double mutants are restricted to Hepatitis B virus strains with an A1757 and are common in genotype D. G1896A pre-core stop mutants, detected in 77 % of e-CHB patients and 85 % of ASCs, showed no association with virus load or aminotransferase levels. 2005 The Journal of general virology Abstract HBV G1896A 0 6 Precore 7 15 Chronic Hepatitis B 52 55 16108169 Chronic hepatitis B--treatment with nucleoside analogues. Adefovir-resistant mutants (rt N236T) are susceptible to lamivudine and entecavir. 2005 The Medical journal of Malaysia Abstract HBV N236T 31 36 RT 28 30 16116655 The influence of N-glycosylation and C-terminal sequence on secretion of HBV large surface antigen from S. cerevisiae. In Saccharomyces cerevisiae, we synthesized and secreted L-HBVsAg (named as pre-S(Met1 to Asn174)::S(Met175 to Ile400)) and three mutants, i.e., pre-S degree degree::S (Asn15Gln and Asn123Gln), pre-S degree degree::S degree (Asn15Gln, Asn123Gln, and Asn320Gln), and pre-S degree degree::S degree degree (Asn15Gln, Asn123Gln, Asn233Gln, and Asn320Gln). 2005 Biotechnology and bioengineering Abstract HBV N15Q;N123Q;N15Q;N123Q;N320Q;N15Q;N123Q;N233Q;N320Q 169;182;225;235;250;304;314;325;340 177;191;233;244;259;312;323;334;349 PreS;PreS;PreS;PreS;S;S;S;S 76;145;194;266;99;166;215;287 81;150;199;271;100;167;216;288 16121373 Heterogeneity analysis of the hepatitis B virus genome in intrauterine infection. The strains without screened mutations such as P21L in the pre-S1 region may infect the fetus more readily. 2005 Journal of medical virology Abstract HBV P21L 47 51 PreS1 59 65 16152756 Cross-resistance testing of next-generation nucleoside and nucleotide analogues against lamivudine-resistant HBV. To investigate this in vitro, we generated novel stable cell lines expressing HBV encoding the four major patterns of lamivudine resistance mutations (rtL180M+rtM204V, rtV173L+rtL180M+rtM204V, rtM204I and rtL180M+ rtM204I). 2005 Antiviral therapy Abstract HBV L180M;M204V;V173L;L180M;M204V;M204I;L180M;M204I 153;161;170;178;186;195;207;216 158;166;175;183;191;200;212;221 RT;RT;RT;RT;RT;RT;RT;RT 151;159;168;176;184;193;205;214 153;161;170;178;186;195;207;216 16168522 Adefovir-resistant hepatitis B can be associated with viral rebound and hepatic decompensation. RESULTS: Eight male patients with pre-existing lamivudine resistance or breakthrough (mean age 47+/-13 years) were found to have adefovir-resistant mutations rtA181V/T or rtN236T. 2005 Journal of hepatology Abstract HBV A181V;A181T;N236T 160;160;173 167;167;178 RT;RT 158;171 160;173 16197491 Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis. Core promoter': the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P=0.03) of group B1 and one of nine (11%; P=0.002) of group B2 patients. 2005 Alimentary pharmacology & therapeutics Abstract HBV G1764A;A1762T 55;48 61;54 Core promoter;BCP 0;27 13;46 16197491 Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis. Precore': the G1896A stop codon mutation was present in seven of eight (87%) of group A and in zero of five (P=0.004) of group B1 and one of nine (11%; P=0.002) of group B2. 2005 Alimentary pharmacology & therapeutics Abstract HBV G1896A 14 21 Precore 0 7 16197491 Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis. RESULTS: 'Polymerase region': M204V/I variants were found in all group A patients, but in none of group B1 (P=0.0007) and in four of nine of group B2 (44%; P=0.02) patients. 2005 Alimentary pharmacology & therapeutics Abstract HBV M204V;M204I 30;30 37;37 P 10 20 16197491 Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis. The L180M substitution was detected in four of eight (50%) of group A and in none of groups B1 and B2. 2005 Alimentary pharmacology & therapeutics Abstract HBV L180M 4 9 16218172 Selection of hepatitis B virus polymerase mutations in HIV-coinfected patients treated with tenofovir. Genotypic analyses from 21 of the patients revealed LAM-associated mutations, and a further two patients developed a novel mutation, rtA194T, along with LAM-resistance-associated mutations. 2005 Antiviral therapy Abstract HBV A194T 135 140 RT 133 135 16218172 Selection of hepatitis B virus polymerase mutations in HIV-coinfected patients treated with tenofovir. In vitro, rtA194T conferred a reduced susceptibility to TDF in the presence of LAM-associated mutations. 2005 Antiviral therapy Abstract HBV A194T 12 17 RT 10 12 16218172 Selection of hepatitis B virus polymerase mutations in HIV-coinfected patients treated with tenofovir. Phenotypic analyses revealed that constructs harbouring rtA194T combined with rtL180M and rtM204V displayed an over 10-fold increase in the IC50 for TDF compared with the wild type. 2005 Antiviral therapy Abstract HBV A194T;L180M;M204V 58;80;92 63;85;97 RT;RT;RT 56;78;90 58;80;92 16220028 Hepatitis B virus DNA quantitation and detection of core promoter, precore and polymerase mutations in chronic hepatitis B: evaluation and clinical usefulness of three new commercial assays. affigene HBV mutant VL (positions G1764A, G1896A) and affigene HBV DE/3TC (positions rtL180M, rtM204V/I) were able to detect a low presence of mutants in a mixed population (wild type and mutant) compared to direct sequencing and Inno-LIPA HBV DR, which identified only the dominant population. 2005 Le infezioni in medicina Abstract HBV L180M;M204V;M204I;G1764A;G1896A 87;96;96;34;42 92;103;103;40;48 RT;RT 85;94 87;96 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. Despite the accumulation of L77R HBsAg in ER-Golgi of transfected Huh7 cells, we detected no increase in Grp78 mRNA and proteins, which are common markers for ER stress response. 2005 Journal of virology Abstract HBV L77R 28 32 S 33 38 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. In addition, the 2.8-fold reduction of the extracellular HBV surface antigen (HBsAg) of mutant L77R from transfected Huh7 cells appeared to be correlated with a 1.7-fold reduction of intracellular HBsAg, as measured by enzyme-linked immunosorbent assay (ELISA). 2005 Journal of virology Abstract HBV L77R 95 99 S;S;S 78;197;61 83;202;68 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. In contrast to HBsAg, the secretion of HBeAg was normal in L77R-transfected cells. 2005 Journal of virology Abstract HBV L77R 59 63 C;S 39;15 44;20 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. In contrast, the L77R mutant HBsAg tends to be highly restricted within the ER and Golgi, often accumulated in the Golgi compartments distal from the nucleus. 2005 Journal of virology Abstract HBV L77R 17 21 S 29 34 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. Mutation L77R alone resulted in >10-fold-reduced secretion of virions. 2005 Journal of virology Abstract HBV L77R 9 13 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. The almost exclusive retention in the ER-Golgi of L77R HBsAg was similar to what was observed when the large envelope protein was overexpressed. 2005 Journal of virology Abstract HBV L77R 50 54 Large S;S 103;55 117;60 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. The discrepancy between ELISA and Western blot data was due to significant accumulation of the mutant L77R HBsAg in the intracellular pellet fraction. 2005 Journal of virology Abstract HBV L77R 102 106 S 107 112 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. These multiple aberrant phenotypes of mutant L77R can be corrected by a second naturally occurring S envelope mutation, W74L. 2005 Journal of virology Abstract HBV L77R;W74L 45;120 49;124 S;S 101;99 109;100 16227269 Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus. We identified two novel naturally occurring mutations (W74L and L77R) in the small S envelope protein of hepatitis B virus (HBV). 2005 Journal of virology Abstract HBV W74L;L77R 55;64 59;68 Small S 77 93 16246191 Community-based epidemiology of hepatitis B virus infection in West Bengal, India: prevalence of hepatitis B e antigen-negative infection and associated viral variants. G1896A PC stop codon mutants were present in 12% of people, BCP mutants in 18% and the remainder (70%) of the HBeAg-negative infections were associated with wild type sequences in these regions. 2005 Journal of gastroenterology and hepatology Abstract HBV G1896A 0 6 BCP;C;Precore 60;110;7 63;115;9 16248943 [Complete HBV DNA clone and sequence from serum samples of severe hepatitis B patients]. Among them, 3 cases had a G to A mutation at nucleotide 1896 in pre-C region and 1 had a double mutation of T1762-A1764 in the core promoter region. 2005 Zhonghua gan zang bing za zhi Abstract HBV G1896A 26 60 Core promoter;Precore 127;64 140;69 16257576 Two subtypes (subgenotypes) of hepatitis B virus genotype C: A novel subtyping assay based on restriction fragment length polymorphism. Some specific mutations were detected in the encapsidation signal; precore stop mutation (A1896), accompanied by a C-to-T substitution at nt 1858, was found in HBV/Ce strains, and another precore mutation (A1898), accompanied by a C-to-T mutation at nt 1856, was found in HBV/Cs. 2005 Hepatology research Abstract HBV C1858T;C1856T 115;231 145;257 Precore;Precore 67;188 74;195 16273841 [Characterisation of an HBsAg mutant of hepatitis B virus (HBV) isolated from a dialysed patient involved in an occupational accident]. RESULTS AND CONCLUSIONS: A threonine to lysine substitution at position 118 of HBsAg (Thrll8Lys) was observed in the analysed viral aminoacid sequence. 2005 La Medicina del lavoro Abstract HBV T118K 27 75 S 79 84 16273841 [Characterisation of an HBsAg mutant of hepatitis B virus (HBV) isolated from a dialysed patient involved in an occupational accident]. They consist most commonly of an aminoacid change from glycine to arginine at position 145 of the highly antigenic a determinant of the surface antigen (HBsAg). 2005 La Medicina del lavoro Abstract HBV G145R 55 90 S;S;S 115;153;136 128;158;143 16299725 Frequency of hepatitis B virus 'a' determinant variants in unselected Spanish chronic carriers. Met133Thr (2.2%); Gln129His, Met133Ile, Phe/Tyr134Asn (1.8%); Phe/Tyr134Leu, Gly145Ala (1.5%), and Pro120Thr (1.1%) were the most frequent. 2006 Journal of medical virology Abstract HBV M133T;Q129H;M133I;F134N;Y134N;F134L;Y134L;G145A;P120T 0;18;29;40;40;62;62;77;99 9;27;38;53;53;75;75;86;108 16299725 Frequency of hepatitis B virus 'a' determinant variants in unselected Spanish chronic carriers. Other substitutions, including Gly145Arg (0.4%), were found at a frequency of less than 1%. 2006 Journal of medical virology Abstract HBV G145R 31 40 16299727 Genotype, phylogenetic analysis, and transmission pattern of occult hepatitis B virus (HBV) infection in families of asymptomatic HBsAg carriers. Mutations in the major hydrophilic loop (MHL) of the S gene region were also detected, including the 'vaccine escape' mutation G145R in three cases. 2006 Journal of medical virology Abstract HBV G145R 127 132 S 53 54 16314804 Heart transplantation in patients with chronic hepatitis B: clinical evolution, molecular analysis, and effect of treatment. Lamivudine treatment was initially effective in all patients; three patients during the second year of treatment developed lamivudine resistance-associated mutations (rt-L180M, rt-M204V) with severe disease reactivation, remitted after switch to adefovir treatment. 2005 Transplantation Abstract HBV L180M;M204V 170;180 175;185 RT;RT 167;177 169;179 16358376 Clinical features of chronic hepatitis B patients with YMDD mutation after lamivudine therapy. Four types of YMDD mutation were observed in this study, rtL180M/M204V mutation was the predominant type (26/63, 41.3%). 2005 Journal of Zhejiang University. Science. B Abstract HBV M204V;L180M 65;59 70;64 RT;P 57;14 59;18 16372296 Characteristics of hepatitis B virus in Ghana: full length genome sequences indicate the endemicity of genotype E in West Africa. Of note, the finding of the G145R escape mutant in an unvaccinated Ghanaian blood donor might raise concern as to the ongoing nation-wide hepatitis B vaccination program in Ghana. 2006 Journal of medical virology Abstract HBV G145R 28 33 16373428 Genotypic resistance to lamivudine among hepatitis B virus isolates in Mexico. The isolate from the haemodialysis patient showed a single mutation at codon position 180 (L180M). 2006 The Journal of antimicrobial chemotherapy Abstract HBV L180M 91 96 16373428 Genotypic resistance to lamivudine among hepatitis B virus isolates in Mexico. The isolate from the hepatitis patient showed a double mutation at codon positions 180 (L180M) and 204 (M204V), thus a 2.6% prevalence of genotypic resistance to lamivudine was found. 2006 The Journal of antimicrobial chemotherapy Abstract HBV L180M;M204V 88;104 93;109 Hepatitis 21 30 16378961 Point mutations upstream of hepatitis B virus core gene affect DNA replication at the step of core protein expression. A naturally occurring G1862T mutation upstream of the core AUG affects the bulge of the epsilon signal and generates a "forbidden" residue at the -3 position of the signal peptide cleavage site. 2006 Journal of virology Abstract HBV G1862T 22 28 C 54 58 16378961 Point mutations upstream of hepatitis B virus core gene affect DNA replication at the step of core protein expression. All these mutations antagonized the G1862T mutation on core protein expression. 2006 Journal of virology Abstract HBV G1862T 36 42 C 55 59 16378961 Point mutations upstream of hepatitis B virus core gene affect DNA replication at the step of core protein expression. Cotransfection of the G1862T mutant with a replication-deficient HBV genome that provides core protein in trans also restored genome replication. 2006 Journal of virology Abstract HBV G1862T 22 28 C 90 94 16378961 Point mutations upstream of hepatitis B virus core gene affect DNA replication at the step of core protein expression. This replication defect was associated with reduced expression of core protein and could be overcome by a G1899A covariation, or by nonsense or frameshift mutation in the precore region. 2006 Journal of virology Abstract HBV G1899A 106 112 C;Precore 66;171 70;178 16378967 Dynamics of hepatitis B virus resistance to lamivudine. Virological breakthrough was preceded by 2 to 4 months by the emergence of quasispecies variants bearing amino acid substitutions at RT position 204, i.e., within the YMDD catalytic motif (rtM204V/I). 2006 Journal of virology Abstract HBV M204V;M204I 191;191 198;198 RT;RT;P 133;189;167 135;191;171 16380661 [The incidence rate of hepatitis B virus surface gene variants in Korean children with immunoprophylaxis failure of perinatal infection]. CONCLUSIONS: In Korea, compared to the previous studies of other nations, gene surface variants such as G145R do not appear to play an important role in perinatal immunoprophylaxis failure. 2005 The Korean journal of hepatology Abstract HBV G145R 104 109 S 79 86 16380661 [The incidence rate of hepatitis B virus surface gene variants in Korean children with immunoprophylaxis failure of perinatal infection]. One case was infected by wild type and variants of I126S, and the other by wild type and S114A+I126S, respectively. 2005 The Korean journal of hepatology Abstract HBV S114A;I126S;I126S 89;51;95 94;56;100 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. CASE PRESENTATION: After 2 years of therapy, a cirrhotic patient developed the rtN236T and rtA181T adefovir resistant mutations. 2006 Comparative hepatology Abstract HBV N236T;A181T 81;93 86;98 RT;RT 79;91 81;93 Liver cirrhosis 47 56 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. Initial reports of the rtN236T mutation showed preserved sensitivity to lamivudine; however, complex mutations are emerging with reduced susceptibility to lamivudine. 2006 Comparative hepatology Abstract HBV N236T 25 30 RT 23 25 16419106 Molecular epidemiology of hepatitis B virus in Dakar, Senegal. The BCP A1762T and G1764A mutations were found in four patients and one patient, respectively; the two mutations were never found in the same patient. 2006 Journal of medical virology Abstract HBV A1762T;G1764A 8;19 14;25 BCP 4 7 16419106 Molecular epidemiology of hepatitis B virus in Dakar, Senegal. The W28* mutation at position 1896 of the core was detected in 19 of the 32 genotyped patients, 18 (83%) of whom had genotype E infection. 2006 Journal of medical virology Abstract HBV W28X 4 8 C 42 46 16419112 Fatal liver failure with the emergence of hepatitis B surface antigen variants with multiple stop mutations after discontinuation of lamivudine therapy. Sequencing of HBV isolates revealed that mutations including G145R and stop codons occurred within the HBsAg coding region. 2006 Journal of medical virology Abstract HBV G145R 61 66 S 103 108 16419114 Hepatitis B virus genotyping, core promoter, and precore/core mutations among Afghan patients infected with hepatitis B: a preliminary report. In parallel, precore G1896A mutation was also determined by an amplification-created restriction site method. 2006 Journal of medical virology Abstract HBV G1896A 21 27 Precore 13 20 16419114 Hepatitis B virus genotyping, core promoter, and precore/core mutations among Afghan patients infected with hepatitis B: a preliminary report. The A1762T/G1764A BCP dual mutation was found in one isolate. 2006 Journal of medical virology Abstract HBV G1764A;A1762T 11;4 17;10 BCP 18 21 16419114 Hepatitis B virus genotyping, core promoter, and precore/core mutations among Afghan patients infected with hepatitis B: a preliminary report. Three isolates presented single mutation in the BCP dual mutation region, whereas two showed a novel G1764T mutation. 2006 Journal of medical virology Abstract HBV G1764T 101 107 BCP 48 51 16420761 [Study of the quasispecies dynamics of serum hepatitis B virus in a patient with acute exacerbations of chronic hepatitis B]. All dominant quasispecies, except the one during the second resolution, carried core P5T, L60V, S155T, and precore G1896A mutations. 2006 Zhonghua gan zang bing za zhi Abstract HBV P5T;L60V;S155T;G1896A 85;90;96;115 88;94;101;121 C;Precore 80;107 84;114 16425408 Distribution of HBV genotypes among HBV carriers in Benin:phylogenetic analysis and virological characteristics of HBV genotype E. Based on the sequences in the basic core promoter (BCP) to precore region of the nine HBV/E isolates compared to those of the other genotypes, a nucleotide substitution in the BCP, G1757A, was observed in HBV/E. 2005 World journal of gastroenterology Abstract HBV G1757A 181 187 BCP;BCP;BCP;Precore 30;51;176;59 49;54;179;66 16425408 Distribution of HBV genotypes among HBV carriers in Benin:phylogenetic analysis and virological characteristics of HBV genotype E. The specific nucleotide substitution G1757A in BCP,which might influence the virological characteristics, is observed in HBV/E. 2005 World journal of gastroenterology Abstract HBV G1757A 37 43 BCP 47 50 16428891 Characterization of naturally occurring and Lamivudine-induced surface gene mutants of hepatitis B virus in patients with chronic hepatitis B in India. Following lamivudine therapy, 14 of 57 (24.5%) patients developed 16 types of S-gene mutations (sP120S, sA128V, sS143L, sW182St., sT189I, sV190A, sS193L, sI195M, sW196L, sW196St., sS207R, sI208T, sS210E, sF219S, sF220L and sC221G). 2006 Intervirology Abstract HBV P120S;A128V;S143L;W182X;T189I;V190A;S193L;I195M;W196L;W196X;S207R;I208T;S210E;F219S;F220L;C221G 96;104;112;120;130;138;146;154;162;170;180;188;196;204;212;223 102;110;118;127;136;144;152;160;168;177;186;194;202;210;218;229 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 78;96;104;112;120;130;138;146;154;162;170;180;188;196;204;212;223 79;97;105;113;121;131;139;147;155;163;171;181;189;197;205;213;224 16428891 Characterization of naturally occurring and Lamivudine-induced surface gene mutants of hepatitis B virus in patients with chronic hepatitis B in India. RESULTS: Two (3.5%) patients had naturally occurring HBV mutants, sP127S and sS143L seen in the 'a' determinant of the S-gene. 2006 Intervirology Abstract HBV P127S;S143L 66;77 72;83 S;S;S;S 97;66;77;119 111;67;78;120 16448607 [Lamivudine and adefovir resistance in a patient with HBeAg negative chronic hepatitis B]. Lamivudine was substituted for adefovir dipivoxil and after 16 months of treatment, in the course of a study to investigate hepatitis B genotypes, the adefovir resistance mutation N236T was detected. 2006 Gastroenterologia y hepatologia Abstract HBV N236T 180 185 16448607 [Lamivudine and adefovir resistance in a patient with HBeAg negative chronic hepatitis B]. We have studied a 49-year-old patient with a HBeAg-negative chronic hepatitis B in whom, after 34 months of treatment with lamivudine and associated with an increase in the serum hepatitis B virus (HBV) DNA, the lamivudine resistance mutations M204I and L180V were detected. 2006 Gastroenterologia y hepatologia Abstract HBV M204I;L180V 244;254 249;259 C 45 50 Chronic Hepatitis B 60 79 16461214 Mechanism of HBV genome variability and replication of HBV mutants. Several core promoter mutants were defective in virion secretion, and mapping experiments revealed three missense mutations in the small envelope protein to be responsible: I110M, G119E, and R169P The effect of I110M and G119E mutations can be relieved by another point mutation that creates a novel N-linked glycosylation site. 2005 Journal of clinical virology Abstract HBV I110M;G119E;R169P;I110M;G119E 173;180;191;211;221 178;185;196;216;226 Core promoter;S 8;131 21;145 16461214 Mechanism of HBV genome variability and replication of HBV mutants. We found point mutations upstream of the precore ATG codon of genotype Aa suppressed HBeAg expression, while the G1862T mutation in the precore region greatly impaired viral replication. 2005 Journal of clinical virology Abstract HBV G1862T 113 119 C;Precore;Precore 85;41;136 90;48;143 16461216 The current management of HBV drug resistance. Add-on adefovir therapy is effective in suppressing rtM204 I/V in both compensated and decompensated patients. 2005 Journal of clinical virology Abstract HBV M204I;M204V 54;54 62;62 RT 52 54 16461216 The current management of HBV drug resistance. However, HBV species with mutations in the tyrosine-methionine-aspartate-aspartate (YMDD) locus of the HBV RNA-dependent DNA polymerase (rtM204 I/V) conferring resistance to lamivudine may emerge after 9-10 months therapy. 2005 Journal of clinical virology Abstract HBV M204I;M204V 139;139 147;147 P;RT;P;P 125;137;43;84 135;139;82;88 16461216 The current management of HBV drug resistance. Serum alanine aminotransferase (ALT) elevation and HBV DNA rebound ( I log) occur in >90% of the patients with rtM204 I/V during continued lamivudine therapy. 2005 Journal of clinical virology Abstract HBV M204I;M204V 113;113 121;121 RT 111 113 16461216 The current management of HBV drug resistance. The initial clinical and histologic improvement may also reverse after emergence of rtM204 IN Studies do suggest that stopping seems better than continuing lamivudine therapy. 2005 Journal of clinical virology Abstract HBV M204I 86 93 RT 84 86 16461216 The current management of HBV drug resistance. The overall incidence of adefovirresistant rtN236T and A181V is low, being 0 after one year and 5.9% after 3 years' therapy. 2005 Journal of clinical virology Abstract HBV N236T;A181V 45;55 50;60 RT 43 45 16461777 Resistance to adefovir dipivoxil in lamivudine resistant chronic hepatitis B patients treated with adefovir dipivoxil. Serial quantification of serum HBV DNA revealed that two patients with the rtA181V mutation, with or without the rtN236T mutation, and one patient with the rtA181T mutation displayed HBV DNA rebound. 2006 Gut Abstract HBV A181V;N236T;A181T 77;115;158 82;120;163 RT;RT;RT 75;113;156 77;115;158 16461777 Resistance to adefovir dipivoxil in lamivudine resistant chronic hepatitis B patients treated with adefovir dipivoxil. The rtA181V, rtN236T, and rtA181T mutations were detected in five, four, and two of the 67 patients at treatment months 12-17, 3-19, and 7-20, respectively. 2006 Gut Abstract HBV A181V;N236T;A181T 6;15;28 11;20;33 RT;RT;RT 4;13;26 6;15;28 16517839 Phylogenetic, virological, and clinical characteristics of genotype C hepatitis B virus with TCC at codon 15 of the precore region. HBV with TCC at nucleotides 1856 to 1858 was associated with the G1898A mutation (64%). 2006 Journal of clinical microbiology Abstract HBV G1898A 65 71 16539393 Inhibition of hepatitis B virus (HBV) replication by pyrimidines bearing an acyclic moiety: effect on wild-type and mutant HBV. These compounds were also found to retain sensitivity against lamivudine-resistant HBV containing a single mutation (M204I) and double mutations (L180M/M204V). 2006 Journal of medicinal chemistry Abstract HBV M204V;L180M;M204I 152;146;117 157;151;122 16549970 Characteristics of drug resistant HBV in an international collaborative study of HIV-HBV-infected individuals on extended lamivudine therapy. The triple polymerase mutant (rtL173V, rtL180M, rtM204V), which behaves as a vaccine escape mutant in vitro, occurred in 17% of viraemic patients. 2006 AIDS (London, England) Abstract HBV L173V;L180M;M204V 32;41;50 37;46;55 P;RT;RT;RT 11;30;39;48 21;32;41;50 16553556 HBsAg diagnostic kits in the detection of hepatitis B virus mutation within "a" determinant. Interestingly, any commercial kits with monoclonal antibody capture and polyclonal antibody detection (mono/poly), but not mono/mono Ab capture and detection, could pick up the common HBsAg Gly145Arg mutant either solely or in combination with other mutations within the "a" determinant. 2006 Viral immunology Abstract HBV G145R 190 199 S 184 189 16567005 Evaluation of a new automated assay for hepatitis B surface antigen (HBsAg) detection VIDAS HBsAg Ultra. The VIDAS HBsAg Ultra (L) did not detect one diluted sample out of six bearing the single aa G145R substitution, and two out of 12 diluted samples harbouring multiple aa substitutions. 2006 Journal of virological methods Abstract HBV G145R 93 98 S 10 15 16571836 Hepatitis B virus particle formation in the absence of pregenomic RNA and reverse transcriptase. The I97L C protein mutant, allowing immature nucleocapsid envelopment in the background of an HBV genome, did not promote the envelopment of capsids lacking a pregenome, suggesting that this mutation is not sufficient to induce secretion competence independently of the pregenome. 2006 Journal of virology Abstract HBV I97L 4 8 C;Capsid 9;141 10;148 16611191 Switching to adefovir monotherapy after emergence of lamivudine-resistant mutations in patients with liver cirrhosis. In conclusion, switching to ADV monotherapy after emergence of LAM-resistant rtM204 I/V is effective and safe in cirrhotic patients, even in those with hepatic decompensation. 2006 Journal of viral hepatitis Abstract HBV M204I;M204V 79;79 87;87 RT 77 79 Liver disease;Liver cirrhosis 152;113 174;122 16611191 Switching to adefovir monotherapy after emergence of lamivudine-resistant mutations in patients with liver cirrhosis. Switching to adefovir (ADV) monotherapy is effective in patients with lamivudine (LAM)-resistant hepatitis B virus (HBV) mutations (rtM204 I/V). 2006 Journal of viral hepatitis Abstract HBV M204I;M204V 134;134 142;142 RT 132 134 16611191 Switching to adefovir monotherapy after emergence of lamivudine-resistant mutations in patients with liver cirrhosis. The clinical, biochemical and virological responses were compared between ADV monotherapy in 18 cirrhotic patients and ADV add-on LAM therapy in 10 comparable cirrhotic patients with LAM-resistant rtM204 I/V. 2006 Journal of viral hepatitis Abstract HBV M204I;M204V 199;199 207;207 RT 197 199 Liver cirrhosis;Liver cirrhosis 96;159 105;168 16611347 Case report of lamivudine-resistant hepatitis B virus infection post liver transplantation from a hepatitis B core antibody donor. De novo HBV infection developed more than 3 years after LT with a lamivudine-resistant polymerase mutant containing the rtM204I and rtl180L/M mutations. 2006 American journal of transplantation Abstract HBV M204I 122 127 P;RT;RT 87;120;132 97;122;134 HBV-HIV coinfections 0 21 16618409 Predominance of hepatitis B virus YMDD mutants is prognostic of viral DNA breakthrough. RFMP exploits differences in molecular masses between wild-type and variant bases of rtM204V/I following PCR amplification of HBV DNA with a lower limit of detection being 100 copies/mL. 2006 Gastroenterology Abstract HBV M204V;M204I 87;87 94;94 RT 85 87 16618410 High prevalence and mapping of pre-S deletion in hepatitis B virus carriers with progressive liver diseases. METHODS: The sequences of the pre-S region and the BCP (A1762T, G1764A) and PC (G1896A) mutations were determined in 46 HBV chronic carriers (CC) and 106 age-matched carriers with different stages of liver diseases, including 38 chronic hepatitis (CH), 18 cirrhosis (LC), and 50 hepatocellular carcinoma (HCC). 2006 Gastroenterology Abstract HBV A1762T;G1764A;G1896A 56;64;80 62;70;86 BCP;Precore;PreS 51;76;30 54;78;35 Liver disease;Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 200;229;248;256;279;305;267 214;246;250;265;303;308;269 16622880 Diagnostic impact of the genetic variability of the hepatitis B virus surface antigen gene. However, they do not guarantee full sensitivity, especially for the detection of the G145R mutation and amino acid insertions or substitutions in positions 120-123. 2006 Journal of medical virology Abstract HBV G145R 85 90 16622880 Diagnostic impact of the genetic variability of the hepatitis B virus surface antigen gene. There is also a need for more complete epidemiological data on the prevalence of HBsAg mutants especially for G145R and assays for the (differential) screening of mutants need to be developed and evaluated. 2006 Journal of medical virology Abstract HBV G145R 110 115 S 81 86 16622882 Infections by hepatitis B surface antigen gene mutants in Europe and North America. In some cases, these mutations have included a glycine to arginine substitution at position 145 (G145R), which results in a conformational change and different reactivity to monoclonal antibody reagents than that of the wild-type virus. 2006 Journal of medical virology Abstract HBV G145R;G145R 47;97 95;102 16622882 Infections by hepatitis B surface antigen gene mutants in Europe and North America. Mutations in the a determinant (but not G145R) also have been reported in European patients with chronic HBV infection who have not received HBV vaccine or HBIG. 2006 Journal of medical virology Abstract HBV G145R 40 45 S 17 30 Chronic HBV infection 97 118 16637865 Association of core promoter/precore mutations and viral load in e antigen-negative chronic hepatitis B patients. Apart from core promoter A1762T/G1764A and precore G1896A mutations, other hepatitis B virus (HBV) mutants are detected in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB). 2006 Journal of viral hepatitis Abstract HBV G1764A;A1762T;G1896A 32;25;51 38;31;57 Core promoter;C;C;Precore 11;135;146;43 24;144;151;50 Chronic Hepatitis B;Chronic Hepatitis B 162;183 181;186 16637865 Association of core promoter/precore mutations and viral load in e antigen-negative chronic hepatitis B patients. However, genotype B was significantly associated with precore G1896A mutation (92.5%), and more mutations within nucleotide 1809-1817 were detected in patients infected by genotype B as compared with those infected by genotype C (18.9%vs 3.8%). 2006 Journal of viral hepatitis Abstract HBV G1896A 62 68 Precore 54 61 16637865 Association of core promoter/precore mutations and viral load in e antigen-negative chronic hepatitis B patients. Triple core promoter mutations T1753C/A1762T/G1764A [corrected] appeared to be linked to genotype C rather than genotype B HBV (19.2%vs 1.9%; P = 0.013). 2006 Journal of viral hepatitis Abstract HBV A1762T;G1764A;T1753C 38;45;31 44;51;37 Core promoter 7 20 16637866 Hepatitis B virus genotypes and G1896A precore mutation in 486 Spanish patients with acute and chronic HBV infection. This study aims to determine the prevalence of hepatitis B virus (HBV) genotypes (A-F) and their association with the G1896A precore mutation in 486 patients positive for HBV surface antigen. 2006 Journal of viral hepatitis Abstract HBV G1896A 118 124 Precore;S 125;175 132;182 16641257 A tryptophan-rich motif in the carboxyl terminus of the small envelope protein of hepatitis B virus is central to the assembly of hepatitis delta virus particles. Here, the W196F S-HBsAg deficiency was assigned to a loss of its ability for interaction with the large HDV antigen (L-HDAg), a major component of the RNP. 2006 Journal of virology Abstract HBV W196F 10 15 S 16 23 16641257 A tryptophan-rich motif in the carboxyl terminus of the small envelope protein of hepatitis B virus is central to the assembly of hepatitis delta virus particles. In addition, a W196S S-HBsAg mutant, which has been described in HBV strains that arose in a few cases of lamivudine-treated HBV-infected patients, was deficient for HDV assembly as a consequence of its impaired capacity for interacting with L-HDAg. 2006 Journal of virology Abstract HBV W196S 15 20 S 21 28 HBV infections 125 137 16641257 A tryptophan-rich motif in the carboxyl terminus of the small envelope protein of hepatitis B virus is central to the assembly of hepatitis delta virus particles. Mutation of W196 to phenylalanine (W196F) was permissive for HBV subviral particle (SVP) secretion but deleterious to HDV virion assembly. 2006 Journal of virology Abstract HBV W196F;W196F 35;12 40;33 16641397 Variant of hepatitis B virus with primary resistance to adefovir. All three cases involved a rare HBV variant with a valine at position 233 of the reverse-transcriptase domain instead of isoleucine (rtI233V), as in the wild-type virus. 2006 The New England journal of medicine Abstract HBV I233V 135 140 RT;RT 81;133 102;135 16673294 Antiviral drug resistance: clinical consequences and molecular aspects. In contrast, resistance to adefovir is associated with mutations at rtN236T +/- rtA181V. 2006 Seminars in liver disease Abstract HBV N236T;A181V 70;82 75;87 RT;RT 68;80 70;82 16673294 Antiviral drug resistance: clinical consequences and molecular aspects. The rtM204I/V is selected by lamivudine and L-nucleosides. 2006 Seminars in liver disease Abstract HBV M204I;M204V 6;6 13;13 RT 4 6 16681927 [Identification of hepatitis B virus genotypes in patients with chronic hepatitis B from different nationalities in ethnic minority areas in Yunnan Province, China]. In 45 CHB patients, C genes was identified to have aa substitutions at the positions V 27, N38, V63, Q135, and A147, due to nt variations of 1979A to G, 2012T to A, 2088G to T, 2304C to A, and 2339A to G transitions respectively. 2006 Zhonghua yi xue za zhi Abstract HBV G2088T;C2304A 165;177 175;187 C 20 21 Chronic Hepatitis B 6 9 16681927 [Identification of hepatitis B virus genotypes in patients with chronic hepatitis B from different nationalities in ethnic minority areas in Yunnan Province, China]. In all subjects, the frequency of aa G145R (0.4%) substitutions was less than 1%. 2006 Zhonghua yi xue za zhi Abstract HBV G145R 37 42 16681927 [Identification of hepatitis B virus genotypes in patients with chronic hepatitis B from different nationalities in ethnic minority areas in Yunnan Province, China]. In the 50 CHB patients, the preS2/S genes were identified to have aa substitutions at the positions R124K (1.1%), L172P (1.3%), M306T (1.5%), and I361M (1.6%), with a frequency of more than 1%. 2006 Zhonghua yi xue za zhi Abstract HBV R124K;L172P;M306T;I361M 100;114;128;146 105;119;133;151 PreS2;S 28;34 33;35 Chronic Hepatitis B 10 13 16681927 [Identification of hepatitis B virus genotypes in patients with chronic hepatitis B from different nationalities in ethnic minority areas in Yunnan Province, China]. Whereas as for the other 5 severe CHB patients, the C gene variations of A to G, and A to C transitions at nt positions 2159 and 2189 led to aa substitutions of S to G and I to L at positions G87 and L97. 2006 Zhonghua yi xue za zhi Abstract HBV A2159C 85 124 C 52 53 Chronic Hepatitis B 34 37 16714855 Sequential accumulation of the basal core promoter and the precore mutations in the progression of hepatitis B virus-related chronic liver disease. The A to T mutation at nucleotide 1762 and/or G to A mutation at nucleotide 1764 were found in 30% in HBeAg(+) ASC, 65.7% in inactive HBsAg carrier, 95% in chronic hepatitis B, and 90% in liver cirrhosis (p < 0.001). 2006 Intervirology Abstract HBV A1762T;G1764A 4;46 38;80 C;S 102;134 107;139 Chronic Hepatitis B;Liver cirrhosis 156;188 175;203 16714855 Sequential accumulation of the basal core promoter and the precore mutations in the progression of hepatitis B virus-related chronic liver disease. The prevalence of the G to A mutation at nucleotide 1896 was 5% in HBeAg(+) ASC, 22.5% in inactive HBsAg carrier, 32.5% in chronic hepatitis B, and 50% in liver cirrhosis, respectively (p < 0.001). 2006 Intervirology Abstract HBV G1896A 22 56 C;S 67;99 72;104 Chronic Hepatitis B;Liver cirrhosis 123;155 142;170 16714855 Sequential accumulation of the basal core promoter and the precore mutations in the progression of hepatitis B virus-related chronic liver disease. The T to C/A mutation at nucleotide 1753 in the BCP and G to A mutation at nucleotide 1899 in the precore were more frequent in liver cirrhosis than in the other clinical statuses (p < 0.05). 2006 Intervirology Abstract HBV G1899A 56 90 BCP;Precore 48;98 51;105 Liver cirrhosis 128 143 16729316 Increased risk of adefovir resistance in patients with lamivudine-resistant chronic hepatitis B after 48 weeks of adefovir dipivoxil monotherapy. In conclusion, the emergence of the rtA181V/T and rtN236T mutations was more common in LAM-resistant patients than in treatment-naive patients after 48 weeks of ADV therapy and was associated with reduced antiviral efficacy to drug treatment. 2006 Hepatology (Baltimore, Md.) Abstract HBV A181V;A181T;N236T 38;38;52 45;45;57 RT;RT 36;50 38;52 16729316 Increased risk of adefovir resistance in patients with lamivudine-resistant chronic hepatitis B after 48 weeks of adefovir dipivoxil monotherapy. We compared the emergence of the ADV-resistant mutations rtA181V/T and rtN236T between LAM-resistant patients and treatment-naive patients at 48 weeks of ADV monotherapy. 2006 Hepatology (Baltimore, Md.) Abstract HBV A181V;A181T;N236T 59;59;73 66;66;78 RT;RT 57;71 59;73 16732904 [Dynamic variations of hepatitis B virus polymerase gene in lamivudine-treated hepatitis B patients]. CONCLUSIONS: D553G mutation is probably one of the reasons which caused non-responsiveness to the lamivudine treatment. 2006 Zhonghua gan zang bing za zhi Abstract HBV D553G 13 18 16732904 [Dynamic variations of hepatitis B virus polymerase gene in lamivudine-treated hepatitis B patients]. RESULTS: Among five patients after 12 months lamivudine treatment, M552I mutations in two patients with HBV DNA rebounding and D553G mutation in one non-responder were detected except in two patients with negative HBV DNA. 2006 Zhonghua gan zang bing za zhi Abstract HBV M552I;D553G 67;127 72;132 16757589 Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). By LiPA analysis, 12 patients (31.5%) were found to have mutations associated with resistance to ADV (rtA181V/T and/or rtN236T). 2006 Journal of clinical microbiology Abstract HBV A181V;A181T;N236T 104;104;121 111;111;126 RT;RT 102;119 104;121 16757589 Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). LiPA detected the rtN236T mutation at least 6 months earlier than its detection by sequencing in patients for whom consecutive serum samples were available. 2006 Journal of clinical microbiology Abstract HBV N236T 20 25 RT 18 20 16757589 Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). The INNO-LiPA HBV DR v2 assay is a very sensitive and specific assay for the detection of the rtN236T mutation associated with resistance to ADV. 2006 Journal of clinical microbiology Abstract HBV N236T 96 101 RT 94 96 16757589 Detection of rtN236T and rtA181V/T mutations associated with resistance to adefovir dipivoxil in samples from patients with chronic hepatitis B virus infection by the INNO-LiPA HBV DR line probe assay (version 2). Twice as many samples were rtN236T positive by LiPA (18 of 124) compared to sequence analysis (9 of 124). 2006 Journal of clinical microbiology Abstract HBV N236T 29 34 RT 27 29 16757620 Unusual naturally occurring humoral and cellular mutated epitopes of hepatitis B virus in a chronically infected argentine patient with anti-HBs antibodies. C107R replacement prevents disulfide bonding, thus disrupting the first loop of the HBsAg. 2006 Journal of clinical microbiology Abstract HBV C107R 0 5 S 84 89 16757620 Unusual naturally occurring humoral and cellular mutated epitopes of hepatitis B virus in a chronically infected argentine patient with anti-HBs antibodies. Observed replacements included both humoral and/or cellular (major histocompatibility complex class I [MHC-I] and MHC-II) HBV mutated epitopes, such as S45A, P46H, L49H, C107R, T125A, M133K, I152F, P153T, T161S, G185E, A194T, G202R, and I213L. 2006 Journal of clinical microbiology Abstract HBV S45A;P46H;L49H;C107R;T125A;M133K;I152F;P153T;T161S;G185E;A194T;G202R;I213L 152;158;164;170;177;184;191;198;205;212;219;226;237 156;162;168;175;182;189;196;203;210;217;224;231;242 16757620 Unusual naturally occurring humoral and cellular mutated epitopes of hepatitis B virus in a chronically infected argentine patient with anti-HBs antibodies. The I213L replacement was the only one observed in the five clones carrying nonsynonymous mutations in the S gene. 2006 Journal of clinical microbiology Abstract HBV I213L 4 9 S 107 108 16789011 Changes in viral loads of lamivudine-resistant mutants and evolution of HBV sequences during adefovir dipivoxil therapy. Changes in rtM204I and rtL180M viral loads were greater than that of the rtM204V, albeit statistically insignificant. 2006 Journal of medical virology Abstract HBV M204I;L180M;M204V 13;25;75 18;30;80 RT;RT;RT 11;23;73 13;25;75 16789011 Changes in viral loads of lamivudine-resistant mutants and evolution of HBV sequences during adefovir dipivoxil therapy. Moreover, the greatest change in viral load was seen for rtM204I without hepatitis B e antigen (HBeAg). 2006 Journal of medical virology Abstract HBV M204I 59 64 C;C;RT 85;96;57 94;101;59 16789011 Changes in viral loads of lamivudine-resistant mutants and evolution of HBV sequences during adefovir dipivoxil therapy. We conclude that the rtM204I may be more sensitive to ADV in vivo. 2006 Journal of medical virology Abstract HBV M204I 23 28 RT 21 23 16789011 Changes in viral loads of lamivudine-resistant mutants and evolution of HBV sequences during adefovir dipivoxil therapy. We determined early viral changes (12 weeks) in YMDD mutants (rtM204I [YIDD sequence], rtM204V [YVDD]) and rtL180M in all 39 patients as well as amino acid changes in the polymerase reverse transcriptase (rt) region and precore/core promoter mutations in 15 patients who received long-term treatment (more than 1 year). 2006 Journal of medical virology Abstract HBV M204I;M204V;L180M 64;89;109 69;94;114 Core promoter;P;Precore;RT;RT;RT;RT;RT;P;P;P 228;171;220;182;62;87;107;205;71;48;96 241;181;227;203;64;89;109;207;75;52;100 16789012 Basal core promoter, precore region mutations of HBV and their association with e antigen, genotype, and severity of liver disease in patients with chronic hepatitis B in India. It is concluded that Pc G1862T mutant is Genotype A-specific but is not always associated with e antigen. 2006 Journal of medical virology Abstract HBV G1862T 24 30 Precore;C 21;95 23;104 16789012 Basal core promoter, precore region mutations of HBV and their association with e antigen, genotype, and severity of liver disease in patients with chronic hepatitis B in India. The Pc G1862T mutation was detected more often in HBeAg-positive than HBeAg-negative (37% vs. 2006 Journal of medical virology Abstract HBV G1862T 7 13 Precore;C;C 4;50;70 6;55;75 16789012 Basal core promoter, precore region mutations of HBV and their association with e antigen, genotype, and severity of liver disease in patients with chronic hepatitis B in India. The Pc G1896A mutation was more common in HBeAg-negative (33% vs. 2006 Journal of medical virology Abstract HBV G1896A 7 13 Precore;C 4;42 6;47 16789016 Detection of a hepatitis B surface antigen variant emerging in a patient with chronic lymphocytic leukaemia treated with fludarabine. Amino-acid sequence comparisons over the alpha determinant region revealed the following substitutions: C124N, G130R, and N146S. 2006 Journal of medical virology Abstract HBV C124N;G130R;N146S 104;111;122 109;116;127 S 41 58 16801428 Intracellular metabolism and in vitro activity of tenofovir against hepatitis B virus. Here we show that the major adefovir resistance mutation, rtN236T, confers three- to fourfold-reduced susceptibility to tenofovir in cell culture; the clinical significance of this susceptibility shift has not yet been determined. 2006 Antimicrobial agents and chemotherapy Abstract HBV N236T 60 65 RT 58 60 16801428 Intracellular metabolism and in vitro activity of tenofovir against hepatitis B virus. The rtA194T HBV polymerase mutation recently identified in tenofovir DF-treated HIV/HBV-coinfected patients did not confer in vitro resistance to tenofovir as a single mutation or in a lamivudine-resistant viral background. 2006 Antimicrobial agents and chemotherapy Abstract HBV A194T 6 11 RT;P 4;16 6;26 HBV-HIV coinfections 80 98 16830379 Mutations in surface and polymerase gene of chronic hepatitis B patients with coexisting HBsAg and anti-HBs. Lamivudine (LMV)-selected mutations were found in three patients who developed anti-HBs, which occurred in amino acid positions (196, 198, 199) of the surface protein and in YMDD motif (M204I/V) of the polymerase protein simultaneously. 2006 World journal of gastroenterology Abstract HBV M204I;M204V 186;186 193;193 S;P;S;P 84;202;151;174 87;212;158;178 16856618 The clinical impact of early detection of the YMDD mutant on the outcomes of long-term lamivudine therapy in patients with chronic hepatitis B. Cumulative viral breakthrough rates at 3 years was 75.0% and 14.3% in patients who had the rtM204I mutant and wild-type virus at 3 months, respectively (P=0.002). 2006 Antiviral therapy Abstract HBV M204I 93 98 RT 91 93 16871563 Tenofovir for patients with lamivudine-resistant hepatitis B virus (HBV) infection and high HBV DNA level during adefovir therapy. Lamivudine-associated mutations (rtV173L, rtL180M, rtM204V/I) could be detected in 6 patients at baseline of TDF, but this obviously did not influence the response. 2006 Hepatology (Baltimore, Md.) Abstract HBV V173L;L180M;M204V;M204I 35;44;53;53 40;49;60;60 RT;RT;RT 33;42;51 35;44;53 16871568 Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection. In in vitro transfection experiments, the replication of Bj clone was markedly enhanced by introducing either G1896A or A1762T/G1764A mutation. 2006 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;G1896A 127;120;110 133;126;116 16871568 Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection. In multivariate analysis, age 34 years or older, Bj, HBeAg-negative, total bilirubin 10.0 mg/dL or greater, and G1896A mutation were independently associated with the fulminant outcome. 2006 Hepatology (Baltimore, Md.) Abstract HBV G1896A 112 118 C 53 58 16871568 Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection. Precore (G1896A) and core-promoter (A1762T/G1764A) mutations were more frequent in patients with fulminant than acute self-limited hepatitis (53% vs. 2006 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;G1896A 43;36;9 49;42;15 Core promoter;Precore 21;0 34;7 Acute Hepatitis B 112 140 16907843 Virological analysis, genotypes and mutational patterns of the HBV precore/core gene in HBV/HCV-related hepatocellular carcinoma. A synonymous T1936C mutation was found in all co-infected HCC cases not related to the presence or absence of circulating HCV, and a hypermutated pre-C strain, characterized by the same mutational pattern, was identified in three HCC cases. 2006 Journal of viral hepatitis Abstract HBV T1936C 13 19 Precore 146 151 Hepatocellular carcinoma;Hepatocellular carcinoma 58;230 61;233 16928212 Association of core promoter mutations with viral breakthrough in chronic hepatitis B patients on long-term lamivudine therapy. Core promoter mutations were seen in five of eight (62.5%) and in six of nine (66.6%); classic double mutations (A1762T/G1764A) of core promoter region were detected in two and three patients and novel double mutations of core promoter (G1764T/C1766G) in one patient each of group Ia and Ib patients, respectively. 2006 Journal of gastroenterology and hepatology Abstract HBV G1764A;C1766G;A1762T;G1764T 120;244;113;237 126;250;119;243 Core promoter;Core promoter;Core promoter 0;131;222 13;144;235 16954295 Detection of hepatitis B virus (HBV) genotype E carried--even in the presence of high titers of anti-HBs antibodies--by an Argentinean patient of African descent who had received vaccination against HBV. Both sisters carried an unusual L209V substitution within HBsAg. 2006 Journal of clinical microbiology Abstract HBV L209V 32 37 S 58 63 16954295 Detection of hepatitis B virus (HBV) genotype E carried--even in the presence of high titers of anti-HBs antibodies--by an Argentinean patient of African descent who had received vaccination against HBV. One of them (who had been vaccinated against HBV) exhibited anti-HBs cocirculating antibodies without HBsAg escape mutants, while her unvaccinated sister showed a D144A HBsAg escape mutant without anti-HBs antibodies. 2006 Journal of clinical microbiology Abstract HBV D144A 163 168 S;S;S;S 65;202;102;169 68;205;107;174 16963200 A unique amino acid substitution, T126I, in human genotype C of hepatitis B virus S gene and its possible influence on antigenic structural change. The results showed that an amino acid substitution within the 'a' determinant, T126I, was unique to genotype C, may affect the antigenicity of the HBsAg, and may result in poorer clinical outcomes of patients infected with genotype C viral strains. 2006 Gene Abstract HBV T126I 79 84 S;S 63;147 77;152 16981258 Detection of YMDD mutation using mutant-specific primers in chronic hepatitis B patients before and after lamivudine treatment. Pair primers specific to rtL180M and rtM204V were selected for YVDD detection. 2006 World journal of gastroenterology Abstract HBV L180M;M204V 27;39 32;44 RT;RT;P 25;37;63 27;39;67 16981258 Detection of YMDD mutation using mutant-specific primers in chronic hepatitis B patients before and after lamivudine treatment. Primer specific to rtM204I with an additional 3'-penultimate base mismatched to both the mutant and wild-type sequence was selected for YIDD detection. 2006 World journal of gastroenterology Abstract HBV M204I 21 26 RT;P 19;136 21;140 16981270 Differential reactivity of mouse monoclonal anti-HBs antibodies with recombinant mutant HBs antigens. Mutations outside the "a" determinant at positions 120 (P-->S), 123(T-->N) and 161 (M-->T) were found to affect reactivity of these mAbs. 2006 World journal of gastroenterology Abstract HBV T123N 64 74 S 60 61 16982790 Emergence of a novel lamivudine-resistant hepatitis B virus variant with a substitution outside the YMDD motif. Here we report a novel lamivudine-resistant strain of HBV with an intact YMDD motif, which included an amino acid substitution, rtA181T, in the reverse transcriptase (RT) domain of HBV polymerase. 2006 Antimicrobial agents and chemotherapy Abstract HBV A181T 130 135 P;RT;RT;RT;P 185;144;128;167;73 195;165;130;169;77 16982790 Emergence of a novel lamivudine-resistant hepatitis B virus variant with a substitution outside the YMDD motif. The detected nucleotide substitution was accompanied by the emergence of an additional nucleotide substitution that induced amino acid change (S331C) in the spacer domain. 2006 Antimicrobial agents and chemotherapy Abstract HBV S331C 143 148 16982790 Emergence of a novel lamivudine-resistant hepatitis B virus variant with a substitution outside the YMDD motif. The rtA181T mutant strain displayed a threefold decrease in susceptibility to lamivudine in in vitro experiments in comparison with the wild type. 2006 Antimicrobial agents and chemotherapy Abstract HBV A181T 6 11 RT 4 6 16982790 Emergence of a novel lamivudine-resistant hepatitis B virus variant with a substitution outside the YMDD motif. The substitution also induced a unique amino acid substitution (W172L) in the overlapping hepatitis B surface (HBs) protein. 2006 Antimicrobial agents and chemotherapy Abstract HBV W172L 64 69 S;S 111;102 114;109 16982790 Emergence of a novel lamivudine-resistant hepatitis B virus variant with a substitution outside the YMDD motif. We developed a method to detect this novel rtA181T mutation and a previously reported rtA181T mutation with the HBs stop codon using restriction fragment length polymorphism PCR and identified one patient with the latter pattern among 40 patients with lamivudine resistance. 2006 Antimicrobial agents and chemotherapy Abstract HBV A181T;A181T 45;88 50;93 RT;RT;S 43;86;112 45;88;115 17020942 Analysis of the cytosolic domains of the hepatitis B virus envelope proteins for their function in viral particle assembly and infectivity. One mutation (P29A) was permissive for synthesis of the S- and M-HBsAg but adversely affected the synthesis or stability of L-HBsAg, thereby preventing the assembly of HBV virions. 2006 Journal of virology Abstract HBV P29A 14 18 S;S;S 124;63;56 131;70;57 17030194 Selection of a multiple drug-resistant hepatitis B virus strain in a liver-transplanted patient. As viral load rose again, a single viral population was progressively selected, harboring the rtV173L+L180M+A181V+N236T and sP120S mutations. 2006 Gastroenterology Abstract HBV V173L;L180M;A181V;N236T;P120S 96;102;108;114;124 101;107;113;119;130 RT;S 94;124 96;125 17030194 Selection of a multiple drug-resistant hepatitis B virus strain in a liver-transplanted patient. Interestingly, among these mutants emerged a population harboring only the rtL180M+A181V mutations, conferring lamivudine-resistance in vitro. 2006 Gastroenterology Abstract HBV L180M;A181V 77;83 82;88 RT 75 77 17030194 Selection of a multiple drug-resistant hepatitis B virus strain in a liver-transplanted patient. RESULTS: At baseline, all HBV genomes carried a wild-type (wt) RT gene but 22% harbored the sP120S and 55% the sC107stop mutations within the surface (S) gene associated with vaccine escape. 2006 Gastroenterology Abstract HBV P120S;C107X 92;111 98;120 RT;S;S;S;S 63;92;111;151;142 65;93;112;152;149 17050029 Nucleotide change of codon 38 in the X gene of hepatitis B virus genotype C is associated with an increased risk of hepatocellular carcinoma. A novel nucleotide change that resulted in a proline to serine substitution at codon 38 in HBx (codon-38 change) was preferentially found in patients with HCC. 2006 Journal of hepatology Abstract HBV P38S 45 87 X 91 94 Hepatocellular carcinoma 155 158 17063521 A low rate of hepatitis B virus vaccine breakthrough infections in Mongolia. A G145A "escape mutant" was found in one HBV carrier child only. 2006 Journal of medical virology Abstract HBV G145A 2 7 17074014 YMDD motif variants in inactive hepatitis B carriers detected by Inno-Lipa HBV DR assay. In two patients, only YIDD and/or YVDD variants plus L180M were detected without the presence of wild YMDD motif. 2006 Journal of gastroenterology and hepatology Abstract HBV L180M 53 58 P;P;P 22;102;34 26;106;38 17074014 YMDD motif variants in inactive hepatitis B carriers detected by Inno-Lipa HBV DR assay. Of the 13 patients, 10 (76.9%) also had accompanying L180M mutation. 2006 Journal of gastroenterology and hepatology Abstract HBV L180M 53 58 17086064 A novel hepatitis B virus mutation with resistance to adefovir but not to tenofovir in an HIV-hepatitis B virus-co-infected patient. A molecular virology analysis performed in an HIV-hepatitis B virus (HBV) co-infected patient showed the emergence of an unusual HBV polymerase gene mutation (rt A181T) under adefovir therapy, conferring resistance to adefovir but not to tenofovir, as proved by in-vitro phenotypic analysis. 2006 AIDS (London, England) Abstract HBV A181T 162 167 P;RT 133;159 143;161 17115304 Analysis of hepatitis B surface antigen mutations in Mongolia: molecular epidemiology and implications for mass vaccination. Pro127Thr and Thr118Ala were the most common substitutions, which occurred in 6 (10.5%) and 3 (5.3%) subjects, respectively; none had Gly145Arg. 2007 Archives of virology Abstract HBV P127T;T118A;G145R 0;14;134 9;23;143 17133475 Entecavir resistance is rare in nucleoside naive patients with hepatitis B. Three ETV rebounds were attributable to LVDr virus present at baseline, with one having a S202G ETV resistance (ETVr) substitution emerge at Week 48. 2006 Hepatology (Baltimore, Md.) Abstract HBV S202G 90 95 17134939 Reactivation of an occult hepatitis B virus escape mutant in an anti-HBs positive, anti-HBc negative lymphoma patient. The virus exhibited three S gene mutations (L109R, C137W, G145R) which led to false negative HBsAg results and diminished binding of vaccine-induced anti-HBs. 2007 Journal of clinical virology Abstract HBV C137W;L109R;G145R 51;44;58 56;49;63 S;S;S 154;93;26 157;98;27 17178796 Two-year assessment of entecavir resistance in Lamivudine-refractory hepatitis B virus patients reveals different clinical outcomes depending on the resistance substitutions present. Prior studies showed that virologic rebound due to ETV resistance (ETVr) required preexisting LVDr HBV reverse transcriptase substitutions M204V and L180M plus additional changes at T184, S202, or M250. 2007 Antimicrobial agents and chemotherapy Abstract HBV M204V;L180M 139;149 144;154 RT 103 124 17187404 Regulation of Toll-like receptor-2 expression in chronic hepatitis B by the precore protein. These results were confirmed in vitro using hepatic cell lines transduced with recombinant HBV baculovirus expressing wild-type HBV (HBeAg-positive), precore stop codon (G1896A) mutant HBV (HBeAg-negative). 2007 Hepatology (Baltimore, Md.) Abstract HBV G1896A 170 176 C;C;Precore 133;190;150 138;195;157 17201657 Hepatitis B virus DNA in unusual serological profiles of hepatitis B surface antigen-positive sera. Among 11 HBV DNA-positive sera, G145A was detected in 2 samples in group I, with the remaining samples identical to the wild-type virus. 2006 Viral immunology Abstract HBV G145A 32 37 17203204 Genotype and variations in core promoter and pre-core regions are related to progression of disease in HBV-infected patients from Northern Vietnam. The presence of the mutation A1762T/G1764A correlated with disease progression. 2007 International journal of molecular medicine Abstract HBV G1764A;A1762T 36;29 42;35 17203204 Genotype and variations in core promoter and pre-core regions are related to progression of disease in HBV-infected patients from Northern Vietnam. The rates of HBeAg seroconversion and G1896A for genotype B were significantly higher than those for genotype C (P<0.05). 2007 International journal of molecular medicine Abstract HBV G1896A 38 44 C 13 18 17203204 Genotype and variations in core promoter and pre-core regions are related to progression of disease in HBV-infected patients from Northern Vietnam. The triple mutation T1753C/A1762T/ G1764A was quite common and was more prevalent in LC and HCC than in CH and ASC. 2007 International journal of molecular medicine Abstract HBV A1762T;T1753C;G1764A 27;20;35 33;26;41 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B 92;85;104 95;87;106 17210268 A new hepatitis B virus vaccine escape mutation in a renal transplant recipient. The sequencing data showed that the HBV strain carried five amino acid substitutions in the major hydrophilic region of the S protein, one (sS143L) located at the "a" determinant. 2007 Journal of clinical virology Abstract HBV S143L 140 146 S;S 124;140 125;141 17211692 Prevalence of hepatitis B virus genotype D in precore mutants among chronic liver disease patients from New Delhi, India. Our objective in this study was to genotype and detect the precore mutant with a point mutation from G to A at nucleotide 1896 using ligase chain reaction (LCR) and direct sequencing. 2007 Digestive diseases and sciences Abstract HBV G1896A 101 126 Precore 59 66 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. Although the rtM204I mutation reduced the production of HBV replicative intermediates, no effect on the level of covalently closed circular DNA or HBV transcripts was observed at late time points. 2007 Journal of virology Abstract HBV M204I 15 20 RT 13 15 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. Coinfection studies with different ratios of wt and rtM204I baculoviruses showed that the rtM204I variant did not produce a product that inhibited HBV replication. 2007 Journal of virology Abstract HBV M204I;M204I 54;92 59;97 RT;RT 52;90 54;92 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. However, the combination of the wt and rtM204I baculoviruses yielded HBV DNA levels at late time points that were greater than those for the wt alone, suggesting that wt polymerase may function in trans to boost rtM204I replication. 2007 Journal of virology Abstract HBV M204I;M204I 41;214 46;219 P;RT;RT 170;39;212 180;41;214 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. In contrast, when the rtM204I mutation was introduced into wt HBV, by day 10 postinfection the levels of intra- and extracellular HBV DNA were markedly reduced compared to those for wt HBV. 2007 Journal of virology Abstract HBV M204I 24 29 RT 22 24 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. In this study, HBV replication in HepG2 cells initiated by transduction with precore (PC), rtM204I, and wild-type (wt) HBV recombinant baculoviruses was compared. 2007 Journal of virology Abstract HBV M204I 93 98 Precore;Precore;RT 86;77;91 88;84;93 17215289 In vitro study of the effects of precore and lamivudine-resistant mutations on hepatitis B virus replication. We concluded that the rtM204I mutation generates a polymerase that is not only resistant to lamivudine but also replicates nucleic acids to lower levels in vitro. 2007 Journal of virology Abstract HBV M204I 24 29 RT;P 22;51 24;61 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. Mutations identified were Y100N, T126I, Q129H and N146K in the asymptomatic group, and F93I and A128V in the symptomatic group. 2007 Virology journal Abstract HBV Y100N;T126I;Q129H;N146K;F93I;A128V 26;33;40;50;87;96 31;38;45;55;91;101 17224847 Hepatitis B virus genotypes and lamivudine resistance mutations in HIV/hepatitis B virus-coinfected patients. The dual L180M + M204V/I mutant was the predominant resistance pattern, although a triple rt173V + 180M + 204V, which acts as a vaccine escape mutant, was found in 1 individual. 2007 Journal of acquired immune deficiency syndromes (1999) Abstract HBV L180M;M204V;M204I 9;17;17 14;24;24 RT 90 92 17237626 [Resistance to adefovir in patients with chronic hepatitis B]. Other mutations in the HBV polymerase (rtP237H, rtN238T/D, rtV84M, rtS85A, rtV214A, rtQ215S) reduce sensitivity to adefovir, but the significance of these mutations is unclear. 2006 The Korean journal of hepatology Abstract HBV P237H;N238T;N238D;V84M;S85A;V214A;Q215S 41;50;50;61;69;77;86 46;57;57;65;73;82;91 P;RT;RT;RT;RT;RT;RT 27;39;48;59;67;75;84 37;41;50;61;69;77;86 17237626 [Resistance to adefovir in patients with chronic hepatitis B]. Two major mutations of adefovir resistance are rtN236T and rtA181V/T. 2006 The Korean journal of hepatology Abstract HBV N236T;A181V;A181T 49;61;61 54;68;68 RT;RT 47;59 49;61 17239478 Stepwise process for the development of entecavir resistance in a chronic hepatitis B virus infected patient. Although the rtL180M+S202G+M204V variant, that prevailed at the end of entecavir therapy, did not show the highest viral genome replication capacity, it conferred one of the strongest resistance levels to entecavir. 2007 Journal of hepatology Abstract HBV L180M;S202G;M204V 15;21;27 20;26;32 RT 13 15 17239478 Stepwise process for the development of entecavir resistance in a chronic hepatitis B virus infected patient. RESULTS: A mixture of lamivudine-resistant HBV strains coexisted following viral breakthrough to lamivudine, all harboring the rtM204V mutation. 2007 Journal of hepatology Abstract HBV M204V 129 134 RT 127 129 17239478 Stepwise process for the development of entecavir resistance in a chronic hepatitis B virus infected patient. The rtV173L+L180M+M204V dominant mutant displayed strong lamivudine-resistance and the highest replication capacity. 2007 Journal of hepatology Abstract HBV V173L;L180M;M204V 6;12;18 11;17;23 RT 4 6 17239478 Stepwise process for the development of entecavir resistance in a chronic hepatitis B virus infected patient. Three years later, the viral load rose again, and a complex mixture of entecavir-resistant strains, all harboring the lamivudine-resistance signature rtL180M+M204V and the rtS202G mutation were observed. 2007 Journal of hepatology Abstract HBV S202G;L180M;M204V 174;152;158 179;157;163 RT;RT 150;172 152;174 17244449 [The rate of hepatitis B virus resistance to adefovir dipivoxil (ADV) and the evolution of hepatitis B virus in lamivudine-resistant chronic hepatitis B patients with ADV monotherapy]. The addition of Lam to the ongoing ADV treatment had poorer antiviral response in the patient with rtA181S or rtA181S+N236T mutant infection; one clone with multi-drug resistant mutations was selected during Lam and ADV combination therapy. 2007 Zhonghua gan zang bing za zhi Abstract HBV A181S;A181S;N236T 101;112;118 106;117;123 RT;RT 99;110 101;112 17244449 [The rate of hepatitis B virus resistance to adefovir dipivoxil (ADV) and the evolution of hepatitis B virus in lamivudine-resistant chronic hepatitis B patients with ADV monotherapy]. The evolution analysis of HBV mutant strains in an ADV-resistant CHB patient showed that the proportion of YMDD mutants gradually decreased with rtA181S mutants increasing over time after ADV monotherapy, and that rtA181S+N236T mutants became the predominant strains during prolonged ADV monotherapy. 2007 Zhonghua gan zang bing za zhi Abstract HBV A181S;A181S;N236T 147;216;222 152;221;227 RT;RT;P 145;214;107 147;216;111 Chronic Hepatitis B 65 68 17245721 Molecular epidemiological study of hepatitis B virus infection in two different ethnic populations from the Solomon Islands. While the prevalence of the BCP mutation (T(1762)A(1764)) tended to be higher in HBV/C, that of the Pre-C mutation (T(1846)) was significantly higher in HBV/D (P < 0.0001). 2007 Journal of medical virology Abstract HBV T1762A 42 49 BCP;Precore 28;100 31;105 17258721 Identification of a hepatitis B virus S gene mutant in lamivudine-treated patients experiencing HBsAg seroclearance. A mutation hot spot, P120A in the S gene, was identified in 6 of the 11 patients. 2007 Gastroenterology Abstract HBV P120A 21 26 S 34 35 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. CONCLUSION: In our community, G1862T mutation was predominantly found in HBV/A1 isolates irrespective of HBeAg status. 2007 Intervirology Abstract HBV G1862T 30 36 C 105 110 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. G1862T was detected in 18 samples, 15 (83%) of them belonged to genotype A (subgenotype HBV/A1), 3 (17%) to genotype D. 2007 Intervirology Abstract HBV G1862T 0 6 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. OBJECTIVE: To study the prevalence of G1862T mutation in hepatitis B virus (HBV) isolates among Eastern Indian patients and its relationship with genotypes, HBeAg status and disease manifestation. 2007 Intervirology Abstract HBV G1862T 38 44 C 157 162 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. The mean viral load was lower in patients with G1862T mutation. 2007 Intervirology Abstract HBV G1862T 47 53 17259736 G1862T mutation among hepatitis B virus-infected individuals: association with viral genotypes and disease outcome in Kolkata, Eastern India. These findings indicate that the G1862T mutation is probably a part of the natural variability of HBV/A1. 2007 Intervirology Abstract HBV G1862T 33 39 17302381 Unusual selection of rtA181V HBV mutants cross-resistant to adefovir following prolonged lamivudine monotherapy: report of two cases. The A181V mutation within the reverse transcriptase (RT) of HBV has been shown to be associated with HBV resistance to adefovir dipivoxil (ADV), and its level of sensitivity to other nucleos(t)ide analogues is an important issue. 2006 Antiviral therapy Abstract HBV A181V 4 9 RT;RT 30;53 51;55 17302381 Unusual selection of rtA181V HBV mutants cross-resistant to adefovir following prolonged lamivudine monotherapy: report of two cases. These observations suggest that rtA181V mutation may unusually emerge under LAM monotherapy, and may be associated with cross resistance to LAM and ADV, but remains sensitive to tenofovir disoproxil fumarate. 2006 Antiviral therapy Abstract HBV A181V 34 39 RT 32 34 17302381 Unusual selection of rtA181V HBV mutants cross-resistant to adefovir following prolonged lamivudine monotherapy: report of two cases. This article reports two cases of chronically HBV infected patients who developed rtA181V HBV mutants following lamivudine (LAM) monotherapy. 2006 Antiviral therapy Abstract HBV A181V 84 89 RT 82 84 HBV infections 46 58 17310821 Virological response and incidence of adefovir resistance in lamivudine-resistant patients treated with adefovir dipivoxil. Of the 46 patients, 11 had ADV resistance (5 rtN236T, 5 rtA181T, 1 rtA181T and rtN236T). 2006 Antiviral therapy Abstract HBV N236T;A181T;A181T;N236T 47;58;69;81 52;63;74;86 RT;RT;RT;RT 45;56;67;79 47;58;69;81 17317127 Dynamic changes of hepatitis B virus polymerase gene including YMDD motif in lamivudine-treated patients with chronic hepatitis B. Among five patients after 12 months of lamivudine treatment, M552I mutations in two patients with HBV DNA rebounding and D553G mutation in one non-responder were detected except two patients with negative HBV DNA consecutively. 2008 Microbiological research Abstract HBV M552I;D553G 61;121 66;126 17317127 Dynamic changes of hepatitis B virus polymerase gene including YMDD motif in lamivudine-treated patients with chronic hepatitis B. In summary, D553G mutation is probably one of the reasons that caused non-responders during lamivudine treatment. 2008 Microbiological research Abstract HBV D553G 12 17 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. HepG2 cells were transfected with the four plasmids and a plasmid expressing G145R HBsAg. 2007 Zhonghua gan zang bing za zhi Abstract HBV G145R 77 82 S 83 88 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. METHODS: Four recombinant plasmids expressing mutant HBsAg (mtHBsAg) P1120T, C121S, K122I and T123N were constructed. 2007 Zhonghua gan zang bing za zhi Abstract HBV P1120T;C121S;K122I;T123N 69;77;84;94 75;82;89;99 S 53 58 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. mtHBsAg with C121S and K122I was not recognized by any mAbs. 2007 Zhonghua gan zang bing za zhi Abstract HBV C121S;K122I 13;23 18;28 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. mtHBsAg with T123N in lysates was recognized by mAb2, but not recognized in the supernatants. 2007 Zhonghua gan zang bing za zhi Abstract HBV T123N 13 18 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. RESULTS: mtHBsAg with P120T was recognized by mAb1 and mAb2. 2007 Zhonghua gan zang bing za zhi Abstract HBV P120T 22 27 17362631 [Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen]. The immunoreactivity of the cells expressing mtHBsAg with P1120T, C121S, K122I, T123N and G145R were detected by immunofluorescence (IF) staining and ELISA with 4 antibodies and 7 HBsAg diagnostic kits respectively. 2007 Zhonghua gan zang bing za zhi Abstract HBV P1120T;C121S;K122I;T123N;G145R 58;66;73;80;90 64;71;78;85;95 S 180 185 17376881 Clinical and virological characteristics of hepatitis B virus subgenotypes Ba, C1, and C2 in China. In contrast, HBV Ba had the highest frequency of 1896A but the lowest of A1762T G1764A, and HBV C2 had intermediate frequencies of these mutations. 2007 Journal of clinical microbiology Abstract HBV A1762T;G1764A 73;80 79;86 17376881 Clinical and virological characteristics of hepatitis B virus subgenotypes Ba, C1, and C2 in China. Multivariate analyses showed that the 1653T, 1753V, and A1762T G1764A mutations and patient age significantly increased the risk of HCC development. 2007 Journal of clinical microbiology Abstract HBV A1762T;G1764A 56;63 62;69 Hepatocellular carcinoma 132 135 17376881 Clinical and virological characteristics of hepatitis B virus subgenotypes Ba, C1, and C2 in China. Therefore, genotyping and detecting the 1653T and 1753V mutations, in addition to the A1762T G1764A double mutation, might have important clinical implications as predictive risk factors for hepatocarcinogenesis. 2007 Journal of clinical microbiology Abstract HBV A1762T;G1764A 86;93 92;99 17376881 Clinical and virological characteristics of hepatitis B virus subgenotypes Ba, C1, and C2 in China. Virologically, HBV C1 had the strongest association with the A1762T G1764A double mutation, while the mutation at position 1896 resulting in A (1896A) was uncommon. 2007 Journal of clinical microbiology Abstract HBV A1762T;G1764A 61;68 67;74 17380283 Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection. In univariate analysis, seronegativity for hepatitis B envelope antigen (HBeAg) and mutations in both the precore (G1896A and/or G1899A) and core promoter (T1753A/C and/or T1754C/G and/or A1762T/G1764A) were associated with FH (odds ratio [OR], 5.60; P=0.0269 and OR, 52.0; P=0.0006; respectively). 2007 Journal of gastroenterology Abstract HBV G1764A;A1762T;G1896A;G1899A;T1753A;T1753C;T1754C;T1754G 195;188;115;129;156;156;172;172 201;194;121;135;164;164;180;180 Core promoter;S;C;Precore 141;55;73;106 154;63;78;113 Fulminant Hepatitis B 224 226 17400303 Adefovir dipivoxil treatment of lamivudine-resistant chronic hepatitis B. The rtN236T, rtA181V/T and rtI233V were not identified before ADV therapy and the genotypic mutation of rtN236T was detected in one (3.4%) patient. 2007 Antiviral research Abstract HBV N236T;A181V;A181T;I233V;N236T 6;15;15;29;106 11;22;22;34;111 RT;RT;RT;RT 4;13;27;104 6;15;29;106 17402992 Early virological suppression is associated with good maintained response to adefovir dipivoxil in lamivudine resistant chronic hepatitis B. Alanine aminotransferase, HBV genotype, rtL80 M mutation and log HBsAg did not affect the HBV DNA response. 2007 Alimentary pharmacology & therapeutics Abstract HBV L80M 42 47 S;RT 65;40 70;42 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Analysis of a large sequence database revealed that rtL80V/I occurred almost exclusively in association with LMV resistance, and 85% of these isolates encoded rtL80I. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80V;L80I;L80I 54;54;161 60;60;165 RT;RT 52;159 54;161 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Collectively, these results suggest that coselection of rtL80V/I and rtM204I/V occurs because the former compensates for the loss of replication efficiency associated with the acquisition of LMV resistance, particularly in the case of rtM204I. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80V;L80I;M204I;M204V;M204I 58;58;71;71;237 64;64;78;78;242 RT;RT;RT 56;69;235 58;71;237 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Coselection of rtL80V/I occurred in 46% of isolates in which LMV resistance was attributable to rtM204I but only 9% of those in which resistance was attributable to rtM204V. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80V;L80I;M204I;M204V 17;17;98;167 23;23;103;172 RT;RT;RT 15;96;165 17;98;167 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Genotyping has shown that LMV treatment can select for HBV rtL80V/I mutants, but their prevalence and phenotype have not been documented. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80V;L80I 61;61 67;67 RT 59 61 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. In vitro phenotyping showed that although the rtL80I mutant by itself replicated less efficiently and was hypersensitive to LMV compared to the replication efficiency and sensitivity of its wild-type parent, the presence of rtL80I enhanced the replication efficiency of rt204I/V mutants without significantly affecting LMV resistance. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80I;L80I 48;226 52;230 RT;RT;RT 46;224;270 48;226;272 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Moreover, rtL80V/I did not occur in HBV genotype A isolates but occurred at similar frequencies in genotype B, C, and D isolates. 2007 Antimicrobial agents and chemotherapy Abstract HBV L80V;L80I 12;12 18;18 RT 10 12 17438047 The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Mutations that result in the replacement of the methionine at position 204 of the deoxynucleoside triphosphate-binding site of the hepatitis B virus (HBV) reverse transcriptase (rt) by isoleucine, valine, or (rarely) serine (rtM204I/V/S) confer high-level resistance to LMV but reduce replication efficiency. 2007 Antimicrobial agents and chemotherapy Abstract HBV M204I;M204V;M204S 227;227;227 236;236;236 RT;RT;RT 155;178;225 176;180;227 17464459 A weak association between occult HBV infection and non-B non-C hepatocellular carcinoma in Japan. In the NBNC-HCC group, the determined nucleotide sequences of the enhancer II/core promoter/precore/core region did not contain any HCC-associated mutations, whereas 25 of 30 patients in the HBV-HCC group carried strains with C1653T, T1753V, and/or A1762T/G1764A mutations. 2007 Journal of gastroenterology Abstract HBV G1764A;A1762T;C1653T;T1753V 256;249;226;234 262;255;232;240 C;Core promoter;Enh II;Precore 100;78;66;92 104;91;77;99 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 12;132;195 15;135;198 17498248 Analysis of the core gene of hepatitis B virus in Korean patients. The frequency of the codon I97F substitutions was the highest in group III. 2007 Liver international Abstract HBV I97F 27 31 17498766 Influences on hepatitis B virus replication by a naturally occurring mutation in the core gene. A HBV clone isolated from a patient with fulminant hepatitis was analyzed, and the features of the particular mutations observed around furin cleavage site in core region (A2339G/G2345A) were assessed using an in vitro replication model. 2007 Virology Abstract HBV G2345A;A2339G 179;172 185;178 C 159 163 Fulminant Hepatitis B 41 60 17498766 Influences on hepatitis B virus replication by a naturally occurring mutation in the core gene. In conclusion, the A2339G mutation was considered as one of the viral factors involved in high replication efficiency. 2007 Virology Abstract HBV A2339G 19 25 17498766 Influences on hepatitis B virus replication by a naturally occurring mutation in the core gene. Replication efficiency of 1.24-fold HBV genome in Huh-7 cells was increased in the presence of A2339G. 2007 Virology Abstract HBV A2339G 95 101 17498766 Influences on hepatitis B virus replication by a naturally occurring mutation in the core gene. The clone belonged to genotype B with precore stop codon mutation (G1896A). 2007 Virology Abstract HBV G1896A 67 73 Precore 38 45 17503077 Hepatitis B virus genotype E surface antigen detection with different immunoassays and diagnostic impact of mutations in the preS/S gene. DNA positive samples with no detectable HBsAg or reduced HBsAg detection signals (<75% of mean signal obtained with HBsAg positive samples) revealed several mutations (V14A, F46S, N48T, L49R, I49T, D51G, A53V, P54L, Q82P, F83C, L127P, A184V, T189I, S204N, V224A), mostly outside the a-determinant. 2007 Medical microbiology and immunology Abstract HBV V14A;F46S;N48T;L49R;I49T;D51G;A53V;P54L;Q82P;F83C;L127P;A184V;T189I;S204N;V224A 168;174;180;186;192;198;204;210;216;222;228;235;242;249;256 172;178;184;190;196;202;208;214;220;226;233;240;247;254;261 S;S;S 40;57;116 45;62;121 17506609 Hepatitis B virus genotype distribution and its lamivudine-resistant mutants in HIV-coinfected patients with chronic and occult hepatitis B. Additionally, two of them exhibited the additional rtV173L mutation. 2007 AIDS research and human retroviruses Abstract HBV V173L 53 58 RT 51 53 17506609 Hepatitis B virus genotype distribution and its lamivudine-resistant mutants in HIV-coinfected patients with chronic and occult hepatitis B. These viral strains showed a methionine-to-valine substitution at codon 204 (rtM204V) in association with an upstream B-domain change at rtL180M. 2007 AIDS research and human retroviruses Abstract HBV M204V;L180M;M204V 79;139;29 84;144;75 RT;RT 77;137 79;139 17526429 Presence of hepatitis B virus core promoter mutations pre-seroconversion predict persistent viral replication after HBeAg loss. Pre-seroconversion mutations in the core promoter region including A1762T and/or G1764A were detected more frequently in group 1 (P=0.031). 2007 Journal of clinical virology Abstract HBV A1762T;G1764A 67;81 73;87 Core promoter 36 49 17567633 Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. All but three patients had baseline rtM204I/V substitutions associated with rtL180M in 23, rtL80I/V in 14, rtV173L in 4, rtT184S in 3, rtQ215S in 2 and rtA181S in 2 cases. 2007 The Journal of antimicrobial chemotherapy Abstract HBV M204I;M204V;L180M;L80I;L80V;V173L;T184S;Q215S;A181S 38;38;78;93;93;109;123;137;154 45;45;83;99;99;114;128;142;159 RT;RT;RT;RT;RT;RT;RT 36;76;91;107;121;135;152 38;78;93;109;123;137;154 17567633 Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. At least one of rtA181S and rtT184S substitutions correlated negatively with IVR and CVR (univariate analysis, P=0.001) and was independently associated with absence of CVR (P = 0.016). 2007 The Journal of antimicrobial chemotherapy Abstract HBV A181S;T184S 18;30 23;35 RT;RT 16;28 18;30 17567633 Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. Four of the six patients (67%) without 24 month CVR showed rtA181S or rtT184S substitutions either alone or with typical lamivudine resistance profiles. 2007 The Journal of antimicrobial chemotherapy Abstract HBV A181S;T184S 61;72 66;77 RT;RT 59;70 61;72 17567633 Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. rtA181S without rtM204I/V was found in one patient. 2007 The Journal of antimicrobial chemotherapy Abstract HBV A181S;M204I;M204V 2;18;18 7;25;25 RT;RT 0;16 2;18 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. However, load changes for rtM204I alone were greater than those for the rtM204I + rtM204V mixed-type (P = 0.042, at both 40 and 52 weeks). 2008 Hepatology research Abstract HBV M204I;M204I;M204V 28;74;84 33;79;89 RT;RT;RT 26;72;82 28;74;84 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. Load changes in rtM204I and rtM204V with G1896A tended to be greater than those without. 2008 Hepatology research Abstract HBV M204I;M204V;G1896A 18;30;41 23;35;47 RT;RT 16;28 18;30 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. Moreover, G1896A was replaced by wild-type virus in two patients at 52 weeks. 2008 Hepatology research Abstract HBV G1896A 10 16 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. RESULTS: Changes in viral loads of rtM204I and rtM204V were similar. 2008 Hepatology research Abstract HBV M204I;M204V 37;49 42;54 RT;RT 35;47 37;49 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. Viral changes in YMDD mutants (rtM204I, rtM204V), amino acid changes in the polymerase reverse transcriptase region and precore/core promoter mutations at 52 weeks were determined in 18 patients. 2008 Hepatology research Abstract HBV M204I;M204V 33;42 38;47 Core promoter;P;Precore;RT;RT;RT;P 128;76;120;87;31;40;17 141;86;127;108;33;42;21 17573951 Changes in viral loads of lamivudine-resistant mutants during entecavir therapy. We investigated viral load changes of YMDD mutant virus (rtM204I [YIDD sequence], rtM204V [YVDD]) in serial serum samples during entecavir treatment for lamivudine-resistant virus and determined changes in viral precore and core promoter mutants. 2008 Hepatology research Abstract HBV M204I;M204V 59;84 64;89 Core promoter;Precore;RT;RT;P;P;P 224;212;57;82;66;38;91 237;219;59;84;70;42;95 17576389 Long-term surveillance of haematopoietic stem cell recipients with resolved hepatitis B: high risk of viral reactivation even in a recipient with a vaccinated donor. A novel HBV surface mutant (D144G/G145E) was isolated from one recipient of stem cells from a donor vaccinated against HBV. 2007 Journal of viral hepatitis Abstract HBV G145E;D144G 34;28 39;33 S 12 19 17576389 Long-term surveillance of haematopoietic stem cell recipients with resolved hepatitis B: high risk of viral reactivation even in a recipient with a vaccinated donor. Another surface mutant (P142L/G145R) was detected in a recipient from a non-immune donor. 2007 Journal of viral hepatitis Abstract HBV G145R;P142L 30;24 35;29 S 8 15 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. Hepatitis B virus (HBV) polymerase mutations associated with virological breakthrough to ADV include rtA181V and rtN236T, which occur alone or in combination. 2007 Antiviral therapy Abstract HBV A181V;N236T 103;115 108;120 P;RT;RT 24;101;113 34;103;115 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. METHODS: To investigate the in vitro activity of adefovir and other anti-HBV agents against these mutants, we generated five stable cell lines that each expressed one of the following HBV mutants: rtN236T, rtA181V, rtA181V + rtN236T, rtA181T + rtN236T and rtA181T. 2007 Antiviral therapy Abstract HBV N236T;A181V;A181V;N236T;A181T;N236T;A181T 199;208;217;227;236;246;258 204;213;222;232;241;251;263 RT;RT;RT;RT;RT;RT;RT 197;206;215;225;234;244;256 199;208;217;227;236;246;258 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. Our results and preliminary clinical data suggest that patients with rtN236T or rtA181V remain susceptible to tenofovir, entecavir and lamivudine. 2007 Antiviral therapy Abstract HBV N236T;A181V 71;82 76;87 RT;RT 69;80 71;82 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. RESULTS: The rtN236T mutant had 7-fold resistance to adefovir but remained sensitive to entecavir, telbivudine and torcitabine (53.2-fold reduced susceptibility). 2007 Antiviral therapy Abstract HBV N236T 15 20 RT 13 15 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. The A181V + rtN236T double mutant was the most highly resistant showing 18-fold resistance to adefovir and higher levels of resistance to other tested drugs with the exception of tenofovir (10-fold reduced susceptibility). 2007 Antiviral therapy Abstract HBV N236T;A181V 14;4 19;9 RT 12 14 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. The A181V mutant had 4.3-fold resistance to adefovir and had reduced susceptibility to multiple other agents ranging from 3.2-fold (tenofovir) to >191-fold (clevudine). 2007 Antiviral therapy Abstract HBV A181V 4 9 17591025 In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents. The rtA181T mutation has also been observed at low frequency, alone or in combination with rtN236T. 2007 Antiviral therapy Abstract HBV A181T;N236T 6;93 11;98 RT;RT 4;91 6;93 17601044 [Impact of amino acid sequence variation of a determinant(s) on the antigenic properties of hepatitis B virus HBsAg]. Eleven recombinant HBsAg variants of wild (adr, ayw2, adw2, adw4, aywl, adw2) and vaccine escape (adw2 T126S, adw2 Q129L, adw2 Q129R, adw2 T143K, adw2 Q145R, aywl Q145A) were obtained. 2007 Voprosy virusologii Abstract HBV T126S;Q129L;Q129R;T143K;Q145R;Q145A 103;115;127;139;151;163 108;120;132;144;156;168 S 19 24 17607789 Virological features of hepatitis B virus-associated nephropathy in Japan. G1862T mutation was observed in the two HBV/A1 patients, resulting in the pre-core amino acid substitution with a switch from valine (Val) to phenylalanine (Phe). 2007 Journal of medical virology Abstract HBV G1862T 0 6 Precore 74 82 17622616 Hepatitis B virus X protein differentially affects the ubiquitin-mediated proteasomal degradation of beta-catenin depending on the status of cellular p53. Interestingly, HBx variants with a Pro-101 to Ser substitution were unable to activate p53 and thus could stabilize beta-catenin irrespective of p53 status. 2007 The Journal of general virology Abstract HBV P101S 35 49 X 15 18 17627632 Impact of viral genotypes and naturally occurring mutations on biological properties of hepatitis B virus. At the step of translation, a G1896A nonsense mutation in the precore region abolishes HBeAg expression. 2007 Hepatology research Abstract HBV G1896A 30 36 C;Precore 87;62 92;69 17627632 Impact of viral genotypes and naturally occurring mutations on biological properties of hepatitis B virus. Subsequent studies by others established the role of polymorphism at nucleotide 1858, rather than genotype, as the determinant for the G1896A mutation. 2007 Hepatology research Abstract HBV G1896A 135 141 17627632 Impact of viral genotypes and naturally occurring mutations on biological properties of hepatitis B virus. We first reportedthat the G1896A mutation rarely occurred in genotype A. 2007 Hepatology research Abstract HBV G1896A 26 32 17627632 Impact of viral genotypes and naturally occurring mutations on biological properties of hepatitis B virus. We found that the hot spot mutations (A1762T/G1764A) only mildly reduced HBeAg expression and enhanced genome replication, while incorporation of additional core promoter mutations intensified both phenotypes. 2007 Hepatology research Abstract HBV G1764A;A1762T 45;38 51;44 Core promoter;C 157;73 170;78 17637268 [A clinical study of adefovir dipivoxil in treating lamivudine refractory HBeAg-positive chronic hepatitis B]. rtN236T and rtA181V mutation was not found in this 48-week study. 2007 Zhonghua nei ke za zhi Abstract HBV N236T;A181V 2;14 7;19 RT;RT 0;12 2;14 17652045 Sequential treatment with lamivudine and alpha-interferon in anti-HBe-positive chronic hepatitis B patients: a pilot study. L180M/M204V mutations were identified during virological breakthrough. 2007 Digestive and liver disease Abstract HBV M204V;L180M 6;0 11;5 17666334 [Construction of whole-genome lamivudine-resistant hepatitis B virus mutant and its replication and expression in HepG2 cells]. The replication of the 3 mutant plasmids with rtG172E, rtG174C and rtG172E/rtG174C mutation decreased significantly in comparison with the wild-type virus. 2007 Nan fang yi ke da xue xue bao Abstract HBV G172E;G174C;G172E;G174C 48;57;69;77 53;62;74;82 RT;RT;RT;RT 46;55;67;75 48;57;69;77 17682718 [A case of chronic hepatitis B with primary adefovir resistance]. On the 11th month resistance to adefovir was analysed and rtA181T mutation was found by DNA sequence analysis (Big Dye Terminator Cycle Sequencing kit, Applied Biosystems, USA). 2007 Mikrobiyoloji bulteni Abstract HBV A181T 60 65 RT 58 60 17687019 In vitro drug susceptibility analysis of hepatitis B virus clinical quasispecies populations. HBV obtained from patients who had developed resistance to adefovir or lamivudine, as demonstrated by development of the rtA181V or rtL180M/M204V mutations in HBV polymerase, respectively, were tested. 2007 Journal of clinical microbiology Abstract HBV M204V;A181V;L180M 140;123;134 145;128;139 P;RT;RT 163;121;132 173;123;134 17687019 In vitro drug susceptibility analysis of hepatitis B virus clinical quasispecies populations. Phenotypic analysis demonstrated that a population containing the HBV rtA181V mutation showed a 2.9-fold increase in the 50% effective concentration (EC(50)) for adefovir compared to the wild-type baseline isolate, while the lamivudine-resistant HBV quasispecies population showed a >1,000-fold increase in the lamivudine EC(50). 2007 Journal of clinical microbiology Abstract HBV A181V 72 77 RT 70 72 17692425 Pooled analysis of amino acid changes in the HBV polymerase in patients from four major adefovir dipivoxil clinical trials. BACKGROUND/AIMS: The rtA181V and rtN236T mutations have been associated with resistance to adefovir dipivoxil (ADV). 2007 Journal of hepatology Abstract HBV A181V;N236T 23;35 28;40 RT;RT 21;33 23;35 17692425 Pooled analysis of amino acid changes in the HBV polymerase in patients from four major adefovir dipivoxil clinical trials. CONCLUSIONS: rtA181V and rtN236T were the only HBV polymerase mutations significantly associated with virologic failure to adefovir dipivoxil. 2007 Journal of hepatology Abstract HBV A181V;N236T 15;27 20;32 RT;RT;P 13;25;51 15;27;61 17692425 Pooled analysis of amino acid changes in the HBV polymerase in patients from four major adefovir dipivoxil clinical trials. The aims of this study were to confirm the role of rtA181V and rtN236T in clinical resistance to ADV and to screen for other potential ADV-R mutations. 2007 Journal of hepatology Abstract HBV A181V;N236T 53;65 58;70 RT;RT 51;63 53;65 17692425 Pooled analysis of amino acid changes in the HBV polymerase in patients from four major adefovir dipivoxil clinical trials. When tested separately, the mutations rtA181V and rtN236T were statistically significant (p<0.0005); no other AA position was associated with VF. 2007 Journal of hepatology Abstract HBV A181V;N236T 40;52 45;57 RT;RT 38;50 40;52 17697019 Association between lamivudine sensitivity and the number of substitutions in the reverse transcriptase region of the hepatitis B virus polymerase. Sequence analysis of the HBV genome revealed that point mutations in the precore region (G1896A) and enhancer I (A1287G/C) were observed more frequently in the good responder group than in the poor responder group (P = 0.002 and 0.019 respectively), and the number of substitutions in the reverse transcriptase domain of the polymerase was significantly higher in the good responders than in the poor responders (P = 0.026). 2007 Journal of viral hepatitis Abstract HBV G1896A;A1287G;A1287C 89;113;113 95;121;121 Enh I;P;Precore;RT 101;325;73;289 111;335;80;310 17711443 Molecular epidemiological study of hepatitis B virus in Thailand based on the analysis of pre-S and S genes. Regarding the "a" determinant, 2/43 (4.65%) and 2/104 (1.92%) samples of vaccinated and non-vaccinated subjects, respectively, displayed mutations, all ofwhich were Thr126Asn. 2008 Hepatology research Abstract HBV T126N 165 174 17713159 A novel mutation pattern emerging during lamivudine treatment shows cross-resistance to adefovir dipivoxil treatment. A novel mutation, A181S, in the reverse transcriptase gene leading to a conversion of W172C in the overlapping surface antigen gene was detected along with a M2041 mutation. 2007 Antiviral therapy Abstract HBV W172C;A181S 86;18 91;23 RT;S 32;111 53;118 17713159 A novel mutation pattern emerging during lamivudine treatment shows cross-resistance to adefovir dipivoxil treatment. CONCLUSION: A new mutation pattern, A181S+M2041, arising under lamivudine treatment confers cross-resistance to ADV both in vivo and in vitro. 2007 Antiviral therapy Abstract HBV A181S 36 41 17713159 A novel mutation pattern emerging during lamivudine treatment shows cross-resistance to adefovir dipivoxil treatment. The complete genome comprising the A181S+M2041 pattern was cloned into an expression vector and its in vitro susceptibility to 3TC, ADV, tenofovir (PMPA), clevudine (L-FMAU) and emtricitabine (FTC) were determined in transiently transfected Huh7 cells. 2007 Antiviral therapy Abstract HBV A181S 35 40 17763322 Replicative competence of the T131I, K141E, and G145R surface variants of hepatitis B Virus. Point mutations leading to sT131I, sK141E, and sG145R amino-acid substitutions were engineered by site-directed mutagenesis into an infectious plasmid clone of the virus. 2007 The Journal of infectious diseases Abstract HBV T131I;K141E;G145R 27;35;47 33;41;53 S;S;S 27;35;47 28;36;48 17763322 Replicative competence of the T131I, K141E, and G145R surface variants of hepatitis B Virus. The sT131I and sG145R variants replicated with efficiency equal to that of the wild type, whereas the sK141E variant was replication impaired. 2007 The Journal of infectious diseases Abstract HBV T131I;G145R;K141E 4;15;102 10;21;108 S;S;S 4;15;102 5;16;103 17825452 Five subgenotypes of hepatitis B virus genotype B with distinct geographic and virological characteristics. In addition to the characteristics of HBV/B(1)-B(5) at some cis-acting elements, the precore stop-codon mutant (G1896A) was significantly different among HBV/B(1), HBV/B(2), and HBV/B(4) (70.3%, 31.7%, 53.0%, P=0.001), while no such mutation was found in HBV/B(3) and B(5). 2007 Virus research Abstract HBV G1896A 112 118 Precore 85 92 17854034 Mutational patterns of hepatitis B virus genome and clinical outcomes after emergence of drug-resistant variants during lamivudine therapy: analyses of the polymerase gene and full-length sequences. Baseline characteristics, alanine aminotransferase (ALT) levels, and HBV DNA levels within 6 months after the emergence of YMDD variants did not differ significantly between patients with rtM204I alone and those with rtL180M/rtM204V. 2007 Journal of medical virology Abstract HBV M204I;L180M;M204V 190;219;227 195;224;232 RT;RT;RT;P 188;217;225;123 190;219;227;127 17854034 Mutational patterns of hepatitis B virus genome and clinical outcomes after emergence of drug-resistant variants during lamivudine therapy: analyses of the polymerase gene and full-length sequences. Between months 5 and 33 of therapy, mutations from methionine to isoleucine at rt204 (rtM204I) were detected in 18 patients, and mutations from methionine to valine at rt204 (rtM204V) were detected in 12. 2007 Journal of medical virology Abstract HBV M204I;M204V 88;177 93;182 RT;RT;RT;RT 79;86;168;175 81;88;170;177 17854034 Mutational patterns of hepatitis B virus genome and clinical outcomes after emergence of drug-resistant variants during lamivudine therapy: analyses of the polymerase gene and full-length sequences. During long term follow-up, the addition of rtL180M to rtM204I was found in four patients 7-31 months after detecting the change at rt204 and was linked to increased ALT levels. 2007 Journal of medical virology Abstract HBV L180M;M204I 46;57 51;62 RT;RT;RT 44;55;132 46;57;134 17854034 Mutational patterns of hepatitis B virus genome and clinical outcomes after emergence of drug-resistant variants during lamivudine therapy: analyses of the polymerase gene and full-length sequences. The rtM204V mutations were always accompanied by mutations from leucine to methionine at rt180 (rtL180M), while rtM204I mutations were not. 2007 Journal of medical virology Abstract HBV M204V;L180M;M204I 6;98;114 11;103;119 RT;RT;RT;RT 4;89;96;112 6;91;98;114 17888035 Analysis of the complete hepatitis B virus genome in patients with genotype C chronic hepatitis and hepatocellular carcinoma. Compared with the wild type X promoter, the mutant type X promoters, M1 (G1317A), M2 (T1341C), and M4 (T1341G) showed increases in activity of 2.3, 3.8, and 1.4 times, respectively, in HepG2 cells. 2007 Cancer science Abstract HBV G1317A;T1341C;T1341G 73;86;103 79;92;109 X promoter;X promoter 28;56 38;67 17888035 Analysis of the complete hepatitis B virus genome in patients with genotype C chronic hepatitis and hepatocellular carcinoma. Substitutions and deletion of nucleotides of the HBV genome, especially the pre-S2 deletion and G1317A and T1341C/A/G mutations may be useful markers for predicting the development of HCC. 2007 Cancer science Abstract HBV G1317A;T1341C;T1341A;T1341G 96;107;107;107 102;117;117;117 PreS2 76 82 Hepatocellular carcinoma 184 187 17888035 Analysis of the complete hepatitis B virus genome in patients with genotype C chronic hepatitis and hepatocellular carcinoma. The number of nucleotide and amino acid substitutions in most regions was higher in the HCC group than in the non-HCC group, and the following substitutions and deletions were found more frequently in the HCC group than in the non-HCC group: G1317A and T1341C/A/G in the X promoter region were detected in 13 and six of the HCC cases, four and none of the non-HCC cases, respectively; and pre-S2 deletion was detected in eight HCC and none of the non-HCC cases. 2007 Cancer science Abstract HBV G1317A;T1341C;T1341A;T1341G 242;253;253;253 248;263;263;263 PreS2;X promoter 389;271 395;281 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 88;205;324;427;114;231;360;451 91;208;327;430;117;234;363;454 17900990 The high prevalence of the I27 mutant HBcAg18-27 epitope in Chinese HBV-infected patients and its cross-reactivity with the V27 prototype epitope. Approximately 93.3% (98/105) of the core genes that were sequenced contained mutations with amino acid substitution at position 27 of the core protein: a mutation from a valine to an isoleucine (V27I). 2007 Clinical immunology (Orlando, Fla.) Abstract HBV V27I 195 199 C;C 36;138 40;142 17913933 Evolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay. A compensatory mutation at position rt80 (L80V/I) was detected in half of these patients. 2007 Journal of clinical microbiology Abstract HBV L80V;L80I 42;42 48;48 RT 36 38 17913933 Evolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay. After 36 months, a compensatory mutation was seen at position rt173 (V173L) in 3/15 patients. 2007 Journal of clinical microbiology Abstract HBV V173L 69 74 RT 62 64 17913933 Evolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay. In all 20 patients, the mutation occurred in the YMDD motif at reverse transcriptase position 204 (rt204; M204V/I) either with or without the compensatory mutation at position rt180 (L180M). 2007 Journal of clinical microbiology Abstract HBV M204V;M204I;L180M 106;106;183 113;113;188 RT;RT;RT;P 63;99;176;49 84;101;178;53 17934636 Hepatitis B virus genotype E detected in Brazil in an African patient who is a frequent traveler. The preC/C region showed G1896A and G1899A mutations but no mutations in the basal core promoter. 2007 Brazilian journal of medical and biological research Abstract HBV G1896A;G1899A 25;36 31;42 BCP;Precore;C 77;4;9 96;8;10 17935165 Successful treatment of an entecavir-resistant hepatitis B virus variant. Direct sequence analysis of the ETV-resistant strain showed appearance of amino acid substitution rtS202G in the reverse transcriptase (RT) domain, together with rtL180M + M204V substitution that had developed at the emergence of LAM-resistant mutant. 2007 Journal of medical virology Abstract HBV S202G;L180M;M204V 100;164;172 105;169;177 RT;RT;RT;RT 113;98;136;162 134;100;138;164 17935165 Successful treatment of an entecavir-resistant hepatitis B virus variant. In conclusion, this study showed that virological and biochemical breakthrough due to ETV could occur in patients infected with LAM-resistant HBV and confirmed that the addition of rtS202G substitution to the rtL180M + M204V mutant strain is responsible for ETV resistance and we could treat the resistant mutant successfully. 2007 Journal of medical virology Abstract HBV S202G;L180M;M204V 183;211;219 188;216;224 RT;RT 181;209 183;211 17935165 Successful treatment of an entecavir-resistant hepatitis B virus variant. In vitro analysis demonstrated that the rtL180M + M204V + S202G mutant strain displayed a 200-fold and a 5-fold reduction in susceptibility to ETV compared with the wild- type and the rtL180M + M204V mutant strain, respectively. 2007 Journal of medical virology Abstract HBV L180M;L180M;M204V;M204V;S202G 42;186;50;194;58 47;191;55;199;63 RT;RT 40;184 42;186 17962902 Prolonged persistence of lamivudine-resistant mutant and emergence of new lamivudine-resistant mutants two years after lamivudine withdrawal in HBsAg-positive chronic hepatitis patient: a case report. We report an unusual case of a male adult patient who showed a prolonged persistence of the M204I mutation up to 24 months after lamivudine withdrawal followed by the emergence of new distinct YMDD mutants (namely M204V, V207L). 2008 Infection Abstract HBV M204I;M204V;V207L 92;214;221 97;219;226 P 193 197 17971947 [Efficacy of adefovir dipivoxil was not related to genotypes B and C of hepatitis B virus: a randomized, double-blind, multicenter clinical study]. rtN236T and rtA181V mutations were confirmed by sequencing. 2007 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV N236T;A181V 2;14 7;19 RT;RT 0;12 2;14 17983801 Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients. The 1-, 2-, 3-, and 4-year cumulative rates of de novo rtA181T were 1%, 2%, 4%, and 4%, respectively. 2007 Gastroenterology Abstract HBV A181T 57 62 RT 55 57 17983801 Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients. The rtA181V/T was the only adefovir-related mutation detected, which occurred in 6 patients at baseline (4%; 1 rtA181V and 5 rtA181T) and in an additional 3 patients (2%; all rtA181T) during treatment. 2007 Gastroenterology Abstract HBV A181V;A181T;A181V;A181T;A181T 6;6;113;127;177 13;13;118;132;182 RT;RT;RT;RT 4;111;125;175 6;113;127;177 17988612 [Adefovir dipivoxil compassionate use program in Spain: efficacy and resistance analysis]. 20% patients developed resistance to adefovir dipivoxil, and the most frequent detected mutations were: A181V, A181T and N236T. 2007 Medicina clinica Abstract HBV A181V;A181T;N236T 104;111;121 109;116;126 17997353 Frequency and significance of hepatitis B virus surface gene variant circulating among 'antiHBc only' individuals in Eastern India. Single or multiple amino acids substitutions were found in 82% samples, however, G145R vaccine escape mutation was rare. 2007 Journal of clinical virology Abstract HBV G145R 81 86 18008227 Hepatitis B virus containing the I233V mutation in the polymerase reverse-transcriptase domain remains sensitive to inhibition by adefovir. An isoleucine-to-valine change at position 233 (rtI233V) of hepatitis B virus (HBV) polymerase was recently reported to cause decreased in vitro susceptibility to, and treatment failure of, adefovir dipivoxil (ADV). 2007 The Journal of infectious diseases Abstract HBV I233V;I233V 50;3 55;46 P;RT 84;48 94;50 18008227 Hepatitis B virus containing the I233V mutation in the polymerase reverse-transcriptase domain remains sensitive to inhibition by adefovir. Phenotypic evaluation of clinical isolates and of a laboratory strain with the rtI233V mutation demonstrated their full susceptibility to adefovir in vitro, and HBV with the rtI233V mutation developed in none of the patients. 2007 The Journal of infectious diseases Abstract HBV I233V;I233V 81;176 86;181 RT;RT 79;174 81;176 18035058 Maternal chronic hepatitis B virus is implicated with low neonatal paraoxonase/arylesterase activities. RESULTS: Serological HBV tests and HBV DNA showed chronic HBV (precore mutant G1896A) in the diseased mothers whereas anti-HBc and anti-HBe were detected in their neonates. 2008 Clinical biochemistry Abstract HBV G1896A 78 84 C;C;Precore 123;136;63 126;139;70 Chronic Hepatitis B 50 61 18036104 Efficacy of hepatitis B virus (HBV) vaccination in treating lamivudine-resistant HBV reactivation following hepatitis B surface antigen seroconversion. Due to the presence of rtM204V resistance mutation, lamivudine was not reintroduced and the patient was treated by HBsAg vaccination. 2007 Liver international Abstract HBV M204V 25 30 S;RT 115;23 120;25 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. The remaining isolate showed a leucine-to-isoleucine substitution at position 127. 2007 BMC microbiology Abstract HBV L127I 31 81 18070286 Hepatitis B virus polymerase variants associated with entecavir drug resistance in treatment-naive patients. Prior to lamivudine treatment, three cases (2.7%) had substitutions in the HBV polymerase gene corresponding to variants associated with ETV resistance (rtS202S/I). 2007 Journal of viral hepatitis Abstract HBV S202S;S202I 155;155 162;162 P;RT 79;153 89;155 18070286 Hepatitis B virus polymerase variants associated with entecavir drug resistance in treatment-naive patients. The aim of this study was to determine the prevalence of HBV variants associated with ETV resistance (rtI169T, rtT184G, rtS202I, rtM250V) in naive patients before and during lamivudine therapy. 2007 Journal of viral hepatitis Abstract HBV I169T;T184G;S202I;M250V 104;113;122;131 109;118;127;136 RT;RT;RT;RT 102;111;120;129 104;113;122;131 18167643 Selection of hepatitis B virus (HBV) vaccine escape mutants in HBV-infected and HBV/HIV-coinfected patients failing antiretroviral drugs with anti-HBV activity. The triple-HBV mutant rtV173L + rtL180M + rtM204V, which has been shown to produce a diminished hepatitis B surface (HBs) antigen-antibody binding, was found in 3 individuals, all coinfected with HIV and HBV. 2007 Journal of acquired immune deficiency syndromes (1999) Abstract HBV V173L;L180M;M204V 24;34;44 29;39;49 S;RT;RT;RT;S 117;22;32;42;108 120;24;34;44;115 18171343 Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case. After 32 months, the rtM204V mutation was predominant, accompanied by the lamivudine-resistant rtL180M mutation. 2008 Journal of gastroenterology and hepatology Abstract HBV M204V;L180M 23;97 28;102 RT;RT 21;95 23;97 18171343 Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case. BACKGROUND AND AIM: Resistance to lamivudine therapy of chronic hepatitis B virus (HBV) infection occurs by mutation in the YMDD motif of the reverse transcriptase (rt) domain (rtM204V/I) of the virus polymerase, and is usually accompanied by rtL180M mutation. 2008 Journal of gastroenterology and hepatology Abstract HBV M204V;M204I;L180M 179;179;245 186;186;250 P;RT;RT;RT;RT;P 201;142;165;177;243;124 211;163;167;179;245;128 Chronic HBV infection 56 97 18171343 Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case. CONCLUSION: The results suggest that substitutions in polymerase (rtS117Y, rtV142A) and surface antigens (L109I, F134L, and I208T), associated with lamivudine-resistant mutations at positions 180 and 204, were involved in this case of fatal hepatitis B. 2008 Journal of gastroenterology and hepatology Abstract HBV S117Y;V142A;L109I;F134L;I208T 68;77;106;113;124 73;82;111;118;129 P;RT;RT;S 54;66;75;88 64;68;77;95 18171343 Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case. Furthermore, two rare polymerase (rtS117Y and rtV142A) and three HBsAg (L109I, F134L, and I208T) substitutions were observed. 2008 Journal of gastroenterology and hepatology Abstract HBV S117Y;V142A;L109I;F134L;I208T 36;48;72;79;90 41;53;77;84;95 S;P;RT;RT 65;22;34;46 70;32;36;48 18171343 Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case. RESULTS: A peak of alanine aminotransferase and aspartate aminotransferase levels occurred after 19 months of lamivudine treatment, associated with the rtM204I mutation. 2008 Journal of gastroenterology and hepatology Abstract HBV M204I 154 159 RT 152 154 18199519 Tenofovir monotherapy is effective in hepatitis B patients with antiviral treatment failure to adefovir in the absence of adefovir-resistant mutations. Among patients with suboptimal virologic response, rtA181T, rtI233V, and rtN236T were present on clonal analysis in 3 patients. 2008 Journal of hepatology Abstract HBV A181T;I233V;N236T 53;62;75 58;67;80 RT;RT;RT 51;60;73 53;62;75 18199519 Tenofovir monotherapy is effective in hepatitis B patients with antiviral treatment failure to adefovir in the absence of adefovir-resistant mutations. RESULTS: ADV-resistant mutations, rtA181V and rtN236T, were detected on direct sequencing in 3 of 8 patients who had virologic breakthrough. 2008 Journal of hepatology Abstract HBV A181V;N236T 36;48 41;53 RT;RT 34;46 36;48 18201182 A valine to phenylalanine mutation in the precore region of hepatitis B virus causes intracellular retention and impaired secretion of HBe-antigen. CONCLUSION: The formation of aggresomes, as a result of the G1862T mutation, may play a contributory role in HBV-induced liver disease. 2008 Hepatology research Abstract HBV G1862T 60 66 Liver disease 121 134 18201182 A valine to phenylalanine mutation in the precore region of hepatitis B virus causes intracellular retention and impaired secretion of HBe-antigen. The G1862T mutation in HBV occurs in the bulge of the encapsidation signal within the pregenomic RNA. 2008 Hepatology research Abstract HBV G1862T 4 10 18205223 Naturally occurring MHR variants in Turkish patients infected with hepatitis B virus. When samples with "a" variants were evaluated by two different commercial HBsAg tests, only the isolate with Ser143Leu variation had a decreased reactivity in the assay using monoclonal antibodies for capture and detection. 2008 Journal of medical virology Abstract HBV S143L 109 118 S 74 79 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. All three showed the double mutation L180M/M204V and displayed a large genetic divergence when compared with other full-length genotype G isolates. 2008 BMC microbiology Abstract HBV M204V;L180M 43;37 48;42 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. Fifteen patients showed the L180M/M204V lamivudine resistant double mutation. 2008 BMC microbiology Abstract HBV M204V;L180M 34;28 39;33 18216102 Genotype-specific genomic markers associated with primary hepatomas, based on complete genomic sequencing of hepatitis B virus. HCC-related mutations T31C, T53C, and A1499G were associated with HBV subgenotype Ce, and mutations G1613A, G1899A, T2170C/G, and T2441C were associated with HBV subgenotype Cs. 2008 Journal of virology Abstract HBV T31C;T53C;A1499G;G1613A;G1899A;T2170C;T2170G;T2441C 22;28;38;100;108;116;116;130 26;32;44;106;114;124;124;136 Hepatocellular carcinoma 0 3 18216102 Genotype-specific genomic markers associated with primary hepatomas, based on complete genomic sequencing of hepatitis B virus. In genotype B HBV, mutations C1165T, A1762T and G1764A, T2712C/A/G, and A/T2525C were associated with HCC. 2008 Journal of virology Abstract HBV C1165T;A1762T;G1764A;T2712C;T2712A;T2712G;A2525C;T2525C 29;37;48;56;56;56;72;72 35;43;54;66;66;66;80;80 Hepatocellular carcinoma 102 105 18221300 Evaluation of initial virological response to adefovir and development of adefovir-resistant mutations in patients with chronic hepatitis B. Five (12%) patients developed ADV-resistant mutations: rtN236T in four cases and one case with an rtV207L change, which has not been previously reported. 2008 Journal of viral hepatitis Abstract HBV N236T;V207L 57;100 62;105 RT;RT 55;98 57;100 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. A novel PCR-RFLP assay based on restriction enzyme HpaI or DraI for on the detection of rtN236T mutant was established, which detected 10% minor strains with 100% specificity. 2008 Zhonghua gan zang bing za zhi Abstract HBV N236T 90 95 RT 88 90 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. CONCLUSIONS: A rapid and easy method was established to detect rtN236T mutants. 2008 Zhonghua gan zang bing za zhi Abstract HBV N236T 65 70 RT 63 65 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. In one patient after stopping the adefovir therapy, 3 months later a wild type virus re-took again the mutant one (rtN236T); in one patient who developed a rt236T mutant after 132 weeks of adefovir treatment, a novel mutant (rtN236V) appeared and then became the dominant one while adefovir treatment continued. 2008 Zhonghua gan zang bing za zhi Abstract HBV N236T;N236V 117;227 122;232 RT;RT;RT 115;156;225 117;158;227 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. Mutants (rtA181V or rtN236T) appeared 0-8 months earlier than the viral breakthrough, then afterwards became the dominant ones. 2008 Zhonghua gan zang bing za zhi Abstract HBV A181V;N236T 11;22 16;27 RT;RT 9;20 11;22 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. OBJECTIVE: The aim was to build a PCR-RFLP method for detecting rtN236T mutants and to observe their kinetics in chronic hepatitis B (CHB) patients. 2008 Zhonghua gan zang bing za zhi Abstract HBV N236T 66 71 RT 64 66 Chronic Hepatitis B;Chronic Hepatitis B 113;134 132;137 18226341 [Kinetics of HBV mutants conferring adefovir resistance (rtn236t) and a method to detect them rapidly]. RESULTS: Three patients had viral breakthrough and one with suboptimal viral response had adefovir-resistance mutants, one had rtA181V mutation and three had rtN236T mutation. 2008 Zhonghua gan zang bing za zhi Abstract HBV A181V;N236T 129;160 134;165 RT;RT 127;158 129;160 18241289 Maternal chronic hepatitis B virus does not affect neonatal biotinidase activity. RESULTS: Serological HBV tests and HBV DNA showed chronic HBV (precore mutant G1896A) in group A, whereas anti-HBc and anti-HBe were detected in their neonates. 2008 Acta paediatrica (Oslo, Norway Abstract HBV G1896A 78 84 C;C;Precore 111;124;63 114;127;70 Chronic Hepatitis B 50 61 18265656 Clinical significance of basal core promoter and precore mutations in chronic hepatitis B. HBeAg-negative samples were associated with precore mutations (G1896A and G1899A). 2007 Hepato-gastroenterology Abstract HBV G1896A;G1899A 63;74 69;80 C;Precore 0;44 5;51 18266648 A complete genomic analysis of hepatitis B virus genotypes and mutations in HBeAg-negative chronic hepatitis B in China. The T2201C mutation was found exclusively among patients (21 of 46 patients, 45%) infected by HBV subgenotype Ce. 2008 Journal of viral hepatitis Abstract HBV T2201C 4 10 18266648 A complete genomic analysis of hepatitis B virus genotypes and mutations in HBeAg-negative chronic hepatitis B in China. Two HBV mutations were identified to associate with severe liver fibrosis (G2858C and C2289A) and one mutation was protective against severe liver fibrosis (T2201C). 2008 Journal of viral hepatitis Abstract HBV G2858C;C2289A;T2201C 75;86;157 81;92;163 Liver fibrosis;Liver fibrosis 59;141 73;155 18283732 [Algorithm of serologic screening and assessment of prevalence of serologically meaningful mutations of HBsAg in hepatitis B virus carriers]. Analysis of primary nucleotide sequence revealed serologically meaningful mutations in S-gene of HBV in all 9 isolates: 3 of them contained substitution mutation G145R, 5--S143L, and one--T143M. 2007 Zhurnal mikrobiologii, epidemiologii i immunobiologii Abstract HBV G145R;T143M;S143L 162;188;172 167;193;177 S 87 88 18283732 [Algorithm of serologic screening and assessment of prevalence of serologically meaningful mutations of HBsAg in hepatitis B virus carriers]. Prevalence of HBsAg mutations in HBV carriers with high level of HBsAg was assessed for the first time: prevalence of G145R, S143L/T143M mutations, and all serologically atypical variants was 0.12%, 0.24%, and 0.76% respectively. 2007 Zhurnal mikrobiologii, epidemiologii i immunobiologii Abstract HBV T143M;S143L;G145R 131;125;118 136;130;123 S;S 14;65 19;70 18291537 Direct detection of lamivudine-resistant hepatitis B virus mutants by a multiplex PCR using dual-priming oligonucleotide primers. Using dual-priming oligonucleotide primer technology, an assay that can detect mutations at codons 180 (L528M) and 204 (YVDD, YIDD, and YSDD) by a single-step multiplex PCR was developed. 2008 Journal of virological methods Abstract HBV L528M 104 109 P;P;P 126;136;120 130;140;124 18329126 Lamivudine compared with lamivudine and adefovir dipivoxil for the treatment of HBeAg-positive chronic hepatitis B. The M204V/I mutation was detected in 43% (15/35) and 15% (6/41) of each group, respectively. 2008 Journal of hepatology Abstract HBV M204V;M204I 4;4 11;11 18331765 Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. In cell culture, the rtA181T/V mutation induced a decreased susceptibility to lamivudine (<10-fold), adefovir (2- to 8-fold) and tenofovir (2- to 3-fold). 2008 Journal of hepatology Abstract HBV A181T;A181V 23;23 30;30 RT 21 23 18331765 Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. In this study, we characterized the main variants harboring the rtA181T/V mutation isolated from 10 consecutive patients who developed lamivudine and/or adefovir resistance. 2008 Journal of hepatology Abstract HBV A181T;A181V 66;66 73;73 RT 64 66 18331765 Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. Interestingly, the association of rtA181T with rtN236T on one clinical isolate genome increased the resistance to these three drugs. 2008 Journal of hepatology Abstract HBV A181T;N236T 36;49 41;54 RT;RT 34;47 36;49 18331765 Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure. RESULTS: Clonal analysis revealed the co-localization on the same HBV genome of rtA181T/V with rtN236T, but not with rtM204V/I mutations following lamivudine, adefovir or lamivudine+adefovir breakthrough. 2008 Journal of hepatology Abstract HBV A181T;A181V;N236T;M204V;M204I 82;82;97;119;119 89;89;102;126;126 RT;RT;RT 80;95;117 82;97;119 18343830 Effect of basal core promoter and pre-core mutations on hepatitis B virus replication. HBeAg was undetectable in all cultures transfected with constructs bearing the G1896A stop-codon mutation, as expected. 2008 The Journal of general virology Abstract HBV G1896A 79 85 C 0 5 18343830 Effect of basal core promoter and pre-core mutations on hepatitis B virus replication. Substitutions A1762T/G1764A and T1753C, C1766T and T1768A in the BCP region, and G1896A and G1899A in the pre-C region, were examined either alone or in combination, using a common genetic background. 2008 The Journal of general virology Abstract HBV G1764A;A1762T;T1753C;C1766T;T1768A;G1896A;G1899A 21;14;32;40;51;81;92 27;20;38;46;57;87;98 BCP;Precore 65;106 68;111 18343830 Effect of basal core promoter and pre-core mutations on hepatitis B virus replication. The double BCP mutation (A1762T/G1764A) and the pre-C mutations (G1896A, G1899A), either alone or in combination, had no appreciable effect on the replication capacity of the virus. 2008 The Journal of general virology Abstract HBV G1764A;A1762T;G1896A;G1899A 32;25;65;73 38;31;71;79 BCP;Precore 11;48 14;53 18373168 Hepatitis B caused by a hepatitis B surface antigen escape mutant. A single amino acid substitution (G145R) within the a determinant of the HBsAg was determined by sequencing of the isolated HBV strain. 2008 Journal of gastroenterology Abstract HBV G145R 34 39 S;S 52;73 65;78 18410611 Detection of HBV core promoter and precore mutations helps distinguish flares of chronic hepatitis from acute hepatitis B. RESULTS: Mutations in the core promoter (A1762T/G1764A) and precore region (G1896A) were more frequent in patients with acute exacerbation of chronic hepatitis than acute hepatitis (81% vs 19%; P < 0.0001 and 58% vs 6%; P < 0.0001, respectively). 2008 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T;G1896A 48;41;76 54;47;82 Core promoter;Precore 26;60 39;67 Chronic Hepatitis B;Acute Hepatitis B 142;165 159;180 18423147 [A study on mutations of the overlapping hepatitis B virus surface and polymerase gene in patients with HBV reinfection after liver transplantations]. Mutations were detected as I126S, T131N, S143T and G145R in 'a' determinant and L110F, I113S, T160K in up- or down-stream of 'a' determinant. 2008 Zhonghua gan zang bing za zhi Abstract HBV I126S;T131N;S143T;G145R;L110F;I113S;T160K 27;34;41;51;80;87;94 32;39;46;56;85;92;99 S;S 61;126 75;140 18428142 Analysis of the entire nucleotide sequence of hepatitis B causing consecutive cases of fatal fulminant hepatitis in Miyagi Prefecture Japan. Amino acid analysis revealed that previously reported Ile97Leu and Pro130Non-Pro in the core region and Trp28Stop in the precore region were present. 2008 Journal of medical virology Abstract HBV I97L;P130Non-P;W28X 54;67;104 62;80;113 C;Precore 88;121 92;128 18428142 Analysis of the entire nucleotide sequence of hepatitis B causing consecutive cases of fatal fulminant hepatitis in Miyagi Prefecture Japan. As for the nucleotides sequences of them, previously reported mutations of G1896A, A1762T, and G1764A were present. 2008 Journal of medical virology Abstract HBV G1896A;A1762T;G1764A 75;83;95 81;89;101 18431229 Viral persistence after liver transplantation for hepatitis B virus: a cross-sectional study. Three of the lamivudine and HBIg cohort had the I126A Hepatitis B surface antigen escape variant. 2008 Transplantation Abstract HBV I126A 48 53 S 66 73 18433023 Safety, efficacy, and pharmacokinetics of adefovir dipivoxil in children and adolescents (age 2 to <18 years) with chronic hepatitis B. No subject developed an ADV-associated mutation that has been linked to HBV DNA rebound (that is, mutations rtN236T or rtA181V). 2008 Hepatology (Baltimore, Md.) Abstract HBV N236T;A181V 110;121 115;126 RT;RT 108;119 110;121 18433925 Low risk of adefovir resistance in lamivudine-resistant chronic hepatitis B patients treated with adefovir plus lamivudine combination therapy: two-year follow-up. At the beginning of ADV therapy, substitutions at rtA181 (rtA181T and rtA181S) were identified in 3 patients (2.3%). 2008 Journal of hepatology Abstract HBV A181T;A181S 60;72 65;77 RT;RT;RT 50;58;70 52;60;72 18433925 Low risk of adefovir resistance in lamivudine-resistant chronic hepatitis B patients treated with adefovir plus lamivudine combination therapy: two-year follow-up. In the remaining 129 patients, the rtM204 mutants were identified at baseline, and two (1.6%) of the 129 patients developed new ADV-resistant mutants; one was rtA181S and another was rtA181T plus rtN236T mutation. 2008 Journal of hepatology Abstract HBV A181S;A181T;N236T 161;185;198 166;190;203 RT;RT;RT;RT 35;159;183;196 37;161;185;198 18434744 A unique amino acid substitution, L215Q, in the hepatitis B virus small envelope protein of a genotype F isolate that inhibits secretion of hepatitis B virus subviral particles. Amino acid substitutions that inhibit HBsAg secretion, such as that characterized in this study (L215Q), should have implications in HBV immunological diagnostics. 2008 Intervirology Abstract HBV L215Q 97 102 S 38 43 18434744 A unique amino acid substitution, L215Q, in the hepatitis B virus small envelope protein of a genotype F isolate that inhibits secretion of hepatitis B virus subviral particles. In this study, we identified a unique amino acid substitution (L215Q) in the carboxyl-terminal end of S-HBsAg of an HBV genotype F isolate that provoked an inhibitory effect on secretion of SVPs. 2008 Intervirology Abstract HBV L215Q 63 68 S 102 109 18435459 Comprehensive evaluation of hepatitis B virus reverse transcriptase substitutions associated with entecavir resistance. Two of these substitutions are associated with lamivudine resistance (LVDr) in the tyrosine-methionine-aspartate-aspartate (YMDD) motif (rtM204V and rtL180M), whereas the other occurs at one or more positions specifically associated with ETV resistance (ETVr): rtT184, rtS202, or rtM250. 2008 Hepatology (Baltimore, Md.) Abstract HBV M204V;L180M 139;151 144;156 RT;RT;RT;RT;RT;P;P 137;149;261;269;280;83;124 139;151;263;271;282;122;128 18504191 [Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients]. Other resistant substitutions included rtL80V/I, rtT184S, and rtA200V, and combined mutation of triple resistant substitutions was detected in HBV RT region of 5 patients by direct sequencing. 2008 Nan fang yi ke da xue xue bao Abstract HBV L80V;L80I;T184S;A200V 41;41;51;64 47;47;56;69 RT;RT;RT;RT 39;49;62;147 41;51;64;149 18504191 [Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients]. RESULTS: Lamivudine resistant mutation was detected in 103 patients, and the major mutations included rtL180M+rtM204V and rtM204I, accounting for 58.3% and 22.3%, respectively. 2008 Nan fang yi ke da xue xue bao Abstract HBV M204I;L180M;M204V 124;104;112 129;109;117 RT;RT;RT 102;110;122 104;112;124 18507754 Clinical significance of precore and core promoter mutations in genotype D hepatitis B-related chronic liver disease. Conversely, the G1757A substitution was associated with protection, being 90% less frequent among patients with AdLD (P = 0.001). 2008 Journal of viral hepatitis Abstract HBV G1757A 16 22 Aggressive Hepatitis and advanced liver disease 112 116 18507754 Clinical significance of precore and core promoter mutations in genotype D hepatitis B-related chronic liver disease. The double mutation A1762T-G1764A was more prevalent in patients with advanced liver disease (AdLD) and was associated with higher alanine aminotransferase and viral load. 2008 Journal of viral hepatitis Abstract HBV A1762T;G1764A 20;27 26;33 Liver disease;Aggressive Hepatitis and advanced liver disease 79;94 92;98 18507754 Clinical significance of precore and core promoter mutations in genotype D hepatitis B-related chronic liver disease. The results indicate that in genotype D CHB, the presence of the A1762T-G1764A mutation was associated with more aggressive liver disease while the G1757A substitution was associated with protection from advanced disease. 2008 Journal of viral hepatitis Abstract HBV A1762T;G1764A;G1757A 65;72;148 71;78;154 Chronic Hepatitis B;Liver disease;Liver disease 40;124;204 43;137;220 18508941 Application of a novel, rapid, and sensitive oligonucleotide ligation assay for detection of cancer-predicting mutations in the precore and basal core promoter of hepatitis B virus. Double mutations in the basal core promoter (BCP) (A1762T and G1764A) and precore (pre-C) (G1896A) regions of the virus are associated with progression to HCC. 2008 Journal of clinical microbiology Abstract HBV A1762T;G1764A;G1896A 51;62;91 57;68;97 BCP;BCP;Precore;Precore 24;45;83;74 43;48;88;81 Hepatocellular carcinoma 155 158 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. CONCLUSION: The rtA181T/sW172* variant has a secretory defect and exerts a dominant negative effect on wild-type HBV virion secretion. 2008 Hepatology (Baltimore, Md.) Abstract HBV W172X;A181T 24;18 30;23 RT;S 16;24 18;25 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. Examination of sequential HBV DNA levels in patients failing lamivudine or adefovir therapy where only the rtA181T change was detected via polymerase chain reaction sequencing revealed that viral load rebound did not occur or was not as large as usually observed with drug-resistant HBV. 2008 Hepatology (Baltimore, Md.) Abstract HBV A181T 109 114 RT 107 109 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. In vitro analysis revealed that the rtA181T/sW172* variant is not only defective in secretion of viral particles causing intracellular retention of surface proteins, it also has a dominant negative effect on virion but not subviral particle secretion when coexpressed with the wild type. 2008 Hepatology (Baltimore, Md.) Abstract HBV W172X;A181T 44;38 50;43 RT;S;S 36;44;148 38;45;155 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. The selection of rtA181T/sW172* reduced the typical extent of virological breakthrough, resulting in a missed diagnosis of drug resistance if viral load was used as the only criterion for drug failure, necessitating HBV polymerase chain reaction sequencing or other genotypic methods to diagnose antiviral drug resistance in these cases. 2008 Hepatology (Baltimore, Md.) Abstract HBV W172X;A181T 25;19 31;24 RT;S 17;25 19;26 18537180 The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. UNLABELLED: The hepatitis B virus (HBV) mutation that encodes rtA181T is selected in the viral polymerase during antiviral drug therapy and can also encode a stop codon in the overlapping surface gene at amino acid 172 (sW172*) resulting in truncation of the last 55 amino acids of the C-terminal hydrophobic region of the surface proteins. 2008 Hepatology (Baltimore, Md.) Abstract HBV A181T;W172X 64;220 69;226 RT;S;P;S;S 62;220;95;188;323 64;221;105;195;330 18551606 Hepatitis B virus X mutations occurring naturally associated with clinical severity of liver disease among Korean patients with chronic genotype C infection. All five mutation types (V5M/L, P38S, H94Y, I127T/N, and K130M and V131I) affecting the six codons were found to be related significantly to clinical severity. 2008 Journal of medical virology Abstract HBV V5M;V5L;P38S;H94Y;I127T;I127N;K130M;V131I 25;25;32;38;44;44;57;67 30;30;36;42;51;51;62;72 18551606 Hepatitis B virus X mutations occurring naturally associated with clinical severity of liver disease among Korean patients with chronic genotype C infection. Among these, two mutation types (V5M/L and K130M and V131I) were observed more frequently in HBeAg negative patients than in HBeAg positive patients. 2008 Journal of medical virology Abstract HBV V5M;V5L;K130M;V131I 33;33;43;53 38;38;48;58 C;C 93;125 98;130 18551606 Hepatitis B virus X mutations occurring naturally associated with clinical severity of liver disease among Korean patients with chronic genotype C infection. In particular, a novel mutation type (V5M/L) discovered firstly during the present study was found to be associated significantly with HCC. 2008 Journal of medical virology Abstract HBV V5M;V5L 38;38 43;43 Hepatocellular carcinoma 135 138 18572757 Antiviral resistance mutations potentiate hepatitis B virus immune evasion through disruption of its surface antigen a determinant. RESULTS: The mutations rtF166L/sF158Y (lamivudine-associated, compensatory) and rtl169T/sF161L (entecavir-associated, primary) acting alone, and the mutations rtV173L/sE164D (lamivudine-associated, compensatory) and rtSilent/sD144E (antibody escape-associated) each when combined with rtM204V/sl195M (lamivudine-associated, primary) led to decreases in antibody reactivity to epitopes in the first or second loop, or in both loops. 2008 Antiviral therapy Abstract HBV F158Y;F161L;E164D;D144E;F166L;V173L;M204V 31;88;167;225;25;161;287 37;94;173;231;30;166;292 RT;RT;RT;RT;S;S;S;S;S 23;80;159;285;31;88;167;225;293 25;82;161;287;32;89;168;226;294 18572757 Antiviral resistance mutations potentiate hepatitis B virus immune evasion through disruption of its surface antigen a determinant. The rtM204V/sl195M + rtV173L/sE164D mutations yielded an epitope-antibody profile similar to the rtR153Q/sG145R vaccine escape mutant. 2008 Antiviral therapy Abstract HBV E164D;G145R;M204V;V173L;R153Q 29;105;6;23;99 35;111;11;28;104 RT;RT;RT;S;S;S 4;21;97;12;29;105 6;23;99;13;30;106 18572757 Antiviral resistance mutations potentiate hepatitis B virus immune evasion through disruption of its surface antigen a determinant. The rtM204V/sl195M mutation combined with the rtF166L/sF158Y or rtR153Q/sG145R mutation restored reactivity to second-loop epitopes previously abrogated by single mutations. 2008 Antiviral therapy Abstract HBV F158Y;G145R;M204V;F166L;R153Q 54;72;6;48;66 60;78;11;53;71 RT;RT;RT;S;S;S 4;46;64;12;54;72 6;48;66;13;55;73 18597996 [Assessment of sensitivity of commercial test-systems for HBsAg immunodetection according to their ability to detect HBsAg-mutants of hepatitis B virus]. Test-systems based only on monoclonal antibodies did not detect HBsAg with G145R substitution in concentration 5 ng/ml. 2008 Zhurnal mikrobiologii, epidemiologii i immunobiologii Abstract HBV G145R 75 80 S 64 69 18605187 [HBV gene variants and polymerse gene mutations in children with chronic hepatitis B in the course of the antiviral therapy]. YIDD mutation appeared to be the single one in the viral polymerase gene, while YVDD mutations in four patients were accompanied by other changes at amino acid sequence of the HBV polymerase: rtL180M, rtN124D and rtL164M. 2007 Medycyna wieku rozwojowego Abstract HBV L180M;N124D;L164M 194;203;215 199;208;220 P;P;RT;RT;RT;P;P 57;180;192;201;213;0;80 67;190;194;203;215;4;84 18605987 Phosphorylation of hepatitis B virus core C-terminally truncated protein (Cp149) by PKC increases capsid assembly and stability. In addition, when pUC1.2x and pUC1.2x/S106A were transfected, mutant virus titre was decreased 2.31-fold compared with WT virus titre. 2008 The Biochemical journal Abstract HBV S106A 38 43 18605987 Phosphorylation of hepatitis B virus core C-terminally truncated protein (Cp149) by PKC increases capsid assembly and stability. In vitro phosphorylation with core mutants (S26A, T70A, S106A and T114A) revealed that the Ser(106) mutation inhibited phosphorylation of core by PKC. 2008 The Biochemical journal Abstract HBV S26A;T70A;S106A;T114A 44;50;56;66 48;54;61;71 C;C 30;138 34;142 18605987 Phosphorylation of hepatitis B virus core C-terminally truncated protein (Cp149) by PKC increases capsid assembly and stability. When either pCMV/FLAG-Cp149[WT (wild-type)] or pCMV/FLAG-S106A Cp149 was transfected into Huh7 human hepatoma cells, mutant capsid level was decreased by 2.06-fold with the S106A mutant when compared with WT, although the same level of total protein was expressed in both cases. 2008 The Biochemical journal Abstract HBV S106A;S106A 57;173 62;178 Capsid;C;C 124;22;63 130;24;65 Hepatocellular carcinoma 101 109 18606836 Rolling circle amplification, a powerful tool for genetic and functional studies of complete hepatitis B virus genomes from low-level infections and for directly probing covalently closed circular DNA. Only the genomes from the last biopsy specimen obtained after the emergence of lamivudine resistance contained the lamivudine resistance-associated mutations rtL180M and rtM204V ("rt" indicates reverse transcriptase domain). 2008 Antimicrobial agents and chemotherapy Abstract HBV L180M;M204V 160;172 165;177 RT;RT;RT;RT 194;158;170;180 215;160;172;182 18617782 Selection of an entecavir-resistant mutant despite prolonged hepatitis B virus DNA suppression, in a chronic hepatitis B patient with preexistent lamivudine resistance: successful rescue therapy with tenofovir. During entecavir treatment, the rtS202G mutation was selected. 2008 European journal of gastroenterology & hepatology Abstract HBV S202G 34 39 RT 32 34 18617782 Selection of an entecavir-resistant mutant despite prolonged hepatitis B virus DNA suppression, in a chronic hepatitis B patient with preexistent lamivudine resistance: successful rescue therapy with tenofovir. Retrospective analysis revealed that during lamivudine treatment three other mutations had been selected as well, namely rtE1D, rtV207L, and rtI220L. 2008 European journal of gastroenterology & hepatology Abstract HBV E1D;V207L;I220L 123;130;143 126;135;148 RT;RT;RT 121;128;141 123;130;143 18617782 Selection of an entecavir-resistant mutant despite prolonged hepatitis B virus DNA suppression, in a chronic hepatitis B patient with preexistent lamivudine resistance: successful rescue therapy with tenofovir. Sequence analysis revealed the presence of rtL180M and rtM204V lamivudine-resistant-associated mutations at the start of entecavir treatment. 2008 European journal of gastroenterology & hepatology Abstract HBV L180M;M204V 45;57 50;62 RT;RT 43;55 45;57 18624719 Occult hepatitis B virus infection in HIV-infected patients: Evaluation of biochemical, virological and molecular parameters. In the second patient, E164D and I195M substitutions in HBsAg, associated with lamivudine-resistance mutations in the polymerase were identified. 2008 Hepatology research Abstract HBV E164D;I195M 23;33 28;38 S;P 56;118 61;128 18647234 Expression of hepatitis B virus nuclear core antigen in young cirrhotic patients is associated with an unfavourable long-term outcome. Sequence analysis revealed mutations on the nuclear localization signal (NLS) of core protein in five cirrhotic patients with nuclear HBcAg (Q171K in four and Q179K in one patients). 2008 Journal of viral hepatitis Abstract HBV Q171K;Q179K 141;159 146;164 C;C 81;134 85;139 Liver cirrhosis 102 111 18647234 Expression of hepatitis B virus nuclear core antigen in young cirrhotic patients is associated with an unfavourable long-term outcome. Site-directed mutagenesis experiments demonstrated that both the Q171K and Q179K mutation enhanced nuclear localization of the core protein. 2008 Journal of viral hepatitis Abstract HBV Q171K;Q179K 65;75 70;80 C 127 131 18647524 [RtL164V, a mutation possibly associated with lamivudine resistant HBV]. (3) An rtL164V mutation in the reverse transcriptase region was observed in all primary non-responders before and after lamivudine therapy and also in rebounders when viral breakthrough occurred, which was not seen in the responders. 2008 Zhonghua gan zang bing za zhi Abstract HBV L164V 9 14 RT;RT 31;7 52;9 18647526 [A five-year analysis of HBV mutations in a multidrug-resistant patient with chronic hepatitis B]. RESULTS: Several mutations were identified in succession, including LAM-resistant mutations M204I/V and L180M+M204V, ETV-resistant mutation S202G, and HBeAg nonsense mutation G1896A. 2008 Zhonghua gan zang bing za zhi Abstract HBV M204I;M204V;L180M;M204V;S202G;G1896A 92;92;104;110;140;175 99;99;109;115;145;181 C 151 156 18649329 Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital. A triple mutation, T1753C/A1762T/G1764A was identified in only one isolate (Irish-3) associated with severe infection. 2008 Journal of medical virology Abstract HBV A1762T;G1764A;T1753C 26;33;19 32;39;25 18649329 Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital. One isolate (Irish-13), collected from a patient with acute asymptomatic infection, had a G1896A mutation and a 243 bp deletion of the polymerase gene. 2008 Journal of medical virology Abstract HBV G1896A 90 96 P 135 145 18649329 Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital. Only four isolates from patients with severe HBV infection harbored the G1896A stop codon mutation. 2008 Journal of medical virology Abstract HBV G1896A 72 78 HBV infections 45 58 18649329 Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital. The latter also had a mutation, A2339G, in the core gene, not previously reported in severe acute infection caused by genotype D. 2008 Journal of medical virology Abstract HBV A2339G 32 38 C 47 51 18649329 Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital. Variations within the S gene were identified in 6 isolates, including Gly145Ala, associated with vaccine immune escape, Asp144Glu, Ser143Leu and Phe134Leu, each associated with failure to detect HBsAg. 2008 Journal of medical virology Abstract HBV G145A;D144E;S143L;F134L 70;120;131;145 79;129;140;154 S;S 195;22 200;23 18649345 Envelope protein variability among HBV-Infected asymptomatic carriers and immunized children with breakthrough infections. The K141E variant found in previous work was not detected and little variation was observed in the immunodominant "a" determinant; a single change was found in one vaccinated patient (Q129H) and nine changes detected among six unvaccinated carriers. 2008 Journal of medical virology Abstract HBV K141E;Q129H 4;184 9;189 18662283 Prevalence and virological features of occult hepatitis B virus infection in female sex workers who work uncontrolled in Turkey. One PC (G1896A) and one BCP (T1762/A1764) mutation was found, but S gene mutation was not detected in any of the samples. 2009 Liver international Abstract HBV G1896A 8 14 BCP;Precore;S 24;4;66 27;6;67 18675784 A1762T/G1764A mutations of hepatitis B virus, associated with the increased risk of hepatocellular carcinoma, reduce basal core promoter activities. A1762T and G1764A mutations in the basal core promoter are often present in HBV patients but seldom in asymptomatic carriers, and are highly correlated with the increased risk of HBV-associated hepatocellular carcinoma (HCC). 2008 Biochemical and biophysical research communications Abstract HBV A1762T;G1764A 0;11 6;17 BCP 35 54 Hepatocellular carcinoma;Hepatocellular carcinoma 179;220 218;223 18675784 A1762T/G1764A mutations of hepatitis B virus, associated with the increased risk of hepatocellular carcinoma, reduce basal core promoter activities. We also show that T1762A and G1764A double mutations synergize the reduction of the promoter activity. 2008 Biochemical and biophysical research communications Abstract HBV T1762A;G1764A 18;29 24;35 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Among participants with a baseline HBV DNA level of at least 10(4) copies/mL, HCC incidence per 100 000 person-years was higher for those with the precore G1896 (wild-type) variant than for those with the G1896A variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4]). 2008 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;G1896A 324;317;205 330;323;211 BCP;BCP;Precore 313;365;147 316;368;154 Hepatocellular carcinoma 78 81 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Participants who had a baseline serum HBV DNA level greater than 10(4) copies/mL (n = 1526) were tested for the precore G1896A and BCP A1762T/G1764A mutants by direct sequencing. 2008 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;G1896A 142;135;120 148;141;126 BCP;Precore 131;112 134;119 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The multivariable-adjusted hazard ratio of developing HCC was 1.76 (95% CI = 1.19 to 2.61) for genotype C vs genotype B, 0.34 (95% CI = 0.21 to 0.57) for precore G1896A vs wild type, and 1.73 (95% CI = 1.13 to 2.67) for BCP A1762T/G1764A vs wild type. 2008 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;G1896A 231;224;162 237;230;168 BCP;Precore 220;154 223;161 Hepatocellular carcinoma 54 57 18713056 Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus. BACKGROUND: Hepatitis B virus (HBV) establishes lamivudine resistance via the resistance-causative rtM204V/I mutation and the replication-compensatory rtL180M mutation. 2008 The Journal of infectious diseases Abstract HBV M204V;M204I;L180M 101;101;153 108;108;158 RT;RT 99;151 101;153 18713056 Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus. CONCLUSIONS: Both the precore-defective mutation and the preS2 deletion may play a supportive role in the replication of lamivudine-resistant HBV, which may be a reason for there being no need for the compensatory rtL180M mutation in lamivudine-resistant HBV possessing the precore and preS2 genomic changes. 2008 The Journal of infectious diseases Abstract HBV L180M 216 221 Precore;Precore;PreS2;PreS2;RT 22;274;57;286;214 29;281;62;291;216 18713056 Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus. However, both lamivudine-resistant viruses with and those without rtL180M can exist in clinical settings. 2008 The Journal of infectious diseases Abstract HBV L180M 68 73 RT 66 68 18713056 Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus. RESULTS: Throughout the HBV genome, a precore-defective A1896 mutation and a short deletion in the preS2 gene were detected more frequently in viruses without rtL180M than in those with it (64% vs. 2008 The Journal of infectious diseases Abstract HBV L180M 161 166 Precore;PreS2;RT 38;99;159 45;104;161 18713056 Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus. To elucidate the differences between viruses with and those without rtL180M, we conducted full-length sequencing analysis of HBV derived from patients with type B chronic hepatitis showing lamivudine resistance. 2008 The Journal of infectious diseases Abstract HBV L180M 70 75 RT 68 70 Chronic Hepatitis B 156 180 18752330 Long-term efficacy and safety of adefovir dipivoxil for the treatment of hepatitis B e antigen-positive chronic hepatitis B. Adefovir resistance mutations A181V or N236T developed in 13 LTSES patients; the first observation was at study week 195. 2008 Hepatology (Baltimore, Md.) Abstract HBV A181V;N236T 30;39 35;44 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In this regard, homology modeled structure of HBV-polymerase was used for minimization, conformational search and induced fit docking followed by binding energy calculation on wild-type as well as on mutant HBV-polymerases (L180M, M204V, M204I, L180M+M204V, L180M-M204I). 2008 Antiviral research Abstract HBV L180M;M204V;M204I;M204V;L180M;L180M;M204I 224;231;238;251;245;258;264 229;236;243;256;250;263;269 P;P 50;211 60;222 18803358 Clinical, virologic and phylogenetic features of hepatitis B infection in Iranian patients. In the HBV S region, the genetic variability was low, and the marked substitution was P120T/S, with a rate of 9.7% (n = 6). 2008 World journal of gastroenterology Abstract HBV P120T;P120S 86;86 93;93 S 11 12 18803358 Clinical, virologic and phylogenetic features of hepatitis B infection in Iranian patients. The G1896A precore (PC) mutant was detected in 58.1% patients. 2008 World journal of gastroenterology Abstract HBV G1896A 4 10 Precore;Precore 20;11 22;18 18813870 Mutation spectra of the surface-protein-coding region of the HBV genome in HBV-vaccinated and non-vaccinated individuals in Hungary. We could not detect the G145R amino acid substitution associated with vaccine escape mutant virus. 2008 Archives of virology Abstract HBV G145R 24 29 18814242 Clinical significance of a set of single nucleotide polymorphisms of hepatitis B virus core gene in Chinese Han patients with chronic hepatitis B. 5 SNPs, A261T, A336C, A336T T337C and T385C, were found to be associated with RFLP patterns change and only SNP A336C or A336T caused the substitution of Glu-83 with Asp in HBcAg. 2008 Journal of medical virology Abstract HBV A261T;A336C;T385C;A336C;A336T;E83D;A336T;T337C 8;15;38;112;121;154;22;28 13;20;43;117;126;169;27;33 C 173 178 18814242 Clinical significance of a set of single nucleotide polymorphisms of hepatitis B virus core gene in Chinese Han patients with chronic hepatitis B. The serum HBV DNA level in RFLP pattern C was higher than that in RFLP pattern G and C/G mixture, respectively, most possibly which associating with aminoacid change, Glu83Asp. 2008 Journal of medical virology Abstract HBV E83D 167 175 18822888 [YMDD motif variants detected by Inno-Lipa HBV DR assay in chronic hepatitis B patients during lamivudine therapy]. In 8 (66.6%) HBV-DNA samples YMDD variants were accompanied with L180M variants. 2008 Mikrobiyoloji bulteni Abstract HBV L180M 65 70 P 29 33 18837083 Virologic characteristics of hepatitis B virus in patients infected via maternal-fetal transmission. The 1762T/1764A double mutation existed in all clones of the mother, 3 of them were also coupled with G1896A mutation, but none were found in the son. 2008 World journal of gastroenterology Abstract HBV G1896A 102 108 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. CONCLUSIONS: HBV A(1762)T, G(1764)A mutations constitute a valuable biomarker to identify a subset of male HBsAg carriers aged >30 yr at extremely high risk of HCC in Guangxi, and likely elsewhere. 2008 The American journal of gastroenterology Abstract HBV A1762T;G1764A 17;26 25;36 S 107 112 Hepatocellular carcinoma 160 163 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Multivariate analyses showed that in men, increasing age and A(1762)T, G(1764)A double mutations are independently associated with developing HCC. 2008 The American journal of gastroenterology Abstract HBV A1762T;G1764A 61;70 69;80 Hepatocellular carcinoma 142 145 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. We reported that 96% of HCC patients but only 24% of controls were infected with the hepatitis B virus (HBV) with A(1762)T, G(1764)A mutations in Guangxi, China. 2008 The American journal of gastroenterology Abstract HBV A1762T;G1764A 114;123 122;133 Hepatocellular carcinoma 24 27 18844687 Molecular epidemiology of hepatitis B virus in Iran. HBsAg (17.2%), precore-G1896A (59.5%) and Basal core promoter (BCP) double mutations (49.2%), whereas no recombination was found. 2008 Clinical microbiology and infection Abstract HBV G1896A 23 29 BCP;BCP;S;Precore 42;63;0;15 61;66;5;22 18939932 Combined mutations in pre-s/surface and core promoter/precore regions of hepatitis B virus increase the risk of hepatocellular carcinoma: a case-control study. CONCLUSIONS: Pre-S deletions, I68T in surface gene, T1762/A1764, and A1899 were independent risk factors for HCC. 2008 The Journal of infectious diseases Abstract HBV I68T 30 34 PreS;S 13;38 18;45 Hepatocellular carcinoma 109 112 18939932 Combined mutations in pre-s/surface and core promoter/precore regions of hepatitis B virus increase the risk of hepatocellular carcinoma: a case-control study. Multivariate analysis showed that pre-S deletions, I68T surface gene, T1762/A1764, and A1899 were independent factors associated with the development of HCC. 2008 The Journal of infectious diseases Abstract HBV I68T 51 55 PreS;S 34;56 39;63 Hepatocellular carcinoma 153 156 18948142 Dynamics of hepatitis B virus resistance to entecavir in a nucleoside/nucleotide-naive patient. Entecavir-resistant quasi-species (rtM204V+/-rtL180M plus S202G) were found after week 112 and gradually became the predominant mutations afterwards. 2009 Antiviral research Abstract HBV M204V;L180M;S202G 37;47;58 42;52;63 RT;RT 35;45 37;47 18948142 Dynamics of hepatitis B virus resistance to entecavir in a nucleoside/nucleotide-naive patient. The lamivudine resistant quasi-species (rtM204V+/-rtL180M), absent at baseline, were emerged as early as 48 weeks after entecavir administration. 2009 Antiviral research Abstract HBV M204V;L180M 42;52 47;57 RT;RT 40;50 42;52 18948142 Dynamics of hepatitis B virus resistance to entecavir in a nucleoside/nucleotide-naive patient. The lamivudine- and entecavir-resistant mutations emerged closely in combination with the rtV207L, rtA222T, rtP237T or rtI163V substitutions. 2009 Antiviral research Abstract HBV V207L;A222T;P237T;I163V 92;101;110;121 97;106;115;126 RT;RT;RT;RT 90;99;108;119 92;101;110;121 18983768 [Multiple-site analysis of HBV drug-resistant mutations in 340 patients with chronic hepatitis B]. LdT-resistance was observed as M204I. 2008 Zhonghua gan zang bing za zhi Abstract HBV M204I 31 36 18983768 [Multiple-site analysis of HBV drug-resistant mutations in 340 patients with chronic hepatitis B]. M204V and M204I were the most common LAM-resistant mutations. 2008 Zhonghua gan zang bing za zhi Abstract HBV M204V;M204I 0;10 5;15 18983768 [Multiple-site analysis of HBV drug-resistant mutations in 340 patients with chronic hepatitis B]. N236T +/- A181 substitution was the most frequently seen ADV-resistant mutation. 2008 Zhonghua gan zang bing za zhi Abstract HBV N236T 0 5 18983768 [Multiple-site analysis of HBV drug-resistant mutations in 340 patients with chronic hepatitis B]. The former usually emerged with L180M while the latter often emerged alone. 2008 Zhonghua gan zang bing za zhi Abstract HBV L180M 32 37 18998047 Molecular epidemiology of hepatitis B virus in an isolated Afro-Brazilian community. A high rate (18.3%) of occult infection was therefore observed that was associated to low HBV loads (mean, 1.8 x 10(4) copies/ml) and to a specific amino acid substitution (C100Y) in the small surface antigen. 2008 Archives of virology Abstract HBV C100Y 173 178 S 187 200 18998047 Molecular epidemiology of hepatitis B virus in an isolated Afro-Brazilian community. The substitution W501R (polymerase), previously reported only in Gambia, was observed in 46% of the HBV/A1 isolates. 2008 Archives of virology Abstract HBV W501R 17 22 P 24 34 19008175 Core promoter mutant HBV non-responding to adefovir after viral breakthrough on lamivudine: rapid virologic response to tenofovir plus lamivudine in a cirrhotic patient. Because of unchanged VL sequence analysis was performed three months later, which showed the mutation (rtS219A) and the concomitant mutation (sS210R) and 2 mutations in core promoter region (A1762T), (G1764A). 2008 European journal of medical research Abstract HBV S219A;S210R;A1762T;G1764A 105;142;191;201 110;148;197;207 Core promoter;RT;S 169;103;142 182;105;143 19028525 Telbivudine, a nucleoside analog inhibitor of HBV polymerase, has a different in vitro cross-resistance profile than the nucleotide analog inhibitors adefovir and tenofovir. Against HBV genomes with known telbivudine-resistance mutations, M204I and L80I/M204I, telbivudine, lamivudine and entecavir lost 353- to >1000-fold activity whereas adefovir and tenofovir exhibited no more than 3-5-fold change. 2009 Antiviral research Abstract HBV M204I;L80I;M204I 80;75;65 85;79;70 19028525 Telbivudine, a nucleoside analog inhibitor of HBV polymerase, has a different in vitro cross-resistance profile than the nucleotide analog inhibitors adefovir and tenofovir. Conversely, against HBV cell lines expressing adefovir resistance mutations N236T and A181V, or the A194T mutant associated with resistance to tenofovir, telbivudine remained active as shown by respective fold-changes of 0.5 (N236T) and 1.0 (A181V and A194T). 2009 Antiviral research Abstract HBV N236T;A181V;A194T;N236T;A181V;A194T 76;86;100;226;242;252 81;91;105;231;247;257 19028525 Telbivudine, a nucleoside analog inhibitor of HBV polymerase, has a different in vitro cross-resistance profile than the nucleotide analog inhibitors adefovir and tenofovir. Telbivudine was not active against HBV strains bearing lamivudine mutations L180M/M204V/I but remained active against the M204V single mutant in vitro, potentially explaining the difference in resistance profiles between telbivudine and lamivudine. 2009 Antiviral research Abstract HBV M204V;M204I;L180M;M204V 82;82;76;122 89;89;81;127 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. Both sF220L and sS207N co-localized in the fourth transmembrane HBsAg domain. 2009 Journal of hepatology Abstract HBV F220L;S207N 5;16 11;22 S;S;S 5;16;64 6;17;69 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. Covariate analysis showed that rtM204V clusters with rtL180M, rtL229V (corresponding to sF220L in the HBsAg), and, interestingly, with HBsAg mutation sS207N (bootstrap=0.95). 2009 Journal of hepatology Abstract HBV M204V;L180M;L229V;F220L;S207N 33;55;64;88;150 38;60;69;94;156 S;S;RT;RT;RT;S;S 102;135;31;53;62;88;150 107;140;33;55;64;89;151 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. In contrast, in genotype D the primary mutations rtM204V and rtM204I occurred with similar prevalence (39.1% versus 45.3%, P=0.47), and showed a distinct pattern of compensatory mutations. 2009 Journal of hepatology Abstract HBV M204V;M204I 51;63 56;68 RT;RT 49;61 51;63 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. Multivariate analysis confirmed that genotype A is the only predictor for rtM204V emergence (OR: 14.5 [95% CI: 1.3-158], P=0.02). 2009 Journal of hepatology Abstract HBV M204V 76 81 RT 74 76 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. RESULTS: In genotype A, the rtM204V (prevalence: 68.2%) was the main sign of lamivudine failure. 2009 Journal of hepatology Abstract HBV M204V 30 35 RT 28 30 19041149 The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes. rtM204V clusters with mutations localized in the RT-B domain (rtV173L, rtL180M, and rtT184A/S) (bootstrap=0.94), while rtM204I clusters with mutations localized in the RT-A domain (rtS53N, rtT54Y, and rtL80I/V) (bootstrap=0.96) (without associations with HBsAg specific mutations). 2009 Journal of hepatology Abstract HBV M204V;V173L;L180M;T184A;T184S;M204I;S53N;T54Y;L80I;L80V 2;64;73;86;86;121;183;191;203;203 7;69;78;93;93;126;187;195;209;209 S;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 255;0;49;62;71;84;119;168;181;189;201 260;2;51;64;73;86;121;170;183;191;203 19041345 Assessment of selective real-time PCR for quantitation of lamivudine and adefovir hepatitis B virus-resistant strains and comparison with direct sequencing and line probe assays. A selective real-time PCR (sPCR) assay has been developed to detect the rtM204V/I and rtN236T mutations of hepatitis B virus (HBV) associated with resistance to lamivudine and adefovir. 2009 Journal of virological methods Abstract HBV M204V;M204I;N236T 74;74;88 81;81;93 RT;RT 72;86 74;88 19043921 The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. BACKGROUND: Previously, a less prevalent lamivudine-resistant mutant (rtA181T) was discovered in Taiwanese patients, in which a stop codon in the surface gene concomitantly occurred, leading to impaired secretion of hepatitis B virus (HBV) surface antigen. 2008 Antiviral therapy Abstract HBV A181T 72 77 RT;S;S 70;146;240 72;153;247 19043921 The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. CONCLUSION: Our data indicate that an HBV polymerase rtA181T/surface truncation mutant could emerge spontaneously without previous antiviral treatment. 2008 Antiviral therapy Abstract HBV A181T 55 60 P;RT;S 42;53;61 52;55;68 19043921 The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. Here, we aimed to evaluate the oncogenic potential of HBV rtA181T/surface truncation mutant. 2008 Antiviral therapy Abstract HBV A181T 60 65 RT;S 58;66 60;73 19043921 The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant. The rtA181T mutant also conferred drug resistance to adefovir. 2008 Antiviral therapy Abstract HBV A181T 6 11 RT 4 6 19065672 Complex dynamics of hepatitis B virus resistance to adefovir. UNLABELLED: In patients with hepatitis B e antigen-negative chronic hepatitis B, adefovir dipivoxil administration selects variants bearing reverse transcriptase rtN236T and/or rtA181V/T substitutions in 29% of cases after 5 years. 2009 Hepatology (Baltimore, Md.) Abstract HBV N236T;A181V;A181T 164;179;179 169;186;186 C;RT;RT;RT 41;140;162;177 50;161;164;179 Chronic Hepatitis B 60 79 19070921 The association of HBV core promoter double mutations (A1762T and G1764A) with viral load differs between HBeAg positive and anti-HBe positive individuals: a longitudinal analysis. BACKGROUND/AIMS: Although there have been a few reports regarding the effect of basal core promoter (BCP) double mutations (A1762T and G1764A) on hepatitis B viral loads, the association remains uncertain. 2009 Journal of hepatology Abstract HBV A1762T;G1764A 124;135 130;141 BCP;BCP 80;101 99;104 19070923 Occult hepatitis B virus infection in hepatitis B vaccinated children in Taiwan. Sequence analyses of S gene showed occult isolates were variants; no G145R but C139S vaccine escape mutant was found. 2009 Journal of hepatology Abstract HBV G145R;C139S 69;79 74;84 S 21 22 19077239 Occult hepatitis B infection: an evolutionary scenario. A single substitution (G173T) that is associated with clade membership alters the local RNA secondary structure and is proposed to affect splicing efficiency at the 202 acceptor site. 2008 Virology journal Abstract HBV G173T 23 28 19077481 [Development of clevudine resistance after switching from lamivudine in a patient with chronic hepatitis B]. After the 6 months of clevudine therapy, the patient developed virologic breakthrough (>1.0chi10(8) copies/mL) as well as biochemical breakthrough, which was associated with the presence of rtM204I plus rtL80I mutant. 2008 The Korean journal of gastroenterology Abstract HBV M204I;L80I 192;205 197;209 RT;RT 190;203 192;205 19098499 Molecular analysis of an HBsAg-negative hepatitis B virus mutant selected in a tenofovir-treated HIV-hepatitis B virus co-infected patient. The molecular analysis performed in an HIV-hepatitis B virus (HBV) coinfected patient revealed selection of an unusual HBV polymerase mutation (rtV191I) during tenofovir-containing therapy, conferring simultaneously immune escape by HBsAg negativity and resistance to lamivudine but not tenofovir. 2009 AIDS (London, England) Abstract HBV V191I 146 151 S;P;RT 233;123;144 238;133;146 19107976 Lamivudine monoprophylaxis and adefovir salvage for liver transplantation in chronic hepatitis B: a seven-year follow-up study. On direct sequencing, four patients had rtM204I mutation and three patients HBV DNA levels were too low for sequencing. 2009 Journal of medical virology Abstract HBV M204I 42 47 RT 40 42 19119245 [The efficacy of adefovir dipivoxil monotherapy and the incidence of genotypic resistance to adefovir dipivoxil in patients with lamivudine-resistant chronic hepatitis B infection]. At 12 months after ADV treatment, the cumulative rates of HBeAg loss and seroconversion were 15.8% and 10.5%, respectively, and the rtN236T and rtA181T/V mutants in HBV DNA polymerase were identified in 25% and 64% of patients, respectively. 2008 The Korean journal of hepatology Abstract HBV N236T;A181T;A181V 134;146;146 139;153;153 C;P;RT;RT 58;173;132;144 63;183;134;146 19125938 Spontaneous HBeAg seroconversion and loss of hepatitis B virus DNA after acute flare due to development of drug resistant mutants during entecavir monotherapy. In contrast to the previously identified ETV resistant mutants, it did not carry the rtM204V/I mutations. 2009 Hepatology research Abstract HBV M204V;M204I 87;87 94;94 RT 85 87 19125938 Spontaneous HBeAg seroconversion and loss of hepatitis B virus DNA after acute flare due to development of drug resistant mutants during entecavir monotherapy. Interestingly, a new mutant type with rtL180M+rtT184L was found alongside rtL180M+rtT184L+rtM204V/I at week 228 and appeared to develop independently, according to the sequence analysis. 2009 Hepatology research Abstract HBV L180M;L180M;T184L;T184L;M204V;M204I 40;76;48;84;92;92 45;81;53;89;99;99 RT;RT;RT;RT;RT 38;46;74;82;90 40;48;76;84;92 19152408 Susceptibility of hepatitis B virus to lamivudine restored by resistance to adefovir. In both patients serial monotherapy caused the replacement in all HBV clones of wild-type virus by classical lamivudine resistant mutants (L180M and M204V/I), which were replaced subsequently by adefovir resistant mutants (A181V and N236T). 2009 Journal of medical virology Abstract HBV L180M;M204V;M204I;A181V;N236T 139;149;149;223;233 144;156;156;228;238 19152408 Susceptibility of hepatitis B virus to lamivudine restored by resistance to adefovir. When finally lamivudine was added to adefovir, the A181V adefovir mutation persisted in all clones and lamivudine-related mutations did not reappear. 2009 Journal of medical virology Abstract HBV A181V 51 56 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. Decrease in mean serum HBV did not differ between patients carrying the rtM204I versus rtM204V mutant at week 24 (-3.3 vs. 2009 Journal of medical virology Abstract HBV M204I;M204V 74;89 79;94 RT;RT 72;87 74;89 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. In addition to the YMDD mutations, the rtL180M, rtL80I, and rtV173L mutations were also present in 78%, 43%, and 11% of patients, respectively. 2009 Journal of medical virology Abstract HBV L180M;L80I;V173L 41;50;62 46;54;67 RT;RT;RT;P 39;48;60;19 41;50;62;23 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. Of the 67 patients with chronic hepatitis B, 65 patients (97%) had lamivudine-resistant mutations in the YMDD motif [27 (41%) rtM204I, 22 (34%) rtM204V, and 16 (25%) rtM204I/V]. 2009 Journal of medical virology Abstract HBV M204I;M204V;M204I;M204V 128;146;168;168 133;151;175;175 RT;RT;RT;P 126;144;166;105 128;146;168;109 Chronic Hepatitis B 24 43 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. The presence of the rtL180M, rtL80I, and rtV173L did not significantly affect viral load reduction during adefovir administration. 2009 Journal of medical virology Abstract HBV L180M;L80I;V173L 22;31;43 27;35;48 RT;RT;RT 20;29;41 22;31;43 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. The rtM204V mutation always accompanied rtL180M, and rtL80I was always observed in conjunction with rtM204I. 2009 Journal of medical virology Abstract HBV M204V;L180M;L80I;M204I 6;42;55;102 11;47;59;107 RT;RT;RT;RT 4;40;53;100 6;42;55;102 19152409 Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B. These results demonstrate that the rtL80I mutant is co-selected with rtM204I as a compensatory mutation in the same manner as rtL180M with rtM204V, and that adefovir shows similar antiviral efficacy against all of the evaluated patterns of lamivudine-resistant HBV mutations. 2009 Journal of medical virology Abstract HBV L80I;M204I;L180M;M204V 37;71;128;141 41;76;133;146 RT;RT;RT;RT 35;69;126;139 37;71;128;141 19178592 Prolonged use of tenofovir in HIV/hepatitis B virus (HBV)-coinfected individuals does not lead to HBV polymerase mutations and is associated with persistence of lamivudine HBV polymerase mutations. The previously identified putative TDF-resistance mutations, rtA194T+rtL180M+rtM204V, were not detected in any individual. 2009 HIV medicine Abstract HBV A194T;L180M;M204V 63;71;79 68;76;84 RT;RT;RT 61;69;77 63;71;79 19178836 [A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding]. CONCLUSION: The point mutation in pre-core region G1896A of HBV dose not affect the positive rate of HBV DNA in breast milk and higher HBV DNA loads in serum of pregnant women might increase the risk of mother-infant transmission. 2008 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV G1896A 50 56 Precore 34 42 19178836 [A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding]. OBJECTIVE: To investigate the relationship between pre-core G1896A point mutation of hepatitis B virus (HBV) and safety of breast feeding. 2008 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV G1896A 60 66 Precore 51 59 19178836 [A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding]. PCR-solid phase hybridization was used to detect the point mutation in pre-core region G1896A of HBV from pregnant women, and HBV DNA loads in sera and breast milk were determined by fluorescence quantitative PCR (FQ-PCR). 2008 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV G1896A 87 93 Precore 71 79 19195324 Adefovir for chronic hepatitis B treatment: identification of virological markers linked to therapy response. BACKGROUND: HBV variants rtA181V/T, rtN236T and rtl233V, which confer resistance to adefovir dipivoxil (ADV), are not detected in many non-responding patients. 2008 Antiviral therapy Abstract HBV A181V;A181T;N236T 27;27;38 34;34;43 RT;RT;RT 25;36;48 27;38;50 19195324 Adefovir for chronic hepatitis B treatment: identification of virological markers linked to therapy response. CONCLUSIONS: Virological pretreatment characteristics (HBeAg, viral genotype and rtL217R polymorphism) are potentially associated with ADV response. 2008 Antiviral therapy Abstract HBV L217R 83 88 C;RT 55;81 60;83 19195324 Adefovir for chronic hepatitis B treatment: identification of virological markers linked to therapy response. On sequencing, variant rt217R (associated with subgenotype A2) was predictive of non-CVR (100%) and non-PVR (72.7%); the rtS219A variant emerged during therapy in three non-PVR patients. 2008 Antiviral therapy Abstract HBV S219A 123 128 RT;RT 23;121 25;123 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. By itself, Cp149-Y132A will not form capsids. 2009 Biochemistry Abstract HBV Y132A 17 22 Capsid;C 37;11 44;13 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Here we use Cp149, the assembly domain of the hepatitis B virus capsid protein, together with an assembly defective mutant, Cp149-Y132A, to examine the limits of the efficacy of assembly inhibitors. 2009 Biochemistry Abstract HBV Y132A 130 135 Capsid;C;C 64;12;124 70;14;126 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. However, Cp-Y132A will coassemble with the wild-type protein on the basis of light scattering and size exclusion chromatography. 2009 Biochemistry Abstract HBV Y132A 12 17 C 9 11 19207682 Hepatitis B virus genotypes and hepatitis B surface antigen mutations in family contacts of hepatitis B virus infected patients with occult hepatitis B virus infection. A128V & T143M mutations were observed in 5 of 13 (38.4%) subjects and A128V & P127S in 2 of 13 (15.3%) patients (P = 0.385). 2009 Journal of gastroenterology and hepatology Abstract HBV A128V;T143M;A128V;P127S 0;8;70;78 5;13;75;83 19207682 Hepatitis B virus genotypes and hepatitis B surface antigen mutations in family contacts of hepatitis B virus infected patients with occult hepatitis B virus infection. A128V mutation was seen in two (15.3%) subjects with D2 genotype, while T143M mutation was seen in three (23.07%) subjects with A1genotype. 2009 Journal of gastroenterology and hepatology Abstract HBV A128V;T143M 0;72 5;77 19207682 Hepatitis B virus genotypes and hepatitis B surface antigen mutations in family contacts of hepatitis B virus infected patients with occult hepatitis B virus infection. None of the subjects had G145R mutation. 2009 Journal of gastroenterology and hepatology Abstract HBV G145R 25 30 19212700 Influence of HBV gene heterogeneity on the failure of immunization with HBV vaccines in eastern China. Interestingly, Thr123Ala and Gly145Arg were observed only in failure-group mothers, whereas Thr126Asn, Thr126Ser, Thr143Asn, Asp144Gly, and Asp144Ala were seen in the success group. 2009 Archives of virology Abstract HBV T123A;G145R;T126N;T126S;T143N;D144G;D144A 15;29;92;103;114;125;140 24;38;101;112;123;134;149 19222103 Hepatitis B virus mutations potentially conferring adefovir/tenofovir resistance in treatment-naive patients. These mutations were rtV214A/rtN238T in one patient and rtA194T in the other. 2009 World journal of gastroenterology Abstract HBV V214A;N238T;A194T 23;31;58 28;36;63 RT;RT;RT 21;29;56 23;31;58 19231002 Entecavir shows limited efficacy in HBeAg-positive hepatitis B patients with a partial virologic response to adefovir therapy. Two lamivudine-experienced patients demonstrated the rtM204I mutation; no other entecavir-resistant substitutions were detected (rtI169, rtT184, rtS202, and rtM250). 2009 Journal of hepatology Abstract HBV M204I 55 60 RT;RT;RT;RT;RT 53;129;137;145;157 55;131;139;147;159 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. Clones harboring rtA194T showed partial resistance to tenofovir in vitro and also to LAM but remained susceptible to telbivudine and entecavir. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T 19 24 RT 17 19 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. CONCLUSION: The rtA194T polymerase mutation is associated with partial tenofovir drug resistance and negatively impacts replication competence of HBV constructs. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T 18 23 RT;P 16;24 18;34 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. In contrast, combination of rtA194T (+/- LAM resistance) with HBeAg-negative PC or BCP mutants increased the replication capacity of the drug-resistant polymerase mutants, thereby restoring the viral replication to similar levels as WT clones. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T 30 35 BCP;C;Precore;P;RT 83;62;77;152;28 86;67;79;162;30 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. The rtA194T polymerase mutation alone or in conjunction with LAM resistance reduced the replication efficiency as compared with wild-type (WT) HBV. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T 6 11 RT;P 4;12 6;22 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. The rtA194T polymerase mutation has been found in HBV/HIV coinfected patients during tenofovir treatment and may be associated with tenofovir resistance. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T 6 11 RT;P 4;12 6;22 HBV-HIV coinfections 50 68 19263474 The rtA194T polymerase mutation impacts viral replication and susceptibility to tenofovir in hepatitis B e antigen-positive and hepatitis B e antigen-negative hepatitis B virus strains. We generated replication-competent HBV constructs harboring rtA194T alone or in addition to lamivudine (LAM) resistance (rt180M + rtM204V), PC mutations, and BCP mutations and assessed their replicative capacity after transient transfection in human hepatoma cells. 2009 Hepatology (Baltimore, Md.) Abstract HBV A194T;M204V 62;132 67;137 BCP;Precore;RT;RT;RT 158;140;60;121;130 161;142;62;123;132 Hepatocellular carcinoma 250 258 1926786 Association of hepatitis B viral precore mutations with fulminant hepatitis B in Japan. We demonstrated that patients with fulminant hepatitis B carried HBV genomes with a G to A mutation at nucleotide positions 1898 (five of five patients; 18 of 18 clones, 100%) and 1901 (five of five patients; 12 of 18 clones, 66%) in the precore region. 1991 Virology Abstract HBV G1898A 84 128 Precore 238 245 Fulminant Hepatitis B 35 54 19272629 Association between genomic heterogeneity of hepatitis B virus and intrauterine infection. Particularly, A1762T/G1764A mutations seemed to be disadvantageous for fetal infection. 2009 Virology Abstract HBV G1764A;A1762T 21;14 27;20 19272629 Association between genomic heterogeneity of hepatitis B virus and intrauterine infection. The clones with mutations such as amino acid P110S in preS1 region, P36L in preS2 region and C107R in S region might infect fetuses more readily. 2009 Virology Abstract HBV P110S;P36L;C107R 45;68;93 50;72;98 PreS1;PreS2;S 54;76;102 59;81;103 19274751 Efficacy of hepatitis B vaccine against antiviral drug-resistant hepatitis B virus mutants in the chimpanzee model. Prior to the HBV mutant challenge of vaccinated chimpanzees, we established virologic, serologic, and pathologic characteristics of infections resulting from intravenous inoculation of the HBV polymerase gene mutant and the sG145R vaccine-escape surface gene mutant. 2009 Hepatology (Baltimore, Md.) Abstract HBV G145R 224 230 P;S;S 193;224;246 203;225;253 19274751 Efficacy of hepatitis B vaccine against antiviral drug-resistant hepatitis B virus mutants in the chimpanzee model. The polymerase gene mutant contained a combination of three mutations (rtV173L, rtL180M, rtM204V), two of which resulted in changes to the overlapping viral envelope of the hepatitis B surface antigen (sE164D, sI195M). 2009 Hepatology (Baltimore, Md.) Abstract HBV V173L;L180M;M204V;E164D;I195M 73;82;91;202;210 78;87;96;208;216 S;P;RT;RT;RT;S;S;S 157;4;71;80;89;202;210;185 165;14;73;82;91;203;211;192 19280622 Long-term monitoring shows hepatitis B virus resistance to entecavir in nucleoside-naive patients is rare through 5 years of therapy. Entecavir (ETV) resistance (ETVr) results from HBV reverse transcriptase substitutions at positions T184, S202, or M250, which emerge in the presence of lamivudine (LVD) resistance substitutions M204I/V +/- L180M. 2009 Hepatology (Baltimore, Md.) Abstract HBV M204I;M204V;L180M 195;195;207 202;202;212 RT 51 72 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. UDPS detected drug-resistance mutations that were not detected by PCR in 10 samples from 5 NRTI-treated patients, including the lamivudine-resistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and S202G (in 1 sample), the adefovir-resistance mutation N236T (in 1 sample), and the lamivudine and adefovir-resistance mutations V173L, L180M, A181T, and M204V (in 1 sample). 2009 The Journal of infectious diseases Abstract HBV V173L;T184S;S202G;N236T;V173L;L180M;A181T;M204V 159;216;241;295;369;376;383;394 164;221;246;300;374;381;388;399 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. A total of 20.6% (7/34) of the clones harbored the rtK212T + rtM250L mutation, and rtA181V was found in 2.9% (1/34) of the clones. 2009 Clinical therapeutics Abstract HBV K212T;M250L;A181V 53;63;85 58;68;90 RT;RT;RT 51;61;83 53;63;85 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. A total of 9.1% (4/44) of the clones harbored the rtL180M + rtT184L + rtM204I mutations. 2009 Clinical therapeutics Abstract HBV L180M;T184L;M204I 52;62;72 57;67;77 RT;RT;RT 50;60;70 52;62;72 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. At week 108, after the patient had been receiving ADV + LDT combination therapy for 22 weeks, rtS202G and rtI269T had emerged, representing 28.9% (13/45) and 8.9% (4/45), respectively, of the viral population during ADV + LDT combination treatment. 2009 Clinical therapeutics Abstract HBV S202G;I269T 96;108 101;113 RT;RT 94;106 96;108 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. At week 18 during LAM treatment, the rtM204I mutation became predominant, being present in 79.5% (35/44) of clones. 2009 Clinical therapeutics Abstract HBV M204I 39 44 RT 37 39 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. At week 22 during ADV treatment, LAM-resistance mutations (rtL180M, rtT184L, rtM204I, rtV191I, and rtL229V) were not detected. 2009 Clinical therapeutics Abstract HBV L180M;T184L;M204I;V191I;L229V 61;70;79;88;101 66;75;84;93;106 RT;RT;RT;RT;RT 59;68;77;86;99 61;70;79;88;101 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. At week 86 during ADV therapy, the rtN236T ADV-resistance mutation was detected in 58.8% (20/34) of clones. 2009 Clinical therapeutics Abstract HBV N236T 37 42 RT 35 37 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. RESULTS: The rtM204V/L LAM-resistance mutation was detected in 4.4% (2/45) of clones prior to LAM treatment. 2009 Clinical therapeutics Abstract HBV M204V;M204L 15;15 22;22 RT 13 15 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. The rtM204I mutation was associated with compensatory mutations (rtL180M and rtT184L). 2009 Clinical therapeutics Abstract HBV M204I;L180M;T184L 6;67;79 11;72;84 RT;RT;RT 4;65;77 6;67;79 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. Two new mutations, rtL229V and rtV191I, were detected in 75.0% (33/44) and 11.4% (5/44) of clones, respectively. 2009 Clinical therapeutics Abstract HBV L229V;V191I 21;33 26;38 RT;RT 19;31 21;33 19302908 Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues. We also detected several polymorphic sites,including rtF221Y, rtS223A, rtI224V, rtN238H, rtL267Q, and rtQ271M, during the sequential treatment. 2009 Clinical therapeutics Abstract HBV F221Y;S223A;I224V;N238H;L267Q;Q271M 55;64;73;82;91;104 60;69;78;87;96;109 RT;RT;RT;RT;RT;RT 53;62;71;80;89;102 55;64;73;82;91;104 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. The A1762T and G1764A mutations in the basal core promoter (BCP) region and the G1896A mutation in the precore (PC) region of hepatitis B virus (HBV) genome are found commonly in HBeAg-negative patients. 2009 Journal of medical virology Abstract HBV A1762T;G1764A;G1896A 4;15;80 10;21;86 BCP;BCP;C;Precore;Precore 39;60;179;112;103 58;63;184;114;110 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. BACKGROUND/AIMS: Lamivudine (LAM) resistance is frequently associated with various types of genomic changes in hepatitis B virus (HBV)-DNA including YMDD mutations (rtM204V/I). 2009 Liver international Abstract HBV M204V;M204I 167;167 174;174 RT;YMDD 165;149 167;153 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. CONCLUSIONS: These results provide evidence that rtL80V/I variants of HBV may be associated with a poor antiviral response to ADV in CHB patients with YMDD mutants. 2009 Liver international Abstract HBV L80V;L80I 51;51 57;57 RT;YMDD 49;151 51;155 Chronic Hepatitis B 133 136 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. However, interestingly, after ADV therapy for 12 months, patients with rtL80V/I achieved a much smaller reduction in serum HBV-DNA titre than those without it (mean, -3.43 vs. 2009 Liver international Abstract HBV L80V;L80I 73;73 79;79 RT 71 73 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. In addition, patients with rtL80V/I had lower rates of undetectable HBV-DNA (20 vs. 2009 Liver international Abstract HBV L80V;L80I 29;29 35;35 RT 27 29 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. RESULTS: All the 97 patients had genotype C HBV associated with rtM204V/I mutations; 63 (65%) rtM204I, 27 (28%) rtM204V and seven (7%) both. 2009 Liver international Abstract HBV M204V;M204I;M204I;M204V 66;66;96;114 73;73;101;119 RT;RT;RT 64;94;112 66;96;114 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. The rtL80V/I and rtL180M variants were identified in 66 (68%) and 67 (69%) patients respectively. 2009 Liver international Abstract HBV L80V;L80I;L180M 6;6;19 12;12;24 RT;RT 4;17 6;19 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. The rtM204I and rtM204V variants were strongly associated with rtL80V/I and rtL180M respectively (P<0.01). 2009 Liver international Abstract HBV M204I;M204V;L80V;L80I;L180M 6;18;65;65;78 11;23;71;71;83 RT;RT;RT;RT 4;16;63;76 6;18;65;78 19323782 Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy. There was no difference in antiviral response at 12 months after ADV therapy between patients in relation to the type of YMDD mutation or the presence of rtL180M. 2009 Liver international Abstract HBV L180M 156 161 RT;YMDD 154;121 156;125 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Introduction of its T1753C, A1762T, G1764A, and C1766T core promoter mutations into the 2A genome greatly enhanced genome replication and suppressed HBeAg expression. 2009 Virology Abstract HBV T1753C;A1762T;G1764A;C1766T 20;28;36;48 26;34;42;54 Core promoter;C 55;149 68;154 19335977 [A study on the treatment of chronic hepatitis B with YMDD mutation]. Two patients had rtN236T mutation in group A, and one patient had rtN236T mutation and another one had rtA181V mutation in group B. 2009 Zhonghua gan zang bing za zhi Abstract HBV N236T;N236T;A181V 19;68;105 24;73;110 RT;RT;RT 17;66;103 19;68;105 19382250 Frequent detection of hepatitis B virus variants associated with lamivudine resistance in treated South African patients infected chronically with different HBV genotypes. Of the 17 patients, 13 (76.5%) carried YMDD mutations: 7 with rtM204I (2 HBeAg-positive and 5 HBeAg-negative) and 6 with rtM204V (4 HBeAg-positive and 2 HBeAg-negative). 2009 Journal of medical virology Abstract HBV M204I;M204V 64;123 69;128 C;C;C;C;RT;RT;P 73;94;132;153;62;121;39 78;99;137;158;64;123;43 19382250 Frequent detection of hepatitis B virus variants associated with lamivudine resistance in treated South African patients infected chronically with different HBV genotypes. Of the 17 patients, 3 carried both pre-C (G1896A) and BCP (A1762T/G1764A) mutants, 1 pre-C only and 1 BCP only. 2009 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 66;59;42 72;65;48 BCP;BCP;Precore;Precore 54;102;35;85 57;105;40;90 19386834 Complete genome sequence and phylogenetic relatedness of hepatitis B virus isolates in Papua, Indonesia. Based on the amino acid alignment, HBV/C6 has subgenotype specific variations (G18V and V47M) in the S region. 2009 Journal of clinical microbiology Abstract HBV G18V;V47M 79;88 83;92 S 101 102 19398648 Alkoxyalkyl esters of 9-(s)-(3-hydroxy-2-phosphonomethoxypropyl) adenine are potent and selective inhibitors of hepatitis B virus (HBV) replication in vitro and in HBV transgenic mice in vivo. HDP-(S)-HPMPA retained full activity against HBV mutants resistant to lamivudine (L180M, M204V), but cross-resistance to a mutant resistant to adefovir (N236T) was detected. 2009 Antimicrobial agents and chemotherapy Abstract HBV L180M;M204V;N236T 82;89;153 87;94;158 19401629 Prevalence of occult hepatitis B virus infection in a general adult population in Korea. Sequencing of HBV S gene in 3 cases revealed one wild-type and two mutant strains (W74S, F85Y; T63I, W74S, T131N substitutions). 2009 Intervirology Abstract HBV W74S;F85Y;T63I;W74S;T131N 83;89;95;101;107 87;93;99;105;112 S 18 19 19413519 Perinatal transmission of hepatitis B virus: an Australian experience. The fourth mother-infant pair had an S gene variant, HBV D144E, which has been previously reported in association with vaccine/HBIG escape. 2009 The Medical journal of Australia Abstract HBV D144E 57 62 S 37 38 19420079 Genetic characterization of hepatitis B virus in peripheral blood leukocytes: evidence for selection and compartmentalization of viral variants with the immune escape G145R mutation. The results of this study revealed the exclusive compartmentalization of HBV subgenotype Ae/A2-specific sequences with a potent immune escape G145R mutation in the PBL of the majority of the subjects. 2009 Journal of virology Abstract HBV G145R 142 147 19420079 Genetic characterization of hepatitis B virus in peripheral blood leukocytes: evidence for selection and compartmentalization of viral variants with the immune escape G145R mutation. These results suggest that subgenotype Ae/A2 is selectively archived in the PBL, and the high prevalence of G145R indicates high immune pressure and high evolutionary rates of HBV DNA in the PBL. 2009 Journal of virology Abstract HBV G145R 108 113 19430095 Association of baseline viral factors with response to lamivudine therapy in chronic hepatitis B patients with high serum alanine aminotransferase levels. RESULTS: The frequency of patients with detectable PC stop codon mutation (G1896A), basal core promoter mutation (A1762T/G1764A) and pre-S deletion at baseline was 22.4%, 21.6% and 12.1%, respectively. 2009 Antiviral therapy Abstract HBV G1764A;G1896A;A1762T 121;75;114 127;81;120 BCP;Precore;PreS 84;51;133 103;53;138 19430100 Identification of nonsense mutations in hepatitis B virus S gene in patients with hepatocellular carcinoma developed after lamivudine therapy. NIH3T3 cells stably expressing sL21*, sW156* and sW172* pre-S/S mutants had increased tumourigenicity in nude mice. 2009 Antiviral therapy Abstract HBV L21X;W156X;W172X 31;38;49 36;44;55 PreS;S;S;S;S 56;62;31;38;49 61;63;32;39;50 19431214 A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan. Compared with the HBsAg-positive HCC controls, occult HBV-infected HCC patients had higher frequencies of M1I and Q2K in pre-S2 gene, G185R and S210N in surface gene, A36T and A44L in X gene, and G1721A in enhancer II gene, and had lower rates of pre-S deletions and A1762T/G1764A, A1846T, G1896A and G1899A in core promoter/precore genes. 2009 International journal of cancer Abstract HBV G1764A;A1762T;G185R;S210N;A36T;A44L;G1721A;A1846T;G1896A;G1899A;M1I;Q2K 274;267;134;144;167;176;196;282;290;301;106;114 280;273;139;149;171;180;202;288;296;307;109;117 Core promoter;Enh II;S;Precore;PreS;PreS2;S;X 311;206;18;325;247;121;153;184 324;217;23;332;252;127;160;185 Hepatocellular carcinoma;Hepatocellular carcinoma;Occult Hepatitis B 33;67;47 36;70;66 19431214 A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan. Moreover, M1I and Q2K in pre-S2 gene and G1721A were more common in occult HBV-infected patients with HCC than in those without HCC. 2009 International journal of cancer Abstract HBV G1721A;M1I;Q2K 41;10;18 47;13;21 PreS2 25 31 Hepatocellular carcinoma;Hepatocellular carcinoma;Occult Hepatitis B 102;128;68 105;131;87 19431214 A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan. Multivariate analysis showed Q2K in pre-S2 gene, G1721A and A1846T were independent factors for occult HBV-infected HCC. 2009 International journal of cancer Abstract HBV G1721A;A1846T;Q2K 49;60;29 55;66;32 PreS2 36 42 Hepatocellular carcinoma;Occult Hepatitis B 116;96 119;115 19431214 A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan. The G1721A, M1I and Q2K in pre-S2 gene may be useful viral markers for HCC in occult HBV carriers. 2009 International journal of cancer Abstract HBV G1721A;M1I;Q2K 4;12;20 10;15;23 PreS2 27 33 Hepatocellular carcinoma 71 74 19439550 Genetic dissection of naturally occurring basal core promoter mutations of hepatitis B virus reveals a silent phenotype in the overlapping X gene. Due to a compact viral genome organization, BCP1 and BCP2 mutations result in amino acids changes in the overlapping X gene: K130M/V131I and F132Y, respectively. 2009 The Journal of general virology Abstract HBV V131I;K130M;F132Y 131;125;141 136;130;146 BCP;BCP;X 44;53;117 47;56;118 19439550 Genetic dissection of naturally occurring basal core promoter mutations of hepatitis B virus reveals a silent phenotype in the overlapping X gene. During chronic hepatitis B virus (HBV) infection, double substitution mutations in the basal core promoter (BCP) region frequently emerge that include A1762T/G1764A and the neighbouring C1766T/T1768A mutations, here termed BCP1 and BCP2, respectively. 2009 The Journal of general virology Abstract HBV G1764A;T1768A;A1762T;C1766T 158;193;151;186 164;199;157;192 BCP;BCP;BCP;BCP 87;108;223;232 106;111;226;235 Chronic HBV infection 7 48 19442845 A sensitive direct sequencing assay based on nested PCR for the detection of HBV polymerase and surface glycoprotein mutations. Direct sequencing was able to show pol mutations not revealed by DR v2, such as rtV214A, rtQ215H/S, and rtM250V. 2009 Journal of virological methods Abstract HBV V214A;Q215H;Q215S;M250V 82;91;91;106 87;98;98;111 P;RT;RT;RT 35;80;89;104 38;82;91;106 19456899 Case-control study for the identification of virological factors associated with fulminant hepatitis B. In multivariate analysis, G1896A mutation (odds ratio [OR], 13.53; 95% confidence interval [CI], 2.75-66.64), serum HBV DNA more than 5.23 log copies/mL (OR, 5.14; 95% CI, 1.10-24.15) and total bilirubin more than 10.35 mg/mL (OR, 7.81; 95% CI, 1.77-34.51) were independently associated with a fulminant outcome by transient HBV infection. 2009 Hepatology research Abstract HBV G1896A 26 32 HBV infections 325 338 19456899 Case-control study for the identification of virological factors associated with fulminant hepatitis B. RESULTS: Higher HBV DNA levels, subgenotype B1/Bj, A1762T/G1764A, G1896A, G1899A and A2339G mutation were significantly more frequent (P < 0.05), while hepatitis B e-antigen was less frequent in the FH-T patients than AHB. 2009 Hepatology research Abstract HBV G1764A;A1762T;G1896A;G1899A;A2339G 58;51;66;74;85 64;57;72;80;91 C 164 173 Acute Hepatitis B;Fulminant Hepatitis B 218;199 221;201 19475333 Lamivudine-to-entecavir switching treatment in type B chronic hepatitis patients without evidence of lamivudine resistance. An entecavir-resistant virus having rtM204V, rtL180M and rtS202G substitutions was detected in this patient. 2009 Journal of gastroenterology Abstract HBV M204V;L180M;S202G 38;47;59 43;52;64 RT;RT;RT 36;45;57 38;47;59 19475624 Effect of HIV co-infection on mutation patterns of HBV in patients with lamivudine-resistant chronic hepatitis B. All patients with the triple mutational pattern showed sE164D + sI195M changes in the envelope gene. 2009 Journal of medical virology Abstract HBV E164D;I195M 55;64 61;70 S;S;Envelope 55;64;86 56;65;94 19475624 Effect of HIV co-infection on mutation patterns of HBV in patients with lamivudine-resistant chronic hepatitis B. Eighty-nine patients infected with HBV (29 co-infected with HIV) with rtM204V or rtM204I mutations were included. 2009 Journal of medical virology Abstract HBV M204V;M204I 72;83 77;88 RT;RT 70;81 72;83 HBV-HIV coinfections 35 63 19475624 Effect of HIV co-infection on mutation patterns of HBV in patients with lamivudine-resistant chronic hepatitis B. In this latter group, the prevalence of the rtV173L + rtL180M + rtM204V triple mutation was 31% versus a prevalence of 3.4% observed among patients infected with HBV only. 2009 Journal of medical virology Abstract HBV V173L;L180M;M204V 46;56;66 51;61;71 RT;RT;RT 44;54;64 46;56;66 19475624 Effect of HIV co-infection on mutation patterns of HBV in patients with lamivudine-resistant chronic hepatitis B. Multivariate analysis demonstrated that HIV co-infection (adjusted OR 11.2, 95% CI 2.0-61.0) and HBV genotype A (adjusted OR 7.2, 95% CI 1.5-34.8) were the only independent variables associated with the chance of harboring rtM204V. 2009 Journal of medical virology Abstract HBV M204V 225 230 RT 223 225 HBV-HIV coinfections 40 56 19475624 Effect of HIV co-infection on mutation patterns of HBV in patients with lamivudine-resistant chronic hepatitis B. Patients with HBV genotype A or HIV co-infection were more likely to harbor the rtM204V mutation. 2009 Journal of medical virology Abstract HBV M204V 82 87 RT 80 82 HBV-HIV coinfections 14 48 19486254 Characterization of hepatitis B virus reverse transcriptase sequences in Chinese treatment naive patients. The M204V/I mutation was found in 1.8% of the strains, 1.2% had L180M+ M204V/I, 0.6% had A181T/V, and only one had all three mutations. 2009 Journal of gastroenterology and hepatology Abstract HBV M204V;M204I;L180M;M204V;M204I;A181T;A181V 4;4;64;71;71;89;89 11;11;70;78;78;96;96 19489434 [Analysis of the relevance of the mutations of the precore and basic core promoter in HBV genome with the DNA amount of HBV viremia]. We assessed the association of continuous viremia with the precore (PC) (G1896A) mutation, basic core promoter (BCP) (A1762T, G1764A) mutations, the viral genotype and the quantity of viral DNA. 2009 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV G1896A;A1762T;G1764A 73;118;126 79;124;132 BCP;BCP;Precore;Precore 91;112;68;59 110;115;70;66 19497198 [Mutation patterns in the RT region of hepatitis B virus P gene in patients treated with nucleoside/nucleotide analogs]. Novel mutations, including A222T, L229V and S256C, were also found. 2009 Zhonghua gan zang bing za zhi Abstract HBV A222T;L229V;S256C 27;34;44 32;39;49 19550344 Monitoring of therapy in patients with chronic hepatitis B virus. In contrast, of the 11 patients treated with ADV, three patients developed mutations (rtN236T; rtA181V; rtA181V plus rtN236T). 2010 European journal of gastroenterology & hepatology Abstract HBV N236T;A181V;A181V;N236T 88;97;106;119 93;102;111;124 RT;RT;RT;RT 86;95;104;117 88;97;106;119 19550344 Monitoring of therapy in patients with chronic hepatitis B virus. In the viral response to treatment, three patients developed substitutions at rtM204I associated with LAM resistance and one of these patients presented rtM204V/I plus rtL180M mutation. 2010 European journal of gastroenterology & hepatology Abstract HBV M204I;M204V;M204I;L180M 80;155;155;170 85;162;162;175 RT;RT;RT 78;153;168 80;155;170 19550344 Monitoring of therapy in patients with chronic hepatitis B virus. With regard to this case, the same results were observed by INNO-LiPA HBV DR v3 and direct sequencing, but by direct sequencing we detected an extra mutation rtQ215S that was present in two patients: one patient who was on treatment with LAM had an rtQ215S mutation in addition to an rtM204I, and the second patient treated with ADV had rtA181V. 2010 European journal of gastroenterology & hepatology Abstract HBV Q215S;Q215S;M204I;A181V 160;251;286;339 165;256;291;344 RT;RT;RT;RT 158;249;284;337 160;251;286;339 19553583 Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. In all samples M204V positive by sequencing (12/12), the mutant variant was detected as the predominant population (range, 82.76 to 99.43%). 2009 Journal of clinical microbiology Abstract HBV M204V 15 20 19553583 Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. Interestingly, in 5 (38%) of 13 samples negative by sequencing, the M204V variant was detected at a ratio above the biological cutoff (0.05 to 28%). 2009 Journal of clinical microbiology Abstract HBV M204V 68 73 19553583 Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. The assay represents an efficient technique for the early detection and quantification of M204V variants before mutant strains emerge to dominate the population. 2009 Journal of clinical microbiology Abstract HBV M204V 90 95 19553583 Quantitative detection of the M204V hepatitis B virus minor variants by amplification refractory mutation system real-time PCR combined with molecular beacon technology. The samples from HBV patients selected for assay evaluation included (i) 57 samples from treatment-naive patients for biological discriminatory ability (cutoff) estimation, (ii) 12 samples from patients with treatment failure that were M204V positive by sequencing, and (iii) 13 samples from patients with treatment failure that were negative for mutation at codon 204 by sequencing. 2009 Journal of clinical microbiology Abstract HBV M204V 236 241 19566788 Naturally occurring amino-acid substitutions to nucleos(t)ide analogues in treatment naive Turkish patients with chronic hepatitis B. Each amino-acid substitution appeared alone and included rtA194T, rtV214A, rtQ215S, rtI233V and rtN236T. 2010 Journal of viral hepatitis Abstract HBV A194T;V214A;Q215S;I233V;N236T 59;68;77;86;98 64;73;82;91;103 RT;RT;RT;RT;RT 57;66;75;84;96 59;68;77;86;98 19570861 A function essential to viral entry underlies the hepatitis B virus "a" determinant. Interestingly, G145R, a substitution often arising under immune pressure selection and detrimental to the "a" determinant, had no effect on infectivity. 2009 Journal of virology Abstract HBV G145R 15 20 19571620 [Analysis of clinical characteristics and S gene mutation of hepatitis B virus (HBV) in patients with hepatitis B surface antigen RIA negative and HBV DNA positive]. G145R mutation was found in 8 patients and G145K, D144G, and D144A were also frequently found. 2009 The Korean journal of laboratory medicine Abstract HBV G145R;G145K;D144G;D144A 0;43;50;61 5;48;55;66 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1653T, T1753V, and A1762T/G1764A were more strongly associated with an increased risk of HCC in hepatitis B e antigen (HBeAg)-positive subjects than in HBeAg-negative subjects. 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;C1653T;T1753V 27;20;0;8 33;26;6;14 C;C;C 109;120;153 118;125;158 Hepatocellular carcinoma 90 93 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. CONCLUSIONS: HBV PreS mutations, C1653T, T1753V, and A1762T/G1764A are associated with an increased risk of HCC. 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;C1653T;T1753V 60;53;33;41 66;59;39;47 PreS 17 21 Hepatocellular carcinoma 108 111 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. PreS mutations were more strongly associated with an increased risk of HCC in subjects who were infected with HBV genotype C than in those who were infected with HBV genotype B, whereas the opposite was true for A1762T/G1764A. 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T 219;212 225;218 PreS 0 4 Hepatocellular carcinoma 71 74 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. PreS mutations, C1653T, C1653T + T1753V, and A1762T/G1764A-based combinations of mutations had specificities greater than 80% for the prediction of HCC. 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;C1653T;C1653T;T1753V 52;45;16;24;33 58;51;22;30;39 PreS 0 4 Hepatocellular carcinoma 148 151 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. PreS mutations, C1653T, T1753V, and A1762T/G1764A accumulated during the progression of chronic HBV infection from the asymptomatic carrier state to HCC (P(trend) < .001 for each mutation). 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;C1653T;T1753V 43;36;16;24 49;42;22;30 P;PreS 154;0 155;4 Chronic HBV infection;Hepatocellular carcinoma 88;149 109;152 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Statistically significant summary odds ratios of HCC were obtained for any PreS mutation (3.77, 95% confidence interval [CI] = 2.57 to 5.52), C1653T in EnhII (2.76, 95% CI = 2.09 to 3.64), T1753V (2.35, 95% CI = 1.63 to 3.40), and A1762T/G1764A in BCP (3.79, 95% CI = 2.71 to 5.29). 2009 Journal of the National Cancer Institute Abstract HBV G1764A;A1762T;C1653T;T1753V 238;231;142;189 244;237;148;195 BCP;Enh II;PreS 248;152;75 251;157;79 Hepatocellular carcinoma 49 52 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The precore mutations G1896A and C1858T were not associated with the risk of HCC, regardless of HBeAg status and HBV genotype. 2009 Journal of the National Cancer Institute Abstract HBV G1896A;C1858T 22;33 28;39 C;Precore 96;4 101;11 Hepatocellular carcinoma 77 80 19578241 Adefovir dipivoxil resistance patterns in patients with lamivudine-resistant chronic hepatitis B. ADV resistance mutations (rtA181V/T and rtN236T) were detected alone or in combination for 11/14 patients, whereas novel substitutions were present in 3 patients. 2009 Antiviral therapy Abstract HBV A181V;A181T;N236T 28;28;42 35;35;47 RT;RT 26;40 28;42 19578241 Adefovir dipivoxil resistance patterns in patients with lamivudine-resistant chronic hepatitis B. Before ADV treatment, apart from 3TC resistance signature mutations, additional changes were found, including the rtA181T mutation, which was already present in 2/14 ADV-resistant patients. 2009 Antiviral therapy Abstract HBV A181T 116 121 RT 114 116 19578241 Adefovir dipivoxil resistance patterns in patients with lamivudine-resistant chronic hepatitis B. CONCLUSIONS: Although most patients showed virological breakthrough because of the well known rtA181V/T and rtN236T substitutions, more complex patterns were also found. 2009 Antiviral therapy Abstract HBV A181V;A181T;N236T 96;96;110 103;103;115 RT;RT 94;108 96;110 19578244 Clinical and virological responses to clevudine therapy in chronic hepatitis B patients: results at 1 year of an open-labelled prospective study. This patient had an HBV polymerase mutation, rtM204I. 2009 Antiviral therapy Abstract HBV M204I 47 52 P;RT 24;45 34;47 19578244 Clinical and virological responses to clevudine therapy in chronic hepatitis B patients: results at 1 year of an open-labelled prospective study. Viral breakthrough associated with the rtM204I mutation in the HBV polymerase gene occurs during long-term clevudine treatment. 2009 Antiviral therapy Abstract HBV M204I 41 46 P;RT 67;39 77;41 19581770 [Long-term clevudine therapy in nucleos(t)ide-naive and lamivudine-experienced patients with hepatitis B virus-related chronic liver diseases]. Proven sites of mutation of HBV DNA polymerase in naive patients were, for example, L80I, L180M, A181V/T, M204I and V207I. 2009 The Korean journal of hepatology Abstract HBV L80I;L180M;A181V;A181T;M204I;V207I 84;90;97;97;106;116 88;95;104;104;111;121 P 36 46 19586679 Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome. BACKGROUND/AIMS: The rtQ215S mutation in the hepatitis B virus (HBV) polymerase has been described as a secondary mutation associated with resistance to lamivudine (LAM) and adefovir (ADV). 2009 Journal of hepatology Abstract HBV Q215S 23 28 RT;P 21;69 23;79 19586679 Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome. Furthermore, rtQ215S, rtQ215P and rtQ215H harbouring constructs remained susceptible towards treatment with LAM or ADV in vitro. 2009 Journal of hepatology Abstract HBV Q215S;Q215P;Q215H 15;24;36 20;29;41 RT;RT;RT 13;22;34 15;24;36 19586679 Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome. In phenotypic assays, rtQ215S, rtQ215P and rtQ215H constructs showed equivalent levels of viral replication as wild-type HBV, whereas LAM- and ADV-resistant mutants had significantly impaired replicative capacities. 2009 Journal of hepatology Abstract HBV Q215S;Q215P;Q215H 24;33;45 29;38;50 RT;RT;RT 22;31;43 24;33;45 19586679 Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome. Replication-competent HBV constructs containing the naturally occurring rtQ215H, rtQ215P and rtQ215S mutations were generated, and compared to wild-type, LAM- (rtM204I, rtL180M/rtM204V) and ADV-resistant (rtN236T) clones. 2009 Journal of hepatology Abstract HBV Q215H;Q215P;Q215S;M204I;N236T;L180M;M204V 74;83;95;162;207;171;179 79;88;100;167;212;176;184 RT;RT;RT;RT;RT;RT;RT 72;81;93;160;169;177;205 74;83;95;162;171;179;207 19586679 Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome. RESULTS: In an Iranian cohort of 249 HBV infected patients, 14.5% (36/249) showed mutations in the rtQ215 locus, namely 6.8% rtQ215S, 3.6% rtQ215P and 4.1% rtQ215H. 2009 Journal of hepatology Abstract HBV Q215S;Q215P;Q215H 127;141;158 132;146;163 RT;RT;RT;RT 99;125;139;156 101;127;141;158 HBV infections 37 49 19590227 First report of genotype e of hepatitis B virus in an Indian population. Amplification and sequencing of the precore region showed 1762(A-T) and 1764(G-A) mutations in 38 and 15% of the samples, respectively. 2009 Intervirology Abstract HBV A1762T;G1764A 58;72 67;81 Precore 36 43 19626618 A serological and molecular survey of hepatitis B in children 15 years after inception of the national hepatitis B vaccination program in eastern China. Mutations of I126T, amino acid 137 (nt553T deletion mutation), G145A, G145R, and F158S were found in the children; the mutations of amino acid 137 and F158S have not been reported previously. 2009 Journal of medical virology Abstract HBV I126T;G145A;G145R;F158S;F158S 13;63;70;81;151 18;68;75;86;156 19634759 [Surveillance for occult HBV infection and HBsAg variants in blood donors]. Mutation(s) in aa124-aa147 existed in 6 (42.9%, 6/14) samples and 4 (66.7%, 4/6)were G145R mutation. 2009 Bing du xue bao Abstract HBV G145R 85 90 19651117 Detection of the rtA181V/T and rtN236T mutations associated with resistance to adefovir dipivoxil using a ligase detection reaction assay. CONCLUSIONS: The PCR-LDR assay can sensitively and specifically detect the rtA181V/T and rtN236T mutations, and may be used for monitoring ADV resistance in patients infected with HBV. 2009 Clinica chimica acta; international journal of clinical chemistry Abstract HBV A181V;A181T;N236T 77;77;91 84;84;96 RT;RT 75;89 77;91 19651117 Detection of the rtA181V/T and rtN236T mutations associated with resistance to adefovir dipivoxil using a ligase detection reaction assay. We developed a sensitive and specific method for detecting the rtA181V/T and rtN236T mutations associated with ADV resistance in chronic hepatitis B patients, based on a ligase detection reaction (LDR). 2009 Clinica chimica acta; international journal of clinical chemistry Abstract HBV A181V;A181T;N236T 65;65;79 72;72;84 RT;RT 63;77 65;79 Chronic Hepatitis B 129 148 19651540 Low pretreatment serum HBsAg level and viral mutations as predictors of response to PEG-interferon alpha-2b therapy in chronic hepatitis B. In HBeAg-positive hepatitis, PEG-IFN response correlated with the appearance of double BCP mutations (A1762T/G1764A) at baseline (P=0.041). 2009 Journal of clinical virology Abstract HBV G1764A;A1762T 109;102 115;108 BCP;C 87;3 90;8 Hepatitis 18 27 19664630 Hepatitis B virus core variants modify natural course of viral infection and hepatocellular carcinoma progression. The longitudinal study further showed that the appearance of 2 such variants (T1938C and T2045A) was preceded by long-term diminished viral load and decreased rate of liver abnormalities and was significantly less frequent in individuals with a prolonged immune clearance phase that associated with spectrum of liver disease than those in inactive carrier or reactivation phase. 2009 Gastroenterology Abstract HBV T1938C;T2045A 78;89 84;95 Liver disease;Liver disease 167;311 186;324 19665408 Lamivudine and adefovir resistance in children and young adults with chronic hepatitis B. Three patients developed ADV-associated mutations (A181T), one after 18 months of ADV; the other two had undergone 18 and 36 months of LAM therapy without ADV exposure. 2010 International journal of infectious diseases Abstract HBV A181T 51 56 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. Both pathways are associated with clusters of secondary mutations that can affect subsequent treatment with NAs (rtT184G, rtS202I) such as ETV. 2008 Hepatology international Abstract HBV T184G;S202I 115;124 120;129 RT;RT 113;122 115;124 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. Finally, in highly drug-experienced patients, clusters of mutations such as rtA181T/I233V/N236T/M250L, all on the one dominant HBV genome, are being detected which are associated with multi-drug resistance. 2008 Hepatology international Abstract HBV I233V;N236T;M250L;A181T 84;90;96;78 89;95;101;83 RT 76 78 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. In naive patients treated with ETV, atleast three mutations arising at the same time are required: rtL180M + rtM204V plus either one of rtT184, rtS202 or rtM250 codon changes. 2008 Hepatology international Abstract HBV L180M;M204V 101;111 106;116 RT;RT;RT;RT;RT 99;109;136;144;154 101;111;138;146;156 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. Several major HBV-evolutionary NA-resistance pathways (rtM204I/V, rtN236T and rtA181T/V) have now been characterised. 2008 Hepatology international Abstract HBV M204I;M204V;N236T;A181T;A181V 57;57;68;80;80 64;64;73;87;87 RT;RT;RT 55;66;78 57;68;80 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. The rtM204V/I pathway is responsible for resistance to the L: -nucleosides, such as lamivudine (LMV), telbivudine (LdT) and clevudine (CLD), and also entecavir (ETV), whilst the rtN236T pathway is responsible for adefovir (ADV) and tenofovir (TFV) resistance. 2008 Hepatology international Abstract HBV M204V;M204I;N236T 6;6;180 13;13;185 RT;RT 4;178 6;180 19669299 Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure. The third pathway, rtA181T/V, is associated with resistance to LMV and ADV and is a potential multi-drug resistance pathway and will probably have an impact on TFV sensitivity, either alone or with the rtN236T. 2008 Hepatology international Abstract HBV A181T;A181V;N236T 21;21;204 28;28;209 RT;RT 19;202 21;204 19669367 Two cases of development of entecavir resistance during entecavir treatment for nucleoside-naive chronic hepatitis B. The ETVr-related substitution (S202G), along with LVD-resistance-related substitutions (L180M and M204V), was detected by sequence analysis at week 124 in both case 1 and case 2. 2009 Hepatology international Abstract HBV S202G;L180M;M204V 31;88;98 36;93;103 19678894 Low efficacy of entecavir therapy in adefovir-refractory hepatitis B patients with prior lamivudine resistance. Higher pretreatment ALT (P = 0.039) and the presence of the rtL180M mutation (P = 0.038) were associated with an initial virologic response. 2010 Journal of viral hepatitis Abstract HBV L180M 62 67 RT 60 62 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. A1762T/G1764A mutation was observed in 1.96% and 5.36%, whereas T1753V mutation was found in 2.94% and 1.79% of HBV/B and HBV/C, respectively. 2009 Virology journal Abstract HBV G1764A;A1762T;T1753V 7;0;64 13;6;70 19705499 Hepatitis B virus subgenotypes and basal core promoter mutations in Indonesia. Double mutation (A1762T/G1764A) in the BCP was significantly higher in LC (59.7%) and HCC (54.2%) than in CH (19.7%), suggesting that this mutation was associated with severity of liver disease. 2009 World journal of gastroenterology Abstract HBV G1764A;A1762T 24;17 30;23 BCP 39 42 Hepatocellular carcinoma;Chronic Hepatitis B;Liver disease;Liver cirrhosis 86;106;180;71 89;108;193;73 19705499 Hepatitis B virus subgenotypes and basal core promoter mutations in Indonesia. Mutations in BCP, such as A1762T/G1764A and T1753V, might have an association with manifestations of liver disease. 2009 World journal of gastroenterology Abstract HBV G1764A;A1762T;T1753V 33;26;44 39;32;50 BCP 13 16 Liver disease 101 114 19705499 Hepatitis B virus subgenotypes and basal core promoter mutations in Indonesia. The T1753V was also higher in LC (46.8%), but lower in HCC (22.9%) and CH (18.0%), suggesting that this mutation may be an indicator of cirrhosis. 2009 World journal of gastroenterology Abstract HBV T1753V 4 10 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 55;71;136;30 58;73;145;32 19710138 Functional surfaces of the hepatitis B virus capsid. We also identified several CP point mutations (e.g., F122V/S/Y and R127D/G) allowing the formation of capsids but preventing the packaging of pregenomic RNA. 2009 Journal of virology Abstract HBV F122V;F122S;F122Y;R127D;R127G 53;53;53;67;67 62;62;62;74;74 Capsid;Core promoter 102;27 109;29 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. By multivariate analysis, high level (>10(5)copies/mL) of serum HBV DNA was inversely associated with the presence of mutations in CTL epitopes of HBc (OR: 0.11, p=0.015), while it was directly associated with the presence of promoter double T(1762)A(1764) mutations together with G(1757) (OR: 16.87, p=0.004). 2009 Journal of clinical virology Abstract HBV T1762A 241 251 C 147 150 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. Substitutions for Ser(21) and Thr12Ser were associated with lower serum levels of HBV DNA (p<0.001). 2009 Journal of clinical virology Abstract HBV T12S 30 38 19759159 The pre-S1 and antigenic loop infectivity determinants of the hepatitis B virus envelope proteins are functionally independent. Finally, we showed that C147S, an AGL infectivity-deficient substitution, exerted a dominant-negative effect on infectivity, likely reflecting an involvement of C147 in intermolecular disulfide bonds. 2009 Journal of virology Abstract HBV C147S 24 29 19785624 Prevalence of hepatitis B virus DNA polymerase mutations in treatment-naive patients with chronic hepatitis B. CONCLUSIONS: No rtM204V/I or rtN236T mutations were observed in our study. 2009 Alimentary pharmacology & therapeutics Abstract HBV M204V;M204I;N236T 18;18;31 25;25;36 RT;RT 16;29 18;31 19785624 Prevalence of hepatitis B virus DNA polymerase mutations in treatment-naive patients with chronic hepatitis B. Some (16.7%) had mutations of unknown clinical significance (rtV207M/L/I) and only 4 patients had rtA181A/S, rtA194S or M250I. 2009 Alimentary pharmacology & therapeutics Abstract HBV V207M;V207L;V207I;A181A;A181S;A194S;M250I 63;63;63;100;100;111;120 72;72;72;107;107;116;125 RT;RT;RT 61;98;109 63;100;111 19785947 [Identification of factors associated with YMDD mutation in patients with chronic hepatitis B receiving lamivudine treatment]. rtM204V mutation in C gene was always accompanied by rtL180M mutation (100%). 2009 Zhonghua gan zang bing za zhi Abstract HBV L180M;M204V 55;2 60;7 C;RT;RT 20;0;53 21;2;55 19785947 [Identification of factors associated with YMDD mutation in patients with chronic hepatitis B receiving lamivudine treatment]. The point mutation of rtM204I and rtL180M appeared only in genotype B group. 2009 Zhonghua gan zang bing za zhi Abstract HBV L180M;M204I 36;24 41;29 RT;RT 22;34 24;36 19785947 [Identification of factors associated with YMDD mutation in patients with chronic hepatitis B receiving lamivudine treatment]. The rate of rtL180M/M204V mutation in genotype C group was significantly higher than that in genotype B group (77.8% to 25.0%), the same was true for the rtL180M/ M204I mutation (22.2% to 12.5%). 2009 Zhonghua gan zang bing za zhi Abstract HBV M204V;L180M;L180M;M204I 20;14;156;163 25;19;161;168 RT;RT 12;154 14;156 19785947 [Identification of factors associated with YMDD mutation in patients with chronic hepatitis B receiving lamivudine treatment]. There are four types of mutation: rtL180M/M204V, rtL180M/M204I, rtM204I, rtL180M. 2009 Zhonghua gan zang bing za zhi Abstract HBV M204V;M204I;L180M;L180M;M204I;L180M 42;57;36;51;66;75 47;62;41;56;71;80 RT;RT;RT;RT 34;49;64;73 36;51;66;75 19786052 Dysregulation of hepatocyte cell cycle and cell viability by hepatitis B virus. Cell viability was reduced and cleaved caspase 3 levels were increased in HBV- and rtM204I-infected cells. 2010 Virus research Abstract HBV M204I 85 90 RT 83 85 19786052 Dysregulation of hepatocyte cell cycle and cell viability by hepatitis B virus. METHODS: We have used a recombinant adeno-HBV model system to investigate the effect of infection with HBV and the replication defective lamivudine resistant mutant rtM204I mutant on hepatocyte cell cycle and cell viability. 2010 Virus research Abstract HBV M204I 167 172 RT 165 167 19786052 Dysregulation of hepatocyte cell cycle and cell viability by hepatitis B virus. Perturbations in these cellular processes are likely to underlie HBV-associated liver oncogenic transformation and may help explain the ongoing risk of developing hepatocellular carcinoma in individuals in whom the lamivudine resistant rtM204I mutant emerges. 2010 Virus research Abstract HBV M204I 238 243 RT 236 238 Hepatocellular carcinoma 163 187 19786052 Dysregulation of hepatocyte cell cycle and cell viability by hepatitis B virus. rAdHBV-M204I-infected Huh7 cells also demonstrated significant up-regulation of phospho-ERK, phospho-Akt, p53 and phospho-Mdm2 compared to mock-infected cells. 2010 Virus research Abstract HBV M204I 7 12 19786052 Dysregulation of hepatocyte cell cycle and cell viability by hepatitis B virus. RESULTS: Huh7 cells synchronised at the G1/S phase of the cell cycle were arrested at the G2/M following infection with rAdHBV-wt and rAdHBV-M204I. 2010 Virus research Abstract HBV M204I 141 146 19795617 [Entecavir resistance in entecavir naive lamivudine treated chronic hepatitis B patients]. In these patients also rtL180M and rtQ215S mutations were detected as compensatory mutations and YVDD and YIDD variants were observed at the 204. 2009 Mikrobiyoloji bulteni Abstract HBV L180M;Q215S 25;37 30;42 RT;RT;YVDD;YIDD 23;35;97;106 25;37;101;110 19795617 [Entecavir resistance in entecavir naive lamivudine treated chronic hepatitis B patients]. rtT184A, rtT1841 and rtT1845 mutations were found related to primary ETV resistance. 2009 Mikrobiyoloji bulteni Abstract HBV T184A 2 7 RT;RT;RT 0;9;21 2;11;23 19795617 [Entecavir resistance in entecavir naive lamivudine treated chronic hepatitis B patients]. Two of the patients in the study group had mutations at the positions sG145R and sC137G in the overlapped S-gene segment. 2009 Mikrobiyoloji bulteni Abstract HBV G145R;C137G 70;81 76;87 S;S;S 106;70;81 107;71;82 19800842 Hepatitis B precore/core promoter mutations in isolates from HBV-monoinfected and HBV-HIV coinfected patients: a 3-yr prospective study. Regardless of the HIV-coexistence, the Pc mutation at G1896A only barely appeared among clone-derived sequences of GtF1 isolates, mainly from HBe(-) HBV-monoinfected patients. 2009 Journal of clinical virology Abstract HBV G1896A 54 60 C;Precore 142;39 145;41 HBV infections 149 165 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. Compared to the patients without this mutation, those with G1896A had lower HAI scores (5.0 +/- 2.8 versus 7.9 +/- 4, p = 0.03). 2009 Viral immunology Abstract HBV G1896A 59 65 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. In 30 HBeAg-negative CHB patients the pre-core region of the HBV genome was amplified and sequenced to determine the presence of the mutation G1896A. 2009 Viral immunology Abstract HBV G1896A 142 148 C;Precore 6;38 11;46 Chronic Hepatitis B 21 24 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. The aim of this study was to investigate the effect of the HBV pre-core mutation G1896A on the expression of HLA class II molecules and the core protein of hepatitis B in liver biopsies of chronic hepatitis B (CHB) infection. 2009 Viral immunology Abstract HBV G1896A 81 87 C;Precore 140;63 144;71 Chronic Hepatitis B;Chronic Hepatitis B 189;210 208;213 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. The study of the expression of HLA-II molecules in our patients revealed that subjects with the G1896A mutation had lower expression of HLA-II compared to wild-type infected subjects (1.87 +/- 0.6 versus 3.27 +/- 1.5, p < 0.01). 2009 Viral immunology Abstract HBV G1896A 96 102 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. These results suggest that the G1896A pre-core mutation may directly interfere with antigen presentation, most likely by decreasing the availability of HLA class II molecules, and this may result in less aggressive liver disease in HBeAg-negative CHB infection. 2009 Viral immunology Abstract HBV G1896A 31 37 C;Precore 232;38 237;46 Liver disease;Chronic Hepatitis B 215;247 228;250 19811086 Downregulation of HLA class II molecules by G1896A pre-core mutation in chronic hepatitis B virus infection. We found that 19 of the 30 patients (63%) harbored the G1896A mutation. 2009 Viral immunology Abstract HBV G1896A 55 61 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. Both T123N and K160N substitutions resulted in additional N-glycosylated forms of HBsAg, while the other mutations produced more glycosylated HBsAg compared with the wild type (wt). 2010 The Journal of general virology Abstract HBV T123N;K160N 5;15 10;20 S;S 82;142 87;147 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. Detection of HBsAg by ELISA and immunofluorescence staining indicated that variant HBsAg (vtHBsAg) with K122I was not recognized by HBsAg immunoassays, while vtHBsAg with T123N, A159G, K160N and A159G/K160N had reduced antigenicity. 2010 The Journal of general virology Abstract HBV K160N;A159G;K122I;T123N;A159G;K160N 201;195;104;171;178;185 206;200;109;176;183;190 S;S;S;S;S 13;83;92;132;160 18;88;97;137;165 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. DNA immunization in BALB/c mice revealed that wtHBsAg and vtHBsAg with T123N and K160N are able to induce antibodies to HBsAg (anti-HBs), whereas K122I and A159G greatly impair the ability of HBsAg to trigger anti-HBs responses. 2010 The Journal of general virology Abstract HBV T123N;K160N;K122I;A159G 71;81;146;156 76;86;151;161 S;S;S;S;S;S 132;214;48;60;120;192 135;217;53;65;125;197 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. In this study, we investigated the significance of naturally occurring amino acid substitutions K122I, T123N, A159G and K160N. 2010 The Journal of general virology Abstract HBV K122I;T123N;A159G;K160N 96;103;110;120 101;108;115;125 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. The amino acid substitution K160N appeared to compensate for the negative effect of A159G on virion production. 2010 The Journal of general virology Abstract HBV K160N;A159G 28;84 33;89 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. The cellular immune response to the HBsAg aa 29-38 epitope was enhanced by the K160N substitution. 2010 The Journal of general virology Abstract HBV K160N 79 84 S 36 41 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. The substitution K122I has been shown to strongly affect HBsAg antigenicity. 2010 The Journal of general virology Abstract HBV K122I 17 22 S 57 62 19812261 Biological significance of amino acid substitutions in hepatitis B surface antigen (HBsAg) for glycosylation, secretion, antigenicity and immunogenicity of HBsAg and hepatitis B virus replication. Using replication competent clones of hepatitis B virus (HBV), T123N and A159G substitutions were shown to strongly reduce virion assembly. 2010 The Journal of general virology Abstract HBV T123N;A159G 63;73 68;78 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. At that time, rtA181T was undetectable and the virus with rtM204V and rtL180M became predominant. 2009 Antiviral therapy Abstract HBV A181T;M204V;L180M 16;60;72 21;65;77 RT;RT;RT 14;58;70 16;60;72 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. Combination therapy with ETV and ADV might have been effective because these drugs share therapeutic roles, that is, ETV affects the rtA181T-related virus and ADV affects the rtM204V-related virus. 2009 Antiviral therapy Abstract HBV A181T;M204V 135;177 140;182 RT;RT 133;175 135;177 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. Efficacy of subsequent combination therapy with ADV and 3TC was limited because of reappearance of the virus with rtA181T, which might confer cross-resistance to 3TC and ADV. 2009 Antiviral therapy Abstract HBV A181T 116 121 RT 114 116 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. ETV resistance was established by an additional rtS202G mutation. 2009 Antiviral therapy Abstract HBV S202G 50 55 RT 48 50 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. Initial 3TC monotherapy offered little benefit and 3TC resistance was established by the virus with rtA181T and not rtM204V/I. 2009 Antiviral therapy Abstract HBV A181T;M204V;M204I 102;118;118 107;125;125 RT;RT 100;116 102;118 19812452 Two types of drug-resistant hepatitis B viral strains emerging alternately and their susceptibility to combination therapy with entecavir and adefovir. Thus, two kinds of mutant viruses (rtM204V-related and rtA181T-related) appeared alternately in this patient. 2009 Antiviral therapy Abstract HBV M204V;A181T 37;57 42;62 RT;RT 35;55 37;57 19817965 Occult hepatitis B virus infection and lamivudine-resistant mutations in isolates from renal patients undergoing hemodialysis. Four of these six HBV isolates contained mutations associated with lamivudine resistance in the DNA polymerase (two with L180M/M204V and two with rt173V/180M/204V) and a specific substitution (Y100C) in the HBV small surface protein. 2010 Journal of gastroenterology and hepatology Abstract HBV M204V;L180M;Y100C 127;121;193 132;126;198 P;RT;S 100;146;211 110;148;224 19818719 Silencing an immunodominant epitope of hepatitis B surface antigen reveals an alternative repertoire of CD8 T cell epitopes of this viral antigen. Comparable levels of wild-type S and mutant S(L39V) were produced by transiently transfected cells, and mice immunized with the pCI/S and pCI/S(L39V) DNA vaccines showed comparable serum antibody responses to HBsAg. 2009 Vaccine Abstract HBV L39V;L39V 46;144 50;148 S;S;S 209;31;44 214;32;45 19818719 Silencing an immunodominant epitope of hepatitis B surface antigen reveals an alternative repertoire of CD8 T cell epitopes of this viral antigen. However, the pCI/S(L39V) DNA vaccine efficiently primed CD8 T cell responses to the subdominant D(d)- and K(b)-restricted epitopes, confirming the immunosuppressive phenotype of the L(d)/S(28-39)-specific CD8 T cell response. 2009 Vaccine Abstract HBV L39V 19 23 S 187 188 19818719 Silencing an immunodominant epitope of hepatitis B surface antigen reveals an alternative repertoire of CD8 T cell epitopes of this viral antigen. The pCI/S but not pCI/S(L39V) DNA vaccination induced L(d)/S(28-39)-specific CD8 T cell responses. 2009 Vaccine Abstract HBV L39V 24 28 S 59 60 19818719 Silencing an immunodominant epitope of hepatitis B surface antigen reveals an alternative repertoire of CD8 T cell epitopes of this viral antigen. We exchanged L to V at position S(39) of HBsAg to construct mutant S(L39V). 2009 Vaccine Abstract HBV L39V 69 73 S;S;S 41;32;67 46;33;68 19850315 Enhanced intracellular retention of a hepatitis B virus strain associated with fulminant hepatitis. The pBFH2 construct with A1762T/G1764A, G1862T, and G1896A showed the largest amount of core particle-associated intracellular HBV DNA, but no significant increase of extracellular HBV DNA in comparison with the wild construct, suggesting that these mutations might work together for retention of the replicative intermediates in the cells. 2009 Virology Abstract HBV G1764A;A1762T;G1862T;G1896A 32;25;40;52 38;31;46;58 C 88 92 19874686 [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients]. CONCLUSIONS: Polymorphism site of rtN118H might be responsible for HBV primary resistance to ADV therapy. 2009 Zhonghua gan zang bing za zhi Abstract HBV N118H 36 41 RT 34 36 19874686 [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients]. RESULTS: 21 out of 30 HBV strains were primary resistant strains, among them 5 HBV strains (23.8%, 5/21) had the polymorphism site of rtN118H. 2009 Zhonghua gan zang bing za zhi Abstract HBV N118H 136 141 RT 134 136 19874686 [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients]. rtM207V variation in HBV RT C domain and other variation sites might play a role in HBV secondary resistance to ADV treatment, and natural resistant quasispecies may be the basis for the ADV quick resistance. 2009 Zhonghua gan zang bing za zhi Abstract HBV M207V 2 7 RT;RT 0;25 2;27 19874686 [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients]. The classic mutation sites such as rtN236T and rtA181V/T were not found. 2009 Zhonghua gan zang bing za zhi Abstract HBV N236T;A181V;A181T 37;49;49 42;56;56 RT;RT 35;47 37;49 19874686 [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients]. While the other 9 HBV strains showed secondary resistance, variations in conservative region C (rtM207V) and other non-conservative regions were found. 2009 Zhonghua gan zang bing za zhi Abstract HBV M207V 98 103 C;RT 93;96 94;98 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 2010 Journal of virology Abstract HBV P120T 13 19 S;S 47;13 52;14 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2010 Journal of virology Abstract HBV P120T 66 72 BCP;C;Precore;S 60;39;57;66 63;44;59;67 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 2010 Journal of virology Abstract HBV M204I;L180M;M204V;G145R;P120T 78;89;97;39;49 83;94;102;45;55 BCP;Precore;BCP;S;S;RT;RT;RT;C;C;Precore 195;187;216;39;49;76;87;95;125;147;178 214;189;219;40;50;78;89;97;130;152;185 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. 2010 Journal of virology Abstract HBV G145R 4 10 BCP;S;Precore;S 176;37;170;4 179;42;172;5 19889778 Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 2010 Journal of virology Abstract HBV G145R;P120T 109;120 115;126 C;S;S 286;109;120 291;110;121 19903586 Surface gene mutations of hepatitis B virus among high-risk patients with occult hepatitis B virus infection. Amino acid substitution at amino acid position 207(S207N) was found in the other isolates. 2010 Diagnostic microbiology and infectious disease Abstract HBV S207N 51 56 19918102 Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir. Combination treatment including potent antiviral agents should be recommended for patients with pre-existing rtM204V/I mutations. 2009 Antiviral therapy Abstract HBV M204V;M204I 111;111 118;118 RT 109 111 19918102 Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir. ETV resistance mutations (rtL180M+rtT184I/L[rtS202G]+rtM204V) were detected in five patients with pre-existing rt204 mutations. 2009 Antiviral therapy Abstract HBV T184I;T184L;L180M;S202G;M204V 36;36;28;46;55 43;43;33;51;60 RT;RT;RT;RT;RT 26;34;44;53;111 28;36;46;55;113 19918102 Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir. Relative abundances of rtM204V/I mutations in total viral populations gradually increased under ETV rescue, whereas those with rtA181V/T and rtN236T mutations decreased. 2009 Antiviral therapy Abstract HBV M204V;M204I;A181V;A181T;N236T 25;25;129;129;143 32;32;136;136;148 RT;RT;RT 23;127;141 25;129;143 19918102 Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir. RESULTS: During 3TC and ADV therapy, 11 patients had rtM204V/I mutations, 2 had rtA181V/T or rtN236T, 7 had both and 2 had no 3TC- or ADV-related mutations. 2009 Antiviral therapy Abstract HBV M204V;M204I;A181V;A181T;N236T 55;55;82;82;95 62;62;89;89;100 RT;RT;RT 53;80;93 55;82;95 19918102 Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir. The limited efficacy might be associated with residual or reselected rtM204V/I mutations leading to ETV resistance. 2009 Antiviral therapy Abstract HBV M204V;M204I 71;71 78;78 RT 69 71 19933798 Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation. Modeling of HBV reverse transcriptase (RT) by docking simulation indicated that a combination of LVDr and ETVr (T184L or S202G) was characterized by a change in the direction of the D205 residue and steric conflict in the binding pocket of ETV triphosphate (ETV-TP), by significantly longer minimal distances (2.2 A and 2.1 A), and by higher potential energy (-117 and -99.8 Kcal/mol) for ETV-TP compared with the wild type (1.3 A; -178 Kcal/mol) and LVDr substitutions (1.5 A; -141 Kcal/mol). 2010 Antimicrobial agents and chemotherapy Abstract HBV T184L;S202G 112;121 117;126 RT;RT 16;39 37;41 19933798 Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation. Multivariate logistic regression analysis adjusted for age, gender, HBV DNA levels, and LVD resistance (LVDr) (L180M and M204V, but not M204I) indicated that T184 substitutions and S202G (not S202C) were a significant factor for BT (adjusted odds ratio [OR], 141.12, and 95% confidence interval [CI], 6.94 to 2,870.20; OR, 201.25, and 95% CI, 11.22 to 3608.65, respectively). 2010 Antimicrobial agents and chemotherapy Abstract HBV L180M;M204V;M204I;S202G;S202C 111;121;136;181;192 116;126;141;186;197 19933798 Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation. Our data suggest that the low binding affinity of ETV-TP for the HBV RT, involving conformational change of the binding pocket of HBV RT by L180M, M204V plus T184L, and S202G, could induce BT. 2010 Antimicrobial agents and chemotherapy Abstract HBV L180M;M204V;T184L;S202G 140;147;158;169 145;152;163;174 RT;RT 69;134 71;136 19940057 Molecular characteristics of occult hepatitis B virus from blood donors in southeast China. G145R was the major variation in the HBV isolates responsible for local occult HBV infections. 2010 Journal of clinical microbiology Abstract HBV G145R 0 5 HBV infections 79 93 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. A homogeneous population of a pre-core mutant strain harbouring the A1896G and A1899G affecting HBeAg expression was invariably found in the liver tissue, plasma and peripheral blood mononuclear cells despite active HBeAg secretion; it was the dominant strain in the liver only, and was characterised by the presence of two point mutations in the direct repeat 1 domain involved in HBV replication activity. 2009 Journal of medical case reports Abstract HBV A1896G;A1899G 68;79 74;85 C;C;Precore 96;216;30 101;221;38 19950231 PreS deletion mutations of hepatitis B virus in chronically infected patients with simultaneous seropositivity for hepatitis-B surface antigen and anti-HBS antibodies. Only two samples in Group I showed G145R/A mutation. 2010 Journal of medical virology Abstract HBV G145R;G145A 35;35 42;42 19998495 Clinical relevance and public health significance of hepatitis B virus genomic variations. HBV mutations in the S genes, especially amino acids substitution at position 145 (G145R), are associated with immune escape, whereas mutations in the PreS or S genes which impair HBsAg secretion could present a risk to blood safety. 2009 World journal of gastroenterology Abstract HBV G145R 83 88 S;PreS;S;S 180;151;21;159 185;155;22;160 19998495 Clinical relevance and public health significance of hepatitis B virus genomic variations. PreS deletions, C1653T, T1753V, and A1762T/G1764A are associated with an increased risk of HCC. 2009 World journal of gastroenterology Abstract HBV G1764A;A1762T;C1653T;T1753V 43;36;16;24 49;42;22;30 PreS 0 4 Hepatocellular carcinoma 91 94 20001517 Short communication: transmission of hepatitis B viruses with lamivudine resistance mutations in newly diagnosed HIV individuals. Two HIV/HBV-coinfected patients showed the lamivudine resistance mutation M204V in HBV while no drug resistance mutations were recognized in HIV. 2009 AIDS research and human retroviruses Abstract HBV M204V 74 79 HBV-HIV coinfections 4 22 20007398 Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. Here, we describe two further patients with chronic HBV infection who were found to develop the rtI233V mutation after initiation of ADF therapy. 2010 Journal of clinical microbiology Abstract HBV I233V 98 103 RT 96 98 Chronic HBV infection 44 65 20007398 Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. Recently, we reported on three patients with chronic hepatitis B virus (HBV) infection for whom adefovir (ADF) therapy virologically failed, most likely due to a preexisting rtI233V HBV polymerase mutation. 2010 Journal of clinical microbiology Abstract HBV I233V 176 181 P;RT 186;174 196;176 Chronic HBV infection 45 86 20007398 Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. These patients represent the first cases known so far in which the rtI233V ADF resistance mutation evolved under persistent HBV replication during HBV therapy with ADF. 2010 Journal of clinical microbiology Abstract HBV I233V 69 74 RT 67 69 20007398 Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. Thus, we provide evidence for the selection and counterselection of the rtI233V ADF resistance mutation during antiviral therapy. 2010 Journal of clinical microbiology Abstract HBV I233V 74 79 RT 72 74 20015989 Testing the balanced electrostatic interaction hypothesis of hepatitis B virus DNA synthesis by using an in vivo charge rebalance approach. HBc ARD IV mutant 173GG and ARD II mutant 173RR/R157A/R158A are arginine deficient and replication defective. 2010 Journal of virology Abstract HBV R157A;R158A 48;54 53;59 C 0 3 20015989 Testing the balanced electrostatic interaction hypothesis of hepatitis B virus DNA synthesis by using an in vivo charge rebalance approach. Similar results were obtained for ARD II mutant 173RR/R157A/R158A. 2010 Journal of virology Abstract HBV R157A;R158A 54;60 59;65 20031483 Reactivation of hepatitis B virus infection with persistently negative HBsAg on three HBsAg assays in a lymphoma patient undergoing chemotherapy. Six amino acid mutations were located in the 'a' determinant, including P120T, K122R, M133T, F134L, D144A and G145A. 2010 Journal of clinical virology Abstract HBV P120T;K122R;M133T;F134L;D144A;G145A 72;79;86;93;100;110 77;84;91;98;105;115 S 46 60 20031483 Reactivation of hepatitis B virus infection with persistently negative HBsAg on three HBsAg assays in a lymphoma patient undergoing chemotherapy. The mutants K122R, F134L and G145A in our patient have not been tested for their sensitivity to Architect and Murex assays by the previous investigators and might represent the escape mutants to these assays. 2010 Journal of clinical virology Abstract HBV K122R;F134L;G145A 12;19;29 17;24;34 20034521 Characterization of potential antiviral resistance mutations in hepatitis B virus reverse transcriptase sequences in treatment-naive Chinese patients. The concomitant AA changes of HBsAg occurred in 16.67% (32/192) isolates including sG145R mutation. 2010 Antiviral research Abstract HBV G145R 83 89 S;S 83;30 84;35 20068337 Impacts of vaccination on hepatitis B viral infections in Korea over a 25-year period. In Korea, there have been no reported cases of HBV surface gene variants such as G145R. 2010 Intervirology Abstract HBV G145R 81 86 S 51 58 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Single mutations including T1753V (C/A/G), A1762T, G1764A, G1896A and G1899A and triple mutations T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A) were more frequently detected in patients with HB-ACLF than in patients with CHB. 2010 Journal of viral hepatitis Abstract HBV A1762T;G1764A;G1764A;C1766T;T1753V;A1762T;G1764A;G1896A;G1899A;A1762T;T1768A;T1753V 105;112;130;137;27;43;51;59;70;123;148;98 111;118;136;143;33;49;57;65;76;129;154;104 Chronic Hepatitis B;Acute on chronic liver failure 233;203 236;210 20074155 Prevalence and clinical characterization of patients with acute hepatitis B induced by lamivudine-resistant strains. LMV-resistance mutations (L180M, M204I) were detected in a patient with subgenotype C2 who had acute self-limited hepatitis. 2010 Journal of gastroenterology and hepatology Abstract HBV L180M;M204I 26;33 31;38 Acute Hepatitis B 95 123 20074155 Prevalence and clinical characterization of patients with acute hepatitis B induced by lamivudine-resistant strains. The other patient with LMV-resistance mutations (L180M, M204V) was infected with subgenotype A2 and had severe hepatitis. 2010 Journal of gastroenterology and hepatology Abstract HBV L180M;M204V 49;56 54;61 Hepatitis 111 120 20077675 [Analysis on mutation of S gene and P gene of hepatitis B virus in two counties of Sichuan Province]. RESULTS: Of 47 serum samples from patients with chronic HBV infection, amino acid mutation in 'a' determinant occurred in 12 samples (25.53%,12/47), correlating with T126A, I126T/S, P127T, T131N, M133L, M133T and T140I; high proportion of mutation clustered in first loop of 'a' determinant (92.86%,13/14), rtV207I mutation in C domain of reverse transcription occured in one sample. 2009 Zhongguo yi miao he mian yi Abstract HBV V207I;T126A;I126T;I126S;P127T;T131N;M133L;M133T;T140I 309;166;173;173;182;189;196;203;213 314;171;180;180;187;194;201;208;218 S;S;RT;RT 95;276;339;307 109;290;360;309 HBV infections 48 69 20080060 Features and clinical implications of hepatitis B virus genotypes and mutations in basal core promoter/precore region in 507 Chinese patients with acute and chronic hepatitis B. CONCLUSION: Patients with genotype B virus, BCP/PC wild-type virus or T1758C mutant virus were more susceptible to develop AHB, whereas high prevalence of the BCP/PC mutations was associated with CHB development. 2010 Journal of clinical virology Abstract HBV T1758C 70 76 BCP;BCP;Precore;Precore 44;159;48;163 47;162;50;165 Acute Hepatitis B;Chronic Hepatitis B 123;196 126;199 20080060 Features and clinical implications of hepatitis B virus genotypes and mutations in basal core promoter/precore region in 507 Chinese patients with acute and chronic hepatitis B. Interestingly, T1758C and A1762T/G1764A appeared mutual restraint. 2010 Journal of clinical virology Abstract HBV G1764A;T1758C;A1762T 33;15;26 39;21;32 20080060 Features and clinical implications of hepatitis B virus genotypes and mutations in basal core promoter/precore region in 507 Chinese patients with acute and chronic hepatitis B. Significantly lower prevalence of A1762T, G1764A, G1896A, and G1899A but higher prevalence of T1758C was found in AHB patients. 2010 Journal of clinical virology Abstract HBV A1762T;G1764A;G1896A;G1899A;T1758C 34;42;50;62;94 40;48;56;68;100 Acute Hepatitis B 114 117 20087936 Molecular evolutionary analysis and mutational pattern of full-length genomes of hepatitis B virus isolated from Belgian patients with different clinical manifestations. Within the immunological domain of the HBsAg gene, the most frequent substitutions were sT125M and sT118A. 2010 Journal of medical virology Abstract HBV T125M;T118A 88;99 94;105 S;S;S 39;88;99 44;89;100 20104776 [The analysis of hepatitis B virus genetic characterization from immuned children and their mother]. Gene of twins has mutation of T143M. 2009 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV T143M 30 35 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Although sW172stop and sL173F mutations were detected, reduced HBsAg titer was not observed. 2010 Journal of Korean medical science Abstract HBV W172X;L173F 9;23 18;29 S;S;S 63;9;23 68;10;24 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. An S gene mutation, sA184V, was found in nine patients, all of whom were in group P. 2010 Journal of Korean medical science Abstract HBV A184V 20 26 S;S 3;20 4;21 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In adefovir (ADV) treated chronic hepatitis B patients carrying rtA181T/rtA181V mutations, overlap with surface gene mutations such as sW172stop/sL173F has been reported. 2010 Journal of Korean medical science Abstract HBV L173F;A181T;A181V;W172X 145;66;74;135 151;71;79;144 RT;RT;S;S;S 64;72;135;145;104 66;74;136;146;111 Chronic Hepatitis B 26 45 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Of the 22 patients included in this study, 13 were ADV-resistant with rtA181T/V mutations (polymerase mutation group, Group P) and nine were antiviral treatment-naive (control group, Group C). 2010 Journal of Korean medical science Abstract HBV A181T;A181V 72;72 79;79 P;RT 91;70 101;72 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The aim of this study was to determine the surface gene sequence in ADV-resistant patients carrying the A181T/V mutation and to describe the clinical significance. 2010 Journal of Korean medical science Abstract HBV A181T;A181V 104;104 111;111 S 43 50 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The Pre-S1 gene mutation, V60A, was detected in 11 patients (Group P=8, Group C=3). 2010 Journal of Korean medical science Abstract HBV V60A 26 30 PreS1 4 10 20130415 Appearance of HbeAg in an occult persistent hepatitis B virus infection. A male patient with severe systemic diseases, positive for anti-HBc and anti-HBs and negative for all other HBV markers, including HBsAg, since at least 4 years, showed a positivity for HBeAg at a follow-up control in November 2008; HBV-DNA testing by real-time PCR evidenced very low levels of viremia (<40 IU/ml), direct sequencing of the surface antigen-coding and Pol/RT coding regions allowed the identification of genotype D, serotype adw2, one immune escape mutation (G145R) and no drug resistance mutations. 2010 Intervirology Abstract HBV G145R 475 480 C;C;S;S;P;RT;S 64;186;77;131;368;372;341 67;191;80;136;371;374;348 20160279 Distribution and hepatocellular carcinoma-related viral properties of hepatitis B virus genotypes in Mainland China: a community-based study. A1762T/G1764A, T1753V, C1653T, and G1896A, except PreS deletion, consecutively increased with increasing age. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV G1764A;A1762T;T1753V;C1653T;G1896A 7;0;15;23;35 13;6;21;29;41 PreS 50 54 20160279 Distribution and hepatocellular carcinoma-related viral properties of hepatitis B virus genotypes in Mainland China: a community-based study. In contrast to G1896A, PreS deletion, T31C, T1753V, and A1762T/G1764A were more frequent in subgenotype C2 than in subgenotype B2. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV G1764A;A1762T;G1896A;T31C;T1753V 63;56;15;38;44 69;62;21;42;50 PreS 23 27 20164224 Identification and characterization of clevudine-resistant mutants of hepatitis B virus isolated from chronic hepatitis B patients. A quadruple mutant (L129M, V173L, M204I, and H337N) was identified that conferred greater replicative ability and strong resistance to both CLV and lamivudine. 2010 Journal of virology Abstract HBV L129M;V173L;M204I;H337N 20;27;34;45 25;32;39;50 20164224 Identification and characterization of clevudine-resistant mutants of hepatitis B virus isolated from chronic hepatitis B patients. In conclusion, the mutation M204I in HBV RT plays a major role in CLV resistance and leads to viral BT during long-term CLV treatment. 2010 Journal of virology Abstract HBV M204I 28 33 RT 41 43 20164224 Identification and characterization of clevudine-resistant mutants of hepatitis B virus isolated from chronic hepatitis B patients. In vitro phenotypic analysis showed that the mutation M204I was predominantly associated with CLV resistance, whereas L229V was a compensatory mutation for the impaired replication of the M204I mutant. 2010 Journal of virology Abstract HBV M204I;L229V;M204I 54;118;188 59;123;193 20164224 Identification and characterization of clevudine-resistant mutants of hepatitis B virus isolated from chronic hepatitis B patients. Several conserved mutations were identified in the RT domain during viral BT, with M204I being the most common. 2010 Journal of virology Abstract HBV M204I 83 88 RT 51 53 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Changes in the HBV polymerase reverse-transcriptase (RT) domain involve lamivudine-resistance (LVDr) substitutions in the conserved YMDD motif (M204V/I +/- L180M), plus an additional ETV-specific change at residues T184, S202 or M250. 2010 PloS one Abstract HBV M204V;M204I;L180M 144;144;156 151;151;161 P;RT;RT;P 19;30;53;132 29;51;55;136 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. METHODS/PRINCIPAL FINDINGS: To determine the mechanistic basis for ETVr, wildtype, lamivudine-resistant (M204V, L180M) and ETVr HBVs were studied using in vitro RT enzyme and cell culture assays, as well as molecular modeling. 2010 PloS one Abstract HBV M204V;L180M 105;112 110;117 RT 161 163 20184927 Molecular characteristics and functional analysis of full-length hepatitis B virus quasispecies from a patient with chronic hepatitis B virus infection. In the basal core promoter, the A1762T/G1764A mutation was found only in 1 clone. 2010 Virus research Abstract HBV G1764A;A1762T 39;32 45;38 BCP 7 26 20184927 Molecular characteristics and functional analysis of full-length hepatitis B virus quasispecies from a patient with chronic hepatitis B virus infection. In the core protein, cI3L, cL60M, and cI97L were detected in 8 of 10 clones and cP130T was detected in all 10 clones. 2010 Virus research Abstract HBV I3L;L60M;I97L;P130T 21;27;38;80 25;32;43;86 C;C;C;C;C 21;27;38;80;7 22;28;39;81;11 20184927 Molecular characteristics and functional analysis of full-length hepatitis B virus quasispecies from a patient with chronic hepatitis B virus infection. In the X protein, xI127M was detected in 5 clones. 2010 Virus research Abstract HBV I127M 18 24 X;X 7;18 8;19 20196797 Diversity of hepatitis B virus infecting Malaysian candidate blood donors is driven by viral and host factors. HBV vaccine escape substitutions (P120S/T, I126N and G145G) were present in six strains. 2011 Journal of viral hepatitis Abstract HBV P120S;P120T;I126N;G145G 34;34;43;53 41;41;48;58 20210630 No increase in prevalence of hepatitis B surface antigen mutant in a population of children and adolescents who were fully covered by universal infant immunization. CONCLUSIONS: Less infectivity of G145R, recombinant vaccine use, and mutant loss with older age seem to decrease the a mutant prevalence in an immunized population over time. 2010 The Journal of infectious diseases Abstract HBV G145R 33 38 20210630 No increase in prevalence of hepatitis B surface antigen mutant in a population of children and adolescents who were fully covered by universal infant immunization. HBV DNA levels were significantly lower in hepatitis B e antigen-positive sera containing the G145R mutant than were levels in sera containing wild-type virus. 2010 The Journal of infectious diseases Abstract HBV G145R 94 99 C 55 64 20222172 Establishment of a new quantitative detection approach to adefovir-resistant HBV and its clinical application. Among the 32 clinical patients, single rtA181 and rtN236T mutation and double rtA181T and rtN236T mutations were detected in 20 and 8, respectively, while ADV-resistant mutations in 6 (including, rtA181V/T mutation alone in 5 patients) and no associated mutations in 26. 2010 World journal of gastroenterology Abstract HBV N236T;A181T;N236T;A181V;A181T 52;80;92;198;198 57;85;97;205;205 RT;RT;RT;RT;RT 39;50;78;90;196 41;52;80;92;198 20222172 Establishment of a new quantitative detection approach to adefovir-resistant HBV and its clinical application. METHODS: Based on the characteristics of rtA181V/T and rtN236T mutations, a new approach based on real-time fluorescent quantitative polymerase chain reaction (RT-PCR) was established for the detection of ADV-resistant HBV quasispecies, total HBV DNA, rtA181 and rtN236 mutations in blood samples from 32 chronic hepatitis B (CHB) patients with unsatisfactory curative effect on ADV and compared with routine HBV DNA sequencing. 2010 World journal of gastroenterology Abstract HBV A181V;A181T;N236T 43;43;57 50;50;62 RT;RT;RT;RT 41;55;252;263 43;57;254;265 Chronic Hepatitis B;Chronic Hepatitis B 305;326 324;329 20231988 Expression of Hepatitis B virus surface antigen (HBsAg) from genotypes A, D and F and influence of amino acid variations related or not to genotypes on HBsAg detection. However, the presence of two single variations, T143M in genotype A, and T125M in genotype D, produced a decrease of 44% and an increase of 34%, respectively, on HBsAg mean values in comparison with their consensus forms. 2009 The Brazilian journal of infectious diseases Abstract HBV T143M;T125M 48;73 53;78 S 162 167 20231988 Expression of Hepatitis B virus surface antigen (HBsAg) from genotypes A, D and F and influence of amino acid variations related or not to genotypes on HBsAg detection. However, unique amino acid substitutions not linked to genotypes, such as T125M and T143M described here, should have more implications in HBV immunological diagnostics than the set of variations characteristic of each HBV genotype. 2009 The Brazilian journal of infectious diseases Abstract HBV T125M;T143M 74;84 79;89 20332649 Response to adefovir depends on mutation patterns in precore region, basal core promoter and reverse transcriptase, and on-treatment responses in Lamivudine-resistant chronic hepatitis B patients. PC mutation, the absence of compensatory mutations (rtL80I/V or rtV173L), and a decrease in serum hepatitis B virus (HBV) DNA by 3 log or greater at 6 months were independent predictors of virologic response. 2010 Intervirology Abstract HBV L80I;L80V;V173L 54;54;66 60;60;71 Precore;RT;RT 0;52;64 2;54;66 20336717 Comparison of the technical and clinical performance of the Elecsys HBsAg II assay with the Architect, AxSym, and Advia Centaur HBsAg screening assays. However, the Elecsys HBsAg II assay recognized a native mutant sample (L94S, L97V, L98V, T123A) that the Architect HBsAg assay failed to detect. 2010 Journal of medical virology Abstract HBV L94S;L97V;L98V;T123A 71;77;83;89 75;81;87;94 S;S 21;115 26;120 20337225 T3098C and T53C mutations of HBV genotype C is associated with HBV infection progress. CONCLUSION: The frequency of genotype C HBV preS T3098C and T53C mutations is associated with hepatitis B infection progression. 2009 Biomedical and environmental sciences Abstract HBV T3098C;T53C 49;60 55;64 PreS 44 48 20337225 T3098C and T53C mutations of HBV genotype C is associated with HBV infection progress. RESULTS: The prevalence of preS T3098C and T53C mutations of genotype C HBV was significantly higher in LC and HCC patients than ASC and CHB patients. 2009 Biomedical and environmental sciences Abstract HBV T3098C;T53C 32;43 38;47 PreS 27 31 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 111;137;104 114;140;106 20337225 T3098C and T53C mutations of HBV genotype C is associated with HBV infection progress. The rate of T3098C mutation in ASC, CHB, LC, and HCC patients were 0.00% (0/24), 3.85% (1/26), 9.09% (2/22), and 30.77% (8/22), respectively (P=0.0015), while the rate of T53C mutation was 12.50% (3/24), 3.85% (1/26), 40.91% (9/22), and 42.31% (11/26), respectively (P=0.0012). 2009 Biomedical and environmental sciences Abstract HBV T3098C;T53C 12;171 18;175 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 36;49;41 39;52;43 2034246 Mutations in the precore region of hepatitis B virus DNA in patients with fulminant and severe hepatitis. RESULTS: Of the nine patients with fatal hepatitis, seven had retrievable hepatitis B DNA: In all seven there was a point mutation from G to A at nucleotide 1896 of the precore region, converting tryptophan (TGG) to a stop codon (TAG). 1991 The New England journal of medicine Abstract HBV G1896A 136 161 Precore 169 176 Hepatitis 41 50 20347609 Establishment of an HBsAg mixed titer performance panel and HBsAg working standard for quality control of HBsAg diagnostic kits in Korea. A G1896A and a T/I126S mutant are included in the positive samples. 2010 Journal of clinical virology Abstract HBV I126S;T126S;G1896A 15;15;2 22;22;8 20367795 Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern. An rtA200V mutation was present in the majority of HBV clones, in addition to the 3TC-resistant mutations of rtL180M+M204V. 2011 Journal of viral hepatitis Abstract HBV A200V;L180M;M204V 5;111;117 10;116;122 RT;RT 3;109 5;111 20367795 Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern. In vitro analysis showed that the rtA200V mutation recovered the impaired replication capacity of the clone with the rtL180M+M204V mutations and induced resistance to ADV. 2011 Journal of viral hepatitis Abstract HBV A200V;L180M;M204V 36;119;125 41;124;130 RT;RT 34;117 36;119 20367795 Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern. Moreover, rtT184S and rtS202C, which are known entecavir-resistant mutations, emerged in some rtL180M+M204V clones without rtA200V or rtN236T. 2011 Journal of viral hepatitis Abstract HBV T184S;S202C;A200V;N236T;L180M;M204V 12;24;125;136;96;102 17;29;130;141;101;107 RT;RT;RT;RT;RT 10;22;94;123;134 12;24;96;125;136 20367795 Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern. The mutation rtA200V with rtL180M+M204V may be sufficient for failure of 3TC+ADV therapy. 2011 Journal of viral hepatitis Abstract HBV A200V;L180M;M204V 15;28;34 20;33;39 RT;RT 13;26 15;28 20367795 Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern. The rtN236T ADV-resistant mutation was observed in only 25% clones. 2011 Journal of viral hepatitis Abstract HBV N236T 6 11 RT 4 6 20374224 Main mutations in the hepatitis B virus basic core promoter (A1762T/G1764A) before HBeAg loss are markers that identify patients who will require long-term treatment. AIMS: To evaluate hepatitis B virus (HBV) genotype and the main mutations in the basic core promoter (BCP, A1762T/G1764A) and precore (G1896A) sequences as markers of persistent HBV-DNA after HBeAg loss. 2010 Alimentary pharmacology & therapeutics Abstract HBV G1764A;A1762T;G1896A 114;107;135 120;113;141 BCP;BCP;C;Precore 81;102;192;126 100;105;197;133 20377434 Hepatitis B virus drug resistance in HIV-1-infected patients taking lamivudine-containing antiretroviral therapy. All 19 patients with HBV-DR had lamivudine resistance with the mutations as follows: M204V/I (95%), L180M/A181T (95%), L80V/I (47%), V173L (32%), and N236T (21%). 2010 AIDS patient care and STDs Abstract HBV A181T;L180M;M204V;M204I;L80V;L80I;V173L;N236T 106;100;85;85;119;119;133;150 111;105;92;92;125;125;138;155 20377825 Highly active antiretroviral therapy improved persistent lamivudine-resistant viremia in acute hepatitis B virus genotype Ae infection with coinfection of human immunodeficiency virus. Sequential genetic analysis revealed that rtL217R, a mutation potentially diminishing the ADV efficacy, was detected before and after the combination therapy. 2010 Hepatology research Abstract HBV L217R 44 49 RT 42 44 20380793 [Polymerase region mutations and hepatitis B virus genotypes in chronic hepatitis B patients with poor response to lamivudine]. M204I mutation in genotype B (20.6%) was more frequent than that in genotype C (13.9%) (x2=4.91, P less than 0.05). 2010 Zhonghua gan zang bing za zhi Abstract HBV M204I 0 5 20380793 [Polymerase region mutations and hepatitis B virus genotypes in chronic hepatitis B patients with poor response to lamivudine]. The overall incidence rate of A181V/T mutation in genotype C (5.3%) was significantly higher than that in genotype B (0.4%) (x2=12.23, P less than 0.01), but the incidence rate of M204I/V, L180M, T184A/G/I/S, S202G/I and V173L mutations was not significantly different between genotype B and C (each P more than 0.05). 2010 Zhonghua gan zang bing za zhi Abstract HBV A181V;A181T;M204I;M204V;L180M;T184A;T184G;T184I;T184S;S202G;S202I;V173L 30;30;180;180;189;196;196;196;196;209;209;221 37;37;187;187;194;207;207;207;207;216;216;226 20382061 Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B. In the NUC therapy group the prevalence was 8.5% (12/142), with the following patterns: sY100C+sI110V, sL109I, sP120T, sP127T, sG130R+sG145X, sS132A+sY134N, sY134N+sG145R, sC137G, sD144E, sG145R. 2010 International journal of infectious diseases Abstract HBV Y100C;G130R;S132A;Y134N;I110V;L109I;P120T;P127T;G145X;Y134N;G145R;C137G;D144E;G145R 88;127;142;157;95;103;111;119;134;149;164;172;180;188 94;133;148;163;101;109;117;125;140;155;170;178;186;194 S;S;S;S;S;S;S;S;S;S;S;S;S;S 88;95;103;111;119;127;134;142;149;157;164;172;180;188 89;96;104;112;120;128;135;143;150;158;165;173;181;189 20382061 Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B. In the treatment-naive group the prevalence was 8.1% (15/185), with the following patterns: sL109I, sI110V, sS117INST, sP120T, sP127T, sM133I, sC137L+sG145R, sS143L. 2010 International journal of infectious diseases Abstract HBV C137L;L109I;I110V;S117I;P120T;P127T;M133I;G145R;S143L 143;92;100;108;119;127;135;150;158 149;98;106;117;125;133;141;156;164 S;S;S;S;S;S;S;S;S 92;100;108;119;127;135;143;150;158 93;101;109;120;128;136;144;151;159 20382061 Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B. Interestingly, the treatment-naive patients had preexisting drug resistance mutations related to lamivudine (rtL180M+rtM204I), adefovir (rtA181V, rtQ215S, rtI233V), entecavir (intermediate susceptibility with rtL180M+rtM204IHBV variant), telbivudine (rtL180M+rtM204I), and tenofovir (rtA194T). 2010 International journal of infectious diseases Abstract HBV A181V;Q215S;I233V;A194T;L180M;L180M;L180M;M204I;M204I;M204I 139;148;157;286;111;211;253;119;219;261 144;153;162;291;116;216;258;124;224;266 RT;RT;RT;RT;RT;RT;RT;RT;RT 109;117;137;146;155;209;251;259;284 111;119;139;148;157;211;253;261;286 20409073 Hepatitis B virus transfusion risk in China: proficiency testing for the detection of hepatitis B surface antigen. The panel included four HBsAg-positive serum samples at concentrations of 0 16, 0 46, 0 9 and 1 73 IU mL(-1) ; three recombinant HBsAg mutants (G145R, T131I and K141E) with defined concentrations and one negative sample. 2010 Transfusion medicine (Oxford, England) Abstract HBV G145R;T131I;K141E 144;151;161 149;156;166 S;S 24;129 29;134 20419326 Significant association of different preS mutations with hepatitis B-related cirrhosis or hepatocellular carcinoma. Combined preS1 mutations had specificities greater than 95%, while C3116T and C7A had moderate sensitivities and specificities, for HCC. 2010 Journal of gastroenterology Abstract HBV C3116T;C7A 67;78 73;81 PreS1 9 14 Hepatocellular carcinoma 132 135 20419326 Significant association of different preS mutations with hepatitis B-related cirrhosis or hepatocellular carcinoma. CONCLUSIONS: C2964A, C3116T, and C7A are novel markers independently associated with an increased risk of HCC, while A2964C and T3116C are novel markers independently associated with an increased risk of cirrhosis. 2010 Journal of gastroenterology Abstract HBV C2964A;C3116T;A2964C;T3116C;C7A 13;21;117;128;33 19;27;123;134;36 Hepatocellular carcinoma;Liver cirrhosis 106;204 109;213 20419326 Significant association of different preS mutations with hepatitis B-related cirrhosis or hepatocellular carcinoma. Multivariate regression analyses showed that C2964A, C3116T, and C7A were novel factors associated with HCC compared with those without HCC, whereas A2964C and T3116C were independently associated with cirrhosis compared with ASCs and the CHB patients. 2010 Journal of gastroenterology Abstract HBV C2964A;C3116T;A2964C;T3116C;C7A 45;53;149;160;65 51;59;155;166;68 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B 104;136;202;239 107;139;211;242 20419834 Application of hepatitis B virus replication mouse model. To identify the model's value in a replication ability study of HBV drug-resistant mutants and a HBx-minus mutant, telbivudine resistance mutants (rtM204I, ayw subtype), adefovir resistance mutants (rtA181V + rtN236T, ayw subtype) and HBx-minus mutants were injected respectively, and their corresponding HBV DNA replication intermediates in mouse liver were assessed. 2010 World journal of gastroenterology Abstract HBV M204I;A181V;N236T 149;201;211 154;206;216 X;X;RT;RT;RT 97;235;147;199;209 100;238;149;201;211 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. S114T, C121Y, T126S/A, Q129K, G130R, T131N, M133T, G145R, N146D substitution and premature stop codon were also found in those clones. 2010 Virology journal Abstract HBV S114T;C121Y;T126S;T126A;Q129K;G130R;T131N;M133T;G145R;N146D 0;7;14;14;23;30;37;44;51;58 5;12;21;21;28;35;42;49;56;63 20513073 Hepatitis B virus BCP, Precore/core, X gene mutations/genotypes and the risk of hepatocellular carcinoma in India. Multivariate analyses showed that the TT1504, V1753, A1762T/G1764A, and the G1914 mutations and the patient's age, sex, and HBeAg status increased the risk of HCC development significantly. 2010 Journal of medical virology Abstract HBV G1764A;A1762T 60;53 66;59 C 124 129 Hepatocellular carcinoma 159 162 20513074 Molecular and clinical characteristics of hepatitis B virus in Korea. A number of amino acid/nucleotide substitutions were associated with HCC, namely sR24K (HBsAg), SI126T (HBsAg), and pcA1846T (precore gene) mutations (P = 0.029, 0.001, and 0.008, respectively). 2010 Journal of medical virology Abstract HBV A1846T;R24K;I126T 116;81;96 124;86;102 S;S;Precore;Precore;S 88;104;116;126;81 93;109;118;133;82 Hepatocellular carcinoma 69 72 20516566 Breakthrough HBV infection in vaccinated children in Taiwan: surveillance for HBV mutants. Among vaccinated individuals with breakthrough HBV infection, sG145R & sT126A/S mutations (which account for 48% of the mutants detected) have become prominent. 2010 Antiviral therapy Abstract HBV G145R;T126A;T126S 62;71;71 68;79;79 S;S 62;71 63;72 HBV infections 47 60 20516567 Development of HBV S gene mutants in chronic hepatitis B patients receiving nucleotide/nucleoside analogue therapy. Among them, the rtA181T/sW172* mutant has a dominant negative secretion effect as well as an increased oncogenic potential. 2010 Antiviral therapy Abstract HBV W172X;A181T 24;18 30;23 RT;S 16;24 18;25 20516568 Infectivity and vaccination efficacy studies in animal models of HBV S and pol gene mutants. Infectious HBV wild-type and mutant clones were produced in vitro with three mutations in pol (rtV173L plus rtL180M plus rtM204V) or with a single mutation in the S gene (sG145R) and inoculated in treatment-naive chimpanzees. 2010 Antiviral therapy Abstract HBV V173L;L180M;M204V;G145R 97;110;123;171 102;115;128;177 P;RT;RT;RT;S;S 90;95;108;121;163;171 93;97;110;123;164;172 20516568 Infectivity and vaccination efficacy studies in animal models of HBV S and pol gene mutants. Intravenous inoculation of these mutants in chimpanzees resulted in HBV infection; the pol mutations remained stable, whereas the sG145R mutation reverted to wild type during viraemia. 2010 Antiviral therapy Abstract HBV G145R 130 136 P;S 87;130 90;131 HBV infections 68 81 20546502 Factors associated with vaccine failure and vertical transmission of hepatitis B among a cohort of Canadian mothers and infants. Of the two cases who were HBeAg negative, one had an undetectable viral load 8 months prior to delivery and a sP120T mutation. 2011 Journal of viral hepatitis Abstract HBV P120T 110 116 C;S 26;110 31;111 20549958 [Genotype distribution of chronic hepatitis B and hepatitis C patients and investigation of the resistance patterns in hepatitis B cases]. Various mutations were detected in 34.1% (15/44) of CHB patients and these were identified as M2041 (n = 6), Q215S (n = 2), L801 + M2041 (n = 1), L80V + M2041 (n = 1), Q215S + M2041 (n = 1) and M2041 + L180M (n = 1) mutations responsible for LAM resistance; V214A (n = 1) and A181T + N236T (n = 1) mutations responsible for adefovir (ADV) resistance, and V84M + V173L (n = 1) mutation responsible for ADV + LAM resistance. 2010 Mikrobiyoloji bulteni Abstract HBV Q215S;L80V;Q215S;L180M;V214A;A181T;N236T;V84M;V173L 109;146;168;202;258;276;284;355;362 114;150;173;207;263;281;289;359;367 Chronic Hepatitis B 52 55 20550526 Nucleotide changes related to hepatocellular carcinoma in the enhancer 1/x-promoter of hepatitis B virus subgenotype C2 in cirrhotic patients. Mutated nucleotides of the Enh1/X-promoter, especially G1053A and G1229A mutations in the HBV subgenotype C2 of patients with cirrhosis, can be risk factors for hepatocarcinogenesis, and this might be due to an increase in the HBx levels through the transactivation of the Enh1/X-promoter. 2010 Cancer science Abstract HBV G1053A;G1229A 55;66 61;72 X;X;X 227;32;278 230;33;279 Liver cirrhosis 126 135 20550526 Nucleotide changes related to hepatocellular carcinoma in the enhancer 1/x-promoter of hepatitis B virus subgenotype C2 in cirrhotic patients. The sites that showed higher mutation rates in the HCC group were G1053A and G1229A, which were found to be independent risk factors through multiple logistic analysis (P < 0.05). 2010 Cancer science Abstract HBV G1053A;G1229A 66;77 72;83 Hepatocellular carcinoma 51 54 20553432 National survey of hepatitis B virus (HBV) polymorphism in asymptomatic HBV blood donors from 1999 to 2007 in France. rtA181T/sW172 stop mutation associated with resistance to nucleos(t)ide analogs was detected in two donors suggesting a transmission of these isolates. 2010 Transfusion Abstract HBV W172X;A181T 8;2 18;7 RT;S 0;8 2;9 20559531 A YIDD Mutation in a Case of Recurrent Hepatitis B after Liver Transplantation Induced by an S-escape Mutant. G145R and K141R mutations in the "a" determinant were detected only in the post-OLT sample. 2010 Gut and liver Abstract HBV G145R;K141R 0;10 5;15 20559531 A YIDD Mutation in a Case of Recurrent Hepatitis B after Liver Transplantation Induced by an S-escape Mutant. Hepatitis B was reactivated with a flare-up, and a M204I mutation (YIDD mutant type) appeared with a higher viral load at 9 months after clevudine treatment. 2010 Gut and liver Abstract HBV M204I 51 56 P 67 71 20572086 Molecular epidemiological study of hepatitis B virus among migrant workers from Cambodia, Laos, and Myanmar to Thailand. Various point mutations in the "a" determinant region were detected in approximately 18% of these samples, of which Ile126Ser/Asn was the most frequent variant. 2010 Journal of medical virology Abstract HBV I126S;I126N 116;116 127;127 20573234 Infection with hepatitis B virus carrying novel pre-S/S gene mutations in female siblings vaccinated at birth: two case reports. Four of these mutations (sL97S, sL98S, sG102R, and sA159P) were novel. 2010 Journal of medical case reports Abstract HBV L97S;L98S;G102R;A159P 25;32;39;51 30;37;45;57 S;S;S;S 25;32;39;51 26;33;40;52 20580309 Acute hepatitis B infection associated with drug-resistant hepatitis B virus. RESULTS: Direct PCR sequencing showed that 14 samples (7.0%) were positive for drug-resistant HBV variants, comprised of 11 with the lamivudine-resistant pattern rtM204I and/or rtM204V in the presence and absence of compensatory mutations rtL80I, rtV173L, and rtL180M; two with the adefovir-resistant pattern rtA181V; and one with the entecavir-resistant pattern rtL180M+rtS202G+rtM204V. 2010 Journal of clinical virology Abstract HBV M204I;M204V;L80I;V173L;L180M;A181V;L180M;S202G;M204V 164;179;241;249;262;311;365;373;381 169;184;245;254;267;316;370;378;386 RT;RT;RT;RT;RT;RT;RT;RT;RT 162;177;239;247;260;309;363;371;379 164;179;241;249;262;311;365;373;381 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. Although three major ADV-resistant mutations of HBV are known, rtA181T/V and rtN236T, HBV mutations associated with ADV resistance have not been fully identified. 2010 Journal of viral hepatitis Abstract HBV A181T;A181V;N236T 65;65;79 72;72;84 RT;RT 63;77 65;79 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. Phenotypic analyses demonstrated that the rtE218G mutation could independently confer resistance to ADV in vitro, with a 50% inhibitory concentration (IC(50)) 5.5-fold higher than wild-type HBV. 2010 Journal of viral hepatitis Abstract HBV E218G 44 49 RT 42 44 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. RtE218G-mutated HBV also showed a decreased replication capacity in vitro, equal to 87% of wild-type HBV. 2010 Journal of viral hepatitis Abstract HBV E218G 2 7 RT 0 2 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. The present study showed that the rtE218G mutation may be a novel ADV-resistant mutation. 2010 Journal of viral hepatitis Abstract HBV E218G 36 41 RT 34 36 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. This mutant exhibited a substitution of glycine for glutamic acid at residue 218 (rtE218G). 2010 Journal of viral hepatitis Abstract HBV E218G;E218G 84;40 89;80 RT 82 84 20586936 rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B. Transient transfection of the HBV replication-competent construct including the rtE218G mutation was performed in HepG2 cells in order to determine the relevance of this mutation to ADV resistance. 2010 Journal of viral hepatitis Abstract HBV E218G 82 87 RT 80 82 20587309 [Detection of HBV resistant mutations related to lamivudine, adefovir and entecavir by reverse hybridization technique]. RESULTS: The specific probes of 10 codon positions related to HBV wild-type and resistant reference strains, including I169T, V173L, L180M, A181T, T184G, S202I, M204V, Q215S, N236T, M250V, were distinguished effectively by reverse hybridization method. 2010 Zhonghua gan zang bing za zhi Abstract HBV I169T;V173L;L180M;A181T;T184G;S202I;M204V;Q215S;N236T;M250V 119;126;133;140;147;154;161;168;175;182 124;131;138;145;152;159;166;173;180;187 20587309 [Detection of HBV resistant mutations related to lamivudine, adefovir and entecavir by reverse hybridization technique]. To detect non-synonymous amino acid substitutions associated with lamivudine, adefovir and entecavir, 26 specific oligonucleotide probes covering ten different codon positions, I169T, V173L/G, L180M, A181T/V, T184G, S202I/G, M204V/I, Q215S, N236T and M250V/I/L were synthesized and immobilized on nylon membranes charged positively. 2010 Zhonghua gan zang bing za zhi Abstract HBV I169T;V173L;V173G;L180M;A181T;A181V;T184G;S202I;S202G;M204V;M204I;Q215S;N236T;M250V;M250I;M250L 177;184;184;193;200;200;209;216;216;225;225;234;241;251;251;251 182;191;191;198;207;207;214;223;223;232;232;239;246;260;260;260 20587311 [Evolution of hepatitis B virus quasispecies during lamivudine-entecavir sequential therapy]. The rtL180M+S202G+M204V triple mutant, which was most likely a descendant of the LAM resistant rtL180M+M204V variant, was closely correlated with ETV resistant in Patient II. 2010 Zhonghua gan zang bing za zhi Abstract HBV L180M;L180M;S202G;M204V;M204V 6;97;12;18;103 11;102;17;23;108 RT;RT 4;95 6;97 20595500 Serologic and molecular characteristics of hepatitis B virus among school children in East Java, Indonesia. A single amino substitution (T126I) in the S region was frequently found. 2010 The American journal of tropical medicine and hygiene Abstract HBV T126I 29 34 S 43 44 20608166 [Liver cirrhosis patogenetics: polymorphism of glutation S-transferase genes]. Association of deletion polymorphism in GSTT1 and GSTM1 genes and polymorphic variant A313G of GSTP1 gene with cirrhosis diseases and 4-year survival rate for the Tomsk region (West Siberia) patients were tested. 2010 Molekuliarnaia biologiia Abstract HBV A313G 86 91 20608166 [Liver cirrhosis patogenetics: polymorphism of glutation S-transferase genes]. The GSTM1 null genotype and GSTP1 gene A313G polymorphic variant correlated with the patients' survival rate. 2010 Molekuliarnaia biologiia Abstract HBV A313G 39 44 20608166 [Liver cirrhosis patogenetics: polymorphism of glutation S-transferase genes]. The patients survived in comparison with the dead had higher frequency of a GSTM1 null genotype (46.6 vs. 30.2%) and GSTP1 AA genotype (63.1 vs. 40.5%), and lower frequency of GSTP1 AG (A313G) genotype (31.1 vs. 51.2%). 2010 Molekuliarnaia biologiia Abstract HBV A313G 186 191 20621632 Lamivudine-resistance mutations can be selected even at very low levels of hepatitis B viraemia. Drug-resistance mutations were observed in 17 (77.2%) LAM-treated patients with virological breakthrough: 8 M204V, 7 M204I, 1 M204I/V, and 1 A181T. 2010 Digestive and liver disease Abstract HBV M204V;M204I;M204I;M204V;A181T 108;117;126;126;141 113;122;133;133;146 20621632 Lamivudine-resistance mutations can be selected even at very low levels of hepatitis B viraemia. Drug-resistance mutations were present also in patients with undetectable serum HBV-DNA: M204I was detected in 2 patients receiving LAM-monotherapy, and V84M in 1 patient receiving LAM+ADV. 2010 Digestive and liver disease Abstract HBV M204I;V84M 89;153 94;157 20631103 Detection of highly prevalent hepatitis B virus coinfection among HIV-seropositive persons in Ghana. HBsAg mutations affected assay performance, including a T123A mutant that escaped detection by Architect. 2010 Journal of clinical microbiology Abstract HBV T123A 56 61 S 0 5 20637763 Occult HBV infection in anti-HBs-positive young adults after neonatal HB vaccination. Only 4/41 (9.8%) showed mutations at the "a" epitope and three of them were G145A. 2010 Vaccine Abstract HBV G145A 76 81 20638744 HBV reactivation after fludarabine chemotherapy identified on investigation of suspected transfusion-transmitted Hepatitis B virus. Correcting the C139Y substitution by site directed mutagenesis of recombinant surface proteins re-established assay reactivity. 2010 Journal of hepatology Abstract HBV C139Y 15 20 S 78 85 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. INTERVENTIONS AND MAIN OUTCOME MEASURE(S): Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). 2010 Virology journal Abstract HBV L180M;V207M;M204V;M204K 318;328;396;412 324;334;401;417 RT;RT;RT;RT;RT;RT;P 316;326;377;387;394;410;403 318;328;379;389;396;412;407 20646776 Lamivudine plus adefovir or entecavir for patients with chronic hepatitis B resistant to lamivudine and adefovir. Multivariable analysis showed that LAM+ADV group (OR=0.08, CI=0.02-0.28) and the presence of the rtA181V/T mutation (OR=0.21, CI=0.05-0.91) were independently associated with a decreased rate of virologic response (HBV DNA <2000 IU/ml) at 12 months. 2010 Journal of hepatology Abstract HBV A181V;A181T 99;99 106;106 RT 97 99 20648600 High frequency of lamivudine resistance mutations in Brazilian patients co-infected with HIV and hepatitis B. LAM resistance substitutions (rtL180M + rtM204V) were detected in 10 (50%) of the 20 patients with viremia. 2010 Journal of medical virology Abstract HBV L180M;M204V 32;42 37;47 RT;RT 30;40 32;42 20648600 High frequency of lamivudine resistance mutations in Brazilian patients co-infected with HIV and hepatitis B. Mutations in the BCP region (A1762T, G1764A) and in the precore region (G1896A, G1899A) were also found. 2010 Journal of medical virology Abstract HBV A1762T;G1764A;G1896A;G1899A 29;37;72;80 35;43;78;86 BCP;Precore 17;56 20;63 20648600 High frequency of lamivudine resistance mutations in Brazilian patients co-infected with HIV and hepatitis B. This pattern and an accompanying rtV173L mutation was found in four patients. 2010 Journal of medical virology Abstract HBV V173L 35 40 RT 33 35 20648600 High frequency of lamivudine resistance mutations in Brazilian patients co-infected with HIV and hepatitis B. Three patients with the triple polymerase substitution pattern (rtV173L + rtL180M + rtM204V) had associated changes in the envelope gene (sE164D + sI195M). 2010 Journal of medical virology Abstract HBV V173L;L180M;M204V;E164D;I195M 66;76;86;138;147 71;81;91;144;153 RT;RT;RT;S;S;Envelope;P 64;74;84;138;147;123;31 66;76;86;139;148;131;41 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. BCP mutations A1762T and G1764A were significantly more frequent in HBV genotype C mono-infection and the -1G frameshift was significantly more frequent in co-infection and was only observed in HBV genotype A co-infection. 2010 Virology Abstract HBV A1762T;G1764A 14;25 20;31 BCP 0 3 HBV infections;HBV infections 68;194 97;221 20675695 Prevalence of occult hepatitis B infection in a highly endemic area for chronic hepatitis B: a study of a large blood donor population. For those with viral sequence generation, none had the common HBsAg mutant G145R. 2010 Gut Abstract HBV G145R 75 80 S 62 67 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. 20% of clones from three serum samples were detected double resistance to LAM and entecavir (ETV) in the combination therapy group, the resistance patterns were M204I+L80I+T184I (2/10), M204V+L180M+T184S (2/10), and M204V+L180M+G173L+S202G (2/10) respectively. 2010 Zhonghua gan zang bing za zhi Abstract HBV T184I;M204I;L80I;T184S;M204V;L180M;M204V;L180M;G173L;S202G 172;161;167;198;186;192;216;222;228;234 177;166;171;203;191;197;221;227;233;239 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. CONCLUSIONS: In the patients with suboptimal viral response to ADV therapy after LAM resistance, the ADV resistance mutation patterns of A181T+N236T, A181V and A181T could easily be selected during ADV monotherapy; while in the patients with combination therapy, the LAM resistance mutation patterns of M204V+L180M, M204V+L180M+L229V, M204I+L80I, and M204V+L180M+V207I were predominant, the ETV resistance mutation T184I/S and S202G could be selected. 2010 Zhonghua gan zang bing za zhi Abstract HBV T184S;N236T;A181T;A181V;A181T;M204V;L180M;M204V;L180M;L229V;M204I;L80I;M204V;L180M;V207I;T184I;S202G 415;143;137;150;160;303;309;316;322;328;335;341;351;357;363;415;427 422;148;142;155;165;308;314;321;327;333;340;345;356;362;368;422;432 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. I269L clones were detected in two serum samples from both two groups and P109S clones also detected in the one from monotherapy group. 2010 Zhonghua gan zang bing za zhi Abstract HBV I269L;P109S 0;73 5;78 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. RESULTS: The ADV resistance mutation patterns of A181T+N236T, A181V, A181T were selected in ADV monotherapy group. 2010 Zhonghua gan zang bing za zhi Abstract HBV N236T;A181T;A181V;A181T 55;49;62;69 60;54;67;74 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. The LAM resistance mutation patterns of M204V+L180M, M204V+L180M+L229V, M204I+L80I, M204V+L180M+V207I were detected in the combination therapy group. 2010 Zhonghua gan zang bing za zhi Abstract HBV M204V;L180M;M204V;L180M;L229V;M204I;L80I;M204V;L180M;V207I 40;46;53;59;65;72;78;84;90;96 45;51;58;64;70;77;82;89;95;101 20678438 [Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance]. The mutation patterns of I269L and P109S may impact the responses to ADV therapy in some patients. 2010 Zhonghua gan zang bing za zhi Abstract HBV I269L;P109S 25;35 30;40 20699378 Comparison study on the complete sequence of hepatitis B virus identifies new mutations in core gene associated with hepatocellular carcinoma. CONCLUSIONS: These results implicate A2189C and G2203W as new predictive markers for HCC. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV A2189C;G2203W 37;48 43;54 Hepatocellular carcinoma 85 88 20699378 Comparison study on the complete sequence of hepatitis B virus identifies new mutations in core gene associated with hepatocellular carcinoma. In the validation study, A2159G, A2189C, and G2203W showed consistent associations with HCC by univariate analysis. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV A2159G;A2189C;G2203W 25;33;45 31;39;51 Hepatocellular carcinoma 88 91 20699378 Comparison study on the complete sequence of hepatitis B virus identifies new mutations in core gene associated with hepatocellular carcinoma. Multivariate analysis showed that A2189C and G2203W were independent risk factors for HCC. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV A2189C;G2203W 34;45 40;51 Hepatocellular carcinoma 86 89 20699378 Comparison study on the complete sequence of hepatitis B virus identifies new mutations in core gene associated with hepatocellular carcinoma. RESULTS: The pre-S deletion and 12 point mutations, namely, the pre-S2 start codon mutation, T53C in the pre-S2 gene, T766A in the S gene, G1613A, C1653T, A1762T, G1764A in the X gene, and G1899A, C2002T, A2159G, A2189C, and G2203W (A or T) in the pre-C/C gene, showed close associations with HCC. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV T53C;T766A;G1613A;C1653T;A1762T;G1764A;G1899A;C2002T;A2159G;A2189C;G2203W;G2203A;G2203T 93;118;139;147;155;163;189;197;205;213;225;225;225 97;123;145;153;161;169;195;203;211;219;231;240;240 Precore;C;PreS;PreS2;PreS2;S;X 248;254;13;64;105;131;177 253;255;18;70;111;132;178 Hepatocellular carcinoma 293 296 20699378 Comparison study on the complete sequence of hepatitis B virus identifies new mutations in core gene associated with hepatocellular carcinoma. The odds ratios (95% confidence interval) were 3.99 (1.61-9.92) and 9.70 (1.17-80.58), respectively, for A2189C and G2203W. 2010 Cancer epidemiology, biomarkers & prevention Abstract HBV A2189C;G2203W 105;116 111;122 20814897 Hepatitis B virus-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma. Assayed factors included the amount of HBV-DNA in the liver tissues; genotype; and the presence of the HBV precore stop codon G1896A mutation, basal core promoter A1762T/G1764A mutation, and pre-S deletions/stop codon mutation. 2010 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;G1896A 170;163;126 176;169;132 BCP;Precore;PreS 143;107;191 162;114;196 20820820 A population-based cohort study for the risk factors of HCC among hepatitis B virus mono-infected subjects in Japan. CONCLUSION: HBV mono-infected subjects with A1762T/G1764A double mutation could be at high risk of HCC development during the natural course of HBV infection. 2011 Journal of gastroenterology Abstract HBV G1764A;A1762T 51;44 57;50 Hepatocellular carcinoma;HBV infections 99;144 102;157 20820820 A population-based cohort study for the risk factors of HCC among hepatitis B virus mono-infected subjects in Japan. Kaplan-Meier method also showed that the probability of HCC occurrence-free was significantly lower in HBV mono-infected subjects with A1762T/G1764A double mutation than those without these mutations. 2011 Journal of gastroenterology Abstract HBV G1764A;A1762T 142;135 148;141 Hepatocellular carcinoma 56 59 20820820 A population-based cohort study for the risk factors of HCC among hepatitis B virus mono-infected subjects in Japan. Multivariate-adjusted Cox hazard model showed that A1762T/G1764A (hazard ratio 7.05 [95% confidence interval (CI) 1.03-48.12, P = 0.046]) was the only independent risk factor for the development of HCC. 2011 Journal of gastroenterology Abstract HBV G1764A;A1762T 58;51 64;57 Hepatocellular carcinoma 198 201 20820820 A population-based cohort study for the risk factors of HCC among hepatitis B virus mono-infected subjects in Japan. Several factors at baseline (male, smoking, alanine aminotransferase, the positivity of HBe antigen and HB core-related antigen, the proportion of HBV DNA >= 5 log copies/mL, T1753V mutation, and A1762T/G1764A double mutation) were significantly associated with HCC among HBV mono-infected subjects. 2011 Journal of gastroenterology Abstract HBV G1764A;A1762T;T1753V 203;196;175 209;202;181 C;C 107;88 111;91 Hepatocellular carcinoma 262 265 20843617 [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors]. AIM: To screen hepatitis B virus (HBV) genotypes and associated basal core promoter (BCP; T1762A/A1764) and precore (PC; A1896) mutations among the 100 HBV surface antigen (HBsAg) positive voluntary blood donors in France. 2011 Pathologie-biologie Abstract HBV T1762A 90 96 BCP;BCP;Precore;S;Precore;S 64;85;117;173;108;156 83;88;119;178;115;163 20843617 [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors]. As HBV infected blood donors were more often asymptomatic carriers, we could speculate that the G1896A mutation may favour the asymptomatic state, supporting previous observations. 2011 Pathologie-biologie Abstract HBV G1896A 96 102 HBV infections 3 15 20843617 [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors]. Three methods were used to detect G1896A mutation: non-commercial real-time PCR (PCRTR , line probe assay (InnoLiPA HBV PreCore, INNOGENETICS( )) and direct sequencing of precore gene. 2011 Pathologie-biologie Abstract HBV G1896A 34 40 Precore;Precore 120;171 127;178 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1896A mutation appears to be independent of infection history. 2010 BMC infectious diseases Abstract HBV G1896A 0 6 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1896A mutation seemed to be involved in liver disease progression independent of the patient age (OR = 3.6, 95% CI: 1.5-8.6; P = 0.004). 2010 BMC infectious diseases Abstract HBV G1896A 0 6 Liver disease 41 54 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Moreover, G1776A mutation was shown to contribute to HBeAg negativity in our study (OR = 8.6, 95% CI: 1.2-44.9; P = 0.01). 2010 BMC infectious diseases Abstract HBV G1776A 10 16 C 53 58 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. The top three multi-mutations were A1762T/G1764A (36%), A1762T/G1764A/G1896A (11%) and T1753(A/C)/A1762T/G1764A/G1896A (8%). 2010 BMC infectious diseases Abstract HBV G1764A;G1764A;G1896A;A1762T;G1764A;G1896A;A1762T;A1762T;T1753A;T1753C 42;63;70;98;105;112;35;56;87;87 48;69;76;104;111;118;41;62;97;97 20857959 Antiviral activity of various 1-(2'-deoxy-beta-D-lyxofuranosyl), 1-(2'-fluoro-beta-D-xylofuranosyl), 1-(3'-fluoro-beta-D-arabinofuranosyl), and 2'-fluoro-2',3'-didehydro-2',3'-dideoxyribose pyrimidine nucleoside analogues against duck hepatitis B virus (DHBV) and human hepatitis B virus (HBV) replication. Intriguingly, 25, 39, 48, and 49 retained sensitivity against lamivudine-resistant HBV containing a single mutation (M204I) and 48 emerged as an effective inhibitor of drug-resistant HBV with an EC(50) of 4.1 muM. 2010 Journal of medicinal chemistry Abstract HBV M204I 117 122 20872711 Mutation pattern of lamivudine resistance in relation to hepatitis B genotypes: hepatitis B genotypes differ in their lamivudine resistance associated mutation pattern. Furthermore, the rtL180M mutation is significantly connected to the rtM204V mutation in genotypes A, B, and C, respectively. 2010 Journal of medical virology Abstract HBV L180M;M204V 19;70 24;75 RT;RT 17;68 19;70 20872711 Mutation pattern of lamivudine resistance in relation to hepatitis B genotypes: hepatitis B genotypes differ in their lamivudine resistance associated mutation pattern. Future studies will need to evaluate whether this will translate into genotype-specific differences in resistance emergence on either entecavir or telbivudine as these antivirals differ in their mutation profile, rtM204V for entecavir and rtM204I for telbivudine. 2010 Journal of medical virology Abstract HBV M204V;M204I 215;241 220;246 RT;RT 213;239 215;241 20872711 Mutation pattern of lamivudine resistance in relation to hepatitis B genotypes: hepatitis B genotypes differ in their lamivudine resistance associated mutation pattern. The literature data revealed that genotype A favors the rtM204V mutation unlike the other major genotypes (P<0.001), which corresponds to a significant difference in the mutation pattern of genotypes endemic in Asian countries and those found in the rest of the world. 2010 Journal of medical virology Abstract HBV M204V 58 63 RT 56 58 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. A similar analysis of ten additional less well-characterized resistance mutations demonstrated a significant association with N(t)RTI treatment for four of the mutations: L82M, S85A, A200V, and Q215S. 2010 Antiviral research Abstract HBV L82M;S85A;A200V;Q215S 171;177;183;194 175;181;188;199 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Among the 10 well-characterized N(t)RTI-resistance mutations, L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were significantly associated with treatment with lamivudine, an l-nucleoside analog, and A181S/T/V and N236T were significantly associated with treatment with adefovir, an acyclic nucleoside phosphonate. 2010 Antiviral research Abstract HBV L80I;L80V;V173L;L180M;A181T;T184S;S202G;M204I;M204V;A181S;A181T;A181V;N236T 62;62;70;77;84;91;98;108;108;206;206;206;220 68;68;75;82;89;96;103;115;115;215;215;215;225 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. Although the S domain is present in all three envelope proteins, the I110M, G119E, and R169P mutations impair virion secretion through the small envelope protein. 2010 Journal of virology Abstract HBV I110M;G119E;R169P 69;76;87 74;81;92 S;S;S 46;13;139 54;14;153 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. Conversely, coexpression of just the small envelope protein of the M133T mutant could rescue virion secretion. 2010 Journal of virology Abstract HBV M133T 67 72 S 37 51 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. Destroying this site by N131Q/T mutation or preventing glycosylation by tunicamycin treatment of transfected cells abrogated the effect of the M133T mutation. 2010 Journal of virology Abstract HBV N131Q;N131T;M133T 24;24;143 31;31;148 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. Here we used transcomplementation assay to confirm that the I110M, G119E, and R169P mutations in the S domain of viral envelope proteins impair virion secretion and that an M133T mutation rescues virion secretion of the I110M and G119E mutants. 2010 Journal of virology Abstract HBV I110M;G119E;R169P;M133T;I110M;G119E 60;67;78;173;220;230 65;72;83;178;225;235 S;S 119;101 127;102 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. In fact, the M133T mutation creates a novel N-linked glycosylation site ((131)NST(133)). 2010 Journal of virology Abstract HBV M133T 13 18 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. The G119E mutation impaired detection of secreted hepatitis B surface antigen (HBsAg), suggesting immune escape. 2010 Journal of virology Abstract HBV G119E 4 9 S;S 79;62 84;69 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. The M133T mutation could also overcome the secretion defect caused by the G145R immune-escape mutation or mutation at N146, the site of N-linked glycosylation. 2010 Journal of virology Abstract HBV M133T;G145R 4;74 9;79 20881037 Impairment of hepatitis B virus virion secretion by single-amino-acid substitutions in the small envelope protein and rescue by a novel glycosylation site. The R169P mutant protein is defective in HBsAg secretion as well and has a dominant negative effect when it is coexpressed with wild-type envelope proteins. 2010 Journal of virology Abstract HBV R169P 4 9 Envelope;S 138;41 146;46 20881176 Hepatitis B virus (HBV) subgenotypes C2 and B2 differ in lamivudine- and adefovir-resistance-associated mutational patterns in HBV-infected Chinese patients. The incidence of adefovir-resistant mutations was similar between the two subsets, but HBV/C2 inclined to show rtA181V (3.6% for C2 versus 0.9% for B2; P<0.01), while HBV/B2 inclined to show rtN236T (4.5% for versus 2.5% for C2; P<0.01). 2010 Journal of clinical microbiology Abstract HBV A181V;N236T 113;193 118;198 RT;RT 111;191 113;193 20881176 Hepatitis B virus (HBV) subgenotypes C2 and B2 differ in lamivudine- and adefovir-resistance-associated mutational patterns in HBV-infected Chinese patients. The incidence of lamivudine-resistant mutations was significantly higher in HBV/C2 compared to HBV/B2 (27.9% versus 19.8%; P<0.01), and the significant difference was observed only for rtM204I and not rtM204V. 2010 Journal of clinical microbiology Abstract HBV M204I;M204V 187;203 192;208 RT;RT 185;201 187;203 20887378 Impact of hepatitis B e antigen-suppressing mutations on the replication efficiency of entecavir-resistant hepatitis B virus strains. In rtS202G mutants (plus lamivudine resistance), addition of either PC or BCP mutations moderately enhanced the reduced replication, without reaching WT HBV levels. 2011 Journal of viral hepatitis Abstract HBV S202G 5 10 BCP;Precore;RT 74;68;3 77;70;5 20887378 Impact of hepatitis B e antigen-suppressing mutations on the replication efficiency of entecavir-resistant hepatitis B virus strains. In rtS202I or rtT184G mutants, PC and BCP mutations did not significantly improve viral fitness. 2011 Journal of viral hepatitis Abstract HBV S202I;T184G 5;16 10;21 BCP;Precore;RT;RT 38;31;3;14 41;33;5;16 20887378 Impact of hepatitis B e antigen-suppressing mutations on the replication efficiency of entecavir-resistant hepatitis B virus strains. Our data demonstrate that HBeAg-suppressing PC or BCP mutations cannot restore the strongly reduced replicative capacity of ETV-resistant HBV mutants to WT level, although they moderately increase replication of rtS202G combination mutants. 2011 Journal of viral hepatitis Abstract HBV S202G 214 219 BCP;C;Precore;RT 50;26;44;212 53;31;46;214 20887378 Impact of hepatitis B e antigen-suppressing mutations on the replication efficiency of entecavir-resistant hepatitis B virus strains. To comprehensively analyse the impact of PC or BCP mutations on viral replication of ETV-resistant HBV mutants, replication-competent HBV constructs were generated harbouring lamivudine resistance (rtM204V/rtL180M, rtM204I) plus ETV resistance (rtS202G, rtS202I or rtT184G) on wild-type (WT)-, PC- and BCP-backgrounds. 2011 Journal of viral hepatitis Abstract HBV M204V;L180M;M204I;S202G;S202I;T184G 200;208;217;247;256;267 205;213;222;252;261;272 BCP;BCP;Precore;Precore;RT;RT;RT;RT;RT;RT 47;302;41;294;198;206;215;245;254;265 50;305;43;296;200;208;217;247;256;267 20927588 Initial virological response and viral mutation with adefovir dipivoxil added to ongoing Lamivudine therapy in Lamivudine-resistant chronic hepatitis B. The lower pretreatment HBV DNA level and virus-containing mutations other than double mutation of rtL180M + rtM204V were significantly associated with IVR (P=0.002 and P=0.014, respectively). 2011 Digestive diseases and sciences Abstract HBV L180M;M204V 100;110 105;115 RT;RT 98;108 100;110 20932594 Evolution of hepatitis B genotype C viral quasi-species during hepatitis B e antigen seroconversion. 0.02, p = 0.0036) that coincided with the dynamics of quasi-species possessing A1762T mutation. 2011 Journal of hepatology Abstract HBV A1762T 79 85 20937597 A classification model for G-to-A hypermutation in hepatitis B virus ultra-deep pyrosequencing reads. For example, two of the most common hepatitis B virus (HBV) reverse transcriptase (RT) drug-resistance mutations, A181T and M204I, arise from G A changes and are routinely detected as low-abundance variants in nearly all HBV deep sequencing samples. 2010 Bioinformatics (Oxford, England) Abstract HBV A181T;M204I 114;124 119;129 RT;RT 60;83 81;85 20937597 A classification model for G-to-A hypermutation in hepatitis B virus ultra-deep pyrosequencing reads. The 2.9% of sequence reads that were classified as hypermutated by our model included most of the reads with A181T and/or M204I, indicating the usefulness of this model for distinguishing viral adaptive changes from host-mediated viral editing. 2010 Bioinformatics (Oxford, England) Abstract HBV A181T;M204I 109;122 114;127 20944991 Hepatitis B genotype G and high frequency of lamivudine-resistance mutations among human immunodeficiency virus/hepatitis B virus co-infected patients in Brazil. In 10 patients with viremia, LAM-resistance mutations in the polymerase gene (rtL180M + rtM204V and rtV173L + rtL180M + rtM204V) were found, accompanied by changes in the envelope gene (sI195M, sW196L and sI195M/sE164D). 2010 Memorias do Instituto Oswaldo Cruz Abstract HBV E164D;L180M;M204V;V173L;L180M;M204V;I195M;I195M;W196L 212;80;90;102;112;122;205;186;194 218;85;95;107;117;127;211;192;200 S;P;RT;RT;RT;RT;RT;S;S;S;S 171;61;78;88;100;110;120;186;194;205;212 179;71;80;90;102;112;122;187;195;206;213 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. However, in Huh7 cells stably expressing WT or the mutated HBc proteins (L60V, S87G or I97L), IFN-alpha could inhibit the extra- and intracellular HBV DNA level and HBsAg secretion to a similar level compared to that in cells transfected with control plasmids. 2010 Virology journal Abstract HBV L60V;S87G;I97L 73;79;87 77;83;91 C;S 59;165 62;170 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In conclusion, HBc protein with I97L mutation may play an special role in suppressing the transcription of MxA gene. 2010 Virology journal Abstract HBV I97L 32 36 C 15 18 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In this study, we investigated whether HBc protein mutations at hot spots (L60V, S87G and I97L) could still inhibit MxA transcription and the potential significance of this inhibition in virus replication in vitro. 2010 Virology journal Abstract HBV L60V;S87G;I97L 75;81;90 79;85;94 C 39 42 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Moreover, the inhibitory effect on MxA gene transcription by the WT or mutated HBc proteins (L60V, S87G and I97L) has no impact on inhibition of HBV replication by IFN-alpha in Huh7 cells. 2010 Virology journal Abstract HBV L60V;S87G;I97L 93;99;108 97;103;112 C 79 82 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Our data indicated that the IFN-induced MxA mRNA expression level and MxA promoter activity was significantly down-regulated by mutant protein of HBc(I97L), compared to WT and the other two mutated HBc proteins(L60V or S87G). 2010 Virology journal Abstract HBV I97L;L60V;S87G 150;211;219 154;215;223 C;C 146;198 149;201 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. A1762T/G1764A had a moderate sensitivity and specificity for HCC. 2011 The American journal of gastroenterology Abstract HBV G1764A;A1762T 7;0 13;6 Hepatocellular carcinoma 61 64 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. A1846T and T1674C/G are novel factors independently associated with cirrhosis and HCC, respectively. 2011 The American journal of gastroenterology Abstract HBV A1846T;T1674C;T1674G 0;11;11 6;19;19 Liver cirrhosis;Hepatocellular carcinoma 68;82 77;85 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. Age, abnormal ALT, HBV DNA (>=10(4) copies/ml), genotype C, C1653T, T1674C/G, T1753V, and A1762T/G1764A were independently associated with HCC compared with those without HCC. 2011 The American journal of gastroenterology Abstract HBV G1764A;A1762T;C1653T;T1674C;T1674G;T1753V 97;90;60;68;68;78 103;96;66;76;76;84 Hepatocellular carcinoma;Hepatocellular carcinoma 139;171 142;174 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. C1673T, A1726C, A1727T, C1730G, C1766T, T1768A, C1773T, and C1799G in genotype C were significantly associated with cirrhosis compared with the CHB patients, whereas these mutations were inversely associated with HCC compared with the cirrhosis patients. 2011 The American journal of gastroenterology Abstract HBV C1673T;A1726C;A1727T;C1730G;C1766T;T1768A;C1773T;C1799G 0;8;16;24;32;40;48;60 6;14;22;30;38;46;54;66 Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 116;144;213;235 125;147;216;244 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. CONCLUSIONS: C1673T, A1726C, A1727T, C1730G, C1766T, T1768A, C1773T, and C1799G in genotype C are specific for cirrhosis. 2011 The American journal of gastroenterology Abstract HBV C1673T;A1726C;A1727T;C1730G;C1766T;T1768A;C1773T;C1799G 13;21;29;37;45;53;61;73 19;27;35;43;51;59;67;79 Liver cirrhosis 111 120 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. Multivariate regression analyses showed that age, male, abnormal alanine aminotransferase (ALT), T1768A, A1762T/G1764A, and A1846T were independently associated with cirrhosis compared with ASCs and the patients with CHB. 2011 The American journal of gastroenterology Abstract HBV G1764A;A1762T;T1768A;A1846T 112;105;97;124 118;111;103;130 Liver cirrhosis;Chronic Hepatitis B 166;217 175;220 20959817 Association between the various mutations in viral core promoter region to different stages of hepatitis B, ranging of asymptomatic carrier state to hepatocellular carcinoma. T1674C/G, C1653T, and T1753V were specific for HCC. 2011 The American journal of gastroenterology Abstract HBV T1674C;T1674G;C1653T;T1753V 0;0;10;22 8;8;16;28 Hepatocellular carcinoma 47 50 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. Application of MboII PRA to samples from 241 Korean patients with chronic liver diseases of different clinical stages confirmed that F141L mutants were significantly related to HCC, even in comparison to liver cirrhosis (HCC, 26.3% of patients, or 26/99; liver cirrhosis, 3.8% of patients, or 2/52; P = 0.001). 2011 Journal of virology Abstract HBV F141L 133 138 Hepatocellular carcinoma;Liver cirrhosis;Hepatocellular carcinoma;Liver cirrhosis 177;204;221;255 180;219;224;270 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. By studying stable cell lines, we found that F141L-LHBs could induce cell cycle progression by downregulating the p53 and p21 pathways and upregulating CDK4 and cyclin A. 2011 Journal of virology Abstract HBV F141L 45 50 S 51 55 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. Furthermore, we found that in a colony-forming assay, the colony-forming rates in cell lines expressing F141L-LHBs were about twice as high as those of the wild type. 2011 Journal of virology Abstract HBV F141L 104 109 S 110 114 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. Here, we describe a novel HCC-related pre-S2 mutation, F141L. 2011 Journal of virology Abstract HBV F141L 55 60 PreS2 38 44 Hepatocellular carcinoma 26 29 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. In conclusion, our results suggest that F141L-LHBs may contribute importantly to the pathogenesis of HCC by inducing cell proliferation and transformation. 2011 Journal of virology Abstract HBV F141L 40 45 S 46 50 Hepatocellular carcinoma 101 104 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. So, the F141L mutation examined in this study could serve as a diagnostic marker for the prognosis of HCC. 2011 Journal of virology Abstract HBV F141L 8 13 Hepatocellular carcinoma 102 105 20962085 Novel F141L pre-S2 mutation in hepatitis B virus increases the risk of hepatocellular carcinoma in patients with chronic genotype C infections. To prove the relationship between the F141L mutation and HCC, molecular epidemiology studies using MboII PCR restriction analysis (PRA) were performed, and the molecular mechanism was investigated through construction of a stable hepatocyte cell line expressing the large surface HB protein (LHB) with the F141L mutation (F141L-LHB). 2011 Journal of virology Abstract HBV F141L;F141L;F141L 38;306;322 43;311;327 S;S;S 266;292;328 279;295;331 Hepatocellular carcinoma 57 60 20970466 Characterization of hepatitis virus B isolated from a multi-drug refractory patient. A precore stop codon mutation of G1896A and basic core promoter (BCP) mutations A1762T/G1764A were detected in a majority of clones. 2011 Virus research Abstract HBV G1764A;A1762T;G1896A 87;80;33 93;86;39 BCP;BCP;Precore 44;65;2 63;68;9 20970466 Characterization of hepatitis virus B isolated from a multi-drug refractory patient. In the core (C) antigen region, a mutation at codon 135 (cP135Q) was detected in 100% of clones. 2011 Virus research Abstract HBV P135Q 57 63 C;C;C 13;57;7 14;58;11 20970466 Characterization of hepatitis virus B isolated from a multi-drug refractory patient. Lamivudine (LAM)-resistant mutations, rtL180M and rtM204V/I were detected in 86.4% of clones. 2011 Virus research Abstract HBV L180M;M204V;M204I 40;52;52 45;59;59 RT;RT 38;50 40;52 20970466 Characterization of hepatitis virus B isolated from a multi-drug refractory patient. Several novel mutations, such as rtT128N, rtA222T, rtS256G, rtL271M, rtS332R, and rtN/T337D, were present in a majority of clones. 2011 Virus research Abstract HBV N337D;T337D;T128N;A222T;S256G;L271M;S332R 84;84;35;44;53;62;71 91;91;40;49;58;67;76 RT;RT;RT;RT;RT;RT 33;42;51;60;69;82 35;44;53;62;71;84 20970466 Characterization of hepatitis virus B isolated from a multi-drug refractory patient. Three mutations in the surface (S) antigen region, sC76Y, sP120T and sI195M, were detected in 100%, 100% and 77.3% of the clones, respectively. 2011 Virus research Abstract HBV C76Y;P120T;I195M 51;58;69 56;64;75 S;S;S;S;S 32;51;58;69;23 33;52;59;70;30 21056552 Variable influence of mutational patterns in reverse-transcriptase domain on replication capacity of hepatitis B virus isolates from antiviral-experienced patients. Compared to wild-type counterpart, mutant rtL217P produced 1.98-fold higher replicative intermediate level, and mutant rtM204I+rtL217P increased the replicative intermediate level to 1.20 fold. 2011 Clinica chimica acta; international journal of clinical chemistry Abstract HBV L217P;M204I;L217P 44;121;129 49;126;134 RT;RT;RT 42;119;127 44;121;129 21056552 Variable influence of mutational patterns in reverse-transcriptase domain on replication capacity of hepatitis B virus isolates from antiviral-experienced patients. CONCLUSIONS: The study offers a practical measurement assay and novel information for replication features of mutant strains; especially, rtL217P substitution likely represents an energetic replication-compensatory mutation. 2011 Clinica chimica acta; international journal of clinical chemistry Abstract HBV L217P 140 145 RT 138 140 21056552 Variable influence of mutational patterns in reverse-transcriptase domain on replication capacity of hepatitis B virus isolates from antiviral-experienced patients. Other mutational patterns (rtV173M, rtA181S/V, rtM204I, rtQ215H, rtL229M, rtN238H, rtV84M+rtA181S+rtM204I, rtV84M+rtM204I, rtA181S+rtM204I, rtA181V+rtL229M, rtQ215H+rtN238H) reduced viral replication capacity to different extents. 2011 Clinica chimica acta; international journal of clinical chemistry Abstract HBV V173M;A181S;A181V;M204I;Q215H;L229M;N238H;V84M;V84M;A181S;A181V;Q215H;A181S;M204I;M204I;M204I;L229M;N238H 29;38;38;49;58;67;76;85;109;125;142;159;92;100;116;133;150;167 34;45;45;54;63;72;81;89;113;130;147;164;97;105;121;138;155;172 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 27;36;47;56;65;74;83;90;98;107;114;123;131;140;148;157;165 29;38;49;58;67;76;85;92;100;109;116;125;133;142;150;159;167 21063480 A case-control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma. By multiple logistic regression analysis, the presence of cirrhosis, A1762T/G1764A and G1899A mutations were independently associated with the risk of HCC. 2010 Hepatology international Abstract HBV G1764A;A1762T;G1899A 76;69;87 82;75;93 Liver cirrhosis;Hepatocellular carcinoma 58;151 67;154 21063480 A case-control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma. CONCLUSION: These data suggested that A1762T/G1764A and G1899A mutations were associated with the development of HCC in Thai patients. 2010 Hepatology international Abstract HBV G1764A;A1762T;G1899A 45;38;56 51;44;62 Hepatocellular carcinoma 113 116 21063480 A case-control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma. No significant difference between groups was found with respect to G1613A, C1653T, C1766T/T1768A, A1846T/C, T1858C, and G1896A mutations. 2010 Hepatology international Abstract HBV T1768A;C1766T;G1613A;C1653T;A1846T;A1846C;T1858C;G1896A 90;83;67;75;98;98;108;120 96;89;73;81;106;106;114;126 21063480 A case-control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma. RESULTS: The prevalence of T1753C/A, A1762T/G1764A and G1899A mutations were significantly higher in the HCC group compared to the non-HCC group (43.3 vs. 2010 Hepatology international Abstract HBV G1764A;A1762T;T1753C;T1753A;G1899A 44;37;27;27;55 50;43;35;35;61 Hepatocellular carcinoma;Hepatocellular carcinoma 105;135 108;138 21063484 Occult hepatitis B in blood donors in Indonesia: altered antigenicity of the hepatitis B virus surface protein. Seven of the viremic samples had nucleotide substitutions (A521G, A551T, C582T, and A562G) in the S gene, causing amino acid mutations (T123A, M133L, and T143M) in the 'a' determinant of HBsAg that resulted in changes in the predicted antigenicity. 2010 Hepatology international Abstract HBV A521G;A551T;C582T;A562G;T123A;M133L;T143M 59;66;73;84;136;143;154 64;71;78;89;141;148;159 S;S;S 169;187;98 183;192;99 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Findings in this study emphasize the significance of variant T143M, the prevalent isolate with highest degree of antigenicity changes found in Indonesian blood donors. 2010 Virology journal Abstract HBV T143M 61 66 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In the pattern T143M, changes in antigenic index were more significant, both in its coverage and magnitude, even when compared to variant T143L. 2010 Virology journal Abstract HBV T143M;T143L 15;138 20;143 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. RESULTS: Three HBV variants (T123A, M133L and T143M) and a wild type sequence were analyzed together with frequently emerged variants T123N, M133I, M133T, M133V, and T143L. 2010 Virology journal Abstract HBV T123A;M133L;T143M;T123N;M133I;M133T;M133V;T143L 29;36;46;134;141;148;155;166 34;41;51;139;146;153;160;171 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. These data were also partially supported by the tertiary structure prediction, in which the pattern T143M showed larger shift in the HBsAg second loop structure compared to the others. 2010 Virology journal Abstract HBV T143M 100 105 S 133 138 21104161 Association of novel mutations and haplotypes in the preS region of hepatitis B virus with hepatocellular carcinoma. As compared with the HBV-infected subjects without HCC, C2875T, G2946C, A3054C, C3060A, T3066C, C3116T, A3120C, G3191A, A1C, C7A, C10A, A31C, C76T, G105C, and G147C in both genotypes were significantly associated with increased risks of HCC. 2010 Frontiers of medicine in China Abstract HBV C2875T;G2946C;A3054C;C3060A;T3066C;C3116T;A3120C;G3191A;A31C;C76T;G105C;G147C;C7A;C10A;A1C 56;64;72;80;88;96;104;112;136;142;148;159;125;130;120 62;70;78;86;94;102;110;118;140;146;153;164;128;134;123 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 51;237;21 54;240;33 21104161 Association of novel mutations and haplotypes in the preS region of hepatitis B virus with hepatocellular carcinoma. C2875A, G2950A, G2951A, A3054T, C3060T, T3066A, T3069G, A3120T, and G3191C were significantly associated with increased risks of HCC in genotype C, whereas these mutations were inversely associated with HCC in genotype B. 2010 Frontiers of medicine in China Abstract HBV C2875A;G2950A;G2951A;A3054T;C3060T;T3066A;T3069G;A3120T;G3191C 0;8;16;24;32;40;48;56;68 6;14;22;30;38;46;54;62;74 Hepatocellular carcinoma;Hepatocellular carcinoma 129;203 132;206 21104161 Association of novel mutations and haplotypes in the preS region of hepatitis B virus with hepatocellular carcinoma. Multivariate regression analyses showed that C76A/T was a novel factor independently associated with an increased risk of HCC, as compared with those without HCC. 2010 Frontiers of medicine in China Abstract HBV C76A;C76T 45;45 51;51 Hepatocellular carcinoma;Hepatocellular carcinoma 122;158 125;161 21108338 A matched case-control study of hepatitis B virus mutations in the preS and core promoter regions associated independently with hepatocellular carcinoma. Conclusively, A2962G and T105C are novel factors associated independently with HCC. 2011 Journal of medical virology Abstract HBV A2962G;T105C 14;25 20;30 Hepatocellular carcinoma 79 82 21108338 A matched case-control study of hepatitis B virus mutations in the preS and core promoter regions associated independently with hepatocellular carcinoma. Multivariate analyses established that genotype C (adjusted odds ratio [AOR] = 3.3; 95% confidence interval [CI] = 1.1-9.8), viral load (>=10(4) copies/ml) (AOR = 2.4; 95% CI = 1.0-5.8), A2962G (AOR = 18.7; 95% CI = 7.5-46.7), preS2 start codon mutation (AOR = 12.5; 95% CI = 3.4-45.5), C105T (AOR = 0.1; 95% CI = 0.0-0.2), T1753V (AOR = 3.1; 95% CI = 1.1-9.2), and A1762T/G1764A (AOR = 2.9; 95% CI = 1.1-7.3) were associated independently with HCC, adjusted for factors including mutations in both regions. 2011 Journal of medical virology Abstract HBV G1764A;A1762T;A2962G;C105T;T1753V 373;366;187;287;324 379;372;193;292;330 PreS2 227 232 Hepatocellular carcinoma 445 448 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. In contrast, Th1/Th2 cytokines producing T cells remained lower in one patient detected with adefovir dipivoxil resistant HBV A181T/V mutation. 2010 Mediators of inflammation Abstract HBV A181T;A181V 126;126 133;133 21149924 Profile of HBV antiviral resistance mutations with distinct evolutionary pathways against nucleoside/nucleotide analogue treatment among Chinese chronic hepatitis B patients. rtM204 mutations (27 rtM204I, 15 rtM204V and 5 rtM204I/V cases) were detected at the highest frequency among 65 mutants (72.30% [47/65]) and found to display 16 combination mutation patterns, in which rtM204I and rtM204V were significantly associated with rtL80I/V and rtL180M, respectively (P<0.01). 2010 Antiviral therapy Abstract HBV M204I;M204V;M204I;M204V;M204I;M204V;L80I;L80V;L180M 23;35;49;49;203;215;258;258;271 28;40;56;56;208;220;264;264;276 RT;RT;RT;RT;RT;RT;RT;RT 0;21;33;47;201;213;256;269 2;23;35;49;203;215;258;271 21159112 Prevention of lamivudine-resistant hepatitis B recurrence after liver transplantation with entecavir plus tenofovir combination therapy and perioperative hepatitis B immunoglobulin only. A 48-year-old male patient with hepatitis B-induced decompensated liver cirrhosis initially improved on lamivudine (LAM) until LAM resistance (rtL180M and rtM204V) emerged followed by renewed decompensation. 2011 Transplant infectious disease Abstract HBV L180M;M204V 145;157 150;162 RT;RT 143;155 145;157 Liver cirrhosis 66 81 21168854 Human interleukin-10 genotypes are associated with different precore/core gene mutation patterns in children with chronic hepatitis B virus infection. C2189A mutation carriers are associated with more viral load decrement from tolerance to inflammatory phase (P = .01) and earlier spontaneous HBeAg seroconversion (P = .01). 2011 The Journal of pediatrics Abstract HBV C2189A 0 6 C 142 147 21168854 Human interleukin-10 genotypes are associated with different precore/core gene mutation patterns in children with chronic hepatitis B virus infection. CONCLUSIONS: The G/G genotype at the IL-10 -1082 polymorphism is associated with higher C2189A mutations, lower HBV viral load at immune inflammatory phase, and earlier spontaneous HBeAg seroconversion than A allele carriers. 2011 The Journal of pediatrics Abstract HBV C2189A 88 94 C 181 186 21168854 Human interleukin-10 genotypes are associated with different precore/core gene mutation patterns in children with chronic hepatitis B virus infection. RESULTS: HBV precore/core gene mutation increased significantly more in the inflammatory phase than in the tolerance phase (G1896A, 76.2% versus 4.8%; C1913A, 33.3% versus 0%; C2189A, 28.6% versus 4.8%; G2304A, 52.4% versus 14.3%) in study group (n = 21) but not the control group (n = 9). 2011 The Journal of pediatrics Abstract HBV G1896A;C1913A;C2189A;G2304A 124;151;176;203 130;157;182;209 C;Precore 21;13 25;20 21168854 Human interleukin-10 genotypes are associated with different precore/core gene mutation patterns in children with chronic hepatitis B virus infection. Subjects with the G/G genotype at the IL-10-1082 polymorphism site had higher C2189A mutation rate than the A allele carriers (P = .02). 2011 The Journal of pediatrics Abstract HBV C2189A 78 84 21177673 Detection of hepatitis B virus genotype A3 and primary drug resistance mutations in African immigrants with chronic hepatitis B in Spain. Interestingly, the lamivudine resistance mutation rtM204V was found in two Africans (6.9%), one infected with HBV-A3 and the other with HBV-E. 2011 The Journal of antimicrobial chemotherapy Abstract HBV M204V 52 57 RT 50 52 21181915 Presence of valine at position 27 of the hepatitis B virus core gene is associated with severe liver inflammation in Chinese patients. In summary, this is the first data showing an association between a specific amino acid mutation (I27V) and severe liver inflammation in patients with chronic hepatitis B. 2011 Journal of medical virology Abstract HBV I27V 98 102 Liver inflammation;Chronic Hepatitis B 115;151 133;170 21181915 Presence of valine at position 27 of the hepatitis B virus core gene is associated with severe liver inflammation in Chinese patients. The frequency of the I27V mutation in the HBV core gene, which produces a core 18-27 peptide capable of binding HLA-A*02, was compared in Chinese patients with severe liver inflammation (n = 77, including 39 with acute-on-chronic liver failure), moderate liver inflammation (n = 44) and inactive disease (n = 45). 2011 Journal of medical virology Abstract HBV I27V 21 25 C;C 46;74 50;78 Liver inflammation;Acute on chronic liver failure;Liver inflammation 167;213;255 185;243;273 21181917 Molecular characterization of hepatitis B virus isolates from Zimbabwean blood donors. Forty-four percent of the Zimbabwean HBV isolates (11/23) were characterized by a G1862C missense mutation, which causes a Val to Leu amino acid substitution at position 17 of the precore region. 2011 Journal of medical virology Abstract HBV G1862C;V17L 82;123 88;172 Precore 180 187 21181918 Molecular epidemiology of chronic hepatitis B virus infection in Greece. Some of the most common mutations occurred at amino acid positions 129, 133, 134, 144, 145, including the "vaccine escape" mutation G145R. 2011 Journal of medical virology Abstract HBV G145R 132 137 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. A1762T/G1764A double mutation rate was 40.0% (18/45), 84.4% (38/45), 73.5% (36/49) and 92.6% (25/27) respectively in different groups. 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 7;0 13;6 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. CONCLUSION: A1762T/G1764A double mutation has a close relationship with the progress of HBV-infection diseases, but is not specific to patients with ACLF. 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 19;12 25;18 HBV infections;Acute on chronic liver failure 88;149 110;153 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. HBV DNA level (log) of patients with A1762T/G1764A double mutation was 5.68 +/- 1.36, lower than but having no significant statistic difference compared to patients without the double mutation (6.14 +/- 1.81, P = 0.075). 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 44;37 50;43 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. However, A1762T/G1764A double mutation rate has no difference between ACLF based on CHB and LC (P = 0.502) and between patients with HBeAg positive and negative (P = 0.735). 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 16;9 22;15 C 133 138 Acute on chronic liver failure;Chronic Hepatitis B;Liver cirrhosis 70;84;92 74;87;94 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. METHODS: HBV BCP A1762T/G1764A double mutation was detected in 166 HBV chronic infection patients by nested PCR and direct DNA sequencing. 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 24;17 30;23 BCP 13 16 Chronic HBV infection 67 88 21186523 [Analysis the relationship of HBV BCP A1762T/G1764A double mutation with HBV related acute on chronic liver failure]. OBJECTIVE: To analysis the relationship between HBV BCP A1762T/G1764A double mutation with acute on chronic liver failure (ACLF). 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV G1764A;A1762T 63;56 69;62 BCP 52 55 Acute on chronic liver failure;Liver disease 123;91 127;121 21186533 [Occult HBV infection in patients with anti-HBc positive alone]. Point mutations within "a" determinant with Q129R/P mutations and co-existence of the mutant type and wild type were found in the two samples. 2010 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV Q129R;Q129P 44;44 51;51 21199523 The clinical implications of hepatitis B virus genotype: Recent advances. HBV genotype C has a higher frequency of basal core promoter (BCP) A1762T/G1764A mutation, pre-S deletion and is associated with higher viral load than genotype B. 2011 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T 74;67 80;73 BCP;BCP;PreS 41;62;91 60;65;96 21199523 The clinical implications of hepatitis B virus genotype: Recent advances. Similarly, genotype D has a higher prevalence of BCP A1762T/G1764A mutation than genotype A. 2011 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T 60;53 66;59 BCP 49 52 21212756 Viral factors and outcomes of chronic HBV infection. The most common core promoter mutations involve a double substitution A1762T and G1764A (TA). 2011 The American journal of gastroenterology Abstract HBV A1762T;G1764A 70;81 76;87 Core promoter 16 29 21264860 Gender disparity in distribution of the major hydrophilic region variants of hepatitis B virus genotype C according to hepatitis B e antigen serostatus. In addition, 2 mutation types (L110I and G145A) related to HBeAg serostatus were found. 2011 Journal of medical virology Abstract HBV L110I;G145A 31;41 36;46 C 59 64 21311107 HBV core region variability: effect of antiviral treatments on main epitopic regions. Codons 74 and 77 were the most polymorphic, and the double change E64D-N67T was significantly observed. 2011 Antiviral therapy Abstract HBV E64D;N67T 66;71 75;75 21311172 Antiviral resistance mutations and genotype-associated amino acid substitutions in treatment-naive hepatitis B virus-infected individuals from the Indian subcontinent. RESULTS: An adefovir-related rtI233V mutation was identified in 4 subjects. 2012 Intervirology Abstract HBV I233V 31 36 RT 29 31 21311172 Antiviral resistance mutations and genotype-associated amino acid substitutions in treatment-naive hepatitis B virus-infected individuals from the Indian subcontinent. The rtS213T lamivudine and entecavir refractory mutant was presented in 3 individuals. 2012 Intervirology Abstract HBV S213T 6 11 RT 4 6 21323729 Natural history of chronic hepatitis B REVEALed. A significant association with risk of cirrhosis and HCC was also observed for HBV genotype, precore G1896A mutant and basal core promoter A1762T/G1764A double mutant. 2011 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T;G1896A 146;139;101 152;145;107 BCP;Precore 119;93 138;100 Liver cirrhosis;Hepatocellular carcinoma 39;53 48;56 21325784 Hepatitis B virus core protein variations differ in tumor and adjacent nontumor tissues from patients with hepatocellular carcinoma. The most frequently occurring mutations in rank were codon P130T (38.8%), I97L (37.8%) and S87G (23.5%). 2012 Intervirology Abstract HBV P130T;I97L;S87G 59;74;91 64;78;95 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Further studies on in vitro replication fitness with the complete genome of HBV isolates displaying or not Y100C substitution may elucidate whether this mutation affects HBV replication and consequently HBsAg production. 2011 Hepatitis research and treatment Abstract HBV Y100C 107 112 S 203 208 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Small hepatitis B virus surface protein (S-HBsAg) variant Y100C has been associated with HBsAg-negative phenotype. 2011 Hepatitis research and treatment Abstract HBV Y100C 58 63 S;S;S 89;41;24 94;48;31 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. To determine whether Y100C substitution yields impaired HBsAg or small amounts of HBsAg that may reduce HBsAg detection by commercial anti-HBsAg antibodies, two eukaryotic expression plasmids, one containing a wild-type S and the other an S gene from a Y100C variant, were constructed and their levels of HBsAg compared by ELISA after transfection of HuH7 cells. 2011 Hepatitis research and treatment Abstract HBV Y100C;Y100C 21;253 26;258 S;S;S;S;S;S;S 56;82;104;139;305;220;239 61;87;109;144;310;221;240 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Unexpectedly, the extracellular HBsAg levels detected with Y100C plasmid were higher than those observed with the wild-type plasmid, but without statistical significance. 2011 Hepatitis research and treatment Abstract HBV Y100C 59 64 S 32 37 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. We concluded that the Y100C substitution alone did not play a role in reducing HBsAg amounts or HBsAg affinity by commercial ELISA assay. 2011 Hepatitis research and treatment Abstract HBV Y100C 22 27 S;S 79;96 84;101 21360549 Impact of universal vaccination on intrafamilial transmission of hepatitis B virus. Sequence analysis of S and pre-S genes showed that HBV isolates of HBsAg-positive vaccinees were variants; no G145R but G145A and other substitutions were found. 2011 Journal of medical virology Abstract HBV G145R;G145A 110;120 115;125 S;S;PreS 21;67;27 22;72;32 21368417 Identification of recombinant intermediates of hepatitis B virus between genotype B and C in vitro. Isolate R2 recombinant intermediate had a break point at nt1740-1 838, and 3 bases changed in different nucleic acid sites: from A to T at nt1740, from C to T at nt1753, and from G to A at nt1838, respectively. 2011 Zhong nan da xue xue bao. Yi xue ban Abstract HBV A1740T;C1753T;G1838A 129;152;179 145;168;195 21368417 Identification of recombinant intermediates of hepatitis B virus between genotype B and C in vitro. Isolate R3 recombinant intermediate had a break point at nt2443-2483, and 4 bases changed in different nucleic acid sites: from C to T at nt2443, from A to G at nt2452, from T to C at nt2480, and from C to T at nt2483, respectively. 2011 Zhong nan da xue xue bao. Yi xue ban Abstract HBV C2443T;A2452G;T2480C;C2483T 128;151;174;201 144;167;190;217 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Double mutations rtM204I and rtL180M were detected more frequently in genotype C than in genotype B virus, and patients infected with this mutant had higher alanine transaminase levels than those infected with mutant containing the rtM204I substitution alone. 2011 Journal of viral hepatitis Abstract HBV M204I;L180M;M204I 19;31;234 24;36;239 RT;RT;RT 17;29;232 19;31;234 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Multidrug-resistant HBV strains were identified in eight patients, including two novel strains with mutational patterns rtL180M + A181V + S202G + M204V + N236T and rtL180M + S202G + M204V + N236T. 2011 Journal of viral hepatitis Abstract HBV L180M;L180M;A181V;S202G;M204V;N236T;S202G;M204V;N236T 122;166;130;138;146;154;174;182;190 127;171;135;143;151;159;179;187;195 RT;RT 120;164 122;166 21396961 HBV DNA replication mediated by cloned patient HBV reverse transcriptase genes from HBV genotypes A-H and its use in antiviral phenotyping assays. Recombinants expressing patient derived RT genes containing the rtL180M+M204V lamivudine resistance (LAM-R) mutations demonstrated a LAM-R phenotype. 2011 Journal of virological methods Abstract HBV L180M;M204V 66;72 71;77 RT;RT 40;64 42;66 21396961 HBV DNA replication mediated by cloned patient HBV reverse transcriptase genes from HBV genotypes A-H and its use in antiviral phenotyping assays. Similarly, patient derived RT genes containing the adefovir resistance (ADV-R) mutations rtA181V or rtN236T demonstrated an ADV-R phenotype. 2011 Journal of virological methods Abstract HBV A181V;N236T 91;102 96;107 RT;RT;RT 27;89;100 29;91;102 21438026 Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival. This study examines the differential activities between wild-type Hepatitis B virus X protein (WtHBx) and a mutant HBx (MutHBx), which bears a hotspot mutation at nucleotides 1,762 and 1,764, resulting in a lysine to methionine change at codon 130 and a valine to isoleucine change at codon 131. 2011 Molecular carcinogenesis Abstract HBV K130M;V131I 207;254 247;294 X;X;X;X 115;97;123;84 118;100;126;85 21442057 Predictors for early HBeAg loss during lamivudine therapy in HBeAg-positive chronic hepatitis B patients with acute exacerbation. Compared to compensated patients, decompensated patients achieved a higher rate of HBeAg loss (25.8 vs. 14.3%; P = 0.0805) at 3 months of therapy, a higher rate of serum HBV DNA negativity (53.2 vs. 29.8%; P = 0.0042), and a lower rate of rtM204V/I mutation (3.2 vs. 16.7%; P = 0.0139) after 12 months of lamivudine therapy. 2010 Hepatology international Abstract HBV M204V;M204I 241;241 248;248 C;RT 83;239 88;241 21445929 Posttransplantation prophylaxis with primary high-dose hepatitis B immunoglobulin monotherapy and complementary preemptive antiviral add-on. The Gly145Arg mutation was found in 11 of 15 (73.3%) patients, whereas 25 of 71 (35.2%), 2 of 29 (6.9%), and 4 of 8 (50%) patients were resistant to lamivudine, adefovir, and entecavir, respectively. 2011 Liver transplantation Abstract HBV G145R 4 13 21455562 Characteristics of occult hepatitis B virus infection in the Solomon Islands. Most of the HBV-DNA-positive individuals were infected with wild-type HBV, and only 3 strains demonstrated specific amino acid substitutions (P121X, T123N, C138S, P142S and D144E) in the alpha determinant region. 2011 International journal of molecular medicine Abstract HBV P121X;T123N;C138S;P142S;D144E 142;149;156;163;173 147;154;161;168;178 S 187 204 21461076 Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection. In addition, the T1753V (p<0.001) and C1485T (p<0.001) mutations were significantly more prevalent in HCC patients than in chronic hepatitis patients. 2011 Gut and liver Abstract HBV T1753V;C1485T 17;38 23;44 Hepatocellular carcinoma;Chronic Hepatitis B 102;123 105;140 21461076 Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection. Only the prevalence of the T1753V mutation increased as the HBV infection progressed from liver cirrhosis to HCC (p=0.023). 2011 Gut and liver Abstract HBV T1753V 27 33 HBV infections;Liver cirrhosis;Hepatocellular carcinoma 60;90;109 73;105;112 21461076 Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection. RESULTS: Each of the mutations G1386M, C1485T, C1653T, T1753V, A1762T, and G1764A was significantly associated with the patient's clinical status. 2011 Gut and liver Abstract HBV A1762T;G1386M;C1485T;C1653T;T1753V;G1764A 63;31;39;47;55;75 69;37;45;53;61;81 21461076 Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection. Specific X gene mutations (G1386M, C1653T, and A1762T/G1764A) were more prevalent in patients with liver cirrhosis and HCC than in chronic hepatitis patients (p<0.005 for all). 2011 Gut and liver Abstract HBV G1764A;G1386M;C1653T;A1762T 54;27;35;47 60;33;41;53 X 9 10 Liver cirrhosis;Hepatocellular carcinoma;Chronic Hepatitis B 99;119;131 114;122;148 21461076 Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection. The T1753V (p<0.001) and A1762T/G1764A (p<0.001) mutations were found more frequently in Hepatitis B e antigen (HBeAg)-negative than in HBeAg-positive patients. 2011 Gut and liver Abstract HBV G1764A;A1762T;T1753V 32;25;4 38;31;10 C;C;C 101;112;136 110;117;141 21462295 Hepatitis B virus quasispecies in hepatic and extrahepatic viral reservoirs in liver transplant recipients on prophylactic therapy. An HBV lamivudine-resistant variant with an M204I mutation was identified in liver (70% and 18% of the clones) and plasma samples (100% of the clones), but a WT sequence was found in 70% and 100% of the PBMC clones. 2011 Liver transplantation Abstract HBV M204I 44 49 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. The precore (G1896A) and core promoter (A1762T, G1764A) mutations of the hepatitis B virus gene are known to be associated with changes in immunologic phase or the progression to complicated liver disease in adults. 2011 Journal of Korean medical science Abstract HBV G1896A;A1762T;G1764A 13;40;48 19;46;54 Core promoter;Precore 25;4 38;11 21480321 Randomized trial of lamivudine versus entecavir in entecavir-treated patients with undetectable hepatitis B virus DNA: outcome at 2 Years. Three patients (12%) had evidence of drug-resistant mutations, of which two patients had rtM204I mutation and one patient had rtM204V mutation. 2011 Hepatology (Baltimore, Md.) Abstract HBV M204I;M204V 91;128 96;133 RT;RT 89;126 91;128 21484144 A comparison of 48-week treatment efficacy between clevudine and entecavir in treatment-naive patients with chronic hepatitis B. Two (3.4%) patients in clevudine group showed virologic breakthrough with rtM204I mutation using direct sequencing analysis. 2011 Hepatology international Abstract HBV M204I 76 81 RT 74 76 21484148 Extended treatment with lamivudine and adefovir dipivoxil in chronic hepatitis B patients with lamivudine resistance. Fifty-two percent of Group A patients on combination treatment continued to have the M204V/I HBV mutation compared to 92% receiving lamivudine alone (p = 0.0013). 2011 Hepatology international Abstract HBV M204V;M204I 85;85 92;92 21485198 [The replication capacity and drug sensitivity of Adefovir dipivoxil-resistant HBV mutants in vivo]. The anti-ADV mutant HBV plasmid of rtA181V and rtN236T, prepared by Multi Site-Directed Mutagenesis Kit, was transferred into mice via the tail vein, and the levels of HBV-DNA replication were detected after Anti-HBV drugs treatment. 2011 Sheng wu yi xue gong cheng xue za zhi Abstract HBV A181V;N236T 37;49 42;54 RT;RT 35;47 37;49 21490166 Impact of hepatitis B virus (HBV) x gene mutations on hepatocellular carcinoma development in chronic HBV infection. The hepatitis B virus (HBV) PreS mutations C1653T, T1753V, and A1762T/G1764A were reported as a strong risk factor of hepatocellular carcinoma (HCC) in a meta-analysis. 2011 Clinical and vaccine immunology Abstract HBV G1764A;A1762T;C1653T;T1753V 70;63;43;51 76;69;49;57 PreS 28 32 Hepatocellular carcinoma;Hepatocellular carcinoma 118;144 142;147 21492508 [Efficacy and safety of lamivudine plus adefovir combination therapy and entecavir monotherapy for chronic hepatitis B patients]. Four patients in monotherapy cohort were found with virological breakthrough at 96 weeks and three cases among were confirmed to be of variants associated with ETV resistance (rtL180M + T184L + M204V). 2011 Zhonghua gan zang bing za zhi Abstract HBV L180M;T184L;M204V 178;186;194 183;191;199 RT 176 178 21494570 Geographical and ethnic distribution of the HBV C/D recombinant on the Qinghai-Tibet Plateau. The predominance of the premature pre-core stop mutation G1896A in patients with the HBV C/D recombinant may account for the higher prevalence of HBeAg in these patients. 2011 PloS one Abstract HBV G1896A 57 63 C;Precore 146;34 151;42 21494570 Geographical and ethnic distribution of the HBV C/D recombinant on the Qinghai-Tibet Plateau. Virologically HBV/CD1 had a significantly lower frequency of G1896A than HBV/C2. 2011 PloS one Abstract HBV G1896A 61 67 21502674 Molecular and serological characterization of occult hepatitis B infection in blood donors from Mexico. No precore stop codon 28 mutant (W28Stop) was identified among the analyzed HBV isolates. 2011 Annals of hepatology Abstract HBV W28X 33 40 Precore 3 10 21503905 Full genome characterization of hepatitis B virus strains from blood donors in Iran. One strain had a 2-amino acid (aa) insertion at position s111 and another sP120Q substitution suggesting a vaccine escape mutant. 2011 Journal of medical virology Abstract HBV P120Q 74 80 S;S 57;74 58;75 21503905 Full genome characterization of hepatitis B virus strains from blood donors in Iran. The double mutations A1762T/G1764A and G1764T/C1766G were found in 20.7% and 24.1% of the strains, respectively. 2011 Journal of medical virology Abstract HBV G1764A;C1766G;A1762T;G1764T 28;46;21;39 34;52;27;45 21503905 Full genome characterization of hepatitis B virus strains from blood donors in Iran. The molecular analysis of the individual genes revealed that the G1896A mutation was present in 86.2% of the strains and in 26 strains (29.9%) this mutation was accompanied by the G1899A mutation. 2011 Journal of medical virology Abstract HBV G1896A;G1899A 65;180 71;186 21503906 Clinical course and predictive factors of virological response in long-term lamivudine plus adefovir dipivoxil combination therapy for lamivudine-resistant chronic hepatitis B patients. Breakthrough hepatitis occurred in three patients without complete viral response and with poor response to the preceding LAM monotherapy, and rtA181A/V substitution was detected in one of the three patients. 2011 Journal of medical virology Abstract HBV A181A;A181V 145;145 152;152 RT 143 145 Fulminant Hepatitis B 0 22 21503912 T1846 and A/G1913 are associated with acute on chronic liver failure in patients infected with hepatitis B virus genotypes B and C. The results of longitudinal study showed that C53T, A1846T, and G1896A were the most common mutations in association with ACLF. 2011 Journal of medical virology Abstract HBV C53T;A1846T;G1896A 46;52;64 50;58;70 Acute on chronic liver failure 122 126 21503942 Emergence of hepatitis B virus S gene mutants in patients experiencing hepatitis B surface antigen seroconversion after peginterferon therapy. In patient 1, an sT125A mutant developed during the HBsAg-negative stage and constituted 11.2% of the viral population. 2011 Hepatology (Baltimore, Md.) Abstract HBV T125A 17 23 S;S 52;17 57;18 21503942 Emergence of hepatitis B virus S gene mutants in patients experiencing hepatitis B surface antigen seroconversion after peginterferon therapy. In patient 2, an sW74* truncation mutation was found during the HBsAg-negative stage and constituted 83.1% of the viral population. 2011 Hepatology (Baltimore, Md.) Abstract HBV W74X 17 22 S;S 64;17 69;18 21513743 Detection of lamivudine- or adefovir-resistant hepatitis B virus mutations by a liquid array. A novel polymerase chain reaction (PCR)-Luminex assay was developed for rapid, accurate, and high-throughput detection of the most important hepatitis B virus (HBV) variants, including those with reverse transcriptase (RT) domain L180M, M204I/V, A181T/V/S, I233V and N236T mutations associated with resistance to lamivudine (LAM) or adefovir (ADV). 2011 Journal of virological methods Abstract HBV L180M;M204I;M204V;A181T;A181V;A181S;I233V;N236T 230;237;237;246;246;246;257;267 235;244;244;255;255;255;262;272 RT;RT 196;219 217;221 21520137 Analysis of carriers of hepatitis B virus from a tertiary referral hospital: does the viral load change during the natural course of infection? Of the 40 HBV DNA-positive cases, 8 had precore/core mutations, [G1896A (10%), T2066A (12.5%), T2050C (10%), and G1888A (7.5%)]. 2011 Journal of medical virology Abstract HBV G1896A;T2066A;T2050C;G1888A 65;79;95;113 71;85;101;119 C;Precore 48;40 52;47 21562108 Ultrasensitive quantification of hepatitis B virus A1762T/G1764A mutant by a SimpleProbe PCR using a wild-type-selective PCR blocker and a primer-blocker-probe partial-overlap approach. Hepatitis B virus (HBV) carrying the A1762T/G1764A double mutation in the basal core promoter (BCP) region is associated with HBe antigen seroconversion and increased risk of liver cirrhosis and hepatocellular carcinoma (HCC). 2011 Journal of clinical microbiology Abstract HBV G1764A;A1762T 44;37 50;43 BCP;BCP;C 74;95;126 93;98;129 Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma 175;195;221 190;219;224 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations occurred in 40/166(24.1%) chronic hepatitis B patients. 2011 Virology journal Abstract HBV A336C;A336T;T337C;A336C;A336T 6;6;12;0;0 11;11;17;7;7 Chronic Hepatitis B 55 74 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. BACKGROUND: A336C/A336T/T337C variations in HBV core gene were demonstrated to relate to the decreases in serum HBV DNA levels and HBV replication in chronic hepatitis B patients. 2011 Virology journal Abstract HBV T337C;A336C;A336T 24;12;12 29;17;17 C 48 52 Chronic Hepatitis B 150 169 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. CONCLUSION/SIGNIFICANCE: A336C/A336T/T337C were naturally occurring polymorphisms in HBV core gene, and moreover, the presence of C336/T336/C337 variants was first demonstrated to be an independent factor associating with spontaneous HBeAg loss in chronic hepatitis B patients. 2011 Virology journal Abstract HBV T337C;A336C;A336T 37;25;25 42;30;30 C;C 89;234 93;239 Chronic Hepatitis B 248 267 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. The aim of the present study was to investigate whether there was correlation between A336C/A336T/T337C variations and spontaneous HBeAg loss METHODOLOGY/PRINCIPAL FINDINGS: A modified PCR-RFLP assay and ELISA were adopted to determine A336C/A336T/T337C variations and serum HBeAg levels in chronic hepatitis B patients without any antiviral therapy, respectively, whereas G1896A variation and HBV genotype were detected using Taqman-PCR assay. 2011 Virology journal Abstract HBV A336C;A336T;T337C;T337C;A336C;A336T;G1896A;A336C;A336T 92;92;98;248;236;236;373;86;86 97;97;103;253;241;241;379;91;91 C;C 131;275 136;280 Chronic Hepatitis B 291 310 21601012 Molecular characterization and phylogenetic analysis of full-genome HBV subgenotype D3 sequences from Serbia. All three isolates have two very rare nucleotide substitutions, A929T and T150A, which indicate the same ancestor. 2011 Infection, genetics and evolution Abstract HBV A929T;T150A 64;74 69;79 21640384 Hepatitis B genotypes/subgenotypes and MHR variants among Moroccan chronic carriers. The global prevalence of MHR variants was 15% (20/134) with substitution P120T/S the most frequent (3.7%, 5/134). 2011 The Journal of infection Abstract HBV P120T;P120S 73;73 80;80 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. BACKGROUND: Hepatitis B virus (HBV) precore G1896A mutation is associated with Hepatitis B e antigen (HBeAg) seroconversion. 2011 Journal of clinical virology Abstract HBV G1896A 44 50 C;C;Precore 91;102;36 100;107;43 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. OBJECTIVES: (1) To develop a reliable and ultrasensitive assay for the quantification of HBV G1896A and/or G1899A mutants. 2011 Journal of clinical virology Abstract HBV G1896A;G1899A 93;107 99;113 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. This mutation and the adjacent G1899A mutation also appear to associate with increased risk of hepatocellular carcinoma. 2011 Journal of clinical virology Abstract HBV G1899A 31 37 Hepatocellular carcinoma 95 119 21671883 Detection of hepatitis B virus variants in HBV monoinfected and HBV/HIV coinfected Iranian patients under lamivudine treatment. Moreover, several mutations (sP105A, sI110S/L, sS136Y and sP127T/L) with significant differences in the frequency were identified in the S region of both cohorts. 2011 Current HIV research Abstract HBV P105A;I110S;I110L;S136Y;P127T;P127L 29;37;37;47;58;58 35;45;45;53;66;66 S;S;S;S;S 29;37;47;58;137 30;38;48;59;138 21671883 Detection of hepatitis B virus variants in HBV monoinfected and HBV/HIV coinfected Iranian patients under lamivudine treatment. While no resistance mutation was detected in HBV/HIV coinfected cohort, LAM-resistance mutations (rtM204I/V in YMDD and rtL180M in FLLA polymerase motifs) were identified in 30% (9 out of 30) and 16.66% (5 out of 30) of HBV monoinfected patients (P<0.05). 2011 Current HIV research Abstract HBV M204I;M204V;L180M 100;100;122 107;107;127 P;RT;RT;P 136;98;120;111 146;100;122;115 HBV-HIV coinfections 45 63 21685535 De novo activation of HBV with escape mutations from hepatitis B surface antibody after living donor liver transplantation. Sequence analysis revealed mutations in the common 'a' determinant region of the surface gene, including G145R, G145A and Q129P, in HBsAg. 2011 Antiviral therapy Abstract HBV G145R;G145A;Q129P 105;112;122 110;117;127 S;S;S 52;132;81 66;137;88 21685546 HBV primary drug resistance in newly diagnosed HIV-HBV-coinfected individuals in Spain. Drug-resistant mutations in the HBV polymerase were found in four (5.5%) patients: two harboured rtL180M, one rtL80V and one rtV173L. 2011 Antiviral therapy Abstract HBV L180M;L80V;V173L 99;112;127 104;116;132 P;RT;RT;RT 36;97;110;125 46;99;112;127 21686872 Polymorphism rtQ215H in primary resistance to adefovir dipivoxil in hepatitis B virus infection: a case report. Finally, we also report that rtQ215H is responsive to tenofovir. 2009 BMJ case reports Abstract HBV Q215H 31 36 RT 29 31 21686872 Polymorphism rtQ215H in primary resistance to adefovir dipivoxil in hepatitis B virus infection: a case report. Virological evaluations showed two well-known LAM-related mutations (rtL180M and rtM204I) in addition to reverse-transcriptase rtQ215H. 2009 BMJ case reports Abstract HBV L180M;M204I;Q215H 71;83;129 76;88;134 RT;RT;RT;RT 105;69;81;127 126;71;83;129 21692935 Large-scale survey of naturally occurring HBV polymerase mutations associated with anti-HBV drug resistance in untreated patients with chronic hepatitis B. Four patients had the rtI233V mutation that may reduce sensitivity to adefovir, and three patients had the rtM250L/V mutation typical of entecavir resistance. 2011 Journal of viral hepatitis Abstract HBV I233V;M250L;M250V 24;109;109 29;116;116 RT;RT 22;107 24;109 21692935 Large-scale survey of naturally occurring HBV polymerase mutations associated with anti-HBV drug resistance in untreated patients with chronic hepatitis B. HBV mutations associated with antiviral drug resistance were detected in 13 (5%) patients: three patients infected with HBV genotype C had the rtM204V + rtL180M mutations associated with lamivudine (LMV) resistance. 2011 Journal of viral hepatitis Abstract HBV M204V;L180M 145;155 150;160 RT;RT 143;153 145;155 21692935 Large-scale survey of naturally occurring HBV polymerase mutations associated with anti-HBV drug resistance in untreated patients with chronic hepatitis B. LMV compensatory mutations rtL80V and rtV173L were seen in two and one patients, respectively. 2011 Journal of viral hepatitis Abstract HBV L80V;V173L 29;40 33;45 RT;RT 27;38 29;40 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. The rtA194T mutation in association with lamivudine resistance may confer resistance to TDF, although both in vivo and in vitro studies regarding this mutation demonstrate conflicting results. 2009 Infection and drug resistance Abstract HBV A194T 6 11 RT 4 6 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. A mixture of lamivudine-resistant genotype A2 HBV strains harboring the rtM204V mutation coexisted in the patient following viral breakthrough to lamivudine. 2011 BMC infectious diseases Abstract HBV M204V 74 79 RT 72 74 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. At the end of the 14-year follow up period, high viral loads were predominant, with viral strains harboring the lamivudine-resistance signature rtL180M+M204V. 2011 BMC infectious diseases Abstract HBV L180M;M204V 146;152 151;157 RT 144 146 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The L180M+M204V dominant mutant displayed strong lamivudine-resistance. 2011 BMC infectious diseases Abstract HBV L180M;M204V 4;10 9;15 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The precore/core frame A1762T and G1764A double mutation was detected before treatment and remaining in this condition during the entire follow-up. 2011 BMC infectious diseases Abstract HBV A1762T;G1764A 23;34 29;40 C;Precore 12;4 16;11 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. METHODS: We constructed a series of HBx mutants with changes in the CP region that correspond to A1762T/G1764A (TA), T1753A, T1768A, or a combination of these (combo) and expressed them, along with wild-type HBx under control of its endogenous promoter, in primary human hepatocytes (PHHs) and HepG2 cells. 2011 Gastroenterology Abstract HBV G1764A;A1762T;T1753A;T1768A 104;97;117;125 110;103;123;131 Core promoter;X;X 68;36;208 70;39;211 21723325 Development and validation of a hepatitis B virus DNA sequencing assay for assessment of antiviral resistance, viral genotype and surface antigen mutation status. The escape mutation sG145R in the surface antigen was identified in 0.8% of patient samples. 2011 Journal of virological methods Abstract HBV G145R 20 26 S;S 20;34 21;41 21734806 Long-term effects of lamivudine treatment in Japanese chronic hepatitis B patients. AIM: To analyze the association between the emergence of tyrosine-methionine-asparatate-asparatate (YMDD) mutants (reverse transcription; rtM204I/V) and deterioration of liver function during long-term lamivudine treatment of Japanese patients with chronic hepatitis B virus (HBV) infection. 2011 World journal of gastroenterology Abstract HBV M204I;M204V 140;140 147;147 RT;RT;P 115;138;100 136;140;104 Chronic HBV infection 249 290 21739444 Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. In conclusion, CHB patients with genotype B, G1896A, and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. 2011 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 64;57;45 70;63;51 Chronic Hepatitis B 15 18 21739444 Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. In genotype B patients, the A1762T/G1764A, A1846T, and G1896A mutations were significantly more prevalent in patients with acute-on-chronic liver failure than CHB (50.7% vs. 2011 Journal of medical virology Abstract HBV G1764A;A1762T;A1846T;G1896A 35;28;43;55 41;34;49;61 Acute on chronic liver failure;Chronic Hepatitis B 123;159 153;162 21739444 Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. In multivariate analysis, the risk factors for acute-on-chronic liver failure were genotype B, A1762T/G1764A, and G1896A. 2011 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 102;95;114 108;101;120 Acute on chronic liver failure 47 77 21739444 Hepatitis B virus genotype B with G1896A and A1762T/G1764A mutations is associated with hepatitis B related acute-on-chronic liver failure. Therefore, HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure. 2011 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 58;51;40 64;57;46 Acute on chronic liver failure 169 199 21743991 Antiviral drug resistance testing in patients with chronic hepatitis B. The detection of rtA181V/I resulted in decision changes in most hepatologists, with the preferred treatment switching from tenofovir to entecavir. 2012 Digestive diseases and sciences Abstract HBV A181V;A181I 19;19 26;26 RT 17 19 21775451 Hepatitis B virus genotype C isolates with wild-type core promoter sequence replicate less efficiently than genotype B isolates but possess higher virion secretion capacity. The A1762T/G1764A core promoter mutations were prevalent in genotype C isolates and correlated with increased replication capacity, while the A1752G/T mutation frequently found in genotype B isolates correlated with a low replication capacity. 2011 Journal of virology Abstract HBV G1764A;A1762T;A1752G;A1752T 11;4;142;142 17;10;150;150 Core promoter 18 31 21775451 Hepatitis B virus genotype C isolates with wild-type core promoter sequence replicate less efficiently than genotype B isolates but possess higher virion secretion capacity. We propose that the low intracellular levels of viral DNA and core protein of wild-type genotype C delay immune clearance and trigger the subsequent emergence of A1762T/G1764A core promoter mutations to upregulate replication; efficient virion secretion compensates for the low replication capacity to ensure the establishment of persistent infection by genotype C. 2011 Journal of virology Abstract HBV G1764A;A1762T 169;162 175;168 C;Core promoter 62;176 66;189 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. CONCLUSIONS: The rtL180M mutation of HBV, as well as a small decrease in HBV-DNA after 1 year of treatment might be closely associated with frequent occurrence of virological resistance to ADV in patients with LAM-resistant CHB. 2012 Journal of gastroenterology and hepatology Abstract HBV L180M 19 24 RT 17 19 Chronic Hepatitis B 224 227 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. However, interestingly, patients carrying rtL180M experienced VB during ADV monotherapy more frequently than those not carrying rtL180M (2-year cumulative probability of VB: 37% vs 3% at 2 years, P < 0.01). 2012 Journal of gastroenterology and hepatology Abstract HBV L180M;L180M 130;44 135;49 RT;RT 42;128 44;130 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. On multivariate Cox proportional hazards analysis, rtL180M (hazard ratio [HR]: 8.62, 95% confidence interval: 1.08-69.09, P = 0.042) and decrease in HBV-DNA for 1 year of treatment (HR: 0.69, 95% CI: 0.51-0.95, P = 0.024) are independently associated with VB. 2012 Journal of gastroenterology and hepatology Abstract HBV L180M 53 58 RT 51 53 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. The rtL180M and rtL80V/I mutations were identified in 68% and 69%, respectively. 2012 Journal of gastroenterology and hepatology Abstract HBV L180M;L80V;L80I 6;18;18 11;24;24 RT;RT 4;16 6;18 21777282 rtL180M mutation of hepatitis B virus is closely associated with frequent virological resistance to adefovir dipivoxil therapy. There was no difference in the occurrence of VB with regard to types of YMDD mutation or rtL80V/I. 2012 Journal of gastroenterology and hepatology Abstract HBV L80V;L80I 91;91 97;97 RT;YMDD 89;72 91;76 21784687 Antiviral drug-associated potential vaccine-escape hepatitis B virus mutants in Turkish patients with chronic hepatitis B. RESULTS: Seven types of ADAPVEM were detected in the total CHB patients: rtM204V/sI195M, rtM204I/sW196S, rtM204I/sW196L, rtV173L/sE164D, rtA181T/sW172*, rtA181T/sW172L, and rtA181V/sL173F. 2011 International journal of infectious diseases Abstract HBV I195M;W196S;W196L;E164D;W172X;W172L;L173F;M204V;M204I;M204I;V173L;A181T;A181T;A181V 81;97;113;129;145;161;181;75;91;107;123;139;155;175 87;103;119;135;151;167;187;80;96;112;128;144;160;180 RT;RT;RT;RT;RT;RT;RT;S;S;S;S;S;S;S 73;89;105;121;137;153;173;81;97;113;129;145;161;181 75;91;107;123;139;155;175;82;98;114;130;146;162;182 Chronic Hepatitis B 59 62 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. While 5 nucleotides variation, and an 18 bp deletion of preS1 have been kept in during at least the first two years, C339T mutation occurring in the hydrophilic region of HBsAg and T770C that caused polymerase V560A substitution were the new point mutations found existing in sequenced clones of the 3rd time point. 2011 Hepatitis research and treatment Abstract HBV C339T;T770C;V560A 117;181;210 122;186;215 S;P;PreS1 171;199;56 176;209;61 21789847 [Variants and quasispecies of reverse transcriptase region in polymerase gene of hepatitis B virus during lamivudine treatment]. The rtL180M variant was found in association with the rtM204I/V variant, HBV variants and wild-type in YMDD motif all existed together in these two groups. 2011 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV L180M;M204I;M204V 6;56;56 11;63;63 RT;RT;P 4;54;103 6;56;107 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In summary, our results suggest the functional consequences of the hotspot G1613A mutation found in HBV. 2011 PloS one Abstract HBV G1613A 75 81 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Intriguingly, RFX1 binds to the G1613A mutant with higher affinity than the wild-type sequence, indicating that the mutation possesses the trans-activating effect to the core promoter via NRE. 2011 PloS one Abstract HBV G1613A 32 38 Core promoter 170 183 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Previously, we demonstrated that the G1613A mutation in the HBV negative regulatory element (NRE) is a hotspot mutation in HCC patients. 2011 PloS one Abstract HBV G1613A 37 43 Hepatocellular carcinoma 123 126 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. We showed that the G1613A mutation significantly suppresses the secretion of e antigen (HBeAg) and enhances the synthesis of viral DNA, which is in consistence to our clinical result that the G1613A mutation associates with high viral load in chronic HBV carriers. 2011 PloS one Abstract HBV G1613A;G1613A 19;192 25;198 C;C 77;88 86;93 Chronic Hepatitis B 243 254 21827734 Nucleotide change of codon 182 in the surface gene of hepatitis B virus genotype C leading to truncated surface protein is associated with progression of liver diseases. CONCLUSIONS: In the present study, we demonstrate that the sW182* of HBV could provide an important contribution to the progression of liver diseases, through molecular epidemiologic and in vitro studies. 2012 Journal of hepatology Abstract HBV W182X 59 65 S 59 60 Liver disease 135 149 21827734 Nucleotide change of codon 182 in the surface gene of hepatitis B virus genotype C leading to truncated surface protein is associated with progression of liver diseases. In addition, an in vitro study using cell lines stable expressing the S protein with sW182* also strongly supported its relationship with HCC. 2012 Journal of hepatology Abstract HBV W182X 85 91 S;S 70;85 71;86 Hepatocellular carcinoma 138 141 21827734 Nucleotide change of codon 182 in the surface gene of hepatitis B virus genotype C leading to truncated surface protein is associated with progression of liver diseases. In this study, novel nucleotide changes (sW182*) that result in a premature stop at codon 182 in the S gene of genotype C are investigated with regards to the development of HCC. 2012 Journal of hepatology Abstract HBV W182X 41 47 S;S 41;101 42;102 Hepatocellular carcinoma 174 177 21827734 Nucleotide change of codon 182 in the surface gene of hepatitis B virus genotype C leading to truncated surface protein is associated with progression of liver diseases. METHODS: A multi-probe real time PCR that enables rapid and reliable detection of sW182* was developed and applied to 292 DNA samples from Korean patients with diverse chronic liver diseases. 2012 Journal of hepatology Abstract HBV W182X 82 88 S 82 83 21827734 Nucleotide change of codon 182 in the surface gene of hepatitis B virus genotype C leading to truncated surface protein is associated with progression of liver diseases. RESULTS: sW182* was detected in a total of 73 patients out of the 275 with positive amplification (26.5%). 2012 Journal of hepatology Abstract HBV W182X 9 15 S 9 10 21831732 Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development. An exception is rtM204I, which can derive from a transition or a transversion. 2011 Digestive and liver disease Abstract HBV M204I 18 23 RT 16 18 21831732 Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development. Genotypes A and G are more prone to develop immune/diagnostic-escape mutations sT114R and sG130N. 2011 Digestive and liver disease Abstract HBV T114R;G130N 79;90 85;96 S;S 79;90 80;91 21831732 Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development. rtL80I/V-rtL180M-rtV173L), whilst most primary mutations (including rtM204V-rtA181T/V-rtI169T-rtA194T) are associated with low genetic barrier. 2011 Digestive and liver disease Abstract HBV L80I;L80V;M204V;L180M;V173L;A181T;A181V;I169T;A194T 2;2;70;11;19;78;78;88;96 8;8;75;16;24;85;85;93;101 RT;RT;RT;RT;RT;RT;RT 0;9;17;68;76;86;94 2;11;19;70;78;88;96 21831732 Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development. Vaccine-escape associated sT131N-mutation is a natural polymorphism in both A and G genotypes. 2011 Digestive and liver disease Abstract HBV T131N 26 32 S 26 27 21840251 Mutations in hepatitis B virus DNA from patients with coexisting HBsAg and anti-HBs. Interestingly, the basal core promoter (BCP) double mutations (A1762T/G1764A) in group I is significantly higher than those in group II as well. 2011 Journal of clinical virology Abstract HBV G1764A;A1762T 70;63 76;69 BCP;BCP 19;40 38;43 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. BACKGROUND: A recent study indicated that addition of the hepatitis B e antigen (HBeAg) precore (PC) or basal core promoter (BCP) mutations to wild-type HBV offset the reduced replication of the HBV polymerase rtA194T+-rtL180M+rtM204V mutations. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T;L180M;M204V 212;221;229 217;226;234 BCP;Precore;BCP;C;RT;RT;RT;C;P;Precore 104;97;125;70;210;219;227;81;199;88 123;99;128;79;212;221;229;86;209;95 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. CONCLUSIONS: PC or BCP mutations increased HBV DNA replication, offset the decreased replication by rtA194T alone, but they did not fully rescue the impaired replication conferred by other RT mutations as compared with wild-type. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T 102 107 BCP;Precore;RT;RT 19;13;100;189 22;15;102;191 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. METHODS: A plasmid containing a wild-type 1.3 genome length genotype D HBV laboratory strain was used as a parent for PC, BCP, rtA194T+-rtL180M+rtM204V, rtL180M+rtM204V and rtM204I mutants. 2011 Antiviral chemistry & chemotherapy Abstract HBV M204I;A194T;L180M;L180M;M204V;M204V 175;129;155;138;146;163 180;134;160;143;151;168 BCP;Precore;RT;RT;RT;RT;RT;RT 122;118;127;136;144;153;161;173 125;120;129;138;146;155;163;175 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. Regardless of the backbone, rtA194T+-rtL180M+rtM204V remained susceptible to tenofovir in vitro. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T;L180M;M204V 30;39;47 35;44;52 RT;RT;RT 28;37;45 30;39;47 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. rtA194T alone remained susceptible to lamivudine, while rtL180M+rtM204V and rtL180M+rtA194T+rtM204V were resistant. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T;L180M;L180M;M204V;A194T;M204V 2;58;78;66;86;94 7;63;83;71;91;99 RT;RT;RT;RT;RT;RT 0;56;64;76;84;92 2;58;66;78;86;94 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. rtA194T reduced replication by <40%, whereas rtL180M+rtM204V, rtL180M+rtA194T+rtM204V or rtM204I each reduced by >75% from their respective wild-type, PC or BCP genome backbone (P<0.05). 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T;M204I;L180M;L180M;M204V;A194T;M204V 2;91;47;64;55;72;80 7;96;52;69;60;77;85 BCP;Precore;RT;RT;RT;RT;RT;RT;RT 157;151;0;45;53;62;70;78;89 160;153;2;47;55;64;72;80;91 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. rtA194T was reportedly associated with tenofovir resistance. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T 2 7 RT 0 2 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. rtA194T+-rtL180M+rtM204V did not confer tenofovir resistance. 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T;L180M;M204V 2;11;19 7;16;24 RT;RT;RT 0;9;17 2;11;19 21860069 The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations. The enhanced replication by PC or BCP offset the reduction by rtA194T; however, the other reverse transcriptase (RT) mutations in PC or BCP backbones remained significantly lower than wild-type (P<0.05). 2011 Antiviral chemistry & chemotherapy Abstract HBV A194T 64 69 BCP;BCP;Precore;Precore;RT;RT;RT 34;136;28;130;90;62;113 37;139;30;132;111;64;115 21863638 [One-year combination therapy de novo of adefovir dipivoxil and lamivudine for decompensated cirrhosis related to HBV]. (3) Virological breakthrough occurred to none in observed group and three cases (16.67%) in control group, all of them were confirmed to be rtM204V variant in the following detection of direct sequencing. 2011 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV M204V 142 147 RT 140 142 21865669 Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. Additionally, the frequency of A1762T/G1764A mutations was higher in the HCC than the non-HCC group [82 (60.7%) versus 30 (22.2%), p < 0.001]. 2012 Intervirology Abstract HBV G1764A;A1762T 38;31 44;37 Hepatocellular carcinoma;Hepatocellular carcinoma 73;90 76;93 21865669 Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. CONCLUSIONS: HCC was associated with preS deletions and A1762T/G1764A mutations, and the combination of both mutations had a stronger association with HCC in Korean patients infected with HBV subgenotype C2. 2012 Intervirology Abstract HBV G1764A;A1762T 63;56 69;62 PreS 37 41 Hepatocellular carcinoma;Hepatocellular carcinoma 13;151 16;154 21865669 Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. For combined mutations, the odds ratio (OR) was highest in patients with both preS deletions and the A1762T/G1764A mutation, with 1 (0.7%) versus 11 (8.1%) patients (p = 0.005; OR 11.887). 2012 Intervirology Abstract HBV G1764A;A1762T 108;101 114;107 PreS 78 82 21865669 Combination of preS deletions and A1762T/G1764A mutations in HBV subgenotype C2 increases the risk of developing HCC. The prevalence of preS deletions and G1896A and A1762T/G1764A mutations was evaluated. 2012 Intervirology Abstract HBV G1764A;A1762T;G1896A 55;48;37 61;54;43 PreS 18 22 21871497 The main hepatitis B virus (HBV) mutants resistant to nucleoside analogs are susceptible in vitro to non-nucleoside inhibitors of HBV replication. Furthermore, the effect of a combination of either AT-61 or AT-130 with BAY41-4109, and the combination of these compounds with tenofovir was studied on wild type HBV as well as on a lamivudine and an adefovir-resistant mutant (rtL180M+M204V and rtN236T, respectively). 2011 Antiviral research Abstract HBV L180M;N236T;M204V 230;248;236 235;253;241 RT;RT 228;246 230;248 21871497 The main hepatitis B virus (HBV) mutants resistant to nucleoside analogs are susceptible in vitro to non-nucleoside inhibitors of HBV replication. HepG2 stable cell lines permanently expressing wild type (WT) HBV or the main HBV mutants resistant to lamivudine and/or adefovir (rtL180M+rtM204V, rtV173L+rtL180M+rtM204V, rtM204I, rtL180M+rtM204I, rtN236T, rtA181V, rtA181V+rtN236T, rtA181T, rtA181T+rtN236T) were treated with AT-61, AT-130 or BAY-41 4109. 2011 Antiviral research Abstract HBV L180M;M204V;V173L;L180M;M204V;M204I;L180M;M204I;N236T;A181V;A181V;N236T;A181T;A181T;N236T 133;141;150;158;166;175;184;192;201;210;219;227;236;245;253 138;146;155;163;171;180;189;197;206;215;224;232;241;250;258 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 131;139;148;156;164;173;182;190;199;208;217;225;234;243;251 133;141;150;158;166;175;184;192;201;210;219;227;236;245;253 21883736 Four-year follow-up of two chronic hepatitis B recipients of hepatitis B surface antigen-positive cadaveric liver grafts from asymptomatic carriers. HBV breakthrough occurred in one recipient at the month 12 post-OLT, with detectable serum HBV-DNA (740 copies/mL) and tyrosine-methionine-aspartate-aspartate motif mutation (rtM204I and rtM204V). 2011 Hepatology research Abstract HBV M204I;M204V 177;189 182;194 RT;RT;P 175;187;119 177;189;158 21911882 Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B. During ADV and LAM treatment, one patient developed ADV plus LAM resistance mutations (rtI163V+rtL180M+rtA181V+rtN236T), in this case, HBV strains harbouring polymerase mutations did not develop LAM associated rtM204V/I primary mutation. 2011 Annals of hepatology Abstract HBV M204V;M204I;I163V;L180M;A181V;N236T 212;212;89;97;105;113 219;219;94;102;110;118 P;RT;RT;RT;RT;RT 158;87;95;103;111;210 168;89;97;105;113;212 21911882 Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B. In addition, ETV resistance mutations (rtL180M+rtT184A+rtS202G+rtM204V) were detected in one patient. 2011 Annals of hepatology Abstract HBV L180M;T184A;S202G;M204V 41;49;57;65 46;54;62;70 RT;RT;RT;RT 39;47;55;63 41;49;57;65 21911882 Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B. RESULTS: Three patients developed LAM resistance mutations (2 presented rtM204I and one rtL180M+rtM204V/I) and one patient showed rtN236T ADV resistance mutation. 2011 Annals of hepatology Abstract HBV M204V;M204I;M204I;N236T;L180M 98;98;74;132;90 105;105;79;137;95 RT;RT;RT;RT 72;88;96;130 74;90;98;132 21915864 Lamivudine resistance mutations in European patients with hepatitis B and patients co-infected with HIV and hepatitis B. LAM substitution mutations L180M + M204V/I were found in six out of seven cases, with an accompanying V173L mutation in three cases. 2011 Journal of medical virology Abstract HBV L180M;M204V;M204I;V173L 27;35;35;102 32;42;42;107 21920388 Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs. Additionally, five polymorphic mutations, with a suggested role in drug resistance, were detected [rtQ215S (12.8%), rtI233V (4.3%), rtV214A (3.6%), rtV191I (0.7%), rtV207L (0.7%)]. 2011 Antiviral research Abstract HBV Q215S;I233V;V214A;V191I;V207L 101;118;134;150;166 106;123;139;155;171 RT;RT;RT;RT;RT 99;116;132;148;164 101;118;134;150;166 21920388 Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs. Amino acid changes at other six RT positions, potentially associated with resistance, were also analyzed (rtV84M-rtV191I-rtV207L-rtV214A-rtQ215S-rtI233V). 2011 Antiviral research Abstract HBV V84M;V191I;V207L;V214A;Q215S;I233V 108;115;123;131;139;147 112;120;128;136;144;152 RT;RT;RT;RT;RT;RT;RT 32;106;113;121;129;137;145 34;108;115;123;131;139;147 21920388 Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs. HBV reverse-transcriptase (RT) region was sequenced and analyzed for 20 mutations, confirmed by in vitro studies as associated with resistance to nucleos(t)ide HBV-RT inhibitors (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-rtM204V/I-rtN236T-rtM250V). 2011 Antiviral research Abstract HBV L80I;L80V;I169T;V173L;L180M;A181T;A181V;A181S;T184A;T184S;T184G;T184C;A194T;S202C;S202G;S202I;M204V;M204I;N236T;M250V 181;181;190;198;206;214;214;214;226;226;226;226;240;248;248;248;260;260;270;278 187;187;195;203;211;223;223;223;237;237;237;237;245;257;257;257;267;267;275;283 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 4;27;164;179;188;196;204;212;224;238;246;258;268;276 25;29;166;181;190;198;206;214;226;240;248;260;270;278 21920388 Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs. Notably, no YMDD mutations, namely rtM204V/I, were found. 2011 Antiviral research Abstract HBV M204V;M204I 37;37 44;44 RT;P 35;12 37;16 21920388 Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs. Overall, only 2/140 (1.4%) patients carried primary drug-resistance mutations [rtA181V (0.7%), and rtA194T (0.7%)], while 3/140 (2.1%) patients harbored the secondary mutations rtV173L (1.4%) and rtL180M (0.7%). 2011 Antiviral research Abstract HBV A181V;A194T;V173L;L180M 81;101;179;198 86;106;184;203 RT;RT;RT;RT 79;99;177;196 81;101;179;198 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. A highly sensitive amplification created restriction enzyme site (ACRES) method was devised to detect small amounts of the rtA181T mutant in the serum. 2011 BMC cancer Abstract HBV A181T 125 130 RT 123 125 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. BACKGROUND: Development of the hepatitis B virus (HBV) rtA181T/sW172* mutant could occur during prolonged lamivudine (LAM) therapy, conferring cross resistance to adefovir. 2011 BMC cancer Abstract HBV W172X;A181T 63;57 69;62 RT;S 55;63 57;64 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. CONCLUSIONS: Emergence of the rtA181T/sW172* mutant in LAM-resistant patients increased the risk of HCC development in the subsequent courses of antiviral therapy. 2011 BMC cancer Abstract HBV W172X;A181T 38;32 44;37 RT;S 30;38 32;39 Hepatocellular carcinoma 100 103 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. During the mean follow-up period of 26.2 +- 16.4 months (range 2 to 108 months), 3 of the 10 (30.0%) rtA181T-positive patients and 2 of the 113 (1.8%) rtA181T-negative patients developed hepatocellular carcinoma (HCC). 2011 BMC cancer Abstract HBV A181T;A181T 103;153 108;158 RT;RT 101;151 103;153 Hepatocellular carcinoma;Hepatocellular carcinoma 187;213 211;216 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Kaplan-Meier analysis indicated that the presence of rtA181T mutation (P < 0.001), age > 50 years (P = 0.001), and liver cirrhosis (P < 0.001) were significantly associated with subsequent occurrence of HCC. 2011 BMC cancer Abstract HBV A181T 55 60 RT 53 55 Liver cirrhosis;Hepatocellular carcinoma 115;203 130;206 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. RESULTS: By use of the highly sensitive ACRES method, the rtA181T mutant was detectable in 10 of the 123 LAM-resistant patients. 2011 BMC cancer Abstract HBV A181T 60 65 RT 58 60 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Virological factors including HBV-DNA level, genotype, precore G1896A, BCP A1762T/G1764A, rtM204I/V, rtA181T and pre-S internal deletion mutations as well as clinical variables including subsequent use of rescue drugs were submitted for outcome analysis. 2011 BMC cancer Abstract HBV G1764A;M204I;M204V;A181T;A1762T;G1896A 82;92;92;103;75;63 88;99;99;108;81;69 BCP;Precore;PreS;RT;RT 71;55;113;90;101 74;62;118;92;103 21941420 Virological response to adefovir monotherapy and the risk of adefovir resistance. RESULTS: At week 48 and 96, eight (10%) and 14 (18%) of 77 LAM-resistant patients developed the ADV-resistant strain (rtA181V/T and/or rtN236T mutations), respectively. 2011 World journal of gastroenterology Abstract HBV A181V;A181T;N236T 120;120;137 127;127;142 RT;RT 118;135 120;137 21950207 Prevalence of hepatitis B genotype and viral basic core promoter and precore mutations among teenagers in Macao: relationship with hepatocellular carcinoma development. The BCP/PreC mutations A1762T, G1764A, G1896A and C1766T were identified in 2.9-11.7% of subjects. 2011 British journal of biomedical science Abstract HBV A1762T;G1764A;G1896A;C1766T 23;31;39;50 29;37;45;56 BCP;Precore 4;8 7;12 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. The overall incidence rate of rtM204I mutation in genotype B (45.61%, 26/57) was more frequent than that in genotype C (20.59%, 7/34) (45.61% vs. 2011 Medical science monitor Abstract HBV M204I 32 37 RT 30 32 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. The pattern of rtM204I alone was predominantly observed (36.26%, 33/91), followed by rtM204V+rtL180M (23.08%, 21/91). 2011 Medical science monitor Abstract HBV M204I;M204V;L180M 17;87;95 22;92;100 RT;RT;RT 15;85;93 17;87;95 21998953 [The cloning, expression, purification and immunological identification of wild-type and mutant hepatitis B virus X gene in pGEX-6P-2 system]. Prokaryotic expression vectors pGEX-6P-2-hbvx(w) and pGEX-6P-2-hbvx(m) (A1762T/G1764A) were constructed and transformed to Trans1-blue; wild and mutant HBxAgs were expressed through IPTG induction respectively; after refolding of inclusion body, the wild and mutant HBxAgs were purified with GSTrap FF; and analysised by SDS-PAGE, Western blot and ELISA. 2011 Bing du xue bao Abstract HBV G1764A;A1762T 79;72 85;78 21998953 [The cloning, expression, purification and immunological identification of wild-type and mutant hepatitis B virus X gene in pGEX-6P-2 system]. The wild and mutant (A1762T/ G1764A) HBV X genes were amplified with polymerase chain reaction (PCR) from HBV genome were inserted into pGEX-6P-2 and confirmed by sequencing respectively. 2011 Bing du xue bao Abstract HBV A1762T;G1764A 21;29 27;35 X 41 42 21998953 [The cloning, expression, purification and immunological identification of wild-type and mutant hepatitis B virus X gene in pGEX-6P-2 system]. To settle the foundation for the future research on the influence of wild and mutant (A1762T/ G1764A) HBV X gene on the progress of chronic HBV infection and hepatic tumorigenicity, wild and mutant (A1762T/G1764A) HBxAgs expression system was constructed. 2011 Bing du xue bao Abstract HBV G1764A;A1762T;G1764A;A1762T 206;86;94;199 212;92;100;205 X 106 107 Chronic HBV infection 132 153 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Additionally, virion and hepatitis B surface antigen secretion of the rtS117F mutant was significantly impaired. 2012 The Journal of antimicrobial chemotherapy Abstract HBV S117F 72 77 RT;S 70;37 72;44 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. CONCLUSIONS: The rtS117F substitution served as a compensatory mutation for rtM204I. 2012 The Journal of antimicrobial chemotherapy Abstract HBV S117F;M204I 19;78 24;83 RT;RT 17;76 19;78 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Emergence of the rtS117F mutation in lamivudine-resistant patients carrying rtM204I was associated with increased hepatitis activities. 2012 The Journal of antimicrobial chemotherapy Abstract HBV S117F;M204I 19;78 24;83 RT;RT 17;76 19;78 Hepatitis 114 123 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Emergence of the rtS117F mutation was associated with an increase in hepatitis activity, whereas prior existence of the rtN124D mutation was associated with decompensated liver function upon development of the rtM204I mutation. 2012 The Journal of antimicrobial chemotherapy Abstract HBV S117F;N124D;M204I 19;122;212 24;127;217 RT;RT;RT 17;120;210 19;122;212 Hepatitis 69 78 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. METHODS: Of 83 lamivudine-resistant patients, 49 and 34 patients harboured the rtM204I and rtM204V mutations, respectively. 2012 The Journal of antimicrobial chemotherapy Abstract HBV M204I;M204V 81;93 86;98 RT;RT 79;91 81;93 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Prior existence of the rtN124D substitution was associated with liver decompensation upon development of the rtM204I mutation. 2012 The Journal of antimicrobial chemotherapy Abstract HBV N124D;M204I 25;111 30;116 RT;RT 23;109 25;111 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. RESULTS: Of the 49 patients carrying the rtM204I mutation, 5 subsequently developed an rtS117F substitution during the follow-up, whereas 4 harboured an rtN124D substitution prior to the development of the rtM204I mutation. 2012 The Journal of antimicrobial chemotherapy Abstract HBV M204I;S117F;N124D;M204I 43;89;155;208 48;94;160;213 RT;RT;RT;RT 41;87;153;206 43;89;155;208 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Site-directed mutagenesis experiments showed that the rtS117F mutation by itself did not confer lamivudine resistance but it compensated for replication deficiency of the rtM204I mutant in HepG2 and Mahlavu cells. 2012 The Journal of antimicrobial chemotherapy Abstract HBV S117F;M204I 56;173 61;178 RT;RT 54;171 56;173 22001270 Identification of hepatitis B virus rtS117F substitution as a compensatory mutation for rtM204I during lamivudine therapy. Such mutations have long been recognized for the rtM204V mutant, while little is known about any compensatory mutation specific to the rtM204I mutant. 2012 The Journal of antimicrobial chemotherapy Abstract HBV M204V;M204I 51;137 56;142 RT;RT 49;135 51;137 22007495 [Effect of Lamivudine on chronic hepatitis B patients with chemotherapy or immunosuppressive agents therapy and research the drug resistance]. The type of genotype mutation were all rtM204I. 2011 Sichuan da xue xue bao. Yi xue ban Abstract HBV M204I 41 46 RT 39 41 22012717 Clonal analysis of hepatitis B viruses among blood donors from Joinville, Brazil: evidence of dual infections, intragenotype recombination and markers of risk for hepatocellular carcinoma. One strain carried the F141L mutation, associated recently with increased risk of hepatocellular carcinoma. 2011 Journal of medical virology Abstract HBV F141L 23 28 Hepatocellular carcinoma 82 106 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A comparison of the nucleotide sequences of the HBV genome between HCC group 1 and non-HCC group 1 revealed that the prevalence of G1613A and C1653T mutations in the core promoter region was significantly higher in the HCC group. 2011 BMC cancer Abstract HBV G1613A;C1653T 131;142 137;148 Core promoter 166 179 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 67;219;87 70;222;90 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A single G1613A mutation was associated with future emergence of HCC. 2011 BMC cancer Abstract HBV G1613A 9 15 Hepatocellular carcinoma 65 68 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. CONCLUSIONS: G1613A and C1653T double mutations were frequently found in patients with HCC. 2011 BMC cancer Abstract HBV G1613A;C1653T 13;24 19;30 Hepatocellular carcinoma 87 90 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. Future emergence of HCC was associated with aging and the presence of a single G1613A mutation. 2011 BMC cancer Abstract HBV G1613A 79 85 Hepatocellular carcinoma 20 23 22037043 Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France. Precore G1896A HBV mutants were detected in both fatal fulminant primary HBV infections. 2012 Clinics and research in hepatology and gastroenterology Abstract HBV G1896A 8 14 Precore 0 7 HBV infections 73 87 22037043 Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France. The impact of the precore G1896A mutation on the severity of AHB deserves to be assessed in larger studies in this country. 2012 Clinics and research in hepatology and gastroenterology Abstract HBV G1896A 26 32 Precore 18 25 Acute Hepatitis B 61 64 22052677 Phenotypic assay of a hepatitis B virus strain carrying an rtS246T variant using a new strategy. Using this strategy, a phenotypic assay was performed on an HBV strain carrying an rtS246T variant isolated from a patient with chronic hepatitis B that was only responsive partially to entecavir therapy. 2012 Journal of medical virology Abstract HBV S246T 85 90 RT 83 85 Chronic Hepatitis B 128 147 22053371 [Identification the relationship between mutation patterns of rtM204I/V in the polymerase gene and genotypes of hepatitis B virus]. OBJECTIVE: To investigate the relationship between the mutation patterns of rtM204V/I (methionine to valine or isoleucine at position rt204 of reverse transcriptase domain) in hepatitis B virus (HBV) polymerase gene and HBV genotypes. 2011 Zhonghua gan zang bing za zhi Abstract HBV M204V;M204I 78;78 85;85 P;RT;RT;RT 200;143;76;134 210;164;78;136 22053371 [Identification the relationship between mutation patterns of rtM204I/V in the polymerase gene and genotypes of hepatitis B virus]. The rtM204V-rtL180M mutations were more frequently found in subgenotype B2 than in subgenotype C2 while the rtM204V-rtL180M-rtV173L mutations were more associated with subgenotype C2 (P < 0.01). 2011 Zhonghua gan zang bing za zhi Abstract HBV M204V;L180M;M204V;L180M;V173L 6;14;110;118;126 11;19;115;123;131 RT;RT;RT;RT;RT 4;12;108;116;124 6;14;110;118;126 22061616 Precore/core promoter mutations and hepatitis B virus genotype in hepatitis B and C dually infected patients treated with interferon-based therapy. Age (HR=1.068, P=0.020), G1896A mutation (HR=0.140, P=0.01) and A1846T mutation (HR=0.086, P=0.018) were associated with HBsAg seroclearance independently. 2012 Antiviral research Abstract HBV G1896A;A1846T 25;64 31;70 S 121 126 22061616 Precore/core promoter mutations and hepatitis B virus genotype in hepatitis B and C dually infected patients treated with interferon-based therapy. Among dually-infected patients, genotype C was associated with a higher frequency of A1762T/G1764A mutation (P<0.001), but with lower HBV DNA (P<0.001) and a lower frequency of A1752T/G (P=0.008), C1799G (P<0.001) and G1896A mutation (P<0.001) than genotype B. 2012 Antiviral research Abstract HBV G1764A;A1762T;A1752T;A1752G;C1799G;G1896A 92;85;177;177;197;218 98;91;185;185;203;224 22061616 Precore/core promoter mutations and hepatitis B virus genotype in hepatitis B and C dually infected patients treated with interferon-based therapy. Based on Cox proportional hazards model, young age (hazard ratio (HR)=0.952, P=0.001), sustained virological response to HCV (HR=4.638, P=0.044), C1766T mutation (HR=5.216, P=0.003) and A1846T mutation (HR=2.332, P=0.031) correlated with HBV DNA reactivation (>=2000IU/ml) after therapy. 2012 Antiviral research Abstract HBV C1766T;A1846T 146;186 152;192 22061616 Precore/core promoter mutations and hepatitis B virus genotype in hepatitis B and C dually infected patients treated with interferon-based therapy. Dually-infected patients had a higher prevalence of genotype C HBV (P=0.022) and a lower frequency of G1896A mutation (P=0.004) as compared with controls. 2012 Antiviral research Abstract HBV G1896A 102 108 22078148 Molecular characterization of a novel entecavir mutation pattern isolated from a multi-drug refractory patient with chronic hepatitis B infection. In this pattern, the S219A and Y245H mutations mainly seem to contribute to the emergence of ETV resistance. 2012 Journal of clinical virology Abstract HBV S219A;Y245H 21;31 26;36 22078148 Molecular characterization of a novel entecavir mutation pattern isolated from a multi-drug refractory patient with chronic hepatitis B infection. RESULTS: Dominance of a clone carrying L80LV, L91I, M204I, S219A, N238D, Y245H changes was detected in the last serum sample of the patient just before his death. 2012 Journal of clinical virology Abstract HBV L91I;M204I;S219A;N238D;Y245H 46;52;59;66;73 50;57;64;71;78 22082274 Antiviral resistance mutations potentiate HBV surface antigen-induced transcription of hfgl2 prothrombinase gene. Luciferase assay showed that the rtM204I/V mutant HBs could activate the transcription of hfgl2 promoter compared with the wild type HBs. 2011 Biochemistry. Biokhimiia Abstract HBV M204I;M204V 35;35 42;42 S;S;RT 50;133;33 53;136;35 22082274 Antiviral resistance mutations potentiate HBV surface antigen-induced transcription of hfgl2 prothrombinase gene. To investigate whether the nucleotide (nucleoside)-induced resistant mutations of HBs potentiate transcription of hfgl2 prothrombinase gene, we generated two mutant HB expression constructs harboring rtM204V/sI195M or rtM204I/sW196L mutations. 2011 Biochemistry. Biokhimiia Abstract HBV I195M;W196L;M204V;M204I 208;226;202;220 214;232;207;225 S;RT;RT;S;S 82;200;218;208;226 85;202;220;209;227 22086128 Novel HBsAg markers tightly correlate with occult HBV infection and strongly affect HBsAg detection. By co-variation analysis, correlations were observed for R122P+S167L (phi=0.68, P=0.01), T116N+S143L (phi=0.53, P=0.03), and Y100S+S143L (phi=0.67, p<0.001). 2012 Antiviral research Abstract HBV R122P;T116N;Y100S;S167L;S143L;S143L 57;89;125;63;95;131 62;94;130;68;100;136 22086128 Novel HBsAg markers tightly correlate with occult HBV infection and strongly affect HBsAg detection. Even more, Y100S and Y100S+S143L supernatants show no detectable-HBsAg (experiments in quadruplicate). 2012 Antiviral research Abstract HBV Y100S;Y100S;S143L 21;11;27 26;16;32 S 65 70 22086128 Novel HBsAg markers tightly correlate with occult HBV infection and strongly affect HBsAg detection. Mutants (obtained by site-directed mutagenesis) carrying T116N, T116N+S143L, R122P, R122P+Q101R, or R122P+S167L strongly decreased HBsAg-reactivity (54.9+-22.6S/CO, 31.2+-12.0S/CO, 6.1+-2.4S/CO, 3.0+-1.0S/CO and 3.9+-1.3S/CO, respectively) compared to wild-type (306.8+-64.1S/CO). 2012 Antiviral research Abstract HBV T116N;R122P;R122P;T116N;S143L;R122P;Q101R;S167L 64;84;100;57;70;77;90;106 69;89;105;62;75;82;95;111 S 131 136 22095534 Mutations within enhancer II and BCP regions of hepatitis B virus in relation to advanced liver diseases in patients infected with subgenotype B3 in Indonesia. Multivariate analysis showed that, in patients older than 45 years, C1638T and T1753V mutations constituted independent risk factors for the advancement of liver diseases. 2012 Journal of medical virology Abstract HBV C1638T;T1753V 68;79 74;85 Liver disease 156 170 22095534 Mutations within enhancer II and BCP regions of hepatitis B virus in relation to advanced liver diseases in patients infected with subgenotype B3 in Indonesia. The presence of C1638T and T1753V mutations may serve as predictive markers for the progression of liver diseases in Indonesia and other countries, where subgenotype B3 infection is prevalent. 2012 Journal of medical virology Abstract HBV C1638T;T1753V 16;27 22;33 Liver disease 99 113 22097597 [Detection and analysis of gene polymorphism in hepatitis B virus C region]. Four hepatitis B patients had mutation nt1896 g-->a, and another 4 patients had 2 mutations, namely, S87G and I97F (or 197L) in HBcAg CTL recognition episome. 2011 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV S87G;I97F 101;110 105;114 C 128 133 22097972 Five years of treatment with adefovir dipivoxil in Chinese patients with HBeAg-positive chronic hepatitis B. Urgent switch or add-on therapy with a nucleoside analogue is necessary if ADV resistant mutations are detected, particularly rtN236T. 2012 Liver international Abstract HBV N236T 128 133 RT 126 128 22097972 Five years of treatment with adefovir dipivoxil in Chinese patients with HBeAg-positive chronic hepatitis B. Virological breakthrough associated with ADV resistant mutations (rtN236T and rtA181V) occurred in 14.6% of subjects. 2012 Liver international Abstract HBV N236T;A181V 68;80 73;85 RT;RT 66;78 68;80 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. CONCLUSION: Biochemical response at 12 months from baseline was better in patients with a rtM204I mutation than rtM204V+ rtM204I/V mutations. 2012 Liver international Abstract HBV M204I;M204V;M204I;M204V 92;114;123;123 97;120;130;130 RT;RT;RT 90;112;121 92;114;123 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. In addition, early treatment failure was more common in patients with rtM204V+ rtM204I/V mutations than a rtM204I mutation. 2012 Liver international Abstract HBV M204V;M204I;M204V;M204I 72;81;81;108 78;88;88;113 RT;RT;RT 70;79;106 72;81;108 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. RESULTS: The baseline tyrosine-methionine-aspartate-aspartate (YMDD) mutation patterns were as follows: rtM204I 45 (57.7%); and rtM204V + rtM204I/V 33 (42.3%). 2012 Liver international Abstract HBV M204I;M204V;M204I;M204V 106;130;140;140 111;135;147;147 RT;RT;RT;YMDD;YMDD 104;128;138;22;63 106;130;140;61;67 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. rtM204IV +rtM204I/V mutations at 3, 6 and 12 months after the initiation of ADV add-on LAM combination treatment. 2012 Liver international Abstract HBV M204I;M204I;M204V 2;12;12 8;19;19 RT;RT 0;10 2;12 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. The decrease in the mean +- standard deviation (SD) serum log(10) HBV-DNA level did not differ between the patients carrying the rtM204I vs. 2012 Liver international Abstract HBV M204I 131 136 RT 129 131 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. The proportion of patients in whom the log(10) HBV-DNA decreased <2 log(10) copies/ml, 6 months after the initiation of ADV add-on LAM combination treatment (non-responders), was significantly higher in patients with a rtM204V + rtM204I/V mutations than rtM204I mutation (7 [21.2%] vs. 2012 Liver international Abstract HBV M204V;M204I;M204V;M204I 221;231;231;256 226;238;238;261 RT;RT;RT 219;229;254 221;231;256 22098177 The influence of YMDD mutation patterns on clinical outcomes in patients with adefovir add-on lamivudine combination treatment. The proportion of patients who achieved ALT normalization (<40 IU/L) 12 months after the initiation of ADV add-on LAM combination treatment were significantly higher in patients with a rtM204I mutation than rtM204V+ rtM204I/V mutations (39 [86.7%] vs. 2012 Liver international Abstract HBV M204I;M204V;M204I;M204V 187;209;218;218 192;215;225;225 RT;RT;RT 185;207;216 187;209;218 22100339 The effect of the G1888A mutation of subgenotype A1 of hepatitis B virus on the translation of the core protein. A distinctive characteristic of subgenotype A1 of hepatitis B virus is G1888A in the precore region. 2012 Virus research Abstract HBV G1888A 71 77 Precore 85 92 22100339 The effect of the G1888A mutation of subgenotype A1 of hepatitis B virus on the translation of the core protein. Our findings indicate that the G1888A mutation, may interfere with initiation at the downstream 1901 core AUG, decreasing core protein translation. 2012 Virus research Abstract HBV G1888A 31 37 C;C 101;122 105;126 22100339 The effect of the G1888A mutation of subgenotype A1 of hepatitis B virus on the translation of the core protein. The aim of this study was to use reporter constructs to determine whether G1888A had any modulating effect on core protein translation. 2012 Virus research Abstract HBV G1888A 74 80 C 110 114 22136288 Mutational complex genotype of the hepatitis B virus X /precore regions as a novel predictive marker for hepatocellular carcinoma. Eight high-frequency mutations (G1613A, C1653T, T1753V, A1762T, G1764A, A1846T, G1896A and G1899A) were significantly associated with HCC. 2012 Cancer science Abstract HBV G1613A;C1653T;T1753V;A1762T;G1764A;A1846T;G1896A;G1899A 32;40;48;56;64;72;80;91 38;46;54;62;70;78;86;97 Hepatocellular carcinoma 134 137 22136288 Mutational complex genotype of the hepatitis B virus X /precore regions as a novel predictive marker for hepatocellular carcinoma. Whereas C1653T, T1753V, G1764A and A1846T were independent mutational factors for HCC, the significance of these individual mutations was negligible when analyzed with all clinico-virological variables. 2012 Cancer science Abstract HBV C1653T;T1753V;G1764A;A1846T 8;16;24;35 14;22;30;41 Hepatocellular carcinoma 82 85 22138369 Late hepatitis B virus reactivation after lamivudine prophylaxis interruption in an anti-HBs-positive and anti-HBc-negative patient treated with rituximab-containing therapy. The patient carried a hepatitis B genotype D virus harbouring a single immune escape mutation, sT118K. 2012 The Journal of infection Abstract HBV T118K 95 101 S 95 96 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Amino acid substitutions at positions rtN238T/D of the hepatitis B virus (HBV) polymerase have been reported as potential mutations associated with adefovir (ADV) resistance. 2012 Antiviral research Abstract HBV N238T;N238D 40;40 47;47 RT;P 38;79 40;89 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Among 1865 enrolled HBV infected patients, 8.8% (165/1865) showed mutations in the rtN238 locus (143 males/22 females, 91 treatment-naive, 42 ADV-treated, 16 LAM-treated and 16 ADV+LAM-treated), namely 86% rtN238H (142/165), 5.5% rtN238S (9/165), 5.5% rtN238T (9/165) and 3% rtN238D (5/165). 2012 Antiviral research Abstract HBV N238H;N238S;N238T;N238D 208;232;254;277 213;237;259;282 RT;RT;RT;RT;RT 83;206;230;252;275 85;208;232;254;277 HBV infections 20 32 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Among the rtN238H mutant strains, there were no significant differences between ADV- or/and LAM- treated patients and treated-naive patients (42% vs. 2012 Antiviral research Abstract HBV N238H 12 17 RT 10 12 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. As rtN238H did neither impair the viral replication efficiency nor susceptibility to LAM or ADV in vitro, rtN238H likely represents background polymorphisms rather than resistance mutations with clinical implications. 2012 Antiviral research Abstract HBV N238H;N238H 5;108 10;113 RT;RT 3;106 5;108 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Importantly, we found that the incidence rate of rtN238H was higher in HBV genotype B infected patients than HBV genotype C subsets (80.3% vs. 2012 Antiviral research Abstract HBV N238H 51 56 RT 49 51 HBV infections 71 94 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. In this study, we characterized the prevalence of the rtN238H mutation and determined the susceptibility to LAM and ADV using phenotypic analyzes in vitro. 2012 Antiviral research Abstract HBV N238H 56 61 RT 54 56 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. Replication-competent HBV constructs containing the naturally occurring rtN238H mutation were generated and replication capacity and susceptibility to LAM and ADV in transiently transfected hepatoma cell lines were determined. 2012 Antiviral research Abstract HBV N238H 74 79 RT 72 74 Hepatocellular carcinoma 190 198 22138714 Prevalence, virology and antiviral drugs susceptibility of hepatitis B virus rtN238H polymerase mutation from 1865 Chinese patients with chronic hepatitis B. The incidence of rtN238H may be associated with HBV genotype. 2012 Antiviral research Abstract HBV N238H 19 24 RT 17 19 22152243 [Evolution of hepatitis B virus quasispecies during antiviral therapy in one chronic hepatitis B patient]. RESULTS: Three mutation patterns detected during antiviral therapy in the patient: rtM204V, rtM204V+rtL180M and rtM204I. 2011 Zhonghua gan zang bing za zhi Abstract HBV M204V;M204V;L180M;M204I 85;94;102;114 90;99;107;119 RT;RT;RT;RT 83;92;100;112 85;94;102;114 22156858 Differential clinical and virologic impact of hepatitis B virus genotypes B and C on HIV-coinfected patients receiving lamivudine-containing highly active antiretroviral therapy. Clinical and immunologic outcomes in the context of HBV genotypes as well as the emergence of HBV DNA mutations conferring lamivudine resistance (rtM204I/V) were determined. 2012 Clinical infectious diseases Abstract HBV M204I;M204V 148;148 155;155 RT 146 148 22166560 Prevalence and resistance pattern of genotype G and H in chronic hepatitis B and HIV co-infected patients in Mexico. As well, rtM204V and rtL180M mutations are common in HBV-HIV co-infected patients with genotype G and ART experience. 2012 Annals of hepatology Abstract HBV M204V;L180M 11;23 16;28 RT;RT 9;21 11;23 HBV-HIV coinfections 57 72 22166560 Prevalence and resistance pattern of genotype G and H in chronic hepatitis B and HIV co-infected patients in Mexico. The most frequent mutations presented in 8 HIV co-infected patients and one mono-infected patient with antiretroviral therapy (ART) experience were rtM204V and six of them showed genotype G (6/9). 2012 Annals of hepatology Abstract HBV M204V 150 155 RT 148 150 HBV-HIV coinfections 43 58 22170538 Comprehensive analysis of the prevalence of hepatitis B virus escape mutations in the major hydrophilic region of surface antigen. Eight important mutations associated with diagnostic failure, P120T, T126S, Q129H, G130N, S143L, D144A, and G145A/R, were prevalent in one or more genotypes, with the frequency of no less than 1%. 2012 Journal of medical virology Abstract HBV P120T;T126S;Q129H;G130N;S143L;D144A;G145A;G145R 62;69;76;83;90;97;108;108 67;74;81;88;95;102;115;115 22170539 Discrepancy of potential antiviral resistance mutation profiles within the HBV reverse transcriptase between nucleos(t)ide analogue-untreated and -treated patients with chronic hepatitis B in a hospital in China. Substitutions at seven non-classical mutation sites were of interest due to either detection only in patients with virologic breakthrough (rtL82 and rtV214), or potential ties with HBV genotypes (rtV191 and rtL229), or coexistence with rtM204I/V (rtL229), or increased mutation trends after NA-treatment (rtT128, rtV207, and rtN/H238). 2012 Journal of medical virology Abstract HBV M204I;M204V 238;238 245;245 RT;RT;RT;RT;RT;RT;RT;RT;RT 139;149;196;207;236;247;305;313;325 141;151;198;209;238;249;307;315;327 22170540 Pre-existing YMDD mutants in treatment-naive patients with chronic hepatitis B are not selected during lamivudine therapy. DPO-based multiplex PCR showed two YMDD mutations in two patients before LAM therapy; rtM204V and rtL180M + rtM204V/I. 2012 Journal of medical virology Abstract HBV M204V;L180M;M204V;M204I 88;100;110;110 93;105;117;117 RT;RT;RT;P 86;98;108;35 88;100;110;39 22170540 Pre-existing YMDD mutants in treatment-naive patients with chronic hepatitis B are not selected during lamivudine therapy. Further, two patients had an rtL180M mutation without an accompanying rtM204V/I mutation. 2012 Journal of medical virology Abstract HBV L180M;M204V;M204I 31;72;72 36;79;79 RT;RT 29;70 31;72 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. CONCLUSIONS: Levels of G1896A and A1762T/G1764A mutants (of genotypes B and C) in the HBeAg-positive patients may predict the time of HBeAg seroconversion. 2012 Journal of hepatology Abstract HBV G1764A;A1762T;G1896A 41;34;23 47;40;29 C;C 86;134 91;139 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. Follow-up of 18 HBeAg-positive patients revealed that the mutant percentage may stay low and stable for many years, followed by a steady increase in the percentage of G1896A and/or A1762T/G1764A mutants, from <10% to 50-100%, within about 3 years prior to seroconversion. 2012 Journal of hepatology Abstract HBV G1764A;A1762T;G1896A 188;181;167 194;187;173 C 16 21 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. Mutant viruses carrying the precore G1896A and/or the basal core promoter (BCP) A1762T/G1764A mutations are associated with HBeAg seroconversion. 2012 Journal of hepatology Abstract HBV G1764A;A1762T;G1896A 87;80;36 93;86;42 BCP;BCP;C;Precore 54;75;124;28 73;78;129;35 22178505 Analysis of hepatitis B virus X gene (HBx) mutants in tissues of patients suffered from hepatocellular carcinoma in China. However, the role of HBx gene mutations at aa L30F/S144A relative to wild type HBx gene is unclear in hepatocarcinogenesis. 2012 Cancer epidemiology Abstract HBV S144A;L30F 51;46 56;50 X;X 21;79 24;82 22178505 Analysis of hepatitis B virus X gene (HBx) mutants in tissues of patients suffered from hepatocellular carcinoma in China. Interestingly, we found that a novel type of HBx linked-mutations, such as at aa L30F/S144A, was 29.5% (13/44) positive in the tumor tissues. 2012 Cancer epidemiology Abstract HBV S144A;L30F 86;81 91;85 X 45 48 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. One patient showed the M204V+ L180M+ V173L+ triple mutation associated with a vaccine escape phenotype, which could be of public health concern in a country with a national HBV vaccination programme. 2011 BMC research notes Abstract HBV M204V;L180M;V173L 23;30;37 29;36;42 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The most common LAM and ETV resistance mutations were rtM204I/V, rtL180M and rtT184A/I/S, respectively, while rtA181T/V and rtN236T substitutions were the most frequently observed ADV resistance mutations. 2011 Hepatitis monthly Abstract HBV M204I;M204V;L180M;T184A;T184I;T184S;A181T;A181V;N236T 56;56;67;79;79;79;112;112;126 63;63;72;88;88;88;119;119;131 RT;RT;RT;RT;RT 54;65;77;110;124 56;67;79;112;126 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Cloning of PCR products allowed detection of the G145R mutant as a minor strain in 7 (group 1: 1 subject, group 2: 6 subjects) of 12 subjects who had overlapped peaks at nt 587 in the electropherogram. 2012 BMC research notes Abstract HBV G145R 49 54 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. However, the G145R mutant was often present as a minor population in children and adults. 2012 BMC research notes Abstract HBV G145R 13 18 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. RESULTS: By mutant-specific real-time PCR, one subject (5.6%) was positive for the G145R mutant in group 1, while the G145 mutant was undetectable in group 2. 2012 BMC research notes Abstract HBV G145R 83 88 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. To detect the G145R and G145A mutants in patients, we designed 3 probes for real-time PCR. 2012 BMC research notes Abstract HBV G145R;G145A 14;24 19;29 22246826 Characterization of hepatitis B virus genome variability in Iranian patients with chronic infection, a nationwide study. Sixty-seven patients (82.7%) were HBeAg negative, and the prevalence of precore mutant isolates (G1896A) was higher in this group than in HBeAg-positive patients. 2012 Journal of medical virology Abstract HBV G1896A 97 103 C;C;Precore 34;138;72 39;143;79 22246826 Characterization of hepatitis B virus genome variability in Iranian patients with chronic infection, a nationwide study. The HBV PC (G1896A) mutation may play an important role in the clinical outcome of the disease by increasing the risk of progressive liver disease among Iranian patients infected with HBV. 2012 Journal of medical virology Abstract HBV G1896A 12 18 Precore 8 10 22246826 Characterization of hepatitis B virus genome variability in Iranian patients with chronic infection, a nationwide study. The most frequent mutation in the major hydrophilic region (MHR) of HBV surface antigen (HBsAg) was sP120S. 2012 Journal of medical virology Abstract HBV P120S 100 106 S;S;S 100;89;72 101;94;79 22251541 Pre-core/basal-core promoter and reverse transcriptase mutations in chronic HBV infected-patients. For combined mutations, A1762T+G1764A (23.43% vs. 11.59 %, p<0.05) and G1896A+ G1899A (21.88% vs. 13.04%, p<0.05) were significantly more frequent in ACLF-HBV than CHB patients. 2012 Hepato-gastroenterology Abstract HBV A1762T;G1764A;G1899A;G1896A 24;31;79;71 30;37;85;77 Chronic Hepatitis B 164 167 22251541 Pre-core/basal-core promoter and reverse transcriptase mutations in chronic HBV infected-patients. In HBV pre-core/ BCP region, the point mutations T1753C (39.06% vs. 21.74%, p<0.01), A1762T (26.56% vs. 13.04%, p<0.05), G1764A (31.25% vs. 18.84%, p<0.01), G1896A (29.69% vs. 15.94%, p<0.05) and G1899 (23.44% vs. 10.14%, p<0.05) were significantly more frequent in the ACLFHBV than CHB patients. 2012 Hepato-gastroenterology Abstract HBV A1762T;G1764A;G1896A;T1753C 85;121;157;49 91;127;163;55 BCP;Precore 17;7 20;15 Chronic Hepatitis B 283 286 22260834 Risk factors of gene-resistant mutations in different nucleosides. In LAM group, rtL180M combined with rtM204V mutations accounted for 32.7% and in ADV group, rtN236T mutation accounted for 12.3%. 2012 Hepato-gastroenterology Abstract HBV L180M;M204V;N236T 16;38;94 21;43;99 RT;RT;RT 14;36;92 16;38;94 22274739 Mutations in the S gene region of hepatitis B virus genotype D in Golestan Province-Iran. 14% of mutations occurred at Major Hydrophilic Region(MHR) area which P120T/S and R122K/T substitutions were the most frequent ones (4%). 2012 Virus genes Abstract HBV P120T;P120S;R122K;R122T 70;70;82;82 77;77;89;89 22274739 Mutations in the S gene region of hepatitis B virus genotype D in Golestan Province-Iran. Mutation in G145R of the S gene was observed in one case. 2012 Virus genes Abstract HBV G145R 12 17 S 25 26 22290465 An improved reverse dot hybridization for simple and rapid detection of adefovir dipivoxil-resistant hepatitis B virus. Thisreverse dot hybridization assay proved to be simple and rapid for detection ofrtA181V/T and rtN236T mutations associated with resistance to adefovirdipivoxil. 2012 Genetics and molecular research Abstract HBV N236T 98 103 RT 96 98 22290465 An improved reverse dot hybridization for simple and rapid detection of adefovir dipivoxil-resistant hepatitis B virus. Wedeveloped an improved reverse dot hybridization test for simple and rapiddetection of the rtA181V/T and rtN236T mutations associated with adefovirdipivoxil resistance in chronic hepatitis B patients. 2012 Genetics and molecular research Abstract HBV A181V;A181T;N236T 94;94;108 101;101;113 RT;RT 92;106 94;108 Chronic Hepatitis B 172 191 22296790 Variable capacity of 13 hepatitis B virus surface antigen assays for the detection of HBsAg mutants in blood samples. Three substitutions: T123, D144A and G145, were negative at all concentrations with at least one assay. 2012 Journal of clinical virology Abstract HBV D144A 27 32 22301154 Amino acid substitutions at positions 122 and 145 of hepatitis B virus surface antigen (HBsAg) determine the antigenicity and immunogenicity of HBsAg and influence in vivo HBsAg clearance. A variety of amino acid substitutions, such as K122I and G145R, have been identified around or within the a determinant of hepatitis B surface antigen (HBsAg), impair HBsAg secretion and antibody binding, and may be responsible for immune escape in patients. 2012 Journal of virology Abstract HBV K122I;G145R 47;57 52;62 S;S;S;S 106;152;167;135 119;157;172;142 22301154 Amino acid substitutions at positions 122 and 145 of hepatitis B virus surface antigen (HBsAg) determine the antigenicity and immunogenicity of HBsAg and influence in vivo HBsAg clearance. Genetic immunization in mice demonstrated that the priming of anti-HBs antibody response was strongly impaired by the substitutions K122I, G145R, and others, like G145I, G145W, and G145E. 2012 Journal of virology Abstract HBV K122I;G145R;G145I;G145W;G145E 132;139;163;170;181 137;144;168;175;186 S 67 70 22301154 Amino acid substitutions at positions 122 and 145 of hepatitis B virus surface antigen (HBsAg) determine the antigenicity and immunogenicity of HBsAg and influence in vivo HBsAg clearance. Only the substitution K122I at position 122 affected HBsAg secretion and recognition by anti-HBs antibodies. 2012 Journal of virology Abstract HBV K122I 22 27 S;S 93;53 96;58 22301217 High-resolution melting and real-time PCR for quantification and detection of drug-resistant HBV mutants in a single amplicon. HRM analysis produced distinct melting temperatures that clearly distinguished the mutants, rtM204V/I (LMV), rtA181V and rtN236T (ADV), and rtT184G and rtM250V (ETV), from their respective wild types. 2012 Antiviral therapy Abstract HBV M204V;M204I;A181V;N236T;T184G;M250V 94;94;111;123;142;154 101;101;116;128;147;159 RT;RT;RT;RT;RT 92;109;121;140;152 94;111;123;142;154 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. alanine aminotransferase (ALT) 60 IU/L, and emergence of drug resistance to ADV (rtN236T). 2010 Hepatitis monthly Abstract HBV N236T 83 88 RT 81 83 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. In the 18th month of the ETV monotherapy, direct sequencing showed reduced susceptibility to ETV (rtL180M+rtM204V). 2010 Hepatitis monthly Abstract HBV L180M;M204V 100;108 105;113 RT;RT 98;106 100;108 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Twelve months after the start of lamivudine (LAM) therapy, virological breakthrough occurred (4.2E+07 IU/ml) and the rtM204V variant was detected in the patient's sera: adefovir (ADV) was added to the therapy. 2010 Hepatitis monthly Abstract HBV M204V 119 124 RT 117 119 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. Fourteen of the 44 patients (31.8%) had mutations in the precore region (G 1896A). 2010 Hepatitis monthly Abstract HBV G1896A 73 80 Precore 57 64 22313146 Reactivation of hepatitis B virus with mutated hepatitis B surface antigen in a liver transplant recipient receiving a graft from an antibody to hepatitis B surface antigen- and antibody to hepatitis B core antigen-positive donor. 4) The replicating HBV encoded two HBsAg mutations, first sQ129R and 4 months later sP127S. 2012 Transfusion Abstract HBV Q129R;P127S 58;84 64;90 S;S;S 35;58;84 40;59;85 22314422 Decreased infectivity of nucleoside analogs-resistant hepatitis B virus mutants. As expected, mutants harboring a sW196Stop mutation in the surface gene did not express small envelope proteins. 2012 Journal of hepatology Abstract HBV W196X 33 42 S;S;S 33;88;59 34;102;66 22314422 Decreased infectivity of nucleoside analogs-resistant hepatitis B virus mutants. METHODS: HBV-resistant mutants (rtL180M+M204V, rtV173L+L180M+M204V, rtM204I, rtL180M+M204I, rtN236T, rtA181V, rtA181V+rtN236T, rtA181T+N236T, and rtA181T) were produced in HepG2 cells permanently expressing the respective viral genomes. 2012 Journal of hepatology Abstract HBV M204I;N236T;A181V;A181T;L180M;V173L;L180M;A181T;A181V;N236T;M204V;L180M;M204V;M204I;N236T 70;94;103;148;34;49;79;129;112;120;40;55;61;85;135 75;99;108;153;39;54;84;134;117;125;45;60;66;90;140 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 32;47;68;77;92;101;110;118;127;146 34;49;70;79;94;103;112;120;129;148 22338219 [The mutation patterns of HBV P gene and genotyping in patients with lanivudine-resistant chronic hepatitis B]. Genetype C was mainly YMDD combined with rtL180M mutations pattern, the rate is 60.7% (48/79); while genetype B was mainly rtM204 mutation pattern, the rate is 66.7% (18/27); there were significant difference between the genetype B and C in mutation pattern (chi2 = 8.4, 7.2, respectively, P < 0. 2011 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV L180M 43 48 RT;RT;P 41;123;22 43;125;26 22338219 [The mutation patterns of HBV P gene and genotyping in patients with lanivudine-resistant chronic hepatitis B]. YMDD mutations happened in 100%, only YMDD mutation were 43 patients, while others were YMDD combined with rtL180M mutations; the HBV genotype among 107chronic hepatitis was mainly B (25.2%) and C (73.8%) and only 1 patient was happend B and C mixed infection. 2011 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV L180M 109 114 RT;P;P;P 107;0;38;88 109;4;42;92 Chronic Hepatitis B 149 169 22340383 Characterization of hepatitis B virus genotypes/subgenotypes in 1,301 patients with chronic hepatitis B in North China. and BCP mutations A1762T+G1764A (65.8% vs. 2011 Chinese medical journal Abstract HBV A1762T;G1764A 18;25 24;31 BCP 4 7 22340383 Characterization of hepatitis B virus genotypes/subgenotypes in 1,301 patients with chronic hepatitis B in North China. HBV/C infection had a higher incidence of lamivudine-resistant mutations rtM204I/V (44.9% vs. 2011 Chinese medical journal Abstract HBV M204I;M204V 75;75 82;82 RT 73 75 HBV infections 0 15 22342116 Hepatitis B virus variant with the a194t substitution within reverse transcriptase before and under adefovir and tenofovir therapy. HBV rtA194T mutants were still the majoritary quasi-species 17 months after being identified for the first time. 2012 Clinics and research in hepatology and gastroenterology Abstract HBV A194T 6 11 RT 4 6 22342116 Hepatitis B virus variant with the a194t substitution within reverse transcriptase before and under adefovir and tenofovir therapy. Retrospective analysis of our local HBV reverse transcriptase (rt) sequence database including 973 sequences recovered from 616 patients identified one unique HBV DNA sequence harbouring amino acid (aa) substitution rtA194T, which has been suspected to confer reduced susceptibility to tenofovir but whose implication in antiviral resistance has not been confirmed. 2012 Clinics and research in hepatology and gastroenterology Abstract HBV A194T 218 223 RT;RT;RT 40;63;216 61;65;218 22358132 Treatment response and evolution of HBV resistance during lamivudine plus adefovir or entecavir therapy in patients with adefovir-resistant mutants. In the LAM+ADV group, patients with single rtN236T resistant mutation had higher rates of undetectable HBV DNA than those with the double mutant rtA181T/V+rtN236T at months 3-18 of therapy. 2012 Antiviral therapy Abstract HBV A181T;A181V;N236T;N236T 147;147;45;157 154;154;50;162 RT;RT;RT 43;145;155 45;147;157 22358132 Treatment response and evolution of HBV resistance during lamivudine plus adefovir or entecavir therapy in patients with adefovir-resistant mutants. LAM+ADV were less effective in patients with the double mutant rtA181T/V+rtN236T than the single rtN236T mutation. 2012 Antiviral therapy Abstract HBV A181T;A181V;N236T;N236T 65;65;75;99 72;72;80;104 RT;RT;RT 63;73;97 65;75;99 22358132 Treatment response and evolution of HBV resistance during lamivudine plus adefovir or entecavir therapy in patients with adefovir-resistant mutants. No virological breakthrough occurred except for one patient with rtN236T resistant mutation who experienced virological and biochemical breakthrough after the emergence of an additional rtA181T mutant under LAM+ADV therapy. 2012 Antiviral therapy Abstract HBV N236T;A181T 67;188 72;193 RT;RT 65;186 67;188 22358356 Hepatitis B virus genotypes, precore mutations, and basal core promoter mutations in HBV-infected Chinese patients with persistently normal alanine aminotransferase and low serum HBV-DNA levels. The most common mutations were G1896A (23.6%), G1764A (9.0%), and A1762T (6.7%). 2012 The Brazilian journal of infectious diseases Abstract HBV G1896A;G1764A;A1762T 31;47;66 37;53;72 22381777 [Clinical application of DNA sequencing for detecting point mutations in hepatitis B virus associated with drug resistance]. RESULTS: Forty out of the 120 patients were found to have one or two point mutations associated with drug resistance, including 17 with L180M and M204V/I mutations (42.5%), 10 with M204V/I mutation (25%), 8 with N236T mutation (20%), 3 with L180M mutation (7.5%), and 1 with both A181V/T and N236T mutations (2.5%), and 1 with A181V/T mutation(2.5%). 2012 Nan fang yi ke da xue xue bao Abstract HBV L180M;M204V;M204I;M204V;M204I;N236T;L180M;A181V;A181T;N236T;A181V;A181T 136;146;146;181;181;212;241;280;280;292;327;327 141;153;153;188;188;217;246;287;287;297;334;334 22398037 The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation. CONCLUSION: The rtL229 substitutions were potentially associated with LAM resistance in Chinese patients and rtL229F had characteristics of a compensatory mutation of rtM204I mutant. 2012 Journal of clinical virology Abstract HBV L229F;M204I 111;169 116;174 RT;RT;RT 16;109;167 18;111;169 22398037 The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation. Functionally, rtL229F did not confer reduced susceptibility to LAM, but could restore replication capacity of rtM204I strain. 2012 Journal of clinical virology Abstract HBV L229F;M204I 16;112 21;117 RT;RT 14;110 16;112 22398037 The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation. Individual substitution incidences were 2.77%, 0.97%, 0.83% and 0.55% for rtL229V, rtL229F, rtL229M and rtL229W, respectively. 2012 Journal of clinical virology Abstract HBV L229V;L229F;L229M;L229W 76;85;94;106 81;90;99;111 RT;RT;RT;RT 74;83;92;104 76;85;94;106 22398037 The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation. Replication-competent viral amplicons which harbored HBV genomes of wild-type, rtM204I, or rtM204I in conjunction with various rtL229 substitutions (rtL229F/W/M/V) were constructed. 2012 Journal of clinical virology Abstract HBV M204I;M204I;L229F;L229W;L229M;L229V 81;93;151;151;151;151 86;98;162;162;162;162 RT;RT;RT;RT 79;91;127;149 81;93;129;151 22398037 The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation. Representative cases follow-up showed that rtL229F developed subsequent to rtM204I emergence during LAM treatment and regressed with rtM204I after LAM withdrawal. 2012 Journal of clinical virology Abstract HBV L229F;M204I;M204I 45;77;135 50;82;140 RT;RT;RT 43;75;133 45;77;135 22417682 Genetic analysis of precore/core and partial pol genes in an unprecedented outbreak of fulminant hepatitis B in India. A1762T, G1764A basal core promoter (BCP) mutations, insertion of isoleucine after nt 1843, stop codon mutation G1896A, G1862T transversion plus seven other mutations in the core gene caused inhibition of HBeAg expression implicating them as circulating precore/BCP mutant virus. 2012 Epidemiology and infection Abstract HBV A1762T;G1764A;G1896A;G1862T 0;8;111;119 6;14;117;125 BCP;BCP;BCP;C;C;Precore 15;36;261;173;204;253 34;39;264;177;209;260 22422696 The perils of relying on anti-hepatitis B total core antibody in screening individuals infected with HIV. High-grade HBV viraemia associated with L180M and M240V drug-resistance mutations was confirmed. 2012 International journal of STD & AIDS Abstract HBV L180M;M240V 40;50 45;55 22442974 [Heterogeneity of hepatitis B virus and diagnostic potential of modern test systems for the detection of HBsAg]. Amino acid substitutions G145A, M133I, S132T localized in the main hydrophilic region and P217L, S207N, V184A localized in the C-end of the protein C that are connected with diagnostic and vaccine escape were identified in 5 isolates. 2012 Zhurnal mikrobiologii, epidemiologii i immunobiologii Abstract HBV G145A;M133I;S132T;P217L;S207N;V184A 25;32;39;90;97;104 30;37;44;95;102;109 C 127 128 22442974 [Heterogeneity of hepatitis B virus and diagnostic potential of modern test systems for the detection of HBsAg]. Approximately equal potential of 6 test systems to detect HBsAg with amino acid substitutions G145A, M133I and S132T localized in the MHR region were shown. 2012 Zhurnal mikrobiologii, epidemiologii i immunobiologii Abstract HBV G145A;M133I;S132T 94;101;111 99;106;116 S 58 63 22445262 New natural variants of hepatitis B virus among Amerindians from Argentina with mainly occult infections. All cases exhibited the polymorphism rtL217R within the RT domain associated to resistance to adefovir. 2012 Journal of clinical virology Abstract HBV L217R 39 44 RT;RT 56;37 58;39 22445262 New natural variants of hepatitis B virus among Amerindians from Argentina with mainly occult infections. Mutations rtD206E and rtV207I associated with lamivudine resistance were found in two MG and three SH respectively. 2012 Journal of clinical virology Abstract HBV D206E;V207I 12;24 17;29 RT;RT 10;22 12;24 22453135 Long-term monitoring drug resistance by ultra-deep pyrosequencing in a chronic hepatitis B virus (HBV)-infected patient exposed to several unsuccessful therapy schemes. Both mutations were statistically associated with rtA200V and rtV207I, respectively. 2012 Antiviral research Abstract HBV A200V;V207I 52;64 57;69 RT;RT 50;62 52;64 22453135 Long-term monitoring drug resistance by ultra-deep pyrosequencing in a chronic hepatitis B virus (HBV)-infected patient exposed to several unsuccessful therapy schemes. Once the entecavir and tenofovir combined therapy was started, polymerase and consequently envelope gene mutations appeared at several positions at a higher frequency than before, including the entecavir resistance-associated mutation rtT184L. 2012 Antiviral research Abstract HBV T184L 237 242 S;P;RT 91;63;235 99;73;237 22453135 Long-term monitoring drug resistance by ultra-deep pyrosequencing in a chronic hepatitis B virus (HBV)-infected patient exposed to several unsuccessful therapy schemes. Under sequential HBV monotherapies including lamivudine, adefovir and entecavir, a high frequency of rtM204I mutation was detected initially as unique and then coexisting with rtM204V. 2012 Antiviral research Abstract HBV M204I;M204V 103;178 108;183 RT;RT 101;176 103;178 22459735 Probable corticosteroid-induced reactivation of latent hepatitis B virus infection in an HIV-positive patient involving immune escape. A genotype A2 strain emerged with 2 major mutations in the S gene, sK122R and sD144E. 2012 The Journal of infectious diseases Abstract HBV K122R;D144E 67;78 73;84 S;S;S 59;67;78 60;68;79 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Besides well known G145R, widely dispersed variations in the MHR of S region, were observed in 20 samples of all the strains sequenced. 2012 Virology journal Abstract HBV G145R 19 24 S 68 69 22510145 Natural history of chronic hepatitis B: what exactly has REVEAL revealed? Genetic features including HBV genotype and basal core promoter A1762T/G1764A mutant, and precore G1896A mutant were documented as predictors of HCC risk. 2012 Liver international Abstract HBV G1764A;A1762T;G1896A 71;64;98 77;70;104 BCP;Precore 44;90 63;97 Hepatocellular carcinoma 145 148 22510694 Convergence and coevolution of hepatitis B virus drug resistance. An analysis of Bayesian networks that connect rtM204I/V to many sites of HBV proteins confirms that lamivudine resistance is a complex trait encoded by the entire HBV genome rather than by a single mutation. 2012 Nature communications Abstract HBV M204I;M204V 48;48 55;55 RT 46 48 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Here we show that the rtM204I/V substitution, although essential, is insufficient for establishing resistance against lamivudine. 2012 Nature communications Abstract HBV M204I;M204V 24;24 31;31 RT 22 24 22510694 Convergence and coevolution of hepatitis B virus drug resistance. The analysis of 639 HBV whole-genome sequences obtained from 11 patients shows that rtM204I/V is independently acquired by more than one intra-host HBV variant, indicating the convergent nature of lamivudine resistance. 2012 Nature communications Abstract HBV M204I;M204V 86;86 93;93 RT 84 86 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Treatment with lamivudine of patients infected with hepatitis B virus (HBV) results in a high rate of drug resistance, which is primarily associated with the rtM204I/V substitution in the HBV reverse transcriptase domain. 2012 Nature communications Abstract HBV M204I;M204V 160;160 167;167 RT;RT 192;158 213;160 22510826 Antiviral therapy against chronic hepatitis B in Brazil: high rates of lamivudine resistance mutations and correlation with HBV genotypes. Genotype D isolates with the rtM204V variant preferentially displayed a triple mutation, while genotype A preferentially displayed a double mutation (p = 0.04). 2012 Memorias do Instituto Oswaldo Cruz Abstract HBV M204V 31 36 RT 29 31 22510826 Antiviral therapy against chronic hepatitis B in Brazil: high rates of lamivudine resistance mutations and correlation with HBV genotypes. Nevertheless, the rtM204V mutation was observed more frequently (12/13, 92%) in genotype A than in the others (p = 0.023). 2012 Memorias do Instituto Oswaldo Cruz Abstract HBV M204V 20 25 RT 18 20 22510826 Antiviral therapy against chronic hepatitis B in Brazil: high rates of lamivudine resistance mutations and correlation with HBV genotypes. Six out of nine isolates that contained the rtM204I mutation belonged to genotype D and half of them displayed a single mutation. 2012 Memorias do Instituto Oswaldo Cruz Abstract HBV M204I 46 51 RT 44 46 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Four of eight (50%) chronic therapy-naive HBeAg-negative patients showed a relatively low prevalence of the G1896A pre-core (pre-C) mutant in the liver tissues, suggesting that other mutations were involved in their HBeAg seroconversion. 2012 PloS one Abstract HBV G1896A 108 114 C;C;Precore;Precore 42;216;125;115 47;221;130;123 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Interestingly, liver tissues in 4 of 5 (80%) of the chronic NA-treated anti-HBe-positive cases had extremely low levels of the G1896A pre-C mutant (0.0%, 0.0%, 0.1%, and 1.1%), suggesting the high sensitivity of the G1896A pre-C mutant to NA. 2012 PloS one Abstract HBV G1896A;G1896A 127;216 133;222 C;Precore;Precore 76;134;223 79;139;228 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Moreover, various abundances of clones resistant to NA were common in both the liver and serum of treatment-na茂ve patients, and the proportion of M204VI mutants resistant to lamivudine and entecavir expanded in response to entecavir treatment in the serum of 35.7% (5/14) of patients, suggesting the putative risk of developing drug resistance to NA. 2012 PloS one Abstract HBV M204V;M204I 146;146 152;152 22538265 Simultaneous emergence of entecavir resistance mutations in a nucleoside-naive chronic hepatitis B patient. The ETV resistance-related substitution (T184A) and lamivudine resistance-related substitutions (L180M and M204V) were detected by sequence analysis at week 96. 2012 Intervirology Abstract HBV T184A;L180M;M204V 41;97;107 46;102;112 22579480 HBV genotypes prevalence, precore and basal core mutants in Morocco. BCP mutants were observed in 65.7% of cases, 22.9% were found to have the T1762/1764A double mutation, 18.6% had A1762/1764T mutation and 22.9% of patients showed the A1762T/G1764A double mutation with either A1762T/G1764T mutation. 2012 Infection, genetics and evolution Abstract HBV G1764A;G1764T;A1762T;A1762T 174;216;167;209 180;222;173;215 BCP 0 3 22579480 HBV genotypes prevalence, precore and basal core mutants in Morocco. In 70 studied strains, HBV mutants were detected in 88.6% of cases; PC mutants were detected in (40%) of patients and 21.5% present a mixture of wild type and G1896A mutation. 2012 Infection, genetics and evolution Abstract HBV G1896A 159 165 Precore 68 70 22585719 Factors influencing inadequate or suboptimal response to adefovir with or without genotypic resistance. In the patients with viral rebound and ADV genotypic resistance, 19 (25.7%) showed rtA181V/T/S + rtN236T substitutions. 2012 Journal of medical virology Abstract HBV A181V;A181T;A181S;N236T 85;85;85;99 94;94;94;104 RT;RT 83;97 85;99 22585719 Factors influencing inadequate or suboptimal response to adefovir with or without genotypic resistance. Multiple logistic regression analysis showed that the rtN236T and time resistant strains occurred during ADV-treatment were statistically significant for influencing rtA181 variation types (P = 0.007 and P = 0.024, respectively), and the occurrence of rtA181T was found to be significantly earlier than rtA181V. 2012 Journal of medical virology Abstract HBV N236T;A181T;A181V 56;254;305 61;259;310 RT;RT;RT;RT 54;166;252;303 56;168;254;305 22585719 Factors influencing inadequate or suboptimal response to adefovir with or without genotypic resistance. Seventy-six patients (47.2%) were found to carry the rtA181V/T/S or rtN236T residue substitution, and most of them had viral rebound. 2012 Journal of medical virology Abstract HBV A181V;A181T;A181S;N236T 55;55;55;70 64;64;64;75 RT;RT 53;68 55;70 22585719 Factors influencing inadequate or suboptimal response to adefovir with or without genotypic resistance. The rtA181T occurs more frequently in patients with the rtN236T and it occurs earlier when compared to the rtA181V. 2012 Journal of medical virology Abstract HBV A181T;N236T;A181V 6;58;109 11;63;114 RT;RT;RT 4;56;107 6;58;109 22585719 Factors influencing inadequate or suboptimal response to adefovir with or without genotypic resistance. The rtN236T was more frequent in patients with genotype B, and the rtA181V/T/S was more common in patients with genotype C (chi(2) = 11.543, P = 0.001). 2012 Journal of medical virology Abstract HBV N236T;A181V;A181T;A181S 6;69;69;69 11;78;78;78 RT;RT 4;67 6;69 22592516 HIV and Hepatitis B coinfection among perinatally HIV-infected Thai adolescents. Among adolescents with chronic HBV infection, 88% have received lamivudine; however, 69% have HBV DNA >10 copies/mL and 75% had the rtM204V/I mutation. 2012 The Pediatric infectious disease journal Abstract HBV M204V;M204I 134;134 141;141 RT 132 134 Chronic HBV infection 23 44 22592516 HIV and Hepatitis B coinfection among perinatally HIV-infected Thai adolescents. HBV DNA quantitation and rtM204V/I mutation analysis (lamivudine resistance-associated mutation) were performed in adolescents with chronic HBV infection. 2012 The Pediatric infectious disease journal Abstract HBV M204V;M204I 27;27 34;34 RT 25 27 Chronic HBV infection 132 153 22595307 The detection of HBsAg mutants expressed in vitro using two different quantitative HBsAg assays. However, HBsAg mutation T123A was under quantified by the Architect, whereas HBsAg mutations P142L, P142S and G145K yielded lower results in the Elecsys system. 2012 Journal of clinical virology Abstract HBV T123A;P142L;P142S;G145K 24;93;100;110 29;98;105;115 S;S 9;77 14;82 22617152 High prevalence of occult hepatitis B virus infection in children born to HBsAg-positive mothers despite prophylaxis with hepatitis B vaccination and HBIG. Ten had G145R mutations. 2012 Journal of hepatology Abstract HBV G145R 8 13 22634131 Influence of mutations in hepatitis B virus surface protein on viral antigenicity and phenotype in occult HBV strains from blood donors. Four out of the 13 mutations (C124R, C124Y, K141E, and D144A) strongly decreased the analytical sensitivity of seven commercial HBsAg immunoassays, and 10 (G119R, C124Y, I126S, Q129R, S136P, C139R, T140I, K141E, D144A, and G145R) significantly impaired virion and/or S protein secretion in both HuH7 cells and mice. 2012 Journal of hepatology Abstract HBV C124R;C124Y;K141E;D144A;G119R;C124Y;I126S;Q129R;S136P;C139R;T140I;K141E;D144A;G145R 30;37;44;55;156;163;170;177;184;191;198;205;212;223 35;42;49;60;161;168;175;182;189;196;203;210;217;228 S;S 128;267 133;268 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In the overlapping surface region, NA-resistant substitutions caused selection of stop codons in a significant percentage of sequences both at pre-treatment and during sequential treatment; the rtA181T substitution, related to sW172stop, predominated during treatment with lamivudine and adefovir. 2012 PloS one Abstract HBV A181T;W172X 196;227 201;236 RT;S;S 194;227;19 196;228;26 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. On linkage analysis of the RT region studied, NA-resistant HBV variants (except for rtA181T) were present in combinations of amino acid substitutions that increased in complexity after viral breakthrough to entecavir, at which time the combined variant rtL180M-S202G-M204V-V207I predominated. 2012 PloS one Abstract HBV A181T;L180M;S202G;M204V;V207I 86;255;261;267;273 91;260;266;272;278 RT;RT;RT 27;84;253 29;86;255 22668794 In vitro inhibition of HBV replication by a novel compound, GLS4, and its efficacy against adefovir-dipivoxil-resistant HBV mutations. To determine the antiviral activity of GLS4 against adefovir dipivoxil (ADV)-resistant HBV mutants, HepG2 cells transiently transfected with PUC-HBV1.2 plasmids that contained one of three major ADV-resistant mutations (rtA181T, rtA181V and rtN236T) were treated with GLS4. 2012 Antiviral therapy Abstract HBV A181T;A181V;N236T 222;231;243 227;236;248 RT;RT;RT 220;229;241 222;231;243 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. The primary LAM resistance mutation (rtM204V/I) occurs in the YMDD motif of HBV polymerase. 2012 BMC microbiology Abstract HBV M204V;M204I 39;39 46;46 P;RT;P 80;37;62 90;39;66 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Besides, the mutations like G1896A and BCP double mutation may be associated with the progression of the liver diseases. 2012 PloS one Abstract HBV G1896A 28 34 BCP 39 42 Liver disease 105 119 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. CONCLUSIONS: Precore mutation G1896A, G1899A, deletions in Pre-S region as well as the other commonly seen mutations correlated with the increased risk of HCC, especially in Asians and may predict the progression of the liver disease. 2012 PloS one Abstract HBV G1896A;G1899A 30;38 36;44 Precore;PreS 13;59 20;64 Hepatocellular carcinoma;Liver disease 155;220 158;233 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Similar correlation existed between BCP double mutation A1762T/G1764A, T1753V, C1653T and HCC. 2012 PloS one Abstract HBV G1764A;A1762T;T1753V;C1653T 63;56;71;79 69;62;77;85 BCP 36 39 Hepatocellular carcinoma 90 93 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Statistically significant correlations were observed in Precore mutation G1896A (OR = 1.46, 95% confidence interval [CI] = 1.15-1.85, P(OR) = 0.002), G1899A (OR = 3.13, 95%CI = 2.38-4.13, P(OR)<0.001) and Pre-S mutation especially Pre-S1 deletion (OR = 2.94, 95%CI = 2.22 to 3.89) and Pre-S2 deletion (OR = 3.02, 95%CI = 2.03 to 4.50). 2012 PloS one Abstract HBV G1896A;G1899A 73;150 79;156 Precore;PreS;PreS1;PreS2 56;205;231;285 63;210;237;291 22686039 [Analysis of the complete hepatitis B virus genomes in a patient for repeated seroconversion to anti-HBe antibody due to co-infection with two virus clones]. However, both clones had mutations in the core promoter(A1762T, G1764A). 2012 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV A1762T;G1764A 56;64 62;70 Core promoter 42 55 22686039 [Analysis of the complete hepatitis B virus genomes in a patient for repeated seroconversion to anti-HBe antibody due to co-infection with two virus clones]. In one HBe antibody-positive clone, a pre-core mutation associated with HBe antigen negativity (G1896A) was found. 2012 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV G1896A 96 102 C;C;Precore 7;72;38 10;75;46 22711345 Molecular analysis of hepatitis B virus associated with vaccine failure in infants and mothers: a case-control study in Thailand. DNA analysis in a pair of HBeAg-negative infant and mother revealed that both were infected with an HBV precore mutant (G1896A). 2012 Journal of medical virology Abstract HBV G1896A 120 126 C;Precore 26;104 31;111 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. In the immunodominant 'a' region of the surface gene, point mutations were identified in 31% (n = 58/187) of sequences, and 2.2% (n = 4/187) and 5.3% (n = 10/187) specimens contained the major vaccine escape mutations G145A/R and P120L/Q/S/T, respectively. 2012 PloS one Abstract HBV G145A;G145R;P120L;P120Q;P120S;P120T 218;218;230;230;230;230 225;225;241;241;241;241 S 40 47 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. The precore mutation G1896A was identified in 35% of all specimens, and was more frequently observed in genotype B (41%) than genotype C (3%; p<0.0001). 2012 PloS one Abstract HBV G1896A 21 27 Precore 4 11 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. 17.9% patients with cirrhosis and 24.6% hepatocellular carcinoma cases were ADV-resistant with rtA181T/V mutations in the S-gene. 2012 PloS one Abstract HBV A181T;A181V 97;97 104;104 S;RT 122;95 123;97 Liver cirrhosis;Hepatocellular carcinoma 20;40 29;64 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. A1896T was found more frequently in fulminant hepatic failure compared to acute viral hepatitis patients (p = 0.038). 2012 PloS one Abstract HBV A1896T 0 6 Acute Hepatitis B 74 95 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. C1914G core gene mutation was associated with the hepatocellular carcinoma (32.2%) compared to other groups. 2012 PloS one Abstract HBV C1914G 0 6 C 7 11 Hepatocellular carcinoma 50 74 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. CONCLUSION: Mutations such as T1762/A1764, T1753V and C1914G were usually associated with advanced forms of liver disease and had an increased risk of HCC. 2012 PloS one Abstract HBV T1753V;C1914G 43;54 49;60 Liver disease;Hepatocellular carcinoma 108;151 121;154 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. T1753V mutation was significantly higher in patients with cirrhosis of liver (34.6%) than in chronic hepatitis (18.9%) and hepatocellular carcinoma patients (21.2%; p = 0.001). 2012 PloS one Abstract HBV T1753V 0 6 Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma 58;93;123 76;110;147 22720699 Effects of mutations in the X gene of hepatitis B virus on the virus replication. Cells bearing the constructs with double mutations A1762T/G1764A contained the lowest levels of hepatitis B e antigen (HBeAg). 2012 Acta virologica Abstract HBV G1764A;A1762T 58;51 64;57 C;C 108;119 117;124 22720699 Effects of mutations in the X gene of hepatitis B virus on the virus replication. Lowest expression of HBV X protein was in constructs that had both A1762T/G1764A and 1726-1730 CTGAG mutations. 2012 Acta virologica Abstract HBV G1764A;A1762T 74;67 80;73 X 25 26 22720699 Effects of mutations in the X gene of hepatitis B virus on the virus replication. The double mutation A1762T/G1764A increased whereas the nt 1726-1730 CTGAG mutations decreased the levels of released virion-associated and intracellular HBV DNA. 2012 Acta virologica Abstract HBV G1764A;A1762T 27;20 33;26 22720699 Effects of mutations in the X gene of hepatitis B virus on the virus replication. To confirm the effects of these mutations on the virus replication efficiency, substitutions nt 1726-1730 CTGAG and A1762T/G1764A in the HBV X (HBX) gene region were investigated alone or in combination. 2012 Acta virologica Abstract HBV G1764A;A1762T 123;116 129;122 X;X 144;141 147;142 22728692 Lamivudine plus adefovir or telbivudine plus adefovir for chronic hepatitis B patients with suboptimal response to adefovir. After 12-month treatment, 8.1% (3/37) of patients in group A and 5.7% (2/35) of patients in group B had VR; among patients in group A, two had rtM204V/I and rtL180M and one had rtN236T, whereas the two patients in group B had rtM204I+rtL180M. 2012 Antiviral therapy Abstract HBV M204V;M204I;L180M;N236T;M204I;L180M 145;145;159;179;228;236 152;152;164;184;233;241 RT;RT;RT;RT;RT 143;157;177;226;234 145;159;179;228;236 22729192 YMDD motif mutations in chronic hepatitis B antiviral treatment naive patients: a multi-center study. YMDD mutation was accompanied by L180M mutation in 154 (76.9%) patients. 2012 The Brazilian journal of infectious diseases Abstract HBV L180M 33 38 P 0 4 22762143 A pilot randomized controlled trial of dual-plasmid HBV DNA vaccine mediated by in vivo electroporation in chronic hepatitis B patients under lamivudine chemotherapy. The incidence of dual-site mutations of rtM204/I/S+rtL180M was significantly lower (P = 0.03) with an identified lower virological breakthrough (VBT) rate (P = 0.03) in patients receiving LAM+DNA vaccine than LAM monotherapy, accompanied with a significant higher positive T-cell response rate in patients receiving LAM+DNA vaccine (P = 0.03). 2012 Journal of viral hepatitis Abstract HBV L180M 53 58 RT;RT;S 40;51;49 42;53;50 22767306 Evaluation of a "home-made" method to determine viral genotype and characterize mutations conferring drug resistance in chronic hepatitis B patients. G173L mutations were not found. 2012 Le infezioni in medicina Abstract HBV G173L 0 5 22767306 Evaluation of a "home-made" method to determine viral genotype and characterize mutations conferring drug resistance in chronic hepatitis B patients. M204I mutations were more frequent in genotype D, M204V in genotype A isolates. 2012 Le infezioni in medicina Abstract HBV M204I;M204V 0;50 5;55 22767306 Evaluation of a "home-made" method to determine viral genotype and characterize mutations conferring drug resistance in chronic hepatitis B patients. The only genotype C isolate tested revealed a different pattern (E263D and I269L). 2012 Le infezioni in medicina Abstract HBV E263D;I269L 65;75 70;80 22767306 Evaluation of a "home-made" method to determine viral genotype and characterize mutations conferring drug resistance in chronic hepatitis B patients. The resistance loci were also reliably detected with mostly combined L180M and M204V/I mutations as the local patterns. 2012 Le infezioni in medicina Abstract HBV L180M;M204V;M204I 69;79;79 74;86;86 22795596 Association between S21 substitution in the core protein of hepatitis B virus and fulminant hepatitis. A newly developed PCR system detecting T1961V showed that HBV/B1 and low viral load were independent factors for the mutation among chronic infection patients. 2012 Journal of clinical virology Abstract HBV T1961V 39 45 Chronic HBV infection 132 149 22795596 Association between S21 substitution in the core protein of hepatitis B virus and fulminant hepatitis. CONCLUSIONS: T1961V/C1962D mutations were found frequently in FHB, especially in HBV/B1. 2012 Journal of clinical virology Abstract HBV C1962D;T1961V 20;13 26;19 Fulminant Hepatitis B 62 65 22795596 Association between S21 substitution in the core protein of hepatitis B virus and fulminant hepatitis. RESULTS: In the analysis of full-genome sequences of HBV/B1 (FHB, n=11; non-FHB, n=35) including those from the databases, mutations at nt 1961 [T1961V (not T)] and nt 1962 [C1962D (not C)], which change S21 in the core protein, were found more frequently in FHB than in non-FHB (100% vs. 2012 Journal of clinical virology Abstract HBV C1962D;T1961V 174;145 180;151 C 215 219 Fulminant Hepatitis B 259 262 22795596 Association between S21 substitution in the core protein of hepatitis B virus and fulminant hepatitis. When our FHB and AHB samples were compared, T1961V and C1962D were significantly more frequent in FHB than in AHB, both in the overall analysis (46% vs. 2012 Journal of clinical virology Abstract HBV C1962D;T1961V 55;44 61;50 Fulminant Hepatitis B;Acute Hepatitis B;Acute Hepatitis B 98;110;17 101;113;20 22825811 Case report: management and HBV sequencing in a patient co-infected with HBV and HIV failing tenofovir. No known mutations, such as rtA181T/V associated with rtN236T or A194T that are associated with reduced susceptibility or resistance to tenofovir were detected. 2012 Journal of medical virology Abstract HBV A181T;A181V;N236T;A194T 30;30;56;65 37;37;61;70 RT;RT 28;54 30;56 22825811 Case report: management and HBV sequencing in a patient co-infected with HBV and HIV failing tenofovir. The rtR192PR, which is located in the B domain near the rtA194T, occurring in a context of a very complex substitutions patterns, might be associated with resistance to tenofovir. 2012 Journal of medical virology Abstract HBV A194T 58 63 RT;RT 4;56 6;58 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. HBV breakthrough was observed only in HBeAg-positive patients and 6 of 7 patients presenting HBV breakthrough had the rtM204I/V mutations associated with 3TC resistance along with rtL180M and/or rtV173L. 2012 PloS one Abstract HBV M204I;M204V;L180M;V173L 120;120;182;197 127;127;187;202 RT;RT;RT;C 118;180;195;38 120;182;197;43 22878399 Clonal analysis of the quasispecies of antiviral-resistant HBV genomes in patients with entecavir resistance during rescue treatment and successful treatment of entecavir resistance with tenofovir. All clones had >=1 of the S202G, T184F, T184A, T184L, T184I and M250V ETV resistance mutations. 2013 Antiviral therapy Abstract HBV S202G;T184F;T184A;T184L;T184I;M250V 26;33;40;47;54;64 31;38;45;52;59;69 22878399 Clonal analysis of the quasispecies of antiviral-resistant HBV genomes in patients with entecavir resistance during rescue treatment and successful treatment of entecavir resistance with tenofovir. Almost all clones had L180M and M204V 3TC resistance mutations before and during combination therapy. 2013 Antiviral therapy Abstract HBV L180M;M204V 22;32 27;37 22878399 Clonal analysis of the quasispecies of antiviral-resistant HBV genomes in patients with entecavir resistance during rescue treatment and successful treatment of entecavir resistance with tenofovir. The percentages of detected clones bearing 3TC (rtL180M and rtM204V) and ETV mutations did not change with rescue 3TC+ADV therapy. 2013 Antiviral therapy Abstract HBV L180M;M204V 50;62 55;67 RT;RT 48;60 50;62 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. And the rtD134E/G/N/S mutations were also higher in chronic hepatitis B patients (22/100, 22.0%) and cirrhotic patients (21/100, 21.0%) than that in hepatocellular carcinoma patients (10/100, 10.0%, P = 0.021 and P = 0.032 respectively). 2012 Liver international Abstract HBV D134E;D134G;D134N;D134S 10;10;10;10 21;21;21;21 RT 8 10 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 52;149;101 71;173;110 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. RESULTS: Among 467 consecutive eligible patients (262 chronic hepatitis B patients, 105 cirrhotic patients and 100 hepatocellular carcinoma patients), the nucleos(t)ide analogues-related mutations (rtI169T, rtV173L, rtL180M, rtA181T, rtS202C, rtM204I/V, rtN236T) were found. 2012 Liver international Abstract HBV I169T;V173L;L180M;A181T;S202C;M204I;M204V;N236T 200;209;218;227;236;245;245;256 205;214;223;232;241;252;252;261 RT;RT;RT;RT;RT;RT;RT 198;207;216;225;234;243;254 200;209;218;227;236;245;256 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 54;115;88 73;139;97 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. rtS106C, rtD134E/G/N/S and A-B interdomain mutations may be associated with necro-inflammation, immune response and cirrhosis development at ages older than 40. 2012 Liver international Abstract HBV S106C;D134E;D134G;D134N;D134S 2;11;11;11;11 7;22;22;22;22 RT;RT 0;9 2;11 Necrotic inflammation;Liver cirrhosis 76;116 94;125 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. The naturally occurring mutation, rtS106C mutation was higher in chronic hepatitis B patients (14/100, 14.0%) and cirrhotic patients (14/100, 14.0%) than that in hepatocellular carcinoma patients (4/100, 4.0%, P = 0.013). 2012 Liver international Abstract HBV S106C 36 41 RT 34 36 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 65;162;114 84;186;123 22892524 Evolution of adefovir-resistant HBV polymerase gene variants after switching to tenofovir disoproxil fumarate monotherapy. Apart from an M204Q mutation in one sample, no new HBV polymerase gene mutations were found. 2012 Antiviral therapy Abstract HBV M204Q 14 19 P 55 65 22892524 Evolution of adefovir-resistant HBV polymerase gene variants after switching to tenofovir disoproxil fumarate monotherapy. METHODS: In 10 HBV-monoinfected patients (9 male, mean age 47 +-11 [range 27-67] years, 6 hepatitis B e antigen-positive) with virological breakthrough during ADV treatment associated with the mutations rtN236T and/or rtA181T/V, HBV polymerase gene variants were studied during up to 24 months of consecutive monotherapy with TDF by population sequencing, line probe assay and clonal analysis. 2012 Antiviral therapy Abstract HBV N236T;A181T;A181V 205;220;220 210;227;227 C;P;RT;RT 102;233;203;218 111;243;205;220 HBV infections 15 31 22892524 Evolution of adefovir-resistant HBV polymerase gene variants after switching to tenofovir disoproxil fumarate monotherapy. To assess the clinical relevance of this cross-resistance, we studied the evolution of HBV polymerase gene variants in patients with genotypic resistance against ADV (rtN236T and/or rtA181V/T) during TDF treatment. 2012 Antiviral therapy Abstract HBV N236T;A181V;A181T 169;184;184 174;191;191 P;RT;RT 91;167;182 101;169;184 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. CP mutations C1653T, T1753V, A1762T/G1764A, and C1766T/T1768A were associated with higher HBV-DNA level and increased liver disease severity. 2012 PloS one Abstract HBV G1764A;T1768A;A1762T;C1766T;C1653T;T1753V 36;55;29;48;13;21 42;61;35;54;19;27 Core promoter 0 2 Liver disease 118 131 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. HBV-DNA levels in patients with G1896A were not significantly different from the other patients carrying wild-type strains (p = 0.84). 2012 PloS one Abstract HBV G1896A 32 38 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Multiple logistic regression analysis showed that older age (>= 40 years), male sex, high viral load (>4.3 log(10) IU/mL) and CP mutations C1653T, T1753V, A1762T/G1764A, and C1766T/T1768A were independent risk factors for AdLD development. 2012 PloS one Abstract HBV G1764A;T1768A;A1762T;C1766T;C1653T;T1753V 162;181;155;174;139;147 168;187;161;180;145;153 Core promoter 126 128 Aggressive Hepatitis and advanced liver disease 222 226 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The pre-C stop codon G1896A mutation was the most frequent (83.9%) and was associated with a lower risk of AdLD development (OR, 0.4; 95% CI, 0.15-1.04; p = 0.04). 2012 PloS one Abstract HBV G1896A 21 27 Precore 4 9 Aggressive Hepatitis and advanced liver disease 107 111 22919746 [Hepatitis B virus (HBV) mutation in enhancer I (HBV Enh I)/X-promoter and the relationship between chronic HBV-related disease spectrum]. (2) In the patients were infected with HBV genotype B, A1123Y mutation in LC was significantly higher than in CHB (30.56% vs. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A1123Y 55 61 Chronic Hepatitis B;Liver cirrhosis 110;74 113;76 22919746 [Hepatitis B virus (HBV) mutation in enhancer I (HBV Enh I)/X-promoter and the relationship between chronic HBV-related disease spectrum]. (3) Multivariate regression analyses showed that A1317G (OR = 5.706, 95% CI [1.770-18.837], P = 0.004) and T1323C (A = 5.810, 95% CI [1.114-30.306], P = 0.037) mutation were risk factors for HCC. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A1317G;T1323C 49;107 55;113 Hepatocellular carcinoma 191 194 22919746 [Hepatitis B virus (HBV) mutation in enhancer I (HBV Enh I)/X-promoter and the relationship between chronic HBV-related disease spectrum]. 8.58%, chi2 = 8.607, P = 0.003, A = 4.324,95% CI [1.544-2.109]); A1317G mutation in HCC was significantly higher than in CHB (30.77% vs. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV A1317G 65 71 Hepatocellular carcinoma;Chronic Hepatitis B 84;121 87;124 22919746 [Hepatitis B virus (HBV) mutation in enhancer I (HBV Enh I)/X-promoter and the relationship between chronic HBV-related disease spectrum]. In the patients were infected with HBV genotype C, T1323C mutation in HCC was significantly higher than in CHB (30.61% vs. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV T1323C 51 57 Hepatocellular carcinoma;Chronic Hepatitis B 70;107 73;110 22930502 Emergence of lamivudine resistance hepatitis B virus mutations in pregnant women infected with HBV and HIV receiving antiretroviral prophylaxis for the prevention of mother-to-infant transmission in Malawi. Resistance mutations (M204I in five cases and L180M + M204I/V in one case) were present in 6 (28.6%) patients. 2012 Journal of medical virology Abstract HBV M204I;M204V;L180M;M204I 22;54;46;54 27;61;51;61 22930503 Clinical characteristics and chronicity of acute hepatitis B induced by lamivudine-resistant strains. Among these patients, six harbored the rtM204I mutation, two harbored the rtL180M + rtM204I mutations, one harbored the rtM204I + rtM204V mutations, one harbored the rtL80I + rtM204I mutations, and one harbored the rtV173L + rtL180M + rtM204V mutations. 2012 Journal of medical virology Abstract HBV M204I;L180M;M204I;M204I;M204V;L80I;M204I;V173L;L180M;M204V 41;76;86;122;132;168;177;217;227;237 46;81;91;127;137;172;182;222;232;242 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 39;74;84;120;130;166;175;215;225;235 41;76;86;122;132;168;177;217;227;237 22930503 Clinical characteristics and chronicity of acute hepatitis B induced by lamivudine-resistant strains. This patient was infected with genotype C HBV that had LAM-resistance mutations (rtL180M + rtM204I). 2012 Journal of medical virology Abstract HBV L180M;M204I 83;93 88;98 RT;RT 81;91 83;93 22941290 High prevalence of the B2+C2 subgenotype mixture in patients with chronic hepatitis B in Eastern China. A double mutation (G1896A) in the PC was significantly more common in subgenotype B2+C2 than in subgenotype B2+C1. 2012 Acta pharmacologica Sinica Abstract HBV G1896A 19 25 Precore 34 36 22960601 Comparison of rescue strategies in lamivudine-resistant patients with chronic hepatitis B. Additionally, the strategy of switching to ADV monotherapy induced more single rtA181T mutations. 2012 Antiviral research Abstract HBV A181T 81 86 RT 79 81 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. In conclusion, HBV basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. 2012 Antiviral research Abstract HBV G1764A;A1762T 56;49 62;55 BCP;C;S 19;146;110 38;151;115 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. The A1762T/G1764A mutations were found to be more prevalent in genotype C than that in genotype B HBV [62.14% (64/103) vs. 2012 Antiviral research Abstract HBV G1764A;A1762T 11;4 17;10 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. The A1762T/G1764A or G1896A mutations were detected in 125specimens (125/192, 65.10%), in which 77 (77/125, 61.60%) existed as subpopulations. 2012 Antiviral research Abstract HBV G1764A;A1762T;G1896A 11;4;21 17;10;27 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. The emergence of A1762T/G1764A mutations was also found to be associated with an older age, an elevated ALT/AST level, and a lower HBsAg level in serum [wild-type vs. 2012 Antiviral research Abstract HBV G1764A;A1762T 24;17 30;23 S 131 136 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. The present study was aimed to obtain baseline information of basal core promoter A1762T/G1764A and precore G1896A mutations of hepatitis B virus (HBV) in 192 HBeAg-positive chronically-infected Chinese patients, who were potential candidates for antiviral treatment. 2012 Antiviral research Abstract HBV G1764A;A1762T;G1896A 89;82;108 95;88;114 BCP;C;Precore 62;159;100 81;164;107 22960603 Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients. There is no statistically significant link between G1896A and genotypes. 2012 Antiviral research Abstract HBV G1896A 51 57 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. Furthermore, the integrated viral sequences in both groups had a similar low frequency of C1653T, T1753V and A1762T/G1764A mutations. 2012 PloS one Abstract HBV G1764A;A1762T;C1653T;T1753V 116;109;90;98 122;115;96;104 22964149 [Clinical characteristics and effect of secondary individualized therapy in chronic hepatitis B patients infected with the rtA181 mutation hepatitis B virus]. RESULTS: The rtA181T mutation was found in 64.8% (35/54) of patients with rtA181 mutation HBV. 2012 Zhonghua gan zang bing za zhi Abstract HBV A181T 15 20 RT;RT 13;74 15;76 22964149 [Clinical characteristics and effect of secondary individualized therapy in chronic hepatitis B patients infected with the rtA181 mutation hepatitis B virus]. The serological index was determined for carriers of the rtA181T/V mutation. 2012 Zhonghua gan zang bing za zhi Abstract HBV A181T;A181V 59;59 66;66 RT 57 59 22964149 [Clinical characteristics and effect of secondary individualized therapy in chronic hepatitis B patients infected with the rtA181 mutation hepatitis B virus]. The serum HBsAg level was higher in carriers of the rtA181T mutation than in carriers of the rtA181V mutation (3.80+/-0.45 vs. 2012 Zhonghua gan zang bing za zhi Abstract HBV A181T;A181V 54;95 59;100 S;RT;RT 10;52;93 15;54;95 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Site-directed mutagenesis was then utilized to introduce three genotype A mutations - M103I, K122R and G145A - associated with occult HBV infection in vivo, alone and in combination, into the wild-type HBsAg vectors. 2012 Journal of viral hepatitis Abstract HBV M103I;K122R;G145A 86;93;103 91;98;108 S 202 207 HBV infections 134 147 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The G145A mutation resulted in significantly decreased extracellular and intracellular HBsAg expression in vitro. 2012 Journal of viral hepatitis Abstract HBV G145A 4 9 S 87 92 22967107 Specific primer sets used to amplify by PCR the hepatitis B virus overlapping S/Pol region select different viral variants. D144A S-escape mutant was detected with two of the primer sets, while the rtL217R mutant within the Pol - conferring resistance to Adefovir - could be picked up with a different pair of primer sets. 2012 Journal of viral hepatitis Abstract HBV L217R;D144A 76;0 81;5 P;RT;S 100;74;6 103;76;7 22997074 Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B. A1679G/C, T1753C/G/A, A1762T/G and A1762T-G1764A were more prevalent in older patients. 2012 Journal of medical virology Abstract HBV A1679G;A1679C;T1753C;T1753G;T1753A;A1762T;A1762G;A1762T;G1764A 0;0;10;10;10;22;22;35;42 8;8;20;20;20;30;30;41;48 22997074 Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B. G1896A (74.8%), G1764A/T/C (71.5%), G1899A (54.4%) and T1678C (52%) were the most common. 2012 Journal of medical virology Abstract HBV G1896A;G1764A;G1764T;G1764C;G1899A;T1678C 0;16;16;16;36;55 6;26;26;26;42;61 22997074 Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B. High DNA levels were associated with G1899A or G1764T/C-C1766G-C1799G and advanced liver disease with mutations at positions 1762, 1764 and/or 1899 alone or in double or triple mutations. 2012 Journal of medical virology Abstract HBV G1764T;G1764C;G1899A;C1766G;C1799G 47;47;37;56;63 55;55;43;62;69 Liver disease 83 96 22997074 Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B. Special attention should be paid to A1703T, T1678C/G-A1703T, and A1652G-A1679G mutations probably specific of Tunisians sequences; they were observed in 40.6%, 41.5% and 30.1% respectively. 2012 Journal of medical virology Abstract HBV T1678C;T1678G;A1703T;A1703T;A1652G;A1679G 44;44;36;53;65;72 52;52;42;59;71;78 23022497 Evaluation of anti-HBV drug resistant mutations among patients with acute symptomatic hepatitis B in the United States. Clonal sequencing was conducted on 192 clones isolated from three patients and showed rtA181T, rtM250V and rtS202G mutations at an overall frequency of 1.54%, 1.39%, and 1.67% respectively. 2013 Journal of hepatology Abstract HBV A181T;M250V;S202G 88;97;109 93;102;114 RT;RT;RT 86;95;107 88;97;109 23023992 Do different lamivudine-resistant hepatitis B genotypes carry the same risk of entecavir resistance? All the patients with rtM204I and rtA181 mutants had undetectable HBV DNA from 18th month. 2013 Journal of medical virology Abstract HBV M204I 24 29 RT;RT 22;34 24;36 23023992 Do different lamivudine-resistant hepatitis B genotypes carry the same risk of entecavir resistance? Compared to the patients with the rtM204I mutant, patients with the rtM204V mutant had increased risk of virologic breakthrough (80% vs. 2013 Journal of medical virology Abstract HBV M204I;M204V 36;70 41;75 RT;RT 34;68 36;70 23023992 Do different lamivudine-resistant hepatitis B genotypes carry the same risk of entecavir resistance? In summary, lamivudine-resistant HBV patients with the rtM204V mutation have the highest risk of developing entecavir resistance, and entecavir monotherapy should be avoided. 2013 Journal of medical virology Abstract HBV M204V 57 62 RT 55 57 23023992 Do different lamivudine-resistant hepatitis B genotypes carry the same risk of entecavir resistance? The presence of a HBV polymerase rtM204V mutation at the baseline was found to be the major risk factor for adverse outcomes. 2013 Journal of medical virology Abstract HBV M204V 35 40 RT;P 33;22 35;32 23023992 Do different lamivudine-resistant hepatitis B genotypes carry the same risk of entecavir resistance? Those with the rtM204I and rtA181V mutations may have lower risks, but regular surveillance for viral breakthrough is required. 2013 Journal of medical virology Abstract HBV M204I;A181V 17;29 22;34 RT;RT 15;27 17;29 23026293 Genotype-specific mutations in the polymerase gene of hepatitis B virus potentially associated with resistance to oral antiviral therapy. Comparison with sequencing data of patients failing LMV or LAM+ADV therapy revealed an higher frequency of novel genotype-specific mutations if compared with naive patients: 3 mutations under LAM monotherapy in HBV-D (rtS85F; rtL91I; rtC256G) and 3 mutations under ADV therapy in HBV-A (rtI53V; rtW153R; rtF221Y). 2012 Antiviral research Abstract HBV S85F;L91I;C256G;I53V;W153R;F221Y 220;228;236;289;297;306 224;232;241;293;302;311 RT;RT;RT;RT;RT;RT 218;226;234;287;295;304 220;228;236;289;297;306 23026293 Genotype-specific mutations in the polymerase gene of hepatitis B virus potentially associated with resistance to oral antiviral therapy. In HBV-D treated patients the dominant resistance mutation was rtL80V (31.4%) and rtM204I (60%) in LAM+ADV group while LAM-treated patients showed a preference of rtM204V (51.9%). 2012 Antiviral research Abstract HBV L80V;M204I;M204V 65;84;165 69;89;170 RT;RT;RT 63;82;163 65;84;165 23026293 Genotype-specific mutations in the polymerase gene of hepatitis B virus potentially associated with resistance to oral antiviral therapy. Interestingly, none of HBV-A patients had mutation rtM204I under ADV add-on treatment but all of them had the "V" AA substitution. 2012 Antiviral research Abstract HBV M204I 53 58 RT 51 53 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Isolates with sV168A occurred more frequently in participants with viral loads >200 IU per ml (p<0.05) and only sS174N occurred more frequently in HBsAg(-ve) than in HBsAg(+ve) individuals (p<0.05). 2012 PloS one Abstract HBV V168A;S174N 14;112 20;118 S;S;S;S 14;112;147;166 15;113;152;171 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Mutations affecting HBeAg expression at the transcriptional (1762T1764A), translational (Kozak 1809-1812, initiation 1814-1816, G1896A with C1858T), or post translational levels (G1862T), were responsible for the high HBeAg-negativity observed. 2012 PloS one Abstract HBV C1858T;G1862T;G1896A 140;179;128 146;185;134 C;C 20;218 25;223 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Prior to initiation of ART, ten percent, 3 of 29 isolates sequenced, had drug resistance mutations rtV173L, rtL180M+rtM204V and rtV214A, respectively. 2012 PloS one Abstract HBV V173L;V214A;L180M;M204V 101;130;110;118 106;135;115;123 RT;RT;RT;RT 99;108;116;128 101;110;118;130 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. ps1I48V/T occurred more frequently in females than males (p<0.05). 2012 PloS one Abstract HBV I48V;I48T 3;3 9;9 PreS1 0 3 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The following mutations occurred significantly more frequently in HBV isolated in this study than in strains of the same cluster of the phylogenetic tree: ps1F25L, ps1V88L/A; ps2Q10R, ps2 R48K/T, ps2A53V and sQ129R/H, sQ164A/V/G/D, sV168A and sS174N (p<0.05). 2012 PloS one Abstract HBV V88L;V88A;F25L;Q10R;R48K;R48T;A53V;Q129R;Q129H;Q164A;Q164V;Q164G;Q164D;V168A;S174N 167;167;158;178;188;188;199;208;208;218;218;218;218;232;243 173;173;162;182;194;194;203;216;216;230;230;230;230;238;249 PreS1;PreS1;PreS2;PreS2;PreS2;S;S;S;S 155;164;175;184;196;208;218;232;243 158;167;178;187;199;209;219;233;244 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The G1862T mutation occurred only in subgenotype A1 isolates, which were found in one third (7/21) of HBsAg(-ve) participants, but in none of the 18 HBsAg(+ve) participants (p<0.05). 2012 PloS one Abstract HBV G1862T 4 10 S;S 102;149 107;154 2304145 Hepatitis B viruses with precore region defects prevail in persistently infected hosts along with seroconversion to the antibody against e antigen. A point mutation from G to A at nucleotide 83, converting Trp-28 (TGG) to a stop codon (TAG), was by far the commonest and was observed in HBV DNA clones from 16 (89%) of 18 carriers seropositive for anti-HBe. 1990 Journal of virology Abstract HBV G83A 22 45 C 205 208 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Six (preC-W28*, C-P5H/L/T, C-E83D, C-I97F/L, C-L100I and C-Q182K/*) and seven types (preC-W28*, preC-G29D, C-D32N/H, C-E43K, C-P50A/H/Y, C-A131G/N/P and C-S181H/P) of mutations in the preC/C region were found to be related to HCC and to affect the HBeAg serostatus, respectively. 2012 PloS one Abstract HBV E83D;I97F;I97L;L100I;Q182K;G29D;D32N;D32H;E43K;A131G;A131N;A131P;S181H;S181P;W28X;P5H;P5L;P5T;Q182X;W28X;P50A;P50H;P50Y 29;37;37;47;59;101;109;109;119;139;139;139;155;155;10;18;18;18;59;90;127;127;127 33;43;43;52;66;105;115;115;123;148;148;148;162;162;14;25;25;25;66;94;135;135;135 C;C;C;C;C;C;C;C;C;C;C;Precore;Precore;Precore;Precore;C 16;27;35;45;57;107;117;125;137;153;248;5;85;96;184;189 17;28;36;46;58;108;118;126;138;154;253;9;89;100;188;190 Hepatocellular carcinoma 226 229 23080492 Influence of B cells in liver fibrosis associated with hepatitis B virus harboring basal core promoter mutations. Coefficients of logistic regression showed that the effect of increasing IgD-positive B cells in rising odds of the liver disease is the same in the patients with BCP mutation A1762T-G1764A and in the patients without mutation, nevertheless the effect of APRIL is not similar in these two groups of patients. 2012 Journal of medical virology Abstract HBV A1762T;G1764A 176;183 182;189 BCP 163 166 Liver disease 116 129 23080492 Influence of B cells in liver fibrosis associated with hepatitis B virus harboring basal core promoter mutations. Logistic regression in patients with BCP A1762T-G1764A mutations demonstrated that increasing one score of APRIL decreased the odds of fibrosis stage about 8%. 2012 Journal of medical virology Abstract HBV A1762T;G1764A 41;48 47;54 BCP 37 40 23080492 Influence of B cells in liver fibrosis associated with hepatitis B virus harboring basal core promoter mutations. Twenty-seven patients (47.4%) harbored the A1762T-G1764A BCP mutations. 2012 Journal of medical virology Abstract HBV A1762T;G1764A 43;50 49;56 BCP 57 60 23096938 Multidrug-resistant hepatitis B virus resulting from sequential monotherapy with lamivudine, adefovir, and entecavir: clonal evolution during lamivudine plus adefovir therapy. Among 6 sets of 20 clones obtained before salvage therapy, all clones harbored the rtM204V mutation, and ETV-resistant mutations were detected with the rtM204V in 108 clones. 2013 Journal of medical virology Abstract HBV M204V;M204V 85;154 90;159 RT;RT 83;152 85;154 23096938 Multidrug-resistant hepatitis B virus resulting from sequential monotherapy with lamivudine, adefovir, and entecavir: clonal evolution during lamivudine plus adefovir therapy. Among 9 sets of 20 clones obtained during salvage therapy, 39 clones harbored rtA181T/V +- rtN236T mutations, which were detected in the absence of rtM204 and ETV-resistant mutations in 37 clones (94.9%). 2013 Journal of medical virology Abstract HBV A181T;A181V;N236T 80;80;93 87;87;98 RT;RT;RT 78;91;148 80;93;150 23096938 Multidrug-resistant hepatitis B virus resulting from sequential monotherapy with lamivudine, adefovir, and entecavir: clonal evolution during lamivudine plus adefovir therapy. Only two clones (5.1%) harbored both rtA181T/V and ETV-resistant mutations. 2013 Journal of medical virology Abstract HBV A181T;A181V 39;39 46;46 RT 37 39 23096938 Multidrug-resistant hepatitis B virus resulting from sequential monotherapy with lamivudine, adefovir, and entecavir: clonal evolution during lamivudine plus adefovir therapy. The rtA181T/V mutation emerged after reversion from ETV-resistant mutants to wild-type HBV. 2013 Journal of medical virology Abstract HBV A181T;A181V 6;6 13;13 RT 4 6 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. RESULTS: The genomic changes such as the G1896A at precore, the A1762T/G1764A at BCP, the C1653T and the T1753V at X gene, and pre-S2 deletion were not significantly associated with postoperative recurrence of HCC or survival of patients after curative resection. 2013 Annals of surgical oncology Abstract HBV G1764A;G1896A;A1762T;C1653T;T1753V 71;41;64;90;105 77;47;70;96;111 BCP;Precore;PreS2;X 81;51;127;115 84;58;133;116 Hepatocellular carcinoma 210 213 23109450 Occult HBV infection among anti-HBc positive HIV-infected patients in apex referral centre, Eastern India. Several mutations were detected but not the common immune escape mutant G145R. 2012 Annals of hepatology Abstract HBV G145R 72 77 23112104 Distinct evolution and predictive value of hepatitis B virus precore and basal core promoter mutations in interferon-induced hepatitis B e antigen seroconversion. UNLABELLED: Precore (PC) (G1896A) and basal core promoter (BCP) (A1762T/G1764A) mutations of the hepatitis B virus (HBV) genome often emerge in chronic hepatitis B (CHB) patients. 2013 Hepatology (Baltimore, Md.) Abstract HBV G1764A;G1896A;A1762T 72;26;65 78;32;71 BCP;BCP;Precore;Precore 38;59;21;12 57;62;23;19 Chronic Hepatitis B;Chronic Hepatitis B 144;165 163;168 23114756 Low-level persistence of drug resistance mutations in hepatitis B virus-infected subjects with a past history of Lamivudine treatment. Sanger sequencing identified >=1 LAM resistance mutations (rtL80I/V, rtM204I, and rtA181T) in samples from 5 (11%) of 46 LAM-experienced and none of 45 LAM-naive subjects (0%; P = 0.06). 2013 Antimicrobial agents and chemotherapy Abstract HBV L80I;L80V;M204I;A181T 61;61;71;84 67;67;76;89 RT;RT;RT 59;69;82 61;71;84 23114756 Low-level persistence of drug resistance mutations in hepatitis B virus-infected subjects with a past history of Lamivudine treatment. UDPS detected >=1 LAM resistance mutations (rtL80I/V, rtV173L, rtL180M, rtA181T, and rtM204I/V) in 10 (22%) of the 46 LAM-experienced subjects, including 5 in whom LAM resistance mutations were not identified by Sanger sequencing. 2013 Antimicrobial agents and chemotherapy Abstract HBV L80I;L80V;V173L;L180M;A181T;M204I;M204V 46;46;56;65;74;87;87 52;52;61;70;79;94;94 RT;RT;RT;RT;RT 44;54;63;72;85 46;56;65;74;87 23134956 [Clinical analysis of hepatitis B virus mutations related to adefovir dipivoxil among patients with chronic hepatitis B virus infection in eastern Zhejiang province]. The mutated sites occur at multiple loci, mostly at rtA181T and rtV214A. 2012 Zhonghua yi xue za zhi Abstract HBV A181T;V214A 54;66 59;71 RT;RT 52;64 54;66 23134956 [Clinical analysis of hepatitis B virus mutations related to adefovir dipivoxil among patients with chronic hepatitis B virus infection in eastern Zhejiang province]. The single mutated site was mostly at rtA181T (46.59%) and at rtV214A (11.36%). 2012 Zhonghua yi xue za zhi Abstract HBV A181T;V214A 40;64 45;69 RT;RT 38;62 40;64 23146520 Hepatitis B reactivation in a renal transplant patient due to a surface antigen mutant strain: a case report. Sequence analysis of the surface (S) antigen corresponding to the amino acid residues 101-186 (including the a-determinant region) revealed a genotype D mutant strain, subtype ayw3 with a single amino acid substitution D144E within the S gene. 2012 Transplantation proceedings Abstract HBV D144E 219 224 S;S;S 34;236;25 35;237;32 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. However, long-term use of NAs increases the possibility of developing drug-resistant viral mutations such as the HBV rtA181T/sW172 mutation, which increases the risk of HCC recurrence. 2012 Hepatitis monthly Abstract HBV A181T 119 124 RT;S 117;125 119;126 Hepatocellular carcinoma 169 172 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. BACKGROUND: The effects of Hepatitis B virus (HBV) rtA181T/sW172* mutation on viral replication and pathogenicity was concerned recently. 2012 Virology journal Abstract HBV W172X;A181T 59;53 65;58 RT;S 51;59 53;60 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. CONCLUSIONS: In the case of the HBV rtA181T/sW172* mutation, the secretion of serum HBsAg was impaired, whereas HBV DNA replication and HBsAg/HBcAg expression were increased in liver. 2012 Virology journal Abstract HBV W172X;A181T 44;38 50;43 C;S;S;RT;S 142;84;136;36;44 147;89;141;38;45 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. METHODS: The rtA181T/sW172* mutant plasmid was constructed using the pHBV4.1 (wild type HBV) as a template. 2012 Virology journal Abstract HBV W172X;A181T 21;15 27;20 RT;S 13;21 15;22 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. This study aimed to investigate the biological characteristics of rtA181T/sW172* mutant strain of HBV in animal model. 2012 Virology journal Abstract HBV W172X;A181T 74;68 80;73 RT;S 66;74 68;75 23180290 A case of hepatitis B reactivation due to the hepatitis B virus escape mutant in a patient undergoing chemotherapy. A sequence revealed HBV genotype C (HBsAg subtype adw) with immune escape mutations, F8L, S34L, F41S, G44V, F93C, V96G, L110I, C149Y and F161Y. 2012 Virologica Sinica Abstract HBV F8L;S34L;F41S;G44V;F93C;V96G;L110I;C149Y;F161Y 85;90;96;102;108;114;120;127;137 88;94;100;106;112;118;125;132;142 S 36 41 23183198 Correlation between hepatitis B virus genotypes and clinical outcomes. Accumulating evidence indicated that higher plasma HBV DNA levels, infection with HBV genotype C, as well as mutations at 1653T, 1753V, and A1762T/G1764A are independently associated with the risk of HCC in Asian men. 2012 Japanese journal of infectious diseases Abstract HBV G1764A;A1762T 147;140 153;146 Hepatocellular carcinoma 200 203 23197889 Clonal evolution of hepatitis B virus polymerase gene mutations during lamivudine-adefovir combination treatment. The emergence of resistance mutations to LMV, such as rtM204V/I and/or rtL180M, were found in all patients. 2012 World journal of gastroenterology Abstract HBV M204V;M204I;L180M 56;56;73 63;63;78 RT;RT 54;71 56;73 23197889 Clonal evolution of hepatitis B virus polymerase gene mutations during lamivudine-adefovir combination treatment. The rtA181V/T mutations were not suppressed by the LMV-ADV combination therapy. 2012 World journal of gastroenterology Abstract HBV A181V;A181T 6;6 13;13 RT 4 6 23197889 Clonal evolution of hepatitis B virus polymerase gene mutations during lamivudine-adefovir combination treatment. The rtA181V/T mutations were predominantly identified during the ADV treatment in the LMV-resistant patients. 2012 World journal of gastroenterology Abstract HBV A181V;A181T 6;6 13;13 RT 4 6 23197889 Clonal evolution of hepatitis B virus polymerase gene mutations during lamivudine-adefovir combination treatment. Thirty-nine of 64 clones showed an rtA181V/T mutation and six clones showed combined mutations in rt181 and rt236. 2012 World journal of gastroenterology Abstract HBV A181V;A181T 37;37 44;44 RT;RT;RT 35;98;108 37;100;110 23207226 [Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure]. Mutations G1899A, T1753V, and A1846T were correlated with disease recovery. 2012 Zhonghua gan zang bing za zhi Abstract HBV G1899A;T1753V;A1846T 10;18;30 16;24;36 23207226 [Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure]. Significant decreases in the MELD score were accompanied by decreases in the A1846T mutation. 2012 Zhonghua gan zang bing za zhi Abstract HBV A1846T 77 83 23207226 [Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure]. Single mutations (A1762T, G1764A, T1753V, G1896A, and G1899A) and combined mutations (A1762T + G1764A, G1896A + G1899A, T1753V+ A1762T + G1764A, G1896A + G1899A + A1762T + G1764A, and A1762T + G1764A + G1896A) were more frequently detected in HB-ACLF patients than in CHB patients (P less than 0.05). 2012 Zhonghua gan zang bing za zhi Abstract HBV A1762T;G1764A;T1753V;G1896A;G1899A;A1762T;G1764A;G1896A;G1899A;T1753V;A1762T;G1764A;G1896A;G1899A;A1762T;G1764A;A1762T;G1764A;G1896A 18;26;34;42;54;86;95;103;112;120;128;137;145;154;163;172;184;193;202 24;32;40;48;60;92;101;109;118;126;134;143;151;160;169;178;190;199;208 Chronic Hepatitis B;Acute on chronic liver failure 268;243 271;250 23207226 [Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure]. The G1899A, T1753C, and A1846T mutations were associated with HB-ACLF response to treatment and improvement in liver function. 2012 Zhonghua gan zang bing za zhi Abstract HBV G1899A;T1753C;A1846T 4;12;24 10;18;30 Acute on chronic liver failure 62 69 23237841 2'-Fluoro-6'-methylene-carbocyclic adenosine phosphoramidate (FMCAP) prodrug: in vitro anti-HBV activity against the lamivudine-entecavir resistant triple mutant and its mechanism of action. FMCA demonstrated significant antiviral activity against wild-type as well as lamivudine-entecavir resistant triple mutant (L180M+M204V+S202G). 2013 Bioorganic & medicinal chemistry letters Abstract HBV L180M;M204V;S202G 124;130;136 129;135;141 23237841 2'-Fluoro-6'-methylene-carbocyclic adenosine phosphoramidate (FMCAP) prodrug: in vitro anti-HBV activity against the lamivudine-entecavir resistant triple mutant and its mechanism of action. Novel 2'-fluoro-6'-methylene-carbocyclic adenosine (FMCA) monophosphate prodrug (FMCAP) was synthesized and evaluated for its in vitro anti-HBV potency against a lamivudine-entecavir resistant clone (L180M+M204V+S202G). 2013 Bioorganic & medicinal chemistry letters Abstract HBV L180M;M204V;S202G 200;206;212 205;211;217 23247054 Single-nucleotide polymorphism genotyping using a novel multiplexed electrochemical biosensor with nonfouling surface. A pre-core mutation in the hepatitis B virus (HBV) genome at G1896A and two adjacent polymorphisms in the human CYP2C19 genome at C680T and G681A were analysed. 2013 Biosensors & bioelectronics Abstract HBV G1896A;C680T;G681A 61;130;140 67;135;145 Precore 2 10 23254298 Hepatitis B virus surface antigen (HBsAg)-positive and HBsAg-negative hepatitis B virus infection among mother-teenager pairs 13 years after neonatal hepatitis B virus vaccination. In comparison with the (hp)HBI cases, those with (hn)HBI had a lower level of HBV load and a higher proportion of genotype-C strains, which were accompanied by differentiated mutations (Q129R, K141E, and Y161N) of the "a" determinant of the HBV surface gene. 2013 Clinical and vaccine immunology Abstract HBV Q129R;K141E;Y161N 186;193;204 191;198;209 S 245 252 23261845 The amino acid substitutions rtP177G and rtF249A in the reverse transcriptase domain of hepatitis B virus polymerase reduce the susceptibility to tenofovir. The HBV mutants with rtP177G and rtF249A were found to have reduced susceptibility to TDF in vitro with a resistance index of 2.53 and 12.16, respectively. 2013 Antiviral research Abstract HBV P177G;F249A 23;35 28;40 RT;RT 21;33 23;35 23261845 The amino acid substitutions rtP177G and rtF249A in the reverse transcriptase domain of hepatitis B virus polymerase reduce the susceptibility to tenofovir. The mutations at rtL77F (sS69C), rtF88L (sF80Y), and rtP177G (sR169G) also significantly affected HBsAg expression. 2013 Antiviral research Abstract HBV L77F;F88L;P177G;S69C;F80Y;R169G 19;35;55;25;41;62 23;39;60;30;46;68 S;RT;RT;RT;S;S;S 98;17;33;53;25;41;62 103;19;35;55;26;42;63 23265059 [The panels of serums, containing various subtypes and mutant forms of HBsAg, to evaluate the diagnostics sensitivity of kits oa reagents detecting HBsAg]. The testing of reagents kits to detect HBsAg using twi panels containing recombinant and native variants of HBsAg, demonstrated that these kits enable to detect various sero-vatriants of HBsAg (ayw2, adw2, ayw3varA, ayw3varB, adrq-) in concentration 0.1-0.01 IU/l and the so called elusive mutant forms of HBsAg of recombinant and native origin (G145R, Q129R, Q129H, Q129L, T143K, T126N, T126S, D144A, M133L, K141E and P142S). 2012 Klinicheskaia laboratornaia diagnostika Abstract HBV G145R;Q129R;Q129H;Q129L;T143K;T126N;T126S;D144A;M133L;K141E;P142S 346;353;360;367;374;381;388;395;402;409;419 351;358;365;372;379;386;393;400;407;414;424 S;S;S;S 39;108;187;306 44;113;192;311 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. Critically, the V124W mutant interfered with replication of wild-type HBV in a dose-dependent manner, mimicking AEf activity. 2013 Journal of virology Abstract HBV V124W 16 21 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. Guided by the structure of an AEf-bound core, we designed a structural mimic of AEf-bound core protein, the V124W mutant. 2013 Journal of virology Abstract HBV V124W 108 113 C;C 40;90 44;94 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. In addition, the V124W mutant was shown to adopt a more compact conformation than that of the wild type, confirming the allosteric regulation in capsid assembly. 2013 Journal of virology Abstract HBV V124W 17 22 Capsid 145 151 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. In biochemical studies, the V124W mutant recapitulated the effects of AEfs, with fast assembly kinetics and a strong protein-protein association energy. 2013 Journal of virology Abstract HBV V124W 28 33 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. In cell culture, the V124W mutant behaved like a potent AEf: expression of HBV carrying the V124W mutant was defective for genome replication. 2013 Journal of virology Abstract HBV V124W;V124W 21;92 26;97 23283960 Genetically altering the thermodynamics and kinetics of hepatitis B virus capsid assembly has profound effects on virus replication in cell culture. Suppression of viral replication by the V124W mutant suggests that mutations that fill the HAP site are not a path for HBV to escape from AEfs. 2013 Journal of virology Abstract HBV V124W 40 45 23296324 Epidemiology of HBV S-gene mutants in the Liguria Region, Italy: Implications for surveillance and detection of new escape variants. Analyzed sequences revealed G145R mutation in 8/256 (3.1%) examined sequences, it was alone in 5 patients and accompanied by other HBsAg mutations in 3 samples. 2013 Human vaccines & immunotherapeutics Abstract HBV G145R 28 33 S 131 136 23296324 Epidemiology of HBV S-gene mutants in the Liguria Region, Italy: Implications for surveillance and detection of new escape variants. HBsAg resulted undetectable by 3 of the 8 samples, derived from patients with multiple mutations: T126I-T131A-C139Y-E/D144G, T126I-M133L, and P120Q-T126I. 2013 Human vaccines & immunotherapeutics Abstract HBV T126I;T131A;C139Y;E144G;D144G;T126I;M133L;P120Q;T126I 98;104;110;116;116;125;131;142;148 103;109;115;123;123;130;136;147;153 S 0 5 23296324 Epidemiology of HBV S-gene mutants in the Liguria Region, Italy: Implications for surveillance and detection of new escape variants. The emergence of these mutants, at least the G145R, has already been addressed as a public health concern because of its capability of escaping the immune system. 2013 Human vaccines & immunotherapeutics Abstract HBV G145R 45 50 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. Baseline samples (n = 105) from adefovir refractory patients were tested for the presence of rtN236T using a highly sensitive allele-specific PCR assay with an rtN236T detection cut-off of 0.5%. 2013 Journal of viral hepatitis Abstract HBV N236T;N236T 95;162 100;167 RT;RT 93;160 95;162 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. Despite low levels of cross-resistance in vitro, TDF similarly suppresses wild-type and rtN236T mutant viruses in vivo. 2013 Journal of viral hepatitis Abstract HBV N236T 90 95 RT 88 90 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. In conclusion, the rtN236T mutant virus showed similar HBV DNA decline kinetics to wild-type virus in adefovir refractory patients who switched to TDF or FTC/TDF. 2013 Journal of viral hepatitis Abstract HBV N236T 21 26 RT 19 21 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. In patients with rtN236T, wild-type and rtN236T mutant virus showed similar rates of HBV DNA decline with no statistically significant difference observed at week 4. 2013 Journal of viral hepatitis Abstract HBV N236T;N236T 19;42 24;47 RT;RT 17;40 19;42 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. In vitro, the rtN236T adefovir dipivoxil (ADV)-associated resistance mutation confers low-level cross-resistance to tenofovir: 3- to 13-fold changes in EC(50) from wild type. 2013 Journal of viral hepatitis Abstract HBV N236T 16 21 RT 14 16 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. Moreover, the proportion of rtN236T remained unchanged in patients in either arm of the study during treatment. 2013 Journal of viral hepatitis Abstract HBV N236T 30 35 RT 28 30 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. The median change in total HBV DNA at week 24 was comparable for patients with rtN236T detected at baseline (-3.7 log(10) copies/mL, n = 14) as compared to patients with wild-type HBV (-3.2 log(10) copies/mL, n = 90). 2013 Journal of viral hepatitis Abstract HBV N236T 81 86 RT 79 81 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. The rtN236T mutation was detected at baseline in 14.3% (14/98) of analysable patient samples (0.5-93.2%, rtN236T percentage range). 2013 Journal of viral hepatitis Abstract HBV N236T;N236T 6;107 11;112 RT;RT 4;105 6;107 23301548 Hepatitis B virus wild-type and rtN236T populations show similar early HBV DNA decline in adefovir refractory patients on a tenofovir-based regimen. This study evaluated the clinical response of rtN236T mutant viruses by comparing their early viral load decay kinetics to wild-type viruses in chronic HBV monoinfected patients harbouring rtN236T prior to initiating TDF or emtricitabine (FTC)/TDF therapy. 2013 Journal of viral hepatitis Abstract HBV N236T;N236T 48;191 53;196 RT;RT 46;189 48;191 Chronic Hepatitis B 144 155 23301549 Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains. All rtN236T- or rtA181V/T-containing constructs, regardless of concomitant PC or BCP mutations, were resistant to adefovir, but remained susceptible to telbivudine, entecavir and tenofovir. 2013 Journal of viral hepatitis Abstract HBV N236T;A181V;A181T 6;18;18 11;25;25 BCP;Precore;RT;RT 81;75;4;16 84;77;6;18 23301549 Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains. HBV rtA181T mutants displayed abolished hepatitis B surface antigen (HBsAg) secretion, owing to a sW172* stop codon in the overlapping envelope gene. 2013 Journal of viral hepatitis Abstract HBV A181T;W172X 6;98 11;104 S;S;RT;S;S 135;69;4;98;52 143;74;6;99;59 23301549 Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains. The adefovir-resistant polymerase mutations rtN236T, rtA181V and rtA181T showed a drastically reduced viral replication compared with WT. 2013 Journal of viral hepatitis Abstract HBV N236T;A181V;A181T 46;55;67 51;60;72 P;RT;RT;RT 23;44;53;65 33;46;55;67 23301549 Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains. Therefore, HBV constructs with wild type (WT) or adefovir-resistant rtN236T, rtA181V and rtA181T mutations, with or without concomitant PC or BCP mutations, were analysed in vitro using molecular assays. 2013 Journal of viral hepatitis Abstract HBV N236T;A181V;A181T 70;79;91 75;84;96 BCP;Precore;RT;RT;RT 142;136;68;77;89 145;138;70;79;91 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. BACKGROUND: To glean insights into the relationship among hepatitis B virus (HBV) genotype/subgenotypes, A1762T/G1764A mutations and advanced liver disease such as liver cirrhosis (LC) and hepatocellular carcinoma (HCC) in Southeast China. 2012 Iranian journal of public health Abstract HBV G1764A;A1762T 112;105 118;111 Liver disease;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 142;164;189;215;181 155;179;213;218;183 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Both subgenotype C2 infection and A1762T/G1764A mutations were associated with LC and HCC with cirrhosis, subgenotype C2 (OR=2.033, 95%CI=1.246-3.323, P=0.003 for LC vs CHB; OR=3.247, 95%CI=1.742-6.096, P=0.001 for HCC with cirrhosis vs CHB; respectively ), and A1762T/G1764A mutations (OR=1.914, 95%CI=1.188-3.085, P=0.005 for LC vs CHB; OR=2.996, 95%CI=1.683-5.353, P=0.002 for HCC with cirrhosis vs CHB; respectively), but no differences in the frequencies of both variants between LC and HCC with cirrhosis groups were found. 2012 Iranian journal of public health Abstract HBV G1764A;G1764A;A1762T;A1762T 41;269;34;262 47;275;40;268 Hepatocellular carcinoma;Liver cirrhosis;Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis;Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 86;95;215;224;237;380;389;402;492;501;79;485;169;334;163;328 89;104;218;233;240;383;398;405;495;510;81;487;172;337;165;330 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. CONCLUSIONS: HBV subgenotype C2 infection and A1762T/G1764A mutations are both risk factors of LC and HCC with cirrhosis development in the patients with CHB in Southeast China, but all no helpful for predicting HCC development in LC patients. 2012 Iranian journal of public health Abstract HBV G1764A;A1762T 53;46 59;52 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 102;111;154;212;95;231 105;120;157;215;97;233 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Fluorescence quantitative polymerase chain reaction (FQ-PCR) was used to detect A1762T/G1764A mutations. 2012 Iranian journal of public health Abstract HBV G1764A;A1762T 87;80 93;86 23322992 Long-term treatment outcomes of clevudine in antiviral-naive patients with chronic hepatitis B. The virologic breakthrough in the clevudine group occurred in 9 (7.6%) patients at weeks 48 and 15 (12.7%) patients at week 96, which primarily corresponded to genotypic mutations of rtM204I and/or rtL180M. 2012 World journal of gastroenterology Abstract HBV M204I;L180M 185;200 190;205 RT;RT 183;198 185;200 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The aim of this study was to assess the HBV genotype distribution pattern and the prevalence of pre-S, T1753V and A1762T/G1764A mutations among the Minangkabau HBV carriers. 2013 Virology journal Abstract HBV G1764A;A1762T;T1753V 121;114;103 127;120;109 PreS 96 101 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The basal core promoter (BCP) region was amplified and directly sequenced to analyze T1753V and A1762T/G1764A mutations. 2013 Virology journal Abstract HBV G1764A;A1762T;T1753V 103;96;85 109;102;91 BCP;BCP 4;25 23;28 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The prevalence of pre-S mutations, including both the pre-S deletion and pre-S2 start codon mutation, was 41.0%, and the T1753V and A1762T/G1764A mutations were found in 51.9% and 71.2% respectively. 2013 Virology journal Abstract HBV G1764A;A1762T;T1753V 139;132;121 145;138;127 PreS;PreS;PreS2 18;54;73 23;59;79 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The prevalence of pre-S, A1762T/G1764A, and T1753V mutations was higher among the Minangkabau compared to Indonesian HBV carriers in general. 2013 Virology journal Abstract HBV G1764A;A1762T;T1753V 32;25;44 38;31;50 PreS 18 23 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. Indeed, 58.8% of patients bearing G1896A mutation were HBeAg-negative while 16.7% were positive. 2012 Hepatitis monthly Abstract HBV G1896A 34 40 C 55 60 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. RESULTS: Twenty-one patients (52.5%) showed PC G1896A mutation and 11 (27.5%) carried A1762T/G1764A double mutations. 2012 Hepatitis monthly Abstract HBV G1764A;A1762T;G1896A 93;86;47 99;92;53 Precore 44 46 23355917 Efficacy of 3 years of adefovir monotherapy in chronic hepatitis B patients with lamivudine resistance. The remaining 49 cases underwent biochemical rebound accompanied by rtM204I/V or rtL180M mutation. 2012 World journal of hepatology Abstract HBV M204I;M204V;L180M 70;70;83 77;77;88 RT;RT 68;81 70;83 23383660 New HBV subgenotype D9, a novel D/C recombinant, identified in patients with chronic HBeAg-negative infection in Eastern India. Interestingly, compared to other subgenotypes of HBV/D, D9 isolates had a higher frequency of mutations (A1762T and G1764A) in the basal core promoter region that had been implicated in the development of hepatocellular carcinoma. 2013 Journal of viral hepatitis Abstract HBV A1762T;G1764A 105;116 111;122 BCP 131 150 Hepatocellular carcinoma 205 229 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Also, the A1762T/G1764A double mutation may act in synergy with C1653T to increase the risk of HCC in patients chronically infected with HBV genotype C2. 2013 Journal of viral hepatitis Abstract HBV G1764A;A1762T;C1653T 17;10;64 23;16;70 Hepatocellular carcinoma 95 98 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. G1896A in the precore region and C1653T mutation in the X region of genotype C2 HBV are important risk factors for HCC development. 2013 Journal of viral hepatitis Abstract HBV G1896A;C1653T 0;33 6;39 X;Precore 56;14 57;21 Hepatocellular carcinoma 115 118 23386590 Interaction of signal transducer and activator of transcription 3 polymorphisms with hepatitis B virus mutations in hepatocellular carcinoma. In multivariate regression analyses, multiplicative interaction of rs1053004 with T1674C/G significantly increased HCC risk, whereas rs2293152 and A1726C interaction reduced it, adjusting for covariates including HBV mutations in the enhancer II/basal core promoter/precore region; the interaction of rs4796793 with preS2 start codon mutation significantly increased HCC risk, adjusting for covariates including HBV mutations in the preS region. 2013 Hepatology (Baltimore, Md.) Abstract HBV T1674C;T1674G;A1726C 82;82;147 90;90;153 BCP;Enh II;Precore;PreS;PreS2 246;234;266;433;316 265;245;273;437;321 Hepatocellular carcinoma;Hepatocellular carcinoma 115;367 118;370 23386590 Interaction of signal transducer and activator of transcription 3 polymorphisms with hepatitis B virus mutations in hepatocellular carcinoma. rs2293152 GG was significantly associated with high viral load (>=1 x 10(4) copies/mL) (AOR, 1.37; 95%, CI 1.01-1.88) and increased frequencies of T1674C/G (AOR, 1.61; 95% CI, 1.06-2.46) and A1762T/G1764A (AOR, 1.64; 95% CI, 1.14-2.35). 2013 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;T1674C;T1674G 198;191;147;147 204;197;155;155 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. The precore G1896A mutation abrogates the expression of HBeAg. 2013 The open virology journal Abstract HBV G1896A 12 18 C;Precore 56;4 61;11 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. The precore mutations (G1896A) and the double mutation (T1762/A1764) in the basal core promoter are important mutations that alter expression of the hepatitis B e antigen (HBeAg). 2013 The open virology journal Abstract HBV G1896A 23 29 BCP;C;C;Precore 76;161;172;4 95;170;177;11 23403838 A novel method for the analysis of drug-resistant phenotypes of hepatitis B virus. A novel resistance test method was developed by co-transfection with pHBV1.3-XhoI and -rtL180M/M204V and treatment with various NA concentrations. 2013 International journal of molecular medicine Abstract HBV M204V;L180M 95;89 100;94 RT 87 89 23403838 A novel method for the analysis of drug-resistant phenotypes of hepatitis B virus. Different bands composed of pHBV1.3-XhoI or -rtL180M/M204V were used to distinguish NA susceptibility. 2013 International journal of molecular medicine Abstract HBV M204V;L180M 53;47 58;52 RT 45 47 23403838 A novel method for the analysis of drug-resistant phenotypes of hepatitis B virus. In this study, a T1699C substitution was introduced into the x gene of pHBV1.3 to generate an additional XhoI site, termed pHBV1.3-XhoI, which is a nonsense mutation and does not influence protein expression, HBV replication ability, or NA susceptibility. 2013 International journal of molecular medicine Abstract HBV T1699C 17 23 X 61 62 23403838 A novel method for the analysis of drug-resistant phenotypes of hepatitis B virus. The bands composed of pHBV1.3 were more sharply reduced by lamivudine (LMV) than -rtL180M/M204V. 2013 International journal of molecular medicine Abstract HBV M204V;L180M 90;84 95;89 RT 82 84 23404231 Characteristics of hepatitis viruses among Egyptian children with acute hepatitis. The A1762T/G1764A double mutation, and the T1846A and G1896A single mutations were common in children with occult HBV infection. 2013 International journal of oncology Abstract HBV G1764A;A1762T;T1846A;G1896A 11;4;43;54 17;10;49;60 HBV infections 114 127 23404231 Characteristics of hepatitis viruses among Egyptian children with acute hepatitis. The Y134F amino acid mutation in the 'alpha' determinant region was detected in all of the patients. 2013 International journal of oncology Abstract HBV Y134F 4 9 S 38 56 23408582 High frequency of complex mutational patterns in lamivudine resistant hepatitis B virus isolates. Both mutations, especially mutation rtM204V, were most often accompanied by compensatory mutations rtV173L and rtL180M but also by mutations conferring entecavir (n = 5) or adefovir resistance (n = 4). 2013 Journal of medical virology Abstract HBV M204V;V173L;L180M 38;101;113 43;106;118 RT;RT;RT 36;99;111 38;101;113 23408582 High frequency of complex mutational patterns in lamivudine resistant hepatitis B virus isolates. Clonal analysis of these seven quasispecies even disclosed the presence of HBV isolates carrying further stop codons and in one case the occurrence of resistance mutation rtA181T without the stop codon mutation sW172*. 2013 Journal of medical virology Abstract HBV A181T;W172X 173;211 178;217 RT;S 171;211 173;212 23408582 High frequency of complex mutational patterns in lamivudine resistant hepatitis B virus isolates. In this study mutational patterns of 60 HBV isolates harboring drug resistance mutations rtM204V or rtM204I were retrospectively analyzed. 2013 Journal of medical virology Abstract HBV M204V;M204I 91;102 96;107 RT;RT 89;100 91;102 23408582 High frequency of complex mutational patterns in lamivudine resistant hepatitis B virus isolates. Interestingly, only one HBV clone carried the resistance mutations rtM204V and rtA181T. 2013 Journal of medical virology Abstract HBV M204V;A181T 69;81 74;86 RT;RT 67;79 69;81 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Notably, classical antiviral resistance mutations (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C /G/I -rtM204V/I-rtN236T-rtM250V) were not detected. 2013 Virology journal Abstract HBV L80I;L80V;M204V;M204I;I169T;V173L;L180M;A181T;A181V;A181S;T184A;T184S;T184G;T184C;A194T;S202C;N236T;M250V;S202G;S202I 53;53;134;134;62;70;78;86;86;86;98;98;98;98;112;120;144;152;120;120 59;59;141;141;67;75;83;95;95;95;109;109;109;109;117;125;149;157;130;130 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 51;60;68;76;84;96;110;118;132;142;150 53;62;70;78;86;98;112;120;134;144;152 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. In this study, it was attempted to evaluate the impact of putative rtI233V substitution on adefovir action by homology modeling and docking studies. 2013 Bioinformation Abstract HBV I233V 69 74 RT 67 69 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The HBVrt nucleotide sequence containing rtI233V mutation was obtained from the treatment-naive chronic hepatitis B subject. 2013 Bioinformation Abstract HBV I233V 43 48 RT 41 43 Chronic Hepatitis B 96 115 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The role of the rtI233V mutation and adefovir resistance remains contradictory. 2013 Bioinformation Abstract HBV I233V 18 23 RT 16 18 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Therefore, it was predicted that rtI233V substitution may not independently affect the antiviral action of adefovir and incoming dNTP binding. 2013 Bioinformation Abstract HBV I233V 35 40 RT 33 35 23432545 Molecular epidemiology of hepatitis B in the Indigenous people of northern Australia. The canonical sG145R vaccine-escape variant was detected in the surface antigen of virus from two patients. 2013 Journal of gastroenterology and hepatology Abstract HBV G145R 14 20 S;S 14;64 15;71 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. FINDINGS: The findings are that 1-48preS/S is secreted, and that removal of the N-terminal myristoylation signal in its G2A variant reduced secretion slightly, but significantly. 2013 Virology journal Abstract HBV G2A 120 123 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. The glycosylation pattern of 1-48preS/S was not affected by the removal of the myristoylation signal (G2A mutant) but was different than natural L protein, whereby N4 of the preS and N3 of the S domain were ectopically glycosylated. 2013 Virology journal Abstract HBV G2A 102 105 S;PreS;S 145;174;193 154;178;194 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Detection of minor variant viral quasispecies of the rtV173L+rtL180M+rtM204V combination mutation in the hepatitis B virus (HBV) polymerase mediating both lamivudine resistance and vaccine escape is potentially important for tracking the development and evolution of resistance within both individuals and populations. 2013 Journal of virological methods Abstract HBV V173L;L180M;M204V 55;63;71 60;68;76 P;RT;RT;RT 129;53;61;69 139;55;63;71 23458523 Efficacy and safety of telbivudine plus adefovir dipivoxil combination therapy and entecavir monotherapy for HBeAg-positive chronic hepatitis B patients with resistance to adefovir dipivoxil. During the 48-week treatment period, two patients in the ETV monotherapy group had viral breakthrough and the strains were confirmed to be of a variant associated with ETV resistance (rtM204V+ rtL180M+ rtT184G), while one patient receiving LdT plus ADV had viral breakthrough and an LdT-associated resistance mutation (rtM204I) was detected. 2013 Journal of viral hepatitis Abstract HBV M204V;L180M;T184G;M204I 186;195;204;321 191;200;209;326 RT;RT;RT;RT 184;193;202;319 186;195;204;321 23462214 Efficacy of entecavir switch therapy in chronic hepatitis B patients with incomplete virological response to telbivudine. Although rtM204I and/or rtL180M was detected in 3 of 7 patients with incomplete virological response to entecavir, none of the patients with HBV DNA<2,000 IU/ml during telbivudine treatment harboured these amino acid substitutions. 2013 Antiviral therapy Abstract HBV M204I;L180M 11;26 16;31 RT;RT 9;24 11;26 23465393 Virology and clinical sequelae of long-term antiviral therapy in a North American cohort of hepatitis B virus (HBV)/human immunodeficiency virus type 1 (HIV-1) co-infected patients. Anti-HBV drug resistant mutations were detected in 54% (6/11) (i.e., any combination of rtV173L, rtL180M, M204V) and 45% (5/11) had an immune escape mutation (sP120S). 2013 Journal of clinical virology Abstract HBV V173L;L180M;M204V;P120S 90;99;106;159 95;104;111;165 RT;RT;S 88;97;159 90;99;160 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. RESULTS: After alignment of protein coding sequences, the rtN236T mutation was observed in two (6.6%) patients, while twenty-eight others had neither rtN236T, nor rtA181V/T mutation. 2013 Iranian journal of microbiology Abstract HBV N236T;N236T;A181V;A181T 60;152;165;165 65;157;172;172 RT;RT;RT 58;150;163 60;152;165 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. The mutations known as causing adefovir resistance, rtN236T and rtA181V/T, are detected within the D and B functional domain of the HBV polymerase, respectively. 2013 Iranian journal of microbiology Abstract HBV N236T;A181V;A181T 54;66;66 59;73;73 P;RT;RT 136;52;64 146;54;66 23485939 Virological response and antiviral resistance mutations in chronic hepatitis B subjects experiencing entecavir therapy: an Indian subcontinent perspective. However, one subject was exclusively detected with rtV173L mutation. 2013 Antiviral research Abstract HBV V173L 53 58 RT 51 53 23485939 Virological response and antiviral resistance mutations in chronic hepatitis B subjects experiencing entecavir therapy: an Indian subcontinent perspective. Molecular modeling, docking and MDS studies revealed that the rtV173L mutation cannot confer resistance to entecavir independently. 2013 Antiviral research Abstract HBV V173L 64 69 RT 62 64 23487374 Prophylactic effect of antiretroviral therapy on hepatitis B virus infection. HBV genotype and LAM-resistant mutation (rtM204V/I) were analyzed in cases that became HBsAg-positive. 2013 Clinical infectious diseases Abstract HBV M204V;M204I 43;43 50;50 S;RT 87;41 92;43 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Resistance to adefovir (rtA181T/V) was detected in 2.7% of patients. 2013 Virology journal Abstract HBV A181T;A181V 26;26 33;33 RT 24 26 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. In multivariate regression analyses, rs4938723 in dominant model increased HCC risk (AOR = 1.62, 95% CI = 1.05-2.49), whereas its multiplicative interaction with C1730G, a HBV mutation inversely associated with HCC risk, reduced HCC risk (AOR = 0.34, 95% CI = 0.15-0.81); rs11614913 strengthened the G1896A effect but attenuated the A3120G/T effect on HCC risk. 2013 PloS one Abstract HBV C1730G;G1896A;A3120G;A3120T 162;300;333;333 168;306;341;341 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 75;211;229;352 78;214;232;355 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. rs4938723 CC genotype and rs11614913 TC genotype were significantly associated with increased frequencies of the HCC-related HBV mutations T1674C/G and G1896A, respectively. 2013 PloS one Abstract HBV T1674C;T1674G;G1896A 139;139;152 147;147;158 Hepatocellular carcinoma 113 116 23517325 Combined core promoter mutations and pre-S deletion of HBV may not increase the risk of HCC: a geographical epidemiological study in Guangxi, China. AIMS: To determine whether the findings that HBV basal core promoter (BCP) A1762T, G1764A double mutations, pre-S deletions and a combination of both are risk factors of HCC are supported by geographical epidemiology. 2013 Liver international Abstract HBV A1762T;G1764A 75;83 81;89 BCP;BCP;PreS 49;70;108 68;73;113 Hepatocellular carcinoma 170 173 23547448 [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. C1673T/C1799G double mutations in Ba were determined in 106 (96. 4%) samples, which was significantly higher than in C1 (14.3%) and C2 (12.5%) subgenotype (P < 0.0001). 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV C1799G;C1673T 7;0 13;6 23547448 [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. CONCLUSION: In Ba subgenotype, double mutations of C1673T/C1799G is much popular than in C1 and C2; the mutation has no effect on HBV replication, and may not be associated with the outcome of chronic HBV infection. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV C1799G;C1673T 58;51 64;57 Chronic HBV infection 193 214 23547448 [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. OBJECTIVE: To explore the biological and clinical significance of the double mutations of C1673T/C1799G in HBV C promoter (CP). 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV C1799G;C1673T 97;90 103;96 Core promoter;Core promoter 111;123 121;125 23547448 [Significance of the double mutations of C1673T/C1799G in HBV C promoter]. The C to T mutation at nucleotide 1673 and C to G at nucleotide 1799 were analyzed in different subgenotypes, and the relationships of C1673T/C1799G double mutations with HBV replication, the expression of HBeAg, and with the severity of liver disease after chronic HBV infection were studied. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV C1799G;C1673T;C1673T;C1799G 142;135;4;43 148;141;38;68 C 206 211 Liver disease;Chronic HBV infection 238;258 251;279 23557465 Entecavir for the treatment of patients with hepatitis B virus-related decompensated cirrhosis. The use of entecavir monotherapy in patients with a known rtM204V lamivudine-resistant mutation should be avoided due to increased risk of developing entecavir resistance and failing treatment. 2013 Expert opinion on pharmacotherapy Abstract HBV M204V 60 65 RT 58 60 23588723 Molecular analysis of the hepatitis B virus presurface and surface gene in patients from eastern China with occult hepatitis B. There were unique amino acid mutations at the G145 position other than G145R. 2013 Journal of medical virology Abstract HBV G145R 71 76 23588725 Snapshot on drug-resistance rate and profiles in patients with chronic hepatitis B receiving nucleos(t)ide analogues in clinical practice. Complex mutational patterns characterized by the co-presence of rtM204V/I-rtA181T/V (impairing the efficacy of all anti-HBV drugs) were detected in four patients (2.7%) with virological rebound. 2013 Journal of medical virology Abstract HBV M204V;M204I;A181T;A181V 66;66;76;76 73;73;83;83 RT;RT 64;74 66;76 23594698 Comparison of INNO-LIPA and TRUGENE assays for genotyping and drug-resistance mutations in chronic hepatitis B virus infection. In relation to drug-resistance mutations, the sensitivity of the line probe assay was lower than TRUGENE because INNO-LIPA could not detect two mutations (S202G and V214A). 2013 Intervirology Abstract HBV S202G;V214A 155;165 160;170 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Mutations related to lamivudine, adefovir, telbivudine, and entecavir occurred in (YMDD) 4% (n = 13), (SVQ) 17.23% (n = 56), (M204I/V + L180M) 2.45% (n = 8) and (M204I) 2.76% (n = 9) of patients, respectively. 2013 Hepatitis monthly Abstract HBV M204I;M204V;L180M;M204I 126;126;136;162 133;133;141;167 P 83 87 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. The predominant mutation of the precore region involves a G to A change at nucleotide1896, which creates a premature stop codon at codon 28. 2013 Hepatitis monthly Abstract HBV G1896A 58 89 Precore 32 39 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. Two mutations of A1762T and G1764A are reported as the most prevalent mutations in the basal core promoter (BCP). 2013 Hepatitis monthly Abstract HBV A1762T;G1764A 17;28 23;34 BCP;BCP 87;108 106;111 23602529 [Low prevalence of hepatitis B virus primary drug resistance in Southern Spain]. RESULTS: rtV173L, a lamivudine compensatory mutation, was detected in two patients (1.9%), rtI233V in one patient, and another one carried the sG145R vaccine escape mutation. 2013 Enfermedades infecciosas y microbiologia clinica Abstract HBV V173L;I233V;G145R 11;93;143 16;98;149 RT;RT;S 9;91;143 11;93;144 23616174 Dynamics of lamivudine-resistant hepatitis B virus strains in patients with entecavir rescue therapy. An additional five patients developed entecavir genotypic resistance, with prior occurrence of lamivudine-resistant mutation (L180 M +- M204 V/I). 2013 Virus genes Abstract HBV L180M;M204V;M204I 126;136;136 132;144;144 23621183 Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. associations between the C1653T mutation and risk of HCC, the results have been inconsistent. 2013 Asian Pacific journal of cancer prevention Abstract HBV C1653T 25 31 Hepatocellular carcinoma 53 56 23621183 Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. However, no significant association was found between the C1653T mutation and HCC risk in HBeAg positive cases. 2013 Asian Pacific journal of cancer prevention Abstract HBV C1653T 58 64 C 90 95 Hepatocellular carcinoma 78 81 23621183 Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. In conclusion, this meta-analysis suggests that the C1653T mutation may be associated with susceptibility to HCC. 2013 Asian Pacific journal of cancer prevention Abstract HBV C1653T 52 58 Hepatocellular carcinoma 109 112 23621183 Hepatitis B virus gene C1653T polymorphism mutation and hepatocellular carcinoma risk: an updated meta-analysis. Seventeen studies with a total of 1,085 HCC cases and 1,365 healthy controls were retrieved.We found a significant association between the C1653T mutation and HCC risk (OR = 2.01, 95%CI= 1.49-2.70). 2013 Asian Pacific journal of cancer prevention Abstract HBV C1653T 139 145 Hepatocellular carcinoma;Hepatocellular carcinoma 40;159 43;162 23627028 [Mutation analysis of the HBV reverse transcriptase in nucleos(t)ide-treated patients with chronic HBV infection]. RtM204 mutations were detected at the highest frequency among 63 mutants (40/63, 63.49%) and found to display 11 combination mutation patterns, in which rtM204I were associated with rtL80I/V and rtL180M, and rtM204V were associated with rtL1l80M, respectively. 2012 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV M204I;L80I;L80V;L180M;M204V 155;184;184;197;210 160;190;190;202;215 RT;RT;RT;RT;RT 0;153;182;195;208 2;155;184;197;210 23637496 Clinical profile, genotype and management updates of hepatitis B virus. The most frequent core promoter mutation is the double A1762T and G1764A nucleotide exchange, which results in a substantial decrease in HBeAg expression but enhanced viral genome replication. 2011 Indian journal of virology Abstract HBV A1762T;G1764A 55;66 61;72 Core promoter;C 18;137 31;142 23658444 Specific amino acid substitutions in the S protein prevent its excretion in vitro and may contribute to occult hepatitis B virus infection. However, the P178R substitution present in all cloned sequences of two OBI strains may contribute significantly to the OBI phenotype. 2013 Journal of virology Abstract HBV P178R 13 18 Occult Hepatitis B;Occult Hepatitis B 71;119 74;122 23658444 Specific amino acid substitutions in the S protein prevent its excretion in vitro and may contribute to occult hepatitis B virus infection. Site-directed-mutagenesis-corrected mutations reversed HBsAg excretion to pattern 1 and, when introduced into a control clone, induced pattern 2 except for Y100S. 2013 Journal of virology Abstract HBV Y100S 156 161 S 55 60 23658444 Specific amino acid substitutions in the S protein prevent its excretion in vitro and may contribute to occult hepatitis B virus infection. The substitution M75T, Y100S, or P178R was present in 4/6 pattern 2 OBI clones. 2013 Journal of virology Abstract HBV M75T;Y100S;P178R 17;23;33 21;28;38 Occult Hepatitis B 68 71 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. In addition, in vitro and in vivo experiments both demonstrated that the HBc L60V variation facilitates viral capsid assembly and increases HBV replication. 2013 Journal of virology Abstract HBV L60V 77 81 Capsid;C 110;73 116;76 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. In this study, we identified the L60V variation in HBc that generates a new HLA-A2-restricted CD8(+) T cell epitope by screening an overlapping 9-mer peptide pool covering HBc and its variants. 2013 Journal of virology Abstract HBV L60V 33 37 C;C 51;172 54;175 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. The HBc L60V variation is correlated with hepatic necroinflammation and higher viral levels, and it may be associated with a poor prognosis in CHB patients. 2013 Journal of virology Abstract HBV L60V 8 12 C 4 7 Chronic Hepatitis B 143 146 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. Therefore, our work provides further dissection of the impact of the HBc L60V variation, which orchestrates HBV replication, viral persistence, and immunopathogenesis during chronic viral infection. 2013 Journal of virology Abstract HBV L60V 73 77 C 69 72 23678186 The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication. These data suggest that the HBc L60V variation can impact both HBV replication and HBV-specific T cell responses. 2013 Journal of virology Abstract HBV L60V 32 36 C 28 31 23679074 Late HBsAg seroreversion of mutated hepatitis B virus after bone marrow transplantation. Despite living without immunosuppressive agents for more than 40 months, she developed a fulminant HBV infection with detection of a mutated hepatitis B virus carrying two immune escape mutations (D144E/G145R) in the HBsAg (HBsIE mutation). 2013 BMC infectious diseases Abstract HBV G145R;D144E 203;197 208;202 S 217 222 HBV infections 99 112 23701433 Sequential analysis of amino acid substitutions with hepatitis B virus in association with nucleoside/nucleotide analog treatment detected by deep sequencing. The lamivudine-resistant mutations at rtL180M and rtM204V and the entecavir-resistant mutation at rtT184L were detected in the first subject. 2014 Hepatology research Abstract HBV L180M;M204V;T184L 40;52;100 45;57;105 RT;RT;RT 38;50;98 40;52;100 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 3, mutations conferring resistance to adefovir at V84I (5%), I169L (1%), and N236H (7%) and entecavir at S202G (2%) were detected. 2013 Gut and liver Abstract HBV V84I;I169L;N236H;S202G 61;72;88;116 65;77;93;121 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 5, M204V/I was detected in 1% and 2% of clones, respectively. 2013 Gut and liver Abstract HBV M204V;M204I 14;14 21;21 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. L80I and V173L were also identified in patient 6. 2013 Gut and liver Abstract HBV L80I;V173L 0;9 4;14 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Patient 2 had substitutions of L80V, W153Q, and L180M. 2013 Gut and liver Abstract HBV L80V;W153Q;L180M 31;37;48 35;42;53 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Patient 4 had mutations at T128N (1%), I169L (1%), V173L (2%), A181V (1%), and Q215H (1%). 2013 Gut and liver Abstract HBV T128N;I169L;V173L;A181V;Q215H 27;39;51;63;79 32;44;56;68;84 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. RESULTS: Among the six patients with LAM failure, the analysis of 100 clones from patient 1 revealed the substitutions L180M in 1% of clones and V173L in 2% of clones. 2013 Gut and liver Abstract HBV L180M;V173L 119;145 124;150 23749665 Global perspective on the natural history of chronic hepatitis B: role of hepatitis B virus genotypes A to J. HBV-genotype C has a higher frequency of basal core promoter (BCP) A1762T/G1764A mutation and preS deletion, and a higher viral load than genotype B. 2013 Seminars in liver disease Abstract HBV G1764A;A1762T 74;67 80;73 BCP;BCP;PreS 41;62;94 60;65;98 23749665 Global perspective on the natural history of chronic hepatitis B: role of hepatitis B virus genotypes A to J. Similarly, genotype D has a higher prevalence of BCP A1762T/G1764A mutation than genotype A. 2013 Seminars in liver disease Abstract HBV G1764A;A1762T 60;53 66;59 BCP 49 52 23773581 Renal transplantation from hepatitis B surface antigen (HBsAg)-positive donors to HBsAg-negative recipients: a case of post-transplant fulminant hepatitis associated with an extensively mutated hepatitis B virus strain and review of the current literature. RESULTS: Molecular analysis revealed multiple mutations in various open reading frames of HBV, the most important being the G145R escape mutation and a frameshift mutation-insertion (1838insA) within the pre-C/C reading frame. 2013 Transplant infectious disease Abstract HBV G145R;1838insA 124;183 129;191 Precore;C 204;210 209;211 23796863 Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen. Furthermore, the HBsAg-mutation sP217L, silent in RT, significantly correlated with M204V/I-related virological-breakthrough and increased HBsAg-quantification in cell-lysate. 2013 The Journal of infection Abstract HBV M204V;M204I;P217L 84;84;32 91;91;38 S;S;RT;S 17;139;50;32 22;144;52;33 23796863 Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen. Indeed, rtS78T (prevalence: 1.1% in drug-naive and 12.2% in adefovir-failing patients) decreased the RT-affinity for adefovir more than the classical adefovir-resistance mutations rtA181 T/V (WT:-9.63 kcal/mol, rtA181T:-9.30 kcal/mol, rtA181V:-7.96 kcal/mol, rtS78T:-7.37 kcal/mol). 2013 The Journal of infection Abstract HBV S78T;A181T;A181V;A181T;A181V;S78T 10;182;182;213;237;261 14;190;190;218;242;265 RT;RT;RT;RT;RT;RT 8;101;180;211;235;259 10;103;182;213;237;261 23796863 Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen. Moreover, rtS78T introduced a stop-codon at HBsAg-position 69, and completely abrogated HBsAg-quantification in both supernatants and cell-lysates, indicating an impaired HBsAg-secretion/production. 2013 The Journal of infection Abstract HBV S78T 12 16 S;S;S;RT 44;88;171;10 49;93;176;12 23796863 Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen. RESULTS: Ten novel RT-mutations (rtN53T-rtS78T-rtS85F-rtS135T-rtA181I-rtA200V-rtK212Q-rtL229V/F-rtM309K) correlated with specific NUC-treatments and classical drug-resistance mutations on divergent evolutionary pathways. 2013 The Journal of infection Abstract HBV N53T;S78T;S85F;S135T;A181I;A200V;K212Q;L229V;L229F;M309K 35;42;49;56;64;72;80;88;88;98 39;46;53;61;69;77;85;95;95;103 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 19;33;40;47;54;62;70;78;86;96 21;35;42;49;56;64;72;80;88;98 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. A plasma sample obtained at the first observation was tested for HBV mutants in the polymerase region by direct sequencing; the antiviral drug-resistant rtM204V/I mutations, the most frequent HBV mutants in Italy, were also sought by the more sensitive allele-specific polymerase chain reaction (PCR). 2013 The Journal of infection Abstract HBV M204V;M204I 155;155 162;162 P;RT 84;153 94;155 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. AIMS: To detect HBV rtM204V/I lamivudine-resistant strains in serum of patients with acute hepatitis B and to assess their biological and clinical significance. 2013 The Journal of infection Abstract HBV M204V;M204I 22;22 29;29 RT 20 22 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. Compared with those with the HBV wild strain, patients with rtM204V/I more frequently showed severe acute hepatitis B (36.4% vs 8.7%; p < 0.05) and lower values of serum HBV DNA (1.77 x 10(6) +- 4.76 x 10(6) vs. 2013 The Journal of infection Abstract HBV M204V;M204I 62;62 69;69 RT 60 62 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. CONCLUSIONS: HBV rtM204V/I lamivudine-resistant strains were detected in serum of 11 (13.7%) patients with acute hepatitis B by allele-specific polymerase chain reaction. 2013 The Journal of infection Abstract HBV M204V;M204I 19;19 26;26 RT 17 19 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. RESULTS: No HBV mutation associated with resistance to nucleos(t)ide analogues was identified by direct sequencing, whereas allele-specific PCR identified HBV strains carrying the substitution rtM204V/I in 11 (13.7%) patients. 2013 The Journal of infection Abstract HBV M204V;M204I 195;195 202;202 RT 193 195 23796869 Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B. The frequent association of rtM204V/I with a more severe acute hepatitis B and with a lower viral load may suggest that greater and/or more prolonged immune pressure might have induced their selection. 2013 The Journal of infection Abstract HBV M204V;M204I 30;30 37;37 RT 28 30 23803196 [Identification of hepatitis B virus YMDD point mutation using peptide nucleic acid clamping PCR]. METHODS: RtM204I (ATT) mutant, rtM204V (GTG) mutant and rtM204 (ATG) wild-type plasmids mixed at different ratios were detected for mutations by PNA clamping PCR assay and direct sequencing, and the sensitivity and specificity of the two methods were compared. 2013 Nan fang yi ke da xue xue bao Abstract HBV M204V 33 38 RT;RT;RT 9;31;56 11;33;58 23804383 Ultrasensitive amplification refractory mutation system real-time PCR (ARMS RT-PCR) assay for detection of minority hepatitis B virus-resistant strains in the era of personalized medicine. The assay showed 100% sensitivity for the detection of mutant variants A181V, T184A, and N236T in samples from 41 chronically HBV-infected patients under antiviral therapy who had developed resistance-associated mutations detected by direct PCR Sanger sequencing. 2013 Journal of clinical microbiology Abstract HBV A181V;T184A;N236T 71;78;89 76;83;94 HBV infections 126 138 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. CONCLUSIONS: Long-term clevudine monotherapy is effective for suppression of serum HBV DNA level and normalization of serum alanine amino transaminase levels, but associated with occurrence of rtM204I mutation. 2013 Hepatitis monthly Abstract HBV M204I 195 200 RT 193 195 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. The rtM204I mutation in HBV polymerase was predominantly detected. 2013 Hepatitis monthly Abstract HBV M204I 6 11 RT;P 4;28 6;38 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. Patients with occult HBVCI had a shorter disease-free (P = 0.002), a shorter overall survival (P = 0.026), a higher bilirubin level (P = 0.003) and a higher prevalence of precore G1896A mutation (P = 0.006) compared with those with overt HBVCI. 2013 PloS one Abstract HBV G1896A 179 185 Precore 171 178 HBV-HCV coinfections;HBV-HCV coinfections 21;238 26;243 23838434 Role of viral genotypes and hepatitis B viral mutants in the risk of hepatocellular carcinoma associated with hepatitis B and C dual infection. CONCLUSIONS: Pre-S deletion, A1762T/G1764A mutation and HCV genotype-1 are important in hepatocarcinogenesis in chronic HBV/HCV dual infection. 2013 Intervirology Abstract HBV G1764A;A1762T 36;29 42;35 PreS 13 18 Hepatocellular carcinoma;HBV-HCV coinfections 88;112 108;123 23838434 Role of viral genotypes and hepatitis B viral mutants in the risk of hepatocellular carcinoma associated with hepatitis B and C dual infection. In the nested case-control study, patients with HCC had a higher HBV DNA level (p < 0.001), a higher frequency of pre-S deletion (p < 0.001) and A1762T/G1764A mutant (p = 0.005), a lower HCV RNA level (p = 0.012) and a higher prevalence of HCV genotype-1 (p = 0.002) than those without. 2013 Intervirology Abstract HBV G1764A;A1762T 152;145 158;151 PreS 114 119 Hepatocellular carcinoma 48 51 23838434 Role of viral genotypes and hepatitis B viral mutants in the risk of hepatocellular carcinoma associated with hepatitis B and C dual infection. Patients with combined HBV mutations (pre-S deletion and A1762T/G1764A mutant) and HCV genotype-1 had a 39-fold increased risk of developing HCC compared to those with A1762T/G1764A and pre-S wild-type strains and HCV genotype non-1. 2013 Intervirology Abstract HBV G1764A;G1764A;A1762T;A1762T 64;175;168;57 70;181;174;63 PreS;PreS 38;186 43;191 Hepatocellular carcinoma 141 144 23838434 Role of viral genotypes and hepatitis B viral mutants in the risk of hepatocellular carcinoma associated with hepatitis B and C dual infection. RESULTS: Age (odds ratio (OR) 1.1), male sex (OR 2.3), pre-S deletion (OR 5.0), A1762T/G1764A mutant (OR 2.5), HCV genotype-1 (OR 2.4) and platelet count <15 x 10(4)/mul (OR 1.9) were independently associated with HCC by stepwise logistic regression analysis. 2013 Intervirology Abstract HBV G1764A;A1762T 87;80 93;86 PreS 55 60 Hepatocellular carcinoma 214 217 23852705 A complete genomic analysis of hepatitis B virus isolated from 516 Chinese patients with different clinical manifestations. Incidences of point mutation T53C (preS1F53L), G1613A (polR841K), G1775A and A1762T + G1764A in the basal core promoter region, G1896A and G1899A in precore region and A2189C (coreI97L) in core region increased along with acute hepatitis B, chronic hepatitis B, and acute-on-chronic liver failure. 2013 Journal of medical virology Abstract HBV T53C;G1613A;G1775A;A1762T;G1764A;G1896A;G1899A;A2189C;F53L;R841K;I97L 29;47;66;77;86;128;139;168;40;55;176 33;53;72;83;92;134;145;174;44;63;184 BCP;C;C;P;Precore;PreS1 100;176;189;55;149;35 119;180;193;58;156;40 Chronic Hepatitis B;Acute on chronic liver failure 241;266 260;296 23852705 A complete genomic analysis of hepatitis B virus isolated from 516 Chinese patients with different clinical manifestations. The mutation G1896A was independently associated with poor survival of patients with acute-on-chronic liver failure. 2013 Journal of medical virology Abstract HBV G1896A 13 19 Acute on chronic liver failure 85 115 23855124 [High-throughout detection and analysis of drug-resistance gene mutation for 2465 cases with chronic hepatitis B in Shenzhen]. Among all samples, rtS202I mutation couldn't be detected. 2013 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV S202I 21 26 RT 19 21 23855124 [High-throughout detection and analysis of drug-resistance gene mutation for 2465 cases with chronic hepatitis B in Shenzhen]. The frequency of Adefovir related mutation was about 8. 19% , among of which rtN236T was 4. 15%. 2013 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV N236T 79 84 23855124 [High-throughout detection and analysis of drug-resistance gene mutation for 2465 cases with chronic hepatitis B in Shenzhen]. The frequency of Lamivudine related mutation was the highest (42.96%), especially on rtL180M (14. 72%), rtL204I (18. 50%), rtL204V (9. 74%). 2013 Zhonghua shi yan he lin chuang bing du xue za zhi Abstract HBV L204I;L204V;L180M 106;125;87 111;129;92 RT;RT;RT 85;104;123 87;106;125 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Basic core promoter/precore region mutations, including the G1896A in 37% of HBeAg-negative individuals, could account for hepatitis B e antigen-negativity. 2013 BMC infectious diseases Abstract HBV G1896A 60 66 BCP;C;C;Precore 0;135;77;20 19;144;82;27 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Three isolates had the vaccine escape mutant sM133T. 2013 BMC infectious diseases Abstract HBV M133T 45 51 S 45 46 23871771 Positive selection signals of hepatitis B virus and their association with disease stages and viral genotypes. Moreover, we found that three substitutions, including A1762T, G1764A, and A2739C, were nearly fixed. 2013 Infection, genetics and evolution Abstract HBV A1762T;G1764A;A2739C 55;63;75 61;69;81 23886144 Hepatitis B virus genetic variation and TP53 R249S mutation in patients with hepatocellular carcinoma in Thailand. By multiple logistic regression analysis, the presence of A1762T/G1764A mutations was independently associated with the risk of HCC in Thai patients. 2013 Asian Pacific journal of cancer prevention Abstract HBV G1764A;A1762T 65;58 71;64 Hepatocellular carcinoma 128 131 23886144 Hepatitis B virus genetic variation and TP53 R249S mutation in patients with hepatocellular carcinoma in Thailand. The prevalences of T1753C/A/G and A1762T/G1764A mutations in the basal core promotor (BCP) region were significantly higher in the HCC group compared to the non-HCC group. 2013 Asian Pacific journal of cancer prevention Abstract HBV G1764A;A1762T;T1753C;T1753A;T1753G 41;34;19;19;19 47;40;29;29;29 BCP;BCP 65;86 84;89 Hepatocellular carcinoma;Hepatocellular carcinoma 131;161 134;164 23892239 HIV-HBV coinfection in Southern Africa and the effect of lamivudine- versus tenofovir-containing cART on HBV outcomes. HBV pol sequencing demonstrated M204I (n = 3) and N236T (n = 1) resistance-associated mutations in 4 of 8 (50%) lamivudine-treated participants and none in tenofovir-treated participants. 2013 Journal of acquired immune deficiency syndromes (1999) Abstract HBV M204I;N236T 32;50 37;55 P 4 7 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Four patterns (C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with LC. 2013 Brazilian journal of medical and biological research Abstract HBV C1810T;A1846T;G1862T;G1896A 15;23;31;43 21;29;37;49 Hepatocellular carcinoma;Liver cirrhosis 86;104 89;106 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Multivariate regression analyses showed that HBV subgenotype C2 and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) were independent risk factors for LC when CHB was the control, and that B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) were independent risk factors for HCC when LC was the control. 2013 Brazilian journal of medical and biological research Abstract HBV C1653T;T1753C;A1762T;G1764A;C1810T;A1846T;G1862T;G1896A 101;109;117;129;242;250;258;270 107;115;123;135;248;256;264;276 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Liver cirrhosis 312;171;179;321 315;173;182;323 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Seven mutation patterns (C1653T, G1719T, G1730C, T1753C, A1762T, G1764A, and G1799C) were associated with C2, and four patterns (C1810T, A1846T, G1862T, and G1896A) were associated with B2. 2013 Brazilian journal of medical and biological research Abstract HBV C1653T;G1719T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A 25;33;41;49;57;65;77;129;137;145;157 31;39;47;55;63;71;83;135;143;151;163 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Six patterns (C1653T, G1730C, T1753C, A1762T, G1764A, and G1799C) were obviously associated with LC, and 10 patterns (C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with CHB. 2013 Brazilian journal of medical and biological research Abstract HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C;C1653T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A 14;22;30;38;46;58;118;126;134;142;150;158;166;174;182;194 20;28;36;44;52;64;124;132;140;148;156;164;172;180;188;200 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 237;255;97 240;258;99 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. Additionally, the mutation pair A1762T/G1764A was found in three samples and the mutation G1896A was detected in an HBeAg-negative subject. 2013 Memorias do Instituto Oswaldo Cruz Abstract HBV G1764A;A1762T;G1896A 39;32;90 45;38;96 C 116 121 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. Secondary mutations associated with drug resistance at positions rtV207L and rtN239T of the reverse transcriptase gene were identified. 2013 Memorias do Instituto Oswaldo Cruz Abstract HBV V207L;N239T 67;79 72;84 RT;RT;RT 65;77;92 67;79;113 23918533 Hepatitis B virus reverse transcriptase mutations in treatment Naive chronic hepatitis B patients. Other common mutations included rtD263E/S, rtM129L, rtF122L/V/I, rtS135Y/H, rtQ149K, rtL91I, rtH126R, rtC256S/G, rtY257W, rtS259T and rtE271D, which were present in 26.5% (9/34), 29.4% (10/34), 20.6% (7/34), 20.6% (7/34), 20.6% (7/34), 17.6% (6/34), 14.7% (5/34), 14.7% (5/34), 11.8% (4/34), 11.8% (4/34) and 11.8% (4/34) patients respectively. 2013 Journal of medical virology Abstract HBV D263E;D263S;M129L;F122L;F122V;F122I;S135Y;S135H;Q149K;L91I;H126R;C256S;C256G;Y257W;S259T;E271D 34;34;45;54;54;54;67;67;78;87;95;104;104;115;124;136 41;41;50;63;63;63;74;74;83;91;100;111;111;120;129;141 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 32;43;52;65;76;85;93;102;113;122;134 34;45;54;67;78;87;95;104;115;124;136 23918533 Hepatitis B virus reverse transcriptase mutations in treatment Naive chronic hepatitis B patients. The rtH248N mutation was the most common mutation, accounting for 47.1% patients. 2013 Journal of medical virology Abstract HBV H248N 6 11 RT 4 6 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. Other mutations (e.g., P5H/L and I97L) associated with severe liver disease were also noticed, some of which were located in the major histocompatibility restricted sites. 2013 Journal of medical virology Abstract HBV I97L;P5H;P5L 33;23;23 37;28;28 Liver disease 62 75 23929069 Long-term efficacy and emergence of multidrug resistance in patients with lamivudine-refractory chronic hepatitis B treated by combination therapy with adefovir plus lamivudine. HBV DNA levels of patients with rtA181S mutation at baseline and emergence of rtA181T + rtN236T double mutation or a wide variety of mutations during combination therapy could not be suppressed. 2014 Journal of gastroenterology Abstract HBV A181S;A181T;N236T 34;80;90 39;85;95 RT;RT;RT 32;78;88 34;80;90 23929069 Long-term efficacy and emergence of multidrug resistance in patients with lamivudine-refractory chronic hepatitis B treated by combination therapy with adefovir plus lamivudine. Moreover, using ultra-deep sequencing, rtA181T/V mutations were detected at baseline in 7 of 10 patients with emergent multidrug resistance during combination therapy, although 6 of these 7 patients had very low frequency (<1 %) variants. 2014 Journal of gastroenterology Abstract HBV A181T;A181V 41;41 48;48 RT 39 41 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. All seven sequences lacked G145R and other escape mutation in S region. 2013 PloS one Abstract HBV G145R 27 32 S 62 63 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. Escape mutation S143L was found in the four sequences of genotype C/D. 2013 PloS one Abstract HBV S143L 16 21 23967738 [Clinical efficacy of various antiviral-based strategies to treat chronic hepatitis patients with positivity for hepatitis B e antigen and rtN236T mutation]. METHODS: Sixty-five adult CHB patients (age range: 20-60 years) who were unresponsive to ADV therapy (HBeAg-positive; HBV DNA >or= 10(5) copies/ml), LAM-naive, and tested positive for the rtN236T HBV mutation were enrolled in the study and randomly divided into two treatment groups: Group A (n = 33), who were administered ADV (10 mg/day, orally) plus peg-IFN (180 microg/week, subcutaneous injection) for 48 weeks; and Group B (n = 32 patients), who received the ADV plus LAM (100 mg/day, orally) for 48 weeks followed by continued LAM treatment for an additional 24 weeks. 2013 Zhonghua gan zang bing za zhi Abstract HBV N236T 190 195 C;RT 102;188 107;190 Chronic Hepatitis B 26 29 23967738 [Clinical efficacy of various antiviral-based strategies to treat chronic hepatitis patients with positivity for hepatitis B e antigen and rtN236T mutation]. OBJECTIVE: To compare the efficacy and safety of the common antivirals, including adefovir dipivoxil (ADV), pegylated-interferon alpha-2a (peg-IFN) and lamivudine (LAM), used as combination therapies to treat chronic hepatitis B (CHB) patients with positivity for the hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) harboring the ADV-resistance mutation, rtN236T, and to explore the factors associated with curative outcome. 2013 Zhonghua gan zang bing za zhi Abstract HBV N236T 367 372 C;C;RT 280;291;365 289;296;367 Chronic Hepatitis B;Chronic Hepatitis B 209;230 228;233 23968804 Dynamics of hepatitis B virus resistance substitutions correlates with virological response in lamivudine-refractory patients with entecavir rescue monotherapy. LMV-resistant mutations (rtL180M and/or rtM204VI) were detected in 9 patients before ETV treatment and not in another 5 patients before and after the treatment. 2013 Virus research Abstract HBV L180M;M204V;M204I 27;42;42 32;48;48 RT;RT 25;40 27;42 23971924 [Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year]. In five of nine samples primary and compensatory multiple mutations (L180M + M204I in one sample, L80I + L180M + M204I in two samples, L80I/V + M204I in one sample) and primary single mutations associated with LVD resistance (M204I/V) in four samples were detected by Inno-Lipa HBV DRv2. 2013 Mikrobiyoloji bulteni Abstract HBV L80I;L80V;M204V;L180M;M204I;L180M;M204I;L80I;M204I;M204I 98;135;226;69;77;105;113;135;144;226 102;141;233;74;82;110;118;141;149;233 23971924 [Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year]. In one sample which had multiple mutations associated with LVD resistance single mutations (S202G, N236T) associated with entecavir resistance and in two other such samples mutations associated with adefovir resistance were detected by SEQ. 2013 Mikrobiyoloji bulteni Abstract HBV S202G;N236T 92;99 97;104 23971924 [Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year]. Multiple mutations that comprise L180M + M204I in four and L180M + M204V in one sample and single mutations (M204I) in three samples were identified by SEQ. 2013 Mikrobiyoloji bulteni Abstract HBV M204I;L180M;L180M;M204V;M204I 41;33;59;67;109 46;38;64;72;114 23971933 [HBV vaccine escape mutations in a chronic hepatitis B patient treated with nucleos(t)ide analogues]. However, multiple HBV vaccine-escape mutations (sS143T + sD144E + sG145R + sE164D + sI195M) have been determined on the HBV overlapping pol/S gene region. 2013 Mikrobiyoloji bulteni Abstract HBV S143T;D144E;G145R;E164D;I195M 48;57;66;75;84 54;63;72;81;90 S;S;S;S;S;S;S 136;140;48;57;66;75;84 139;141;49;58;67;76;85 23971933 [HBV vaccine escape mutations in a chronic hepatitis B patient treated with nucleos(t)ide analogues]. Primary drug resistance mutations (rtV173L + rtL180M + rtM204V) to lamivudine and telbivudine and a compensatory mutation (rtQ215H) to lamivudine and adefovir were described in the HBV pol gene sequence. 2013 Mikrobiyoloji bulteni Abstract HBV V173L;L180M;M204V;Q215H 37;47;57;125 42;52;62;130 P;RT;RT;RT;RT 185;35;45;55;123 188;37;47;57;125 23978387 Genotyping and molecular characterization of hepatitis B virus in liver disease patients in Kenya. HBeAg-negativity was a result of G1896A in genotype D isolates, whereas in subgenotype A1, the HBeAg-negativity was a result of mutations in the Kozak region (1809-1812) or precore start codon (1814-1816). 2013 Infection, genetics and evolution Abstract HBV G1896A 33 39 C;C;Precore 0;95;173 5;100;180 24006435 HLA-DP polymorphisms affect the outcomes of chronic hepatitis B virus infections, possibly through interacting with viral mutations. HLA-DP polymorphisms promoting HBV clearance were associated with a lower prevalence of mutations increasing HCC risk (C1653T, T1674C/G, A1846T, G1896A and pre-S2 mutations and pre-S deletion in genotype C) and a higher prevalence of mutations decreasing HCC risk (G1652A, T1673C, T1674C, G1719T, G1730C, and G1799C in genotype B and A1727T in genotype C). 2013 Journal of virology Abstract HBV C1653T;T1674C;T1674G;A1846T;G1896A;G1652A;T1673C;G1719T;G1730C;G1799C;A1727T;T1674C 119;127;127;137;145;265;273;289;297;309;334;281 125;135;135;143;151;271;279;295;303;315;340;287 PreS;PreS2 177;156 182;162 Hepatocellular carcinoma;Hepatocellular carcinoma 109;255 112;258 24006435 HLA-DP polymorphisms affect the outcomes of chronic hepatitis B virus infections, possibly through interacting with viral mutations. The interaction of rs9277535 AA with the T1674C/G or G1719T mutation in genotype C significantly decreased HCC risk. 2013 Journal of virology Abstract HBV T1674C;T1674G;G1719T 41;41;53 49;49;59 Hepatocellular carcinoma 107 110 24006435 HLA-DP polymorphisms affect the outcomes of chronic hepatitis B virus infections, possibly through interacting with viral mutations. The interactions of C1653T, T1674C/G, and G1896A mutations with HLA-DP polymorphisms promoting HBV clearance significantly decreased cirrhosis risk. 2013 Journal of virology Abstract HBV C1653T;T1674C;T1674G;G1896A 20;28;28;42 26;36;36;48 Liver cirrhosis 133 142 24006443 Change in hepatitis B virus large surface antigen variant prevalence 13 years after implementation of a universal vaccination program in China. The prevalence of "alpha" determinant mutants in the children increased from 6.5% in 1992 to 14.8% in 2005, where the G145R mutant occurred most frequently. 2013 Journal of virology Abstract HBV G145R 118 123 24009186 Unique surface gene variants of hepatitis B virus isolated from patients in the Philippines. No G145R mutation was observed. 2014 Journal of medical virology Abstract HBV G145R 3 8 24009186 Unique surface gene variants of hepatitis B virus isolated from patients in the Philippines. The amino acid substitution M133T which was associated with failure of HBsAg detection was found in one isolate (7%, 1/15), while the amino acid substitution D144A which was associated with vaccine escape was observed in one isolate (7%, 1/15). 2014 Journal of medical virology Abstract HBV M133T;D144A 28;158 33;163 S 71 76 24009186 Unique surface gene variants of hepatitis B virus isolated from patients in the Philippines. Unique sequence variants at amino acid positions M103I, L109P, S117R, F134I, and S136L found in this study have not yet been reported. 2014 Journal of medical virology Abstract HBV M103I;L109P;S117R;F134I;S136L 49;56;63;70;81 54;61;68;75;86 24021712 Hepatitis B virus in the State of Alagoas, Brazil: genotypes characterization and mutations of the precore and basal core promoter regions. The aims of this study were to investigate the genotypes of hepatitis B virus and to identify the precore G1896A and basal core promoter A1762T/G1764A mutations in HBsAg and anti-HBc-positive patients. 2013 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T;G1896A 144;137;106 150;143;112 BCP;S;C;Precore 117;164;179;98 136;169;182;105 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. All of the W4P/R mutants were found in males only. 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 11;11 16;16 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. The novel HBV pre-S1 mutations, W4P/R, may be associated with disease severity in male patients chronically infected with HBV genotype C. 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 32;32 37;37 PreS1 14 20 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. The W4P/R mutations may provide in part an explanation for the relatively high ratio of male to female incidence in HCC generation in South Korean chronic HBV patients. 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 4;4 9;9 Hepatocellular carcinoma;Chronic Hepatitis B 116;147 119;158 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. W4P/R mutants were found to be significantly related to severe liver diseases (hepatocellular carcinoma [HCC] and liver cirrhosis, 12.4% [19/153] of patients, versus chronic hepatitis and asymptomatic carriage, 1.1% [1/94] of patients) (P < 0.001). 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 0;0 5;5 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B 63;79;105;114;166 77;103;108;129;183 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. We aimed to elucidate the relationships of the novel pre-S1 mutations, W4P/R, with the progression of liver diseases and male predominance in a South Korean chronic cohort by use of a molecular epidemiologic study. 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 71;71 76;76 PreS1 53 59 Liver disease 102 116 24025913 Male-specific W4P/R mutation in the pre-S1 region of hepatitis B virus, increasing the risk of progression of liver diseases in chronic patients. We developed a fluorescence resonance energy transfer (FRET)-based real-time PCR (RT-PCR) assay for the detection of the W4P/R mutations and applied it to 292 chronic HBV patients. 2013 Journal of clinical microbiology Abstract HBV W4P;W4R 121;121 126;126 Chronic Hepatitis B 159 170 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Serum pre-S1 and the precore G1896A mutation were simultaneously detected in most of Chinese HBeAg-negative patients. 2009 Brazilian journal of microbiology Abstract HBV G1896A 29 35 C;Precore;PreS1 93;21;6 98;28;12 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The overall prevalence of the precore G1896A mutation was 72.6% in HBeAg-negative Chinese patients with detectable serum HBV DNA. 2009 Brazilian journal of microbiology Abstract HBV G1896A 38 44 C;Precore 67;30 72;37 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The prevalence of the precore G1896A is significantly higher in Chinese HBeAg-negative patients with chronic hepatitis B than that in inactive HBV carriers with detectable serum HBV DNA. 2009 Brazilian journal of microbiology Abstract HBV G1896A 30 36 C;Precore 72;22 77;29 Chronic Hepatitis B 101 120 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. This study investigated the prevalence of the precore G1896A mutation in Chinese patients with hepatitis B e antigen (HBeAg) negative HBV infection and its relation to serum HBV pre-S1 antigen. 2009 Brazilian journal of microbiology Abstract HBV G1896A 54 60 C;C;Precore;PreS1 107;118;46;178 116;123;53;184 HBV infections 134 147 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. All five ELISA kits manifested similar avidity, which were demonstrated by the slope of the curves, for the sT118M mutant, and sT118M-rtM204I (sT118M-sI195M) and sT118M-rtM204V (sT118M-sW196S) double mutants, suggesting that drug-resistant YMDD mutants caused negligible losses in the antigenicity of immune-escaped sT118M HBsAg. 2013 Virology journal Abstract HBV M204I;M204V;T118M;T118M;T118M;I195M;T118M;T118M;W196S;T118M 136;171;108;127;143;150;162;178;185;316 141;176;114;132;148;156;167;183;191;322 S;RT;RT;S;S;S;S;S;S;S;S;P 323;134;169;108;127;143;150;162;178;185;316;240 328;136;171;109;128;144;151;163;179;186;317;244 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Because of the overlap of the open reading frame (ORF) S for the HBsAg and ORF P for viral polymerase, rtM204I and rtM204V mutations in the polymerase would produce sI195M and sW196S in the HBsAg. 2013 Virology journal Abstract HBV M204I;M204V;I195M;W196S 105;117;165;176 110;122;171;182 S;S;P;P;P;RT;RT;S;S;S 65;190;79;91;140;103;115;55;165;176 70;195;80;101;150;105;117;56;166;177 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. CONCLUSIONS: Drug-resistant mutations rtM204I (sI195M) and rtM204V (sW196S) caused significant reduction in antigenicity for the immune-escaped HBsAg mutants sG145K and sG145R, which may hamper HBV diagnosis and disease control from HBV blood-transfusion transmissions in China. 2013 Virology journal Abstract HBV M204I;M204V;I195M;W196S;G145K;G145R 40;61;47;68;158;169 45;66;53;74;164;175 S;RT;RT;S;S;S;S 144;38;59;47;68;158;169 149;40;61;48;69;159;170 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. In contrast, the presence of the rtM204I (sI195M) mutation, but not rtM204V (sW196S) in combination with the sG145K mutation significantly reduced the avidity of sG145K HBsAg. 2013 Virology journal Abstract HBV M204I;M204V;I195M;W196S;G145K;G145K 35;70;42;77;109;162 40;75;48;83;115;168 S;RT;RT;S;S;S;S 169;33;68;42;77;109;162 174;35;70;43;78;110;163 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The combined effects of immune-escaped mutations (sT118M, sG145K, sG145R) and drug-resistant mutations (rtM204I, rtM204V) on the antigenicity profiles of HBsAg has not been widely explored. 2013 Virology journal Abstract HBV M204I;M204V;T118M;G145K;G145R 106;115;50;58;66 111;120;56;64;72 S;RT;RT;S;S;S 154;104;113;50;58;66 159;106;115;51;59;67 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The rtM204I (sI195M) mutation also decreased the antigenicity profiles for sG145R HBsAg. 2013 Virology journal Abstract HBV M204I;I195M;G145R 6;13;75 11;19;81 RT;S;S;S 4;13;75;82 6;14;76;87 24064642 Mutation analysis of hepatitis B virus reverse transcriptase region among untreated chronically infected patients in Ahvaz city (South-West of Iran). Of these, 3 (6.6%) patients had primary resistance mutation (rtM204I, rtA181T and rtA181S) and 20 (44.4%) patients had secondary resistance mutations. 2013 Indian journal of medical microbiology Abstract HBV M204I;A181T;A181S 63;72;84 68;77;89 RT;RT;RT 61;70;82 63;72;84 24076590 Construction and expression of hepatitis B surface antigen escape variants within the "a" determinant by site directed mutagenesis. RESULTS: Ten HBsAg mutants having single mutation within the "a" determinant including P120E, T123N, Q129H, M133L, K141E, P142S, D144A, G145R, N146S and C147S together with a wt form were successfully constructed and expressed in CHO cells. 2013 Iranian journal of immunology Abstract HBV P120E;T123N;Q129H;M133L;K141E;P142S;D144A;G145R;N146S;C147S 87;94;101;108;115;122;129;136;143;153 92;99;106;113;120;127;134;141;148;158 S 13 18 24100506 Efficacy of adefovir-based combination therapy for patients with Lamivudine- and entecavir-resistant chronic hepatitis B virus infection. Virologic breakthrough was observed in 9 patients, and rtA181V substitution was newly detected in one patient. 2013 Antimicrobial agents and chemotherapy Abstract HBV A181V 57 62 RT 55 57 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. All rtA181V+rtN236T isolates conferred reduced susceptibility to ADV (FC values 2.3-4.2). 2014 Liver international Abstract HBV A181V;N236T 6;14 11;19 RT;RT 4;12 6;14 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. Clinical isolates containing the rtA181T+rtN236T double mutant remained sensitive to TFV in genotype D but exhibited reduced susceptibility to TFV in genotypes B and C. 2014 Liver international Abstract HBV A181T;N236T 35;43 40;48 RT;RT 33;41 35;43 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. CONCLUSIONS: Genotype B, C and D isolates with single ADV resistance mutations remained fully sensitive to TFV, while the double mutants rtA181T+rtN236T and rtA181V+rtN236T exhibited either no change or low-level reduced susceptibility to TFV across genotypes. 2014 Liver international Abstract HBV A181T;A181V;N236T;N236T 139;159;147;167 144;164;152;172 RT;RT;RT;RT 137;145;157;165 139;147;159;167 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. METHODS: Full-length HBV isolates from patients infected with genotype B, C and D virus had rtA181T, rtA181V, rtN236T, rtA181T+rtN236T and rtA181V+rtN236T mutations introduced by site-directed mutagenesis. 2014 Liver international Abstract HBV A181T;A181V;N236T;A181T;A181V;N236T;N236T 94;103;112;121;141;129;149 99;108;117;126;146;134;154 RT;RT;RT;RT;RT;RT;RT 92;101;110;119;127;139;147 94;103;112;121;129;141;149 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. RESULTS: Clinical HBV isolates containing rtA181T, rtA181V or rtN236T as single mutants remained sensitive to TFV across genotypes B, C and D. 2014 Liver international Abstract HBV A181T;A181V;N236T 44;53;64 49;58;69 RT;RT;RT 42;51;62 44;53;64 24118725 HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D. Viruses containing the double mutant rtA181V+rtN236T in genotypes B and D exhibited reduced susceptibility to TFV with EC50 fold changes (FC) of 3.8 and 2.5, respectively, while genotype C viruses containing rtA181V+rtN236T either remained sensitive (FC=1.3) or exhibited reduced susceptibility to TFV (FC=2.9) depending on the isolate. 2014 Liver international Abstract HBV A181V;A181V;N236T;N236T 39;210;47;218 44;215;52;223 RT;RT;RT;RT 37;45;208;216 39;47;210;218 24118778 Association of a potential functional pre-miR-218 polymorphism and its interaction with hepatitis B virus mutations with hepatocellular carcinoma risk. CONCLUSION: rs11134527 may be a novel genetic risk factor of HCC in HBV-exposed subjects, can facilitate HBV preS deletion generation and predispose the host to the effect of T1674C/G and preS1 start codon mutation in hepatocarcinogenesis. 2014 Liver international Abstract HBV T1674C;T1674G 175;175 183;183 PreS;PreS1 109;188 113;193 Hepatocellular carcinoma 61 64 24118778 Association of a potential functional pre-miR-218 polymorphism and its interaction with hepatitis B virus mutations with hepatocellular carcinoma risk. In multivariate regression analyses, rs11134527 in dominant model was associated with HCC risk (OR = 1.50, 95% CI = 1.05-2.13), whereas its multiplicative interaction with viral mutation T1674C/G was inversely associated with HCC risk (OR = 0.44, 95% CI = 0.21-0.96), adjusting for covariates including HBV mutations in the enhancer II-precore region; its interaction with HBV preS1 start codon mutation was associated with HCC risk (OR = 4.44, 95% CI = 1.27-15.55), adjusting for covariates including HBV mutations in the preS region. 2014 Liver international Abstract HBV T1674C;T1674G 187;187 195;195 Enh II;Precore;PreS;PreS1 324;336;523;377 335;343;527;382 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 86;226;424 89;229;427 24119014 Clinical and virological features of occult hepatitis B in patients with HBsAg seroclearance post-treatment or spontaneously. CONCLUSIONS: One mutation, C3050T (preS1T68I), decreased S promoter activity; nevertheless, other factors may play more important role in the clearance of HBsAg in these OHB patients. 2014 Liver international Abstract HBV C3050T;T68I 27;40 33;44 S;PreS1;S promoter 155;35;57 160;40;67 Occult Hepatitis B 170 173 24119014 Clinical and virological features of occult hepatitis B in patients with HBsAg seroclearance post-treatment or spontaneously. One mutation in surface promoter/polymerase region, C3050T (preS1T68I), was identified to be associated with the seroclearance of HBsAg in six cases. 2014 Liver international Abstract HBV C3050T;T68I 52;65 58;69 S;P;PreS1;S 130;33;60;16 135;43;65;23 24119014 Clinical and virological features of occult hepatitis B in patients with HBsAg seroclearance post-treatment or spontaneously. The S promoter activity was significantly lower in the construct containing C3050T mutation as compared with the wild-type (P = 0.0008). 2014 Liver international Abstract HBV C3050T 76 82 S promoter 4 14 24141768 A modified murine model based on hydrodynamic injection for the analysis of chronic human hepatitis B virus infection. In the present study, T378C was introduced into the pAAV-HBV1.3 plasmid and was confirmed to affect HBsAg production and secretion, and HBV replication in vivo, which was in agreement with the previous in vitro results. 2013 Molecular medicine reports Abstract HBV T378C 22 27 S 100 105 24141768 A modified murine model based on hydrodynamic injection for the analysis of chronic human hepatitis B virus infection. The highly conserved ATG S5 was mutated to ACG by T378C, which led to the substitution sM75T and inhibition of the production and secretion of the hepatitis B surface antigen (HBsAg), and subsequent inhibition of HBV replication. 2013 Molecular medicine reports Abstract HBV M75T;T378C 87;50 92;55 S;S;S 176;87;159 181;88;166 24157033 Analysis of S gene mutation of the hepatitis B virus in adult liver transplant recipients showing resistance to hepatitis B immunoglobulin therapy. RESULTS: Various mutations in the MHR were observed in 14/15 samples: Gly145Arg mutation in 8/13 Adr subtype and 1/2 Ayw subtype samples (60%). 2013 Transplantation proceedings Abstract HBV G145R 70 79 24157033 Analysis of S gene mutation of the hepatitis B virus in adult liver transplant recipients showing resistance to hepatitis B immunoglobulin therapy. The next most common mutation was Gly165Trp in 8/13 Adr subtype but neither of 2 Ayw subtype samples (53.3%). 2013 Transplantation proceedings Abstract HBV G165W 34 43 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Among LAM/LdT based therapies, HBV rtM204I was significantly associated with HBV rtL80I/V mutations [rtM204I+rtL80I/V (50.0%, 32/64) vs. rtM204V+rtL80I/V (27.3%,9/33), P=0.032] 2013 Virology journal Abstract HBV L80I;L80V;M204I;L80I;L80V;M204I;L80I;L80V;M204V 111;111;37;83;83;103;147;147;139 117;117;42;89;89;108;153;153;144 RT;RT;RT;RT;RT;RT 35;81;101;109;137;145 37;83;103;111;139;147 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. while the HBV rtM204V mutations was significantly associated with HBV rtL180M mutations [rtM204V+rtL180M (100%, 33/33) vs. rtM204I+rtL180M (60.9%, 39/64), P<0.001]. 2013 Virology journal Abstract HBV L180M;M204I;L180M;M204V;L180M;M204V 133;125;99;91;72;16 138;130;104;96;77;21 RT;RT;RT;RT;RT;RT 14;70;89;97;123;131 16;72;91;99;125;133 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. The mutations detected were as follows: sM133L + sI195T (2.94%), sI195M (2.94%), sP120T (2.94%), sY100S/F (2.94%), sY100C (17.64%), sI/T126P + sQ129P (2.94%), sM198I + sF183C (2.94%) and sS210R (5.88%). 2013 Virology journal Abstract HBV I126P;T126P;M133L;I195T;I195M;P120T;Y100S;Y100F;Y100C;Q129P;M198I;F183C;S210R 132;132;40;49;65;81;97;97;115;143;159;168;187 140;140;46;55;71;87;105;105;121;149;165;174;193 S;S;S;S;S;S;S;S;S;S;S 40;49;65;81;97;115;132;143;159;168;187 41;50;66;82;98;116;133;144;160;169;188 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. The other samples showed only compensatory mutations, such as rtL80F (5.88%), rtL80V (2.94%), rtL82V + rtV207L (2.94%), rtT128P (5.88%), rtT128N/S (2.94%) and rtS219A (5.88%). 2013 Virology journal Abstract HBV L80F;L80V;L82V;V207L;T128P;T128N;T128S;S219A 64;80;96;105;122;139;139;161 68;84;100;110;127;146;146;166 RT;RT;RT;RT;RT;RT;RT 62;78;94;103;120;137;159 64;80;96;105;122;139;161 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. We were able to detect one sample with the resistance mutation to lamivudine rtM204V + rtL180M (2.94%), which was found in a volunteer blood donor that has never used antiviral drugs. 2013 Virology journal Abstract HBV M204V;L180M 79;89 84;94 RT;RT 77;87 79;89 24175223 Antiviral treatment to prevent chronic hepatitis B or C-related hepatocellular carcinoma. Of the NA resistance-associated mutants, A181T mutant significantly increases the risk of HCC development during the subsequent course of NA therapy. 2012 World journal of virology Abstract HBV A181T 41 46 Hepatocellular carcinoma 90 93 24175847 Prevelance of common YMDD motif mutations in long term treated chronic HBV infections in a Turkish population. Eight of the 17 samples (19.5%) having rtM204V/I/A missense transition and/or transversion point mutations and resistance to lamivudin. 2013 Asian Pacific journal of cancer prevention Abstract HBV M204V;M204I;M204A 41;41;41 50;50;50 RT 39 41 24175847 Prevelance of common YMDD motif mutations in long term treated chronic HBV infections in a Turkish population. Six of the the mutated samples (14.6%) having rtL180M missense transversion mutation and resistance to combined adefovir and lamivudin. 2013 Asian Pacific journal of cancer prevention Abstract HBV L180M 48 53 RT 46 48 24175847 Prevelance of common YMDD motif mutations in long term treated chronic HBV infections in a Turkish population. The current results provide evidence that rtL180M and rtM204V/I/A mutations of HBV-DNA may be associated with a poor antiviral response and HBV chronicity during conventional therapy in Turkish patients. 2013 Asian Pacific journal of cancer prevention Abstract HBV L180M;M204V;M204I;M204A 44;56;56;56 49;65;65;65 RT;RT 42;54 44;56 24175847 Prevelance of common YMDD motif mutations in long term treated chronic HBV infections in a Turkish population. Three of the mutated samples (7.5%) having codon rtL181W due to the missense transversion point mutations and showed resistance to combined adefovir and lamivudin. 2013 Asian Pacific journal of cancer prevention Abstract HBV L181W 51 56 RT 49 51 24175847 Prevelance of common YMDD motif mutations in long term treated chronic HBV infections in a Turkish population. Three of the mutated samples (7.5%) having rtG215H by the double base substituation and resistance to adefovir. 2013 Asian Pacific journal of cancer prevention Abstract HBV G215H 45 50 RT 43 45 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 +- 2.9 versus 3.4 +- 2.2 ng/mL, P = 0.03). 2013 Advances in virology Abstract HBV G1896A 4 10 Precore 11 19 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. 2013 Advances in virology Abstract HBV G1896A 39 45 Precore 46 54 24237431 [Investigation of baseline antiviral resistance in treatment-naive chronic hepatitis B cases]. Mutations conferring resistance to entecavir + lamivudine (S202G, M204V, L180M, T184N) were identified in one patient whereas L180P, A181Q and A194V substitutions associated with probable lamivudin + adefovir and tenofovir resistance, respectively, were detected in other patients. 2013 Mikrobiyoloji bulteni Abstract HBV S202G;M204V;L180M;T184N;L180P;A181Q;A194V 59;66;73;80;126;133;143 64;71;78;85;131;138;148 24249691 Variability in the precore and core promoter region of the hepatitis B virus genome. A novel association of mutation C1773T with G1764T, C1766A, and G1757A was also found within a site already suggested to be a putative binding site for HNF-3. 2014 Journal of medical virology Abstract HBV C1773T;G1764T;C1766A;G1757A 32;44;52;64 38;50;58;70 24249691 Variability in the precore and core promoter region of the hepatitis B virus genome. A rare double mutation (C1857T together with G1897A) was observed, and C1856T was found together with the emerging G1898A mutation, which itself was found to be more widespread geographically than previously described. 2014 Journal of medical virology Abstract HBV C1857T;G1897A;C1856T;G1898A 24;45;71;115 30;51;77;121 24249691 Variability in the precore and core promoter region of the hepatitis B virus genome. The study confirmed that core promoter and precore mutations occur at key positions (A1762T, G1764A, G1896A, and G1899A), and that the proportions of strains with seroconvertion in patients differ between the four HBV genotypes. 2014 Journal of medical virology Abstract HBV A1762T;G1764A;G1896A;G1899A 85;93;101;113 91;99;107;119 Core promoter;Precore 25;43 38;50 24249691 Variability in the precore and core promoter region of the hepatitis B virus genome. This novel association is proposed by us to be of importance for additional binding of HNH-2 to this site and is a better indicator of the emergence of the double mutation G1764T and C1766A than the G1757A mutation proposed previously. 2014 Journal of medical virology Abstract HBV G1764T;C1766A;G1757A 172;183;199 178;189;205 24249691 Variability in the precore and core promoter region of the hepatitis B virus genome. We found a novel mutation (T1850C), never before observed in human HBV strains but known from woodchuck hepatitis virus (WHV). 2014 Journal of medical virology Abstract HBV T1850C 27 33 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In the BCP region, the double mutation A1762T/G1764A and the G1757A substitution were detected respectively in 26/228 patients (11.4%) and 189/228 patients (82.8%). 2013 PloS one Abstract HBV G1764A;A1762T;G1757A 46;39;61 52;45;67 BCP 7 10 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In the PC region, 83/228 patients (36.4%) harbored a G1896A mutant or mixed phenotype virus. 2013 PloS one Abstract HBV G1896A 53 59 Precore 7 9 24273041 The impact of hepatitis B virus precore/core gene carboxyl terminal mutations on viral biosynthesis and the host immune response. CONCLUSIONS: The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. 2014 The Journal of infectious diseases Abstract HBV P135Q 22 27 C 95 100 24273041 The impact of hepatitis B virus precore/core gene carboxyl terminal mutations on viral biosynthesis and the host immune response. RESULTS: The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). 2014 The Journal of infectious diseases Abstract HBV P135Q;G1896A 14;24 19;30 C;C 70;113 75;118 24273041 The impact of hepatitis B virus precore/core gene carboxyl terminal mutations on viral biosynthesis and the host immune response. The P135Q mutant peptide induced less interferon-gamma expression in CD3+ CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). 2014 The Journal of infectious diseases Abstract HBV P135Q 4 9 C 96 101 24273041 The impact of hepatitis B virus precore/core gene carboxyl terminal mutations on viral biosynthesis and the host immune response. The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. 2014 The Journal of infectious diseases Abstract HBV P135Q 4 9 Capsid;C;C 62;38;117 68;43;122 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S, N123S, and N177S mutated LHBs proteins could induce overexpression of EDEM in L02 cells. 2013 Hepatitis monthly Abstract HBV N15S;N123S;N177S 4;10;21 8;15;26 S 35 39 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N320K may be the key sites N-linked glycosylation modification of LHBs. 2013 Hepatitis monthly Abstract HBV N320K 4 9 Large S 70 74 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The secretion of LHBs was blocked by N320K mutation, which could induce an increase in G1 phase and inhibition of S phase, and inhibited mitotic entry. 2013 Hepatitis monthly Abstract HBV N320K 37 42 S 17 21 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. CONCLUSIONS: Our findings suggest that CHB or LC patients infected with HBV A1846T and C1913A/G mutants are more susceptible to develop ACLF. 2013 Hepatitis monthly Abstract HBV A1846T;C1913A;C1913G 76;87;87 82;95;95 Acute on chronic liver failure;Chronic Hepatitis B;Liver cirrhosis 136;39;46 140;42;48 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In addition, there were no significant differences in mutations at T1753V, A1762T, G1764A, G1896A, and G1899A which were found between either CHB and ACLF-CHB or LC and ACLF-LC patients, suggesting no associations of these mutations with ACLF development. 2013 Hepatitis monthly Abstract HBV T1753V;A1762T;G1764A;G1896A;G1899A 67;75;83;91;103 73;81;89;97;109 Chronic Hepatitis B;Chronic Hepatitis B;Acute on chronic liver failure;Acute on chronic liver failure;Liver cirrhosis;Liver cirrhosis 142;155;238;169;162;174 145;158;242;173;164;176 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Multivariable analysis indicated that A1846T and C1913A/G mutations were independent factors for ACLF (OR = 2.86 and 5.93, respectively), suggesting an association between the mutations and development of ACLF. 2013 Hepatitis monthly Abstract HBV A1846T;C1913A;C1913G 38;49;49 44;57;57 Acute on chronic liver failure;Acute on chronic liver failure 97;205 101;209 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. RESULTS: Our results revealed significantly higher incidences (P < 0.05) of genotype B with C1913A/G or A1846T in patients with ACLF-CHB than those with CHB; genotype C with C1913A/G or A1846T in patients with ACLF-CHB and ACLF-LC than those with CHB and LC, respectively. 2013 Hepatitis monthly Abstract HBV C1913A;C1913G;A1846T;C1913A;C1913G;A1846T 92;92;104;174;174;186 100;100;110;182;182;192 Chronic Hepatitis B;Acute on chronic liver failure;Chronic Hepatitis B;Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 133;128;153;247;215;228;255 136;132;156;250;218;230;257 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Considerable prevalence of differential BCP (1752C, 1753C, 1762T/1764A, 1753C+1762T/1764A, 1773C, and 1814C) and reverse transcriptase (rt) gene (rtI91L, rtL93P, rtS106C, rtR110G, rtN118T, rtS119T, rtY126H, rtG127W/R, rtC136R, and rtY158H) mutations was identified. 2013 TheScientificWorldJournal Abstract HBV I91L;L93P;S106C;R110G;N118T;S119T;Y126H;G127W;G127R;C136R;Y158H 148;156;164;173;182;191;200;209;209;220;233 152;160;169;178;187;196;205;216;216;225;238 BCP;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 40;113;136;146;154;162;171;180;189;198;207;218;231 43;134;138;148;156;164;173;182;191;200;209;220;233 24304458 Full genome ultra-deep pyrosequencing associates G-to-A hypermutation of the hepatitis B virus genome with the natural progression of hepatitis B. Additionally, we found that for HBeAg-positive chronic hepatitis G-to-A hypermutation rates were significantly associated with the relative prevalence of the G1764A mutation, which is related to HBeAg seroconversion. 2013 Journal of viral hepatitis Abstract HBV G1764A 158 164 C;C 32;195 37;200 Chronic Hepatitis B 37 64 24316031 Amino acid similarities and divergences in the small surface proteins of genotype C hepatitis B viruses between nucleos(t)ide analogue-naive and lamivudine-treated patients with chronic hepatitis B. Interestingly, another newly-identified truncation mutation sC69stop/rtS78T decreased from 7.91% (11/139) in NA-naive cohort to 2.70% (2/74) in LMV-treated one. 2014 Antiviral research Abstract HBV S78T;C69X 71;60 75;68 RT;S 69;60 71;61 24316031 Amino acid similarities and divergences in the small surface proteins of genotype C hepatitis B viruses between nucleos(t)ide analogue-naive and lamivudine-treated patients with chronic hepatitis B. With little influence on immune escape-associated mutation frequencies within 'a' determinant, LMV-monotherapy significantly induced classical LMVr-associated mirror changes sE164D/rtV173L, sI195M/rtM204V and sW196L/S/rtM204I, as well as non-classical ones sG44E/rtS53N, sT47K/A/rtH55R/Q and sW182stop/rtV191I outside 'a' determinant. 2014 Antiviral research Abstract HBV V173L;M204V;M204I;S53N;H55R;H55Q;V191I;E164D;I195M;W196L;W196S;G44E;T47K;T47A;W182X 183;199;220;265;281;281;304;174;190;209;209;257;271;271;292 188;204;225;269;287;287;309;180;196;217;217;262;278;278;301 S;S;RT;RT;RT;RT;RT;RT;S;S;S;S;S;S 79;319;181;197;218;263;279;302;174;190;209;257;271;292 93;333;183;199;220;265;281;304;175;191;210;258;272;293 24329944 Short duration of lamivudine for the prevention of hepatitis B virus transmission in pregnancy: lack of potency and selection of resistance mutations. These viral variants were detected mostly at low frequencies (0.63-5.92%) at EOT, but one LMV-treated mother had an rtA181T variant that increased from 2.2% pretherapy to 25.59% at EOT. 2014 Journal of viral hepatitis Abstract HBV A181T 118 123 RT 116 118 24329944 Short duration of lamivudine for the prevention of hepatitis B virus transmission in pregnancy: lack of potency and selection of resistance mutations. This mother was also infected with the vaccine escape variant (sG145R), which was inhibited by LMV treatment. 2014 Journal of viral hepatitis Abstract HBV G145R 63 69 S 63 64 24329944 Short duration of lamivudine for the prevention of hepatitis B virus transmission in pregnancy: lack of potency and selection of resistance mutations. UDPS showed that LMV therapy resulted in increased viral quasispecies diversity and positive selection of HBV variants with reverse transcriptase amino acid substitutions at sites associated with primary LMV resistance (rtM204I/V and rtA181T) in four (19%) women. 2014 Journal of viral hepatitis Abstract HBV M204I;M204V;A181T 222;222;236 229;229;241 RT;RT;RT 220;234;124 222;236;145 24338810 Genetic variability of hepatitis B and C viruses in Brazilian patients with and without hepatocellular carcinoma. Core promoter T1753V, A1762T, and G1764A mutations were more frequent in patients with HCC than in those without, although with no statistical difference. 2014 Journal of medical virology Abstract HBV T1753V;A1762T;G1764A 14;22;34 20;28;40 Core promoter 0 13 Hepatocellular carcinoma 87 90 24338810 Genetic variability of hepatitis B and C viruses in Brazilian patients with and without hepatocellular carcinoma. However, a significant correlation was observed between T1753V mutation and elevation of transaminases levels (P < 0.05). 2014 Journal of medical virology Abstract HBV T1753V 56 62 24342744 Mutations in HBV DNA polymerase associated with nucleos(t)ide resistance are rare in treatment-naive patients. Mutations in HBV DNA polymerase were found in 2 patients (1%), rtI233V (n = 1) and rtM250M/L (n = 1). 2014 Clinical gastroenterology and hepatology Abstract HBV I233V;M250M;M250L 65;85;85 70;92;92 P;RT;RT 21;63;83 31;65;85 24344773 Combinations of eight key mutations in the X/preC region and genomic activity of hepatitis B virus are associated with hepatocellular carcinoma. Accumulation of eight key mutations located in the X/preC regions of the hepatitis B virus (HBV) genome (G1613A, C1653T, T1753V, A1762T, G1764A, A1846T, G1896A and G1899A) is a risk marker for the development of hepatocellular carcinoma (HCC). 2014 Journal of viral hepatitis Abstract HBV G1613A;C1653T;T1753V;A1762T;G1764A;A1846T;G1896A;G1899A 105;113;121;129;137;145;153;164 111;119;127;135;143;151;159;170 X;Precore 51;53 52;57 Hepatocellular carcinoma;Hepatocellular carcinoma 212;238 236;241 24344773 Combinations of eight key mutations in the X/preC region and genomic activity of hepatitis B virus are associated with hepatocellular carcinoma. Analyses were focused on patient >=40 years of age infected by HBV genotype C with A1762T and G1764A mutations in the basal core promoter region (BCP double mutation). 2014 Journal of viral hepatitis Abstract HBV A1762T;G1764A 83;94 89;100 BCP;BCP 118;146 137;149 24344773 Combinations of eight key mutations in the X/preC region and genomic activity of hepatitis B virus are associated with hepatocellular carcinoma. In patients with >=6 mutations, the combination of [G1613A + C1653T + A1846T + G1896A] mutations was closely linked to HCC, whereas no specific single or double mutation combination was associated with HCC. 2014 Journal of viral hepatitis Abstract HBV G1613A;C1653T;A1846T;G1896A 52;61;70;79 58;67;76;85 Hepatocellular carcinoma;Hepatocellular carcinoma 119;202 122;205 24344773 Combinations of eight key mutations in the X/preC region and genomic activity of hepatitis B virus are associated with hepatocellular carcinoma. Of the BCP double mutation-based HBV mutant types, combinations of >=6 mutations that include G1613A + C1653T + A1846T + G1896A, and combinations of <=5 mutations with reduced HBeAg production, may be more specific indicators of HCC risk than only the number of mutations or any specific combination(s). 2014 Journal of viral hepatitis Abstract HBV G1613A;C1653T;A1846T;G1896A 94;103;112;121 100;109;118;127 BCP;C 7;176 10;181 Hepatocellular carcinoma 229 232 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. RESULTS: The dual mutations K130M/V131I enhanced the functionality of HBx as they upregulated the expression and transcriptional activity of HIF-1alpha. 2014 British journal of cancer Abstract HBV V131I;K130M 34;28 39;33 X 70 73 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Among them, rtQ267H was often observed in patients receiving LMV administration. 2013 Hepatitis monthly Abstract HBV Q267H 14 19 RT 12 14 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. CONCLUSIONS: The result suggested that rtQ267H is a potential adaptive mutation of HBV to LMV. 2013 Hepatitis monthly Abstract HBV Q267H 41 46 RT 39 41 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The in vitro susceptibility analysis showed that the existence of rtQ267H in WT and LMV-resistant (LMVr) HBV were responsible for the reduced susceptibility to LMV to varying degrees, and enhanced HBV replication capacity. 2013 Hepatitis monthly Abstract HBV Q267H 68 73 RT 66 68 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The rtQ267H substitution enhanced HBV replication not merely in single-site mutation, but also in multisite mutations. 2013 Hepatitis monthly Abstract HBV Q267H 6 11 RT 4 6 24368224 Randomized comparison of tenofovir disoproxil fumarate vs emtricitabine and tenofovir disoproxil fumarate in patients with lamivudine-resistant chronic hepatitis B. Patients were hepatitis B e antigen (HBeAg)-positive or HBeAg-negative, with levels of HBV DNA >=3 log10 IU/mL and lamivudine resistance mutations (HBV polymerase or reverse transcriptase amino acid substitutions rtM204I/V +- rtL180M by INNO-LiPA Multi-DR v3; Innogenetics, Inc, Alpharetta, GA). 2014 Gastroenterology Abstract HBV M204I;M204V;L180M 215;215;228 222;222;233 C;C;C;P;RT;RT;RT 26;37;56;152;166;213;226 35;42;61;162;187;215;228 24369590 [Clinical evaluation of a newly developed high-sensitive detection of hepatitis B virus surface antigen by a semi-automated immune complex transfer chemiluminescent enzyme immunoassay]. The sensitivity of wild type and HBsAg escape mutants (I126S, D144A, G145R) by ICT-CLEIA was 2- -5 to 2- -6 times higher than that of Architect HBsAg QT. 2013 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV I126S;D144A;G145R 55;62;69 60;67;74 S;S 33;144 38;149 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Sequence analysis of S, pre-S, and overlapped polymerase (P) genes showed that HBV isolates of HBsAg-positive vaccinees were variants; no G145R but G145A and other substitutions were found in the "a" determinant. 2013 TheScientificWorldJournal Abstract HBV G145R;G145A 138;148 143;153 S;P;P;PreS;S 95;58;46;24;21 100;59;56;29;22 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Several immune-epitope mutants, such as S45T/A, N131T, I194V, and S207N in S, were detected in all isolates. 2013 TheScientificWorldJournal Abstract HBV S45T;S45A;N131T;I194V;S207N 40;40;48;55;66 46;46;53;60;71 S 75 76 24389280 Detection of hepatitis B virus A1762T/G1764A mutant by amplification refractory mutation system. However, the percentage of A1762T/G1764A double mutation in hepatitis B e antigen-negative (58.3%) samples was almost the same as in hepatitis B e antigen-positive (61%) samples. 2014 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 34;27 40;33 C;C 72;145 81;154 24389280 Detection of hepatitis B virus A1762T/G1764A mutant by amplification refractory mutation system. METHODS: We developed an accurate and fast real-time amplification refractory mutation system to detect A1762T/G1764A double mutation. 2014 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 111;104 117;110 24389280 Detection of hepatitis B virus A1762T/G1764A mutant by amplification refractory mutation system. OBJECTIVE: To study the role of hepatitis B virus with A1762T/G1764A double mutation in liver cirrhosis and hepatocellular carcinoma, and create a sensitive, fast, accurate assay for detection of A1762T/G1764A double mutation. 2014 The Brazilian journal of infectious diseases Abstract HBV G1764A;G1764A;A1762T;A1762T 62;203;196;55 68;209;202;61 Liver cirrhosis;Hepatocellular carcinoma 88;108 103;132 24399391 Antiviral efficacy of adefovir dipivoxil in the treatment of chronic hepatitis B subjects from Indian subcontinent. On sequence analysis, two subjects were identified with rtI169L and rtA181V mutation after 9 months and 18 months of adefovir treatment, respectively. 2014 Indian journal of medical microbiology Abstract HBV I169L;A181V 58;70 63;75 RT;RT 56;68 58;70 24406435 Clinical significance of hepatitis B virus precore and core promoter variants in Korean patients with chronic hepatitis B. METHODS: We assessed serum HBeAg, HBV DNA levels, alanine transferase (ALT) levels, and progression of liver fibrosis in 226 Korean CHB patients, presumed to be infected with genotype C HBV, to analyze HBV variants in the preC region (G1896A) and CP regions (A1762T, G1764A). 2015 Journal of clinical gastroenterology Abstract HBV G1896A;A1762T;G1764A 235;259;267 241;265;273 Core promoter;C;Precore 247;27;222 249;32;226 Liver fibrosis;Chronic Hepatitis B 103;132 117;135 24409056 Hepatitis B virus subgenotype A1 predominates in liver disease patients from Kerala, India. Mutation A1762T/G1764A was significantly associated with HCC in both genotypes A and D. 2013 World journal of gastroenterology Abstract HBV G1764A;A1762T 16;9 22;15 Hepatocellular carcinoma 57 60 24409056 Hepatitis B virus subgenotype A1 predominates in liver disease patients from Kerala, India. Mutation C1766T/T1768A was significantly associated with genotype A (P = 0.05) and HCC (P = 0.03). 2013 World journal of gastroenterology Abstract HBV T1768A;C1766T 16;9 22;15 Hepatocellular carcinoma 83 86 24409056 Hepatitis B virus subgenotype A1 predominates in liver disease patients from Kerala, India. Mutation G1862T was more frequent in subgenotype A1 (P < 0.0001), and in combination with A1762T/G1764A, it was significantly associated with HBV from HCC patients. 2013 World journal of gastroenterology Abstract HBV G1764A;A1762T;G1862T 97;90;9 103;96;15 Hepatocellular carcinoma 151 154 24409056 Hepatitis B virus subgenotype A1 predominates in liver disease patients from Kerala, India. The preS2 start codon M1T/I mutation was unique to genotype A strains (15.6%) from all disease groups and occurred at a higher frequency in isolates from HCC patients (P = 0.076). 2013 World journal of gastroenterology Abstract HBV M1T;M1I 22;22 27;27 PreS2 4 9 Hepatocellular carcinoma 154 157 24409056 Hepatitis B virus subgenotype A1 predominates in liver disease patients from Kerala, India. The preS2:F22L mutation was found in genotypes A and D. 2013 World journal of gastroenterology Abstract HBV F22L 10 14 PreS2 4 9 24444423 Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies. Multiple mutations occurred in the S gene during the flare-up of HBV as shown by sequencing, including I103T, K122R, M133I, F134V, D144E, V164E and L175S. 2014 Virology journal Abstract HBV I103T;K122R;M133I;F134V;D144E;V164E;L175S 103;110;117;124;131;138;148 108;115;122;129;136;143;153 S 35 36 24478474 Rapid detection of hepatitis B virus variants associated with lamivudine and adefovir resistance by multiplex ligation-dependent probe amplification combined with real-time PCR. Based on the results of MLP-RT-PCR, the mutations rtM204V, rtM204I, rtA181T, rtA181V, and rtN236T were 95.7% (111/116 patients), 98.3% (114/116 patients), 99.1% (115/116 patients), 98.3% (114/116 patients), and 99.1% (115/116 patients) concordant, respectively, with those of direct sequencing. 2014 Journal of clinical microbiology Abstract HBV M204V;M204I;A181T;A181V;N236T 52;61;70;79;92 57;66;75;84;97 RT;RT;RT;RT;RT 50;59;68;77;90 52;61;70;79;92 24478474 Rapid detection of hepatitis B virus variants associated with lamivudine and adefovir resistance by multiplex ligation-dependent probe amplification combined with real-time PCR. For this study, a multiplex ligation-dependent probe real-time PCR (MLP-RT-PCR) method was developed to simultaneously detect lamivudine (LAM)- and adefovir (ADV)-resistant HBV mutants (those with the mutations rtM204V/I, rtA181V/T, and rtN236T). 2014 Journal of clinical microbiology Abstract HBV M204V;M204I;A181V;A181T;N236T 213;213;224;224;239 220;220;231;231;244 RT;RT;RT 211;222;237 213;224;239 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. A number of significant drug resistant mutations were found in five patients including S202I, N236T, M250L, L180M/V, M204I, A181T, T184G, M250V, and V173L. 2014 Hepatitis monthly Abstract HBV S202I;N236T;M250L;L180M;L180V;M204I;A181T;T184G;M250V;V173L 87;94;101;108;108;117;124;131;138;149 92;99;106;115;115;122;129;136;143;154 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Of these, L180M/V and M204I were most frequently detected (80%) and associated with lamivudine in combination with emtricitabine and telbivudine drug resistance. 2014 Hepatitis monthly Abstract HBV L180M;L180V;M204I 10;10;22 17;17;27 24517926 Efficacy of tenofovir in adefovir-experienced patients compared with treatment-naive patients with chronic hepatitis B. Patients with primary ADV-R mutations had either A181T/V or N236T mutations or both. 2014 Antiviral therapy Abstract HBV A181T;A181V;N236T 49;49;60 56;56;65 24518026 [Effect of PTPRD rs2279776 gene and interaction with hepatitis B virus mutations on the risk of hepatocellular carcinoma]. However, the interactions of GC genotype on HBV mutations T1753V and preS deletion significantly increased on the risk of HCC in female HBV-infected subjects. 2013 Zhonghua liu xing bing xue za zhi Abstract HBV T1753V 58 64 PreS 69 73 Hepatocellular carcinoma;HBV infections 122;136 125;148 24518026 [Effect of PTPRD rs2279776 gene and interaction with hepatitis B virus mutations on the risk of hepatocellular carcinoma]. The interaction of rs2279776 GC genotype with G1896A could reduce the risk of HCC in HBV genotype B infected subjects and the interaction of CC genotype with A1652G significantly reduced the risk of HCC in HBV genotype C infected subjects. 2013 Zhonghua liu xing bing xue za zhi Abstract HBV G1896A;A1652G 46;158 52;164 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 78;199;85 81;202;108 24583110 Generation of a human hepatoma cell line supporting efficient replication of a lamivudine resistant hepatitis B virus. Accordingly, a human hepatoma (HepG2)-derived cell line was established by stable transfection of a plasmid containing a 1.2 unit length of HBV genome harboring rtL180M and rtM204V mutations that confer LAM resistance. 2014 Journal of virological methods Abstract HBV L180M;M204V 163;175 168;180 RT;RT 161;173 163;175 Hepatocellular carcinoma 21 29 24583247 Entecavir vs. lamivudine in chronic hepatitis B patients with severe acute exacerbation and hepatic decompensation. The T1753C/A mutation was also an independent predictor associated with overall and liver-related mortality at week 24. 2014 Journal of hepatology Abstract HBV T1753C;T1753A 4;4 12;12 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. By contrast, rtM204I mutant in the sample had lower replication capacity and higher LAM resistance (46.3% and 1396-fold increased LAM EC50 of the wild-type strain) compared to rtM204Q mutant. 2014 PloS one Abstract HBV M204I;M204Q 15;178 20;183 RT;RT 13;176 15;178 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. By contrast, rtM204I/rtM204V mutations were detected in 2,502 patients' samples. 2014 PloS one Abstract HBV M204I;M204V 15;23 20;28 RT;RT 13;21 15;23 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing verified that rtM204Q mutant was predominant in viral quasispecies of these samples. 2014 PloS one Abstract HBV M204Q 34 39 RT 32 34 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. CONCLUSION: rtM204Q is suggested to be a novel LAM-resistance-associated mutation. 2014 PloS one Abstract HBV M204Q 14 19 RT 12 14 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. It conferred a moderate resistance with higher competent natural replication capacity compared to rtM204I mutation. 2014 PloS one Abstract HBV M204I 100 105 RT 98 100 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Phenotypic analysis showed that rtM204Q mutant had 89.9% of replication capacity and 76-fold increased LAM EC50 of the concomitant wild-type strain. 2014 PloS one Abstract HBV M204Q 34 39 RT 32 34 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. rtM204Q mutant was susceptible to adefovir dipivoxil (ADV) in vitro and ADV/ADV+LAM rescue therapy in clinic. 2014 PloS one Abstract HBV M204Q 2 7 RT 0 2 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. rtM204Q mutation was detected in seven LAM-refractory patients. 2014 PloS one Abstract HBV M204Q 2 7 RT 0 2 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204Q emerged either alone or in concomitance with rtM204I/rtM204V, and all were accompanied with virologic breakthrough in clinical course. 2014 PloS one Abstract HBV M204Q;M204I;M204V 6;59;67 11;64;72 RT;RT;RT 4;57;65 6;59;67 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The study aimed to clarify whether a newly-found rtM204Q mutation from patients was associated with the drug resistance. 2014 PloS one Abstract HBV M204Q 51 56 RT 49 51 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Functional studies of the above 3 non-sense mutations all demonstrated higher cell proliferation activities and transformation abilities than wild type S, especially sW182*. 2014 PloS one Abstract HBV W182X 166 172 S;S 152;166 153;167 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. sW182* and sL216* were recurrently found in the 25 HBcAg (-) HCC tumor tissue, too. 2014 PloS one Abstract HBV W182X;L216X 0;11 6;17 C;S;S 51;0;11 56;1;12 Hepatocellular carcinoma 61 64 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Three nonsense mutations of S gene (sL95*, sW182*, and sL216*) were identified in the HBcAg(+) HCC tumor tissues. 2014 PloS one Abstract HBV L95X;W182X;L216X 36;43;55 41;49;61 C;S;S;S;S 86;28;36;43;55 91;29;37;44;56 Hepatocellular carcinoma 95 98 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Tumorigenicity analysis by xenograft experiments and in vitro migration assay showed potent oncogenic activity of sW182* mutant. 2014 PloS one Abstract HBV W182X 114 120 S 114 115 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. The rtM204I (ATT coding for isoleucine) is one of the most important resistance mutation sites. 2014 PloS one Abstract HBV M204I 6 11 RT 4 6 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Furthermore, the frequently occurring mutations in the major hydrophilic loop of the S gene include the T125M, A128V and M133I/L. 2014 PloS one Abstract HBV T125M;A128V;M133I;M133L 104;111;121;121 109;116;128;128 S 85 86 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Moreover, the prevalence of G1896A was considerably high among the HBeAg negative HIV/HBV co-infected subjects compared to HBV mono-infection. 2014 PloS one Abstract HBV G1896A 28 34 C 67 72 HBV infections;HBV-HIV coinfections 123;82 141;101 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The main amino acid substitutions within the MHC class II restricted T-cell epitope of HBcAg includes the T12S (15.8%) and T67N (12.3%) mutation and the V27I (10.5%) mutation in the MHC class I restricted T-cell epitope. 2014 PloS one Abstract HBV T12S;T67N;V27I 106;123;153 110;127;157 C 87 92 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The major mutations affecting HBeAg expression includes the A1762T/G1764A (13.6%), G1896A (22%) and G1862T mutation (33.9%) which was predominantly associated with HBV/A1. 2014 PloS one Abstract HBV G1764A;A1762T;G1896A;G1862T 67;60;83;100 73;66;89;106 C 30 35 24589944 Lamivudine and Adefovir Motif Variants Detected in chronic Hepatitis B patients. This mutations; responsible for lamivudine resistance YMDD+YVDD (n=10), YMDD+YIDD (n=12), YIDD (n=2), YVDD (=1); responsible for adefovir resistance N236T (n=3), A181T (n=5); responsible for lamivudine and adefovir resistance YMDD+YIDD+N236T (n=1). 2014 La Clinica terapeutica Abstract HBV N236T;A181T;N236T 149;162;236 154;167;241 P;P;P;P;P;P;P;P 77;90;231;54;72;226;59;102 81;94;235;58;76;230;63;106 24630522 Analysis of potential antiviral resistance mutation profiles within the HBV reverse transcriptase in untreated chronic hepatitis B patients using an ultra-deep pyrosequencing method. However, NAr mutations found in 6 isolates (37.5%) involved 7 positions including rtL91I, rtT128I, rtQ215P, rtF221Y, rtN238D, rtC256S, and rtI266G. 2014 Diagnostic microbiology and infectious disease Abstract HBV L91I;T128I;Q215P;F221Y;N238D;C256S;I266G 84;92;101;110;119;128;141 88;97;106;115;124;133;146 RT;RT;RT;RT;RT;RT;RT 82;90;99;108;117;126;139 84;92;101;110;119;128;141 24630522 Analysis of potential antiviral resistance mutation profiles within the HBV reverse transcriptase in untreated chronic hepatitis B patients using an ultra-deep pyrosequencing method. However, the relationship between rtI266G mutation and NA drug resistance was not previously reported. 2014 Diagnostic microbiology and infectious disease Abstract HBV I266G 36 41 RT 34 36 24630522 Analysis of potential antiviral resistance mutation profiles within the HBV reverse transcriptase in untreated chronic hepatitis B patients using an ultra-deep pyrosequencing method. One patient with rtI266G mutation also developed drug resistance after lamivudine (LAM) therapy. 2014 Diagnostic microbiology and infectious disease Abstract HBV I266G 19 24 RT 17 19 24630522 Analysis of potential antiviral resistance mutation profiles within the HBV reverse transcriptase in untreated chronic hepatitis B patients using an ultra-deep pyrosequencing method. Substitutions at 3 NAr mutation sites (rtT128I, rtN238D, and rtC256S) were detected in 3 unresponsive patients developing drug resistance after NA treatment. 2014 Diagnostic microbiology and infectious disease Abstract HBV T128I;N238D;C256S 41;50;63 46;55;68 RT;RT;RT 39;48;61 41;50;63 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. Five specific mutations, namely small S protein T57I, polymerase Q177H, G245W and M612L, and X protein V30L, were observed in 79-96% of the isolates of the separate lineage, compared to a frequency of 0-12% among the other HBV/E African isolates. 2014 PloS one Abstract HBV T57I;Q177H;G245W;M612L;V30L 48;65;72;82;103 52;70;77;87;107 P;S;X 54;32;93 64;39;94 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Drug Associated mutations were detected in 22% of the patient group and T36A and G50R mutations in X gene were found to be associated with HCC. 2014 PloS one Abstract HBV T36A;G50R 72;81 76;85 X 99 100 Hepatocellular carcinoma 139 142 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Few mutations in X gene (T36A and G50R) showed high frequency of association with HCC. 2014 PloS one Abstract HBV T36A;G50R 25;34 29;38 X 17 18 Hepatocellular carcinoma 82 85 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. A gene expression microarray in combination with gene set enrichment analysis (GSEA) revealed differentially expressed gene sets in the sW182* cells, including those related to cell-cycle regulation, deoxyribonucleic acid repair, and genome instability. 2014 Biochimica et biophysica acta Abstract HBV W182X 136 142 S 136 137 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. Among them, the sW182* mutant (the stop codon for tryptophan 182) showed the most potent oncogenicity in a mouse xenograft model using stably transfected mouse fibroblast cells. 2014 Biochimica et biophysica acta Abstract HBV W182X 16 22 S 16 17 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. Exogenous expression of TGFBI alleviated the oncogenic activity of the sW182* cells. 2014 Biochimica et biophysica acta Abstract HBV W182X 71 77 S 71 72 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. Of the differentially expressed genes, the transforming growth factor-beta-induced (TGFBI) gene was further validated to be dysregulated in the sW182* cells. 2014 Biochimica et biophysica acta Abstract HBV W182X 144 150 S 144 145 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. The level of cyclin D1, a negatively regulated TGFBI target, was highly elevated in the sW182* mutant cells, which is consistent with the potent oncogenicity. 2014 Biochimica et biophysica acta Abstract HBV W182X 88 94 S 88 89 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. These results suggest that dysregulation of TGFBI is involved in the oncogenic activity of the sW182* mutant of the hepatitis B virus S gene. 2014 Biochimica et biophysica acta Abstract HBV W182X 95 101 S;S 95;134 96;135 24662304 Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*. This study is aimed at understanding the molecular mechanisms leading to the oncogenic activity of the sW182* mutant. 2014 Biochimica et biophysica acta Abstract HBV W182X 103 109 S 103 104 24693312 The Effect of HBV Genotype C on the Development of HCC Differs Between Wild-Type Viruses and Those With BCP Double Mutations (T(1762)A(1764)). HBV basal core promoter (BCP) double mutations (T(1762)A(1764)) are very strong confounding factors of genotypes B and C in HCC development. 2014 Hepatitis monthly Abstract HBV T1762A 48 55 BCP;BCP 4;25 23;28 Hepatocellular carcinoma 124 127 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. A series of mutant clones containing rtA181T and/or rtI233V mutations were constructed and determined the effect of these mutations on the replication ability and drug resistance. 2014 Journal of virology Abstract HBV A181T;I233V 39;54 44;59 RT;RT 37;52 39;54 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Among drug-resistant mutations, the single rtA181T mutation is known to confer cross-resistance to antiviral drugs. 2014 Journal of virology Abstract HBV A181T 45 50 RT 43 45 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. An in vitro study revealed that the effect of the rtA181T mutation on viral replication and drug resistance is dependent on the mutations in the overlapping surface gene. 2014 Journal of virology Abstract HBV A181T 52 57 RT;S 50;157 52;164 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Compared to the rtA181T surface missense mutation (rtA181T/sW172S), the introduction of rtA181T surface nonsense mutation (rtA181T/sW172*) resulted in decreased viral replication and increased drug resistance. 2014 Journal of virology Abstract HBV W172S;W172X;A181T;A181T;A181T;A181T 59;131;18;90;53;125 65;137;23;95;58;130 RT;RT;RT;RT;S;S;S;S 16;51;88;123;59;131;24;96 18;53;90;125;60;132;31;103 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Complementation assay revealed that the truncated PreS1 is responsible for reduced replication of rtA181T/sW172* mutant. 2014 Journal of virology Abstract HBV W172X;A181T 106;100 112;105 RT;S;PreS1 98;106;50 100;107;55 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. In this study, we analyzed the evolution of drug-resistant mutations and characterized the effects of the rtA181T and rtI233V mutations on viral replication and drug resistance. 2014 Journal of virology Abstract HBV A181T;I233V 108;120 113;125 RT;RT 106;118 108;120 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Moreover, the clinical occurrence of the rtA181T mutation during antiviral therapy is also high. 2014 Journal of virology Abstract HBV A181T 43 48 RT 41 43 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Moreover, the rtA181T/sW172* mutant exhibited a defect in viral particle secretion. 2014 Journal of virology Abstract HBV W172X;A181T 22;16 28;21 RT;S 14;22 16;23 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Our data suggest that the impact of the rtA181T mutation on replication and drug resistance differs based on the mutation status of the corresponding surface gene. 2014 Journal of virology Abstract HBV A181T 42 47 RT;S 40;150 42;157 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. Our study revealed that the effect of the rtA181T mutation on viral replication and drug resistance is dependent on the mutations in the overlapping surface gene. 2014 Journal of virology Abstract HBV A181T 44 49 RT;S 42;149 44;156 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. The rtI233V mutation also affects replication ability and drug resistance. 2014 Journal of virology Abstract HBV I233V 6 11 RT 4 6 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. The rtI233V mutation that emerged during adefovir therapy reduced viral replication and conferred resistance to adefovir. 2014 Journal of virology Abstract HBV I233V 6 11 RT 4 6 24696492 The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene. This observation suggests the need for genotypic analysis of overlapping surface genes to manage antiviral drug resistance if clinical isolates harbor the rtA181T mutation. 2014 Journal of virology Abstract HBV A181T 157 162 RT;S 155;73 157;80 24697270 Stereoselective synthesis of 2'-fluoro-6'-methylene carbocyclic adenosine via Vince lactam. FMCA demonstrated excellent anti-HBV activity against both adefovir-resistant and lamivudine-resistant double (rtL180M/rtM204V) mutants as well as in lamivudine/entecavir triple mutants (L180M+S202G+M204V) in vitro. 2014 The Journal of organic chemistry Abstract HBV L180M;M204V;L180M;S202G;M204V 113;121;187;193;199 118;126;192;198;204 RT;RT 111;119 113;121 24700252 HBV whole-genome mutation profile in HIV-1/HBV coinfected patients in a long-term follow-up study. Known mutants Y100C, P127T and P120A associated to Y134H and S143T and new S mutants, which may potentially affect HBsAg expression and secretion and anti-HBs binding, were detected in baseline sera persisting up to the end of 9 years follow-up. 2014 Infection Abstract HBV Y100C;P127T;P120A;Y134H;S143T 14;21;31;51;61 19;26;36;56;66 S;S;S 155;115;75 158;120;76 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. BACKGROUND: The study aimed to clarify whether rtN236V mutation of HBV derived from adefovir dipivoxil (ADV)-refractory patients was associated with drug resistance. 2014 Antiviral therapy Abstract HBV N236V 49 54 RT 47 49 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. CONCLUSIONS: rtN236V was a novel infrequently occurring ADV-resistance-associated mutation. 2014 Antiviral therapy Abstract HBV N236V 15 20 RT 13 15 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. RESULTS: rtN236V was detected in six ADV-refractory patients; signature ADV-resistant mutations rtA181V and rtN236T were detected in 1,311 patients. 2014 Antiviral therapy Abstract HBV N236V;A181V;N236T 11;98;110 16;103;115 RT;RT;RT 9;96;108 11;98;110 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. rtN236V mutants emerged predominantly with virological breakthrough in the clinical course of the six patients. 2014 Antiviral therapy Abstract HBV N236V 2 7 RT 0 2 24710668 Screening and identification of a novel adefovir dipivoxil resistance associated mutation, rtN236V, of HBV from a large cohort of HBV-infected patients. rtN236V mutants from patient 1 and patient 2 exhibited 3.90-fold and 3.10-fold decreased susceptibility to ADV, respectively, compared to the wild-type virus; by contrast, rtN236T mutants from the patients had 4.50-fold and 4.75-fold decreased susceptibility, respectively. 2014 Antiviral therapy Abstract HBV N236V;N236T 2;174 7;179 RT;RT 0;172 2;174 24715933 Prevalence and molecular analysis of occult hepatitis B virus infection isolated in a sample of cryptogenic cirrhosis patients in iran. All patients who acquired Y134F contained S207R (within HLA-A2-restricted CTL epitope) as a combination. 2014 Oman medical journal Abstract HBV Y134F;S207R 26;42 31;47 24715933 Prevalence and molecular analysis of occult hepatitis B virus infection isolated in a sample of cryptogenic cirrhosis patients in iran. There were 14 mutations found in 5 patients; 6 were in the major hydrophilic region, of which 4 were Y134F assigning for the "a" determinant region. 2014 Oman medical journal Abstract HBV Y134F 101 106 24748463 Association of miRNA-122-binding site polymorphism at the interleukin-1 alpha gene and its interaction with hepatitis B virus mutations with hepatocellular carcinoma risk. Although rs3783553 did not significantly affect genetic susceptibility to HBV-related HCC, its variant allele may predispose the host to selecting HBV C7A mutation during evolution and significantly reduce the risk of HCC caused by HBV preS deletion. 2014 Frontiers of medicine Abstract HBV C7A 151 154 PreS 236 240 Hepatocellular carcinoma;Hepatocellular carcinoma 86;218 89;221 24748463 Association of miRNA-122-binding site polymorphism at the interleukin-1 alpha gene and its interaction with hepatitis B virus mutations with hepatocellular carcinoma risk. However, the TTCA insertion allele of rs3783553 was significantly associated with an increased frequency of HBV C7A mutation compared with homozygous TTCA deletion carriers [(del/ins + ins/ins) vs. 2014 Frontiers of medicine Abstract HBV C7A 112 115 24763132 Higher proportion of viral basal core promoter mutant increases the risk of liver cirrhosis in hepatitis B carriers. BACKGROUND AND OBJECTIVE: Precore (PC) variant (G1896A) and basal core promoter (BCP) variant (A1762T/G1764A) of HBV are associated with risk of hepatocellular carcinoma in HBV carriers. 2015 Gut Abstract HBV G1764A;G1896A;A1762T 102;48;95 108;54;101 BCP;BCP;Precore;Precore 60;81;35;26 79;84;37;33 Hepatocellular carcinoma 145 169 24777553 Amino acid polymorphism in the reverse transcriptase region of hepatitis B virus and the relationship with nucleos(t)ide analogues treatment for preventing mother-to-infant transmission. The primary drug mutation rtA181T/V was detected in three HBeAg-negative women with an HBV DNA level of <4 log IU/ml. 2014 Journal of medical virology Abstract HBV A181T;A181V 28;28 35;35 RT;C 26;58 28;63 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A pooled analysis of samples revealed that A799G, A987G, and T1055A were independent risk factors for HCC, with adjusted odds ratios of 5.53 [95% confidence interval (CI), 1.69-18.10], 4.20 (95%CI, 1.15-15.35), and 3.78 (95%CI, 1.45-9.86), respectively. 2014 PloS one Abstract HBV A799G;A987G;T1055A 43;50;61 48;55;67 Hepatocellular carcinoma 102 105 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. RESULTS: There were 15 candidate mutations identified from the discovery set, with A799G and T1055A being consistently associated with HCC across all studies. 2014 PloS one Abstract HBV A799G;T1055A 83;93 88;99 Hepatocellular carcinoma 135 138 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. The remaining showed the following mutation patterns: rtM204I/V (50.2%), rtL180M (39.2%), and rtA181T/V (19.6%). 2014 Annals of laboratory medicine Abstract HBV M204I;M204V;L180M;A181T;A181V 56;56;75;96;96 63;63;80;103;103 RT;RT;RT 54;73;94 56;75;96 24797477 Molecular epidemiological study of hepatitis B virus genotypes in Southwest, China. 67.5% (56/83) of genotype C/D was Hepatitis B surface antigen (HBsAg) positive/Hepatitis B e antigen (HBeAg) positive/HBV DNA>=20,000 IU/ml, BCP A1762T/G1764A double mutation was frequent in genotype C and C/D, and G1896A was frequent in B and B/C. 2014 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 152;145;215 158;151;221 BCP;C;C;S;S 141;91;102;63;46 144;100;107;68;53 24797477 Molecular epidemiological study of hepatitis B virus genotypes in Southwest, China. C/D recombinant exhibits higher frequency with HBeAg positive, high level of HBV DNA and BCP A1762T/G1764A double mutation. 2014 Journal of medical virology Abstract HBV G1764A;A1762T 100;93 106;99 BCP;C 89;47 92;52 24797477 Molecular epidemiological study of hepatitis B virus genotypes in Southwest, China. HBV infectious markers, HBV DNA and mutations in the basic core promoter (BCP) A1762T/G1764A and G1896A were analyzed. 2014 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 86;79;97 92;85;103 BCP;BCP 53;74 72;77 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. CONCLUSIONS: Reactivation from occult HBV infection is characterized by low genetic heterogeneity, with the wild-type G1896 or G1896A variant prevalent. 2014 Journal of hepatology Abstract HBV G1896A 127 133 HBV infections 38 51 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. Prevalence of the G1896A variant in latently infected livers was determined among 44 healthy individuals that were HBsAg-negative but anti-HBc-positive. 2014 Journal of hepatology Abstract HBV G1896A 18 24 S;C 115;139 120;142 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. The G1896A variant was detected in 42.9% (6/14) of cases, including two cases with fatal liver failure. 2014 Journal of hepatology Abstract HBV G1896A 4 10 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. The G1896A variant was observed in the liver tissue of 11.4% (5/44) of individuals with occult HBV infection. 2014 Journal of hepatology Abstract HBV G1896A 4 10 HBV infections 95 108 24798622 Reactivation from occult HBV carrier status is characterized by low genetic heterogeneity with the wild-type or G1896A variant prevalence. The reactivated viruses in each case were almost exclusively the wild-type G1896 or G1896A variant. 2014 Journal of hepatology Abstract HBV G1896A 84 90 24814823 Nucleoside/nucleotide analog inhibitors of hepatitis B virus polymerase: mechanism of action and resistance. Major mutational patterns conferring nucleoside/nucleotide analog resistance include the combinations rtL180M/rtM204(I/V) (for lamivudine, entecavir, telbivudine and clevudine) and rtA181V/rtN236T (for adefovir and tenofovir). 2014 Current opinion in virology Abstract HBV L180M;A181V;N236T 104;183;191 109;188;196 RT;RT;RT;RT 102;110;181;189 104;112;183;191 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Especially the lamivudine resistance mutations rtL180M/rtM204V and rtM204I were detected. 2014 PloS one Abstract HBV M204I;L180M;M204V 69;49;57 74;54;62 RT;RT;RT 47;55;67 49;57;69 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Two patients showed the described HBV vaccine escape mutation sP120T. 2014 PloS one Abstract HBV P120T 62 68 S 62 63 24836314 Viral evolutionary changes during tenofovir treatment in a chronic hepatitis B patient with sequential nucleos(t)ide therapy. A 54-year-old man diagnosed with HBeAg-positive chronic hepatitis B (CHB) was treated with entecavir (ETV) 1mg/day following an initial unsuccessful lamivudine (LAM) treatment (rtL180M, rtM204V/I). 2014 Journal of clinical virology Abstract HBV L180M;M204V;M204I 179;188;188 184;195;195 C;RT;RT 33;177;186 38;179;188 Chronic Hepatitis B;Chronic Hepatitis B 33;69 67;72 24836314 Viral evolutionary changes during tenofovir treatment in a chronic hepatitis B patient with sequential nucleos(t)ide therapy. However, this patient experienced virological breakthrough under TDF with a HBV strain bearing rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I combined mutations without rtA194T mutation. 2014 Journal of clinical virology Abstract HBV L80M;L180M;M204V;M204I;A200V;F221Y;S223A;T184A;T184L;R153Q;V191I;A194T 97;105;114;114;125;134;143;152;152;163;176;211 101;110;121;121;130;139;148;159;159;168;181;216 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 95;103;112;123;132;141;150;161;174;209 97;105;114;125;134;143;152;163;176;211 24836314 Viral evolutionary changes during tenofovir treatment in a chronic hepatitis B patient with sequential nucleos(t)ide therapy. Subsequently, virological breakthrough with ETV mutation (rtT184A/L) developed. 2014 Journal of clinical virology Abstract HBV T184A;T184L 60;60 67;67 RT 58 60 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. HCC patients also had a lower frequency of T31C mutation in pre-S2 gene, compared with control subjects (0.524; 95% CI 0.280-0.982). 2014 PloS one Abstract HBV T31C 43 47 PreS2 60 66 Hepatocellular carcinoma 0 3 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. RESULTS: After adjustment for age, history of cigarette smoking and alcohol consumption, HBeAg positivity, pre-S deletions, pre-S2 start codon mutations, and T53C mutation were significantly associated with HCC, showing adjusted odds ratios (ORs) from 1.914 to 3.199. 2014 PloS one Abstract HBV T53C 158 162 C;PreS;PreS2 89;107;124 94;112;130 Hepatocellular carcinoma 207 210 24850741 Phosphoacceptors threonine 162 and serines 170 and 178 within the carboxyl-terminal RRRS/T motif of the hepatitis B virus core protein make multiple contributions to hepatitis B virus replication. Individual alanine substitution of threonine 162 significantly decreased minus-strand, plus-strand, and relaxed-circular DNA synthesis, demonstrating that this residue plays multiple roles in HBV DNA synthesis. 2014 Journal of virology Abstract HBV T162A 11 48 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. Allele-specific PCR assays capable of detecting rtM204V or rtM204I subpopulations as low as 0.5% were developed and used to assess patient samples from a Phase 3b study evaluating TDF and FTC/TDF treatment in LAM-R patients. 2014 Journal of medical virology Abstract HBV M204V;M204I 50;61 55;66 RT;RT 48;59 50;61 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. Baseline samples (n = 280) were quantified for rtM204V/I subpopulations and rtM204V or rtM204I subpopulations were detected in 269/273 (98.5%) baseline samples with a range of 0.7% to >95%. 2014 Journal of medical virology Abstract HBV M204V;M204I;M204V;M204I 49;49;78;89 56;56;83;94 RT;RT;RT 47;76;87 49;78;89 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. In conclusion, rtM204V/I subpopulations demonstrate similar early HBV DNA decline kinetics to WT subpopulations during treatment with either TDF or FTC/TDF. 2014 Journal of medical virology Abstract HBV M204V;M204I 17;17 24;24 RT 15 17 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. On-treatment analyses were conducted for seventeen patients (TDF, n = 8; FTC/TDF, n = 9) that harbored baseline WT and either rtM204V or rtM204I (no rtM204V/I mixtures) and HBV DNA >=1,000 copies/ml at/after week 4. 2014 Journal of medical virology Abstract HBV M204V;M204I;M204V;M204I 128;139;151;151 133;144;158;158 RT;RT;RT 126;137;149 128;139;151 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. Tenofovir disoproxil fumarate (TDF) is recommended as treatment for chronic hepatitis B patients harboring lamivudine-associated resistance mutations (LAM-R, rtM204V/I +- rtL180M). 2014 Journal of medical virology Abstract HBV M204V;M204I;L180M 160;160;173 167;167;178 RT;RT 158;171 160;173 Chronic Hepatitis B 68 87 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. The median change in HBV DNA through week 12 for WT and rtM204V/I subpopulations was similar, -2.64 and -3.30 log10copies/ml, respectively, with no significant difference between TDF and FTC/TDF treatment. 2014 Journal of medical virology Abstract HBV M204V;M204I 58;58 65;65 RT 56 58 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. These results demonstrate that TDF is similarly active against both WT and rtM204V/I subpopulations in vivo. 2014 Journal of medical virology Abstract HBV M204V;M204I 77;77 84;84 RT 75 77 24861361 Evaluation of HBV DNA decay kinetics in patients containing both rtM204V/I mutant and wild-type HBV subpopulations during tenofovir DF (TDF) monotherapy or combination therapy with emtricitabine (FTC)/TDF. This study evaluated the clinical response of rtM204V and rtM204I subpopulations to TDF by comparing their early viral load decay kinetics to wild-type (WT) subpopulations in chronic hepatitis B patients harboring rtM204V/I prior to initiating TDF or emtricitabine (FTC)/TDF therapy. 2014 Journal of medical virology Abstract HBV M204V;M204I;M204V;M204I 48;60;216;216 53;65;223;223 RT;RT;RT 46;58;214 48;60;216 Chronic Hepatitis B 175 194 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. Among 9 patients on antiretroviral treatment (ART), one patient had the [L180M, M204V] mutation associated with lamivudine resistance. 2014 PloS one Abstract HBV L180M;M204V 73;80 78;85 24930916 Clinical and virological characteristics associated with severe acute hepatitis B. The 19 patients with severe or fulminant AVH-B more frequently than the 119 with a normal course stated intravenous drug use (63.2% versus 36.1%, p 0.04) and were HBV-DNA negative (31.6% versus 11.8%, p 0.03) and anti-hepatitis C virus (HCV) positive (57.9% versus 19.3%, p 0.0008); the prevalences of different HBV genotypes and of the rtM204V/I mutant were similar in these three forms of AVH-B. 2014 Clinical microbiology and infection Abstract HBV M204V;M204I 339;339 346;346 RT 337 339 Acute Hepatitis B 391 394 24930916 Clinical and virological characteristics associated with severe acute hepatitis B. The HBV mutants in the polymerase region were sought in 110 (87%) patients by direct sequencing, and the rtM204V/I mutations also by an allele-specific PCR. 2014 Clinical microbiology and infection Abstract HBV M204V;M204I 107;107 114;114 P;RT 23;105 33;107 24973814 Mother-to-child transmission of hepatitis B virus: evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era. In the 56 mother-child pairs with 1-15 year-old children acquired the infection from their mothers, the frequencies of HBV mutations including A1762T/G1764A and G1896A in genotype B2 or C2 increased consecutively with increasing age of children. 2014 Journal of clinical virology Abstract HBV G1764A;A1762T;G1896A 150;143;161 156;149;167 24973814 Mother-to-child transmission of hepatitis B virus: evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era. T1753V, C1653T, and G1899A were infrequent in the mother-child pairs. 2014 Journal of clinical virology Abstract HBV T1753V;C1653T;G1899A 0;8;20 6;14;26 24973814 Mother-to-child transmission of hepatitis B virus: evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era. The HCC-risk mutations including A1762T/G1764A were present in the mothers' and cord blood but mostly absent in the 7-month-old infants'. 2014 Journal of clinical virology Abstract HBV G1764A;A1762T 40;33 46;39 Hepatocellular carcinoma 4 7 24973814 Mother-to-child transmission of hepatitis B virus: evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era. These mutations including A1762T/G1764A in genotype C2 and G1896A in genotype B2 were more frequent in mothers than in children (P<0.001). 2014 Journal of clinical virology Abstract HBV G1764A;A1762T;G1896A 33;26;59 39;32;65 24976702 HBeAg negative variants and their role in the natural history of chronic hepatitis B virus infection. The appearance of the precore stop codon (with G-for-A substitution at position 1896) and basal core promoter (BCP) (with A-for-T and G-for-A, at positions 1762 and 1764, respectively) variants which reduce or abrogate hepatitis B e antigen (HBeAg) production, heralds the initiation of the seroconversion phase from HBeAg to anti-HBe positivity. 2014 World journal of gastroenterology Abstract HBV A1896G 47 84 BCP;BCP;C;C;C;C;Precore 90;111;231;331;242;317;22 109;114;240;334;247;322;29 24992206 Investigation into drug-resistant mutations of HBV from 845 nucleoside/nucleotide analogue-naive Chinese patients with chronic HBV infection. A follow-up study showed that the presence of pre-existing rtM204I strain in one patient increased from 20% at baseline to 85% after 13 months of entecavir treatment with corresponding recession of wild-type strain in the viral pool. 2015 Antiviral therapy Abstract HBV M204I 61 66 RT 59 61 24992206 Investigation into drug-resistant mutations of HBV from 845 nucleoside/nucleotide analogue-naive Chinese patients with chronic HBV infection. Clonal sequencing identified 13 drug-resistant HBV strains: rtL80I+M204I, rtL80I+M204V, rtL180M+M204I, rtL180M+M204V, rtM204I, rtM204V, rtL80I+L180M+M204I, rtL80I+L180M+M204V, rtA181V, rtA181V+M204I, rtA181T+N236T, rtA181V+N236T and rtN236T. 2015 Antiviral therapy Abstract HBV M204I;M204V;A181V;N236T;L180M;L80I;L80I;A181V;A181V;L80I;L80I;L180M;A181T;M204V;L180M;M204I;L180M;M204V;M204I;N236T;M204I;M204V;M204I;N236T 120;129;178;235;105;138;158;187;217;62;76;90;202;111;143;149;163;169;193;223;67;81;96;208 125;134;183;240;110;142;162;192;222;66;80;95;207;116;148;154;168;174;198;228;72;86;101;213 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 60;74;88;103;118;127;136;156;176;185;200;215;233 62;76;90;105;120;129;138;158;178;187;202;217;235 24992206 Investigation into drug-resistant mutations of HBV from 845 nucleoside/nucleotide analogue-naive Chinese patients with chronic HBV infection. Phenotypic analysis showed that two pre-existing lamivudine-resistant strains (rtL80I+M204I, rtL180M+M204V) had >1,000-fold resistance to lamivudine, and one pre-existing adefovir-resistant strain (rtA181V+N236T) had 15.4-fold resistance to adefovir compared with the wild-type strain. 2015 Antiviral therapy Abstract HBV L80I;L180M;A181V;M204I;M204V;N236T 81;95;200;86;101;206 85;100;205;91;106;211 RT;RT;RT 79;93;198 81;95;200 24992206 Investigation into drug-resistant mutations of HBV from 845 nucleoside/nucleotide analogue-naive Chinese patients with chronic HBV infection. RESULTS: Drug-resistant mutations were detected in 2.01% (17/845) of the patients by direct sequencing, including 15 with lamivudine-resistant mutations (rtM204V, rtM204I), one with adefovir-resistant mutation (rtA181V), and one with both lamivudine- and adefovir-resistant mutations (rtA181V, rtM204I). 2015 Antiviral therapy Abstract HBV M204V;M204I;A181V;A181V;M204I 156;165;213;287;296 161;170;218;292;301 RT;RT;RT;RT;RT 154;163;211;285;294 156;165;213;287;296 24993731 Adefovir and lamivudine combination therapy in patients with entecavir-resistant chronic hepatitis B: antiviral responses and evolution of mutations. An ADV- and LMV-resistant mutant (rtA181T) emerged in 2 patients (11.7%). 2014 Intervirology Abstract HBV A181T 36 41 RT 34 36 24993731 Adefovir and lamivudine combination therapy in patients with entecavir-resistant chronic hepatitis B: antiviral responses and evolution of mutations. The rtT184L/I/A/F (50%), rtS202G (25%) and mixed ETV-resistant mutations (25%) were detected at enrollment. 2014 Intervirology Abstract HBV T184L;T184I;T184A;T184F;S202G 6;6;6;6;27 17;17;17;17;32 RT;RT 4;25 6;27 25019072 Hidden secret in hepatitis B viral X protein mutation and hypoxia-inducible factor-1alpha in hepatocarcinoma cancer. The C-terminal region of amino acids 119-140 was important for the stability and transactivation, and the point mutations K130M/V131I enhance the functionality of HIF-1alpha, while C-terminal truncation diminish the HIF-1alpha function. 2014 Hepatobiliary surgery and nutrition Abstract HBV V131I;K130M 128;122 133;127 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. A high prevalence of the rtI187V polymerase substitution of hepatitis B virus (HBV) was detected in nucleoside/nucleotide-analogue-naive and -treated chronic hepatitis B (CHB) patients. 2014 The Journal of general virology Abstract HBV I187V 27 32 RT;P 25;33 27;43 Chronic Hepatitis B;Chronic Hepatitis B 150;171 169;174 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. Furthermore, rtI187V HBV remained susceptible towards treatment with LAM or ADV in vitro whereas the combination of the rtI187V substitution with LAM-resistant mutations rendered HBV resistant to LAM but still sensitive to ADV. 2014 The Journal of general virology Abstract HBV I187V;I187V 15;122 20;127 RT;RT 13;120 15;122 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. However, the emergence of the rtI187V substitution significantly impaired viral replication but without affecting drug sensitivity in vitro. 2014 The Journal of general virology Abstract HBV I187V 32 37 RT 30 32 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. In vitro phenotypic assays showed that the viruses bearing the rtI187V substitution had impaired replication efficacy when compared with the WT and the virus carrying rtI187V combined with LAM-resistant single or double mutations showed even more significantly impaired replicative capacities. 2014 The Journal of general virology Abstract HBV I187V;I187V 65;169 70;174 RT;RT 63;167 65;169 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. Of note, the rtI187V prevalence in HBV genotype B was significantly higher than that in HBV genotype C (95.2 vs 4.8 %). 2014 The Journal of general virology Abstract HBV I187V 15 20 RT 13 15 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. Our study revealed that the rtI187V substitution in the HBV polymerase frequently occurred in CHB patients, particularly those with HBV genotype B. 2014 The Journal of general virology Abstract HBV I187V 30 35 P;RT 60;28 70;30 Chronic Hepatitis B 94 97 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. Replication-competent HBV constructs containing rtI187V and combined with LAM-resistant (rtM204I, rtL180M/rtM204V) mutations were generated, and compared with WT, LAM-resistant single (rtM204I) or double (rtL180M/rtM204V) and ADV-resistant (rtN236T) clones. 2014 The Journal of general virology Abstract HBV I187V;M204I;M204I;N236T;L180M;L180M;M204V;M204V 50;91;187;243;100;207;108;215 55;96;192;248;105;212;113;220 RT;RT;RT;RT;RT;RT;RT;RT 48;89;98;106;185;205;213;241 50;91;100;108;187;207;215;243 25028473 Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility. We aimed at assessing the replicative capacity and susceptibility to lamivudine (LAM) and adefovir (ADV) in vitro of HBV harbouring rtI187V alone or in conjunction with LAM- or ADV-resistant mutations. 2014 The Journal of general virology Abstract HBV I187V 134 139 RT 132 134 25040474 Genetic characterization and genotyping of hepatitis B virus (HBV) isolates from donors with an occult HBV infection. Mutations in the S region (100%) were found especially in loop 1 of the major hydrophilic loop (MHL) at positions I110L, T114S, T126I and S113T, whereas mutations in the C region (65%) were within the basal core promoter region (position A1762T/G1764A) and precore region (position G1896A). 2014 Vox sanguinis Abstract HBV G1764A;A1762T;I110L;T114S;T126I;S113T;G1896A 245;238;114;121;128;138;282 251;244;119;126;133;143;288 BCP;C;Precore;S 201;170;257;17 220;171;264;18 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Amino acid substitutions of rtL180M, rtS202G, and rtM204V emerged and were associated with an increase in serum HBV DNA at virologic breakthrough. 2014 Drug design, development and therapy Abstract HBV L180M;S202G;M204V 30;39;52 35;44;57 RT;RT;RT 28;37;50 30;39;52 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. At the start of combination therapy, amino acid substitutions of the reverse transcriptase (rt) gene, rtL180M, rtT184I/M, and rtM204V, were detected. 2014 Drug design, development and therapy Abstract HBV L180M;T184I;T184M;M204V 104;113;113;128 109;120;120;133 RT;RT;RT;RT;RT 69;92;102;111;126 90;94;104;113;128 25100867 Hepatitis B virus sub-genotype A1 infection is characterized by high replication levels and rapid emergence of drug resistance in HIV-positive adults receiving first-line antiretroviral therapy in Malawi. At 6 months, M204I was detected in 8/46 (17%) and 16/17 (94%) subjects using Sanger and deep sequencing, respectively. 2014 Clinical infectious diseases Abstract HBV M204I 13 18 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. All rtA181S-positive patients had received nucleos(t)ide analogues. 2015 Journal of viral hepatitis Abstract HBV A181S 6 11 RT 4 6 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. Genotype C and genotype B HBV infection occupied 91.8% and 8.2% in rtA181S-positive patients, in contrast to 84.6% and 15.4% in rtA181S-negative patients (P < 0.01). 2015 Journal of viral hepatitis Abstract HBV A181S;A181S 69;130 74;135 RT;RT 67;128 69;130 HBV infections 26 39 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. Phenotypic analysis of patient-derived viral strains showed that rtA181S, rtA181S+N236T, rtN236T and rtA181V strains had 68.5%, 49.9%, 71.4% and 66.2% of natural replication capacity of wild-type strain, and 3.7-fold, 9.8-fold, 7.9-fold and 5.6-fold increased EC(50) to adefovir dipivoxil (ADV). 2015 Journal of viral hepatitis Abstract HBV A181S;N236T;A181V;A181S;N236T 67;91;103;76;82 72;96;108;81;87 RT;RT;RT;RT 65;74;89;101 67;76;91;103 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. Rescue therapy with entecavir or combination therapy was effective in rtA181S-related ADV-refractory patients. 2015 Journal of viral hepatitis Abstract HBV A181S 72 77 RT 70 72 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. rtA181S was detected in multiple patients with virologic breakthrough. 2015 Journal of viral hepatitis Abstract HBV A181S 2 7 RT 0 2 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. The rtA181S mutation confers moderate resistance to ADV. 2015 Journal of viral hepatitis Abstract HBV A181S 6 11 RT 4 6 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. The rtA181S strain remained susceptible to lamivudine, entecavir and tenofovir, and ADV susceptibility was restored after the mutation was eliminated through site-directed mutagenesis. 2015 Journal of viral hepatitis Abstract HBV A181S 6 11 RT 4 6 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. The rtA181S was detected in 98 patients with 12 kinds of mutational patterns. 2015 Journal of viral hepatitis Abstract HBV A181S 6 11 RT 4 6 25132017 The rtA181S mutation of hepatitis B virus primarily confers resistance to adefovir dipivoxil. The study aimed to clarify clinical significance of hepatitis B virus (HBV) rtA181S mutation in Chinese HBV-infected patients. 2015 Journal of viral hepatitis Abstract HBV A181S 78 83 RT 76 78 HBV infections 104 116 25132075 Molecular analysis of the interspousal transmission of hepatitis B virus in two Japanese patients who acquired fulminant hepatitis B after 50 and 49 years of marriage. These four isolates shared a precore mutation of G1896A known to be associated with fulminant hepatitis B. 2014 Journal of medical virology Abstract HBV G1896A 49 55 Precore 29 36 Fulminant Hepatitis B 84 103 25170961 Correlation between the promoter basal core and precore mutations and HBsAg quantification in French blood donors infected with hepatitis B virus. As the study was conducted in healthy subjects who could be considered as asmptomatic carriers, these results suggest a possible protective effect of the G1896A mutation against severe liver lesions. 2015 Journal of medical virology Abstract HBV G1896A 154 160 Liver disease 185 198 25170961 Correlation between the promoter basal core and precore mutations and HBsAg quantification in French blood donors infected with hepatitis B virus. Direct sequencing of precore/core gene was used to detect A1762T/G1764A mutations in the BCP and G1896A in the PC region. 2015 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 65;58;97 71;64;103 BCP;C;Precore;Precore 89;29;111;21 92;33;113;28 25208639 Performance of LigAmp assay for sensitive detection of drug-resistant hepatitis B virus minor variants in comparison with standard nucleotide sequencing. Among these subjects, rtM204V and rtM204I (ATT) mutations were identified by standard sequencing in 10 (25%) and 12 (30%) subjects, respectively. 2014 Molecular diagnosis & therapy Abstract HBV M204V;M204I 24;36 29;41 RT;RT 22;34 24;36 25208639 Performance of LigAmp assay for sensitive detection of drug-resistant hepatitis B virus minor variants in comparison with standard nucleotide sequencing. CONCLUSIONS: This data shows significantly higher sensitivity of LigAmp for detection of minority rtM204V and rtM204I (ATT) mutations over standard sequencing. 2014 Molecular diagnosis & therapy Abstract HBV M204V;M204I 100;112 105;117 RT;RT 98;110 100;112 25208639 Performance of LigAmp assay for sensitive detection of drug-resistant hepatitis B virus minor variants in comparison with standard nucleotide sequencing. LigAmp detected both rtM204V and rtM204I (ATT) mutations in 13 (32.5%) subjects, rtM204I mutation in 12 (30%) subjects and rtM204V mutation in 1 (2.5%) subject, respectively. 2014 Molecular diagnosis & therapy Abstract HBV M204V;M204I;M204I;M204V 23;35;83;125 28;40;88;130 RT;RT;RT;RT 21;33;81;123 23;35;83;125 25208639 Performance of LigAmp assay for sensitive detection of drug-resistant hepatitis B virus minor variants in comparison with standard nucleotide sequencing. RESULTS: A total of 80 reactions of LigAmp assay were performed for rtM204V and rtM204I (ATT) mutant detection. 2014 Molecular diagnosis & therapy Abstract HBV M204V;M204I 70;82 75;87 RT;RT 68;80 70;82 25218700 Occult hepatitis B virus infection with positive hepatitis B e antigen. The HBV had double mutations (A1762T and G1764A) in the basal core promoter but had no mutation in the pre C/C gene in both patients. 2015 Clinica chimica acta; international journal of clinical chemistry Abstract HBV A1762T;G1764A 30;41 36;47 BCP;Precore 56;103 75;108 25223483 Effect of functional nuclear factor-kappaB genetic polymorphisms on hepatitis B virus persistence and their interactions with viral mutations on the risk of hepatocellular carcinoma. In the genotype C HBV-infected subjects, rs2233406 variant genotypes were significantly associated with an increased risk of HCC [CT versus CC: age-, gender-adjusted odds ratio (AOR), 1.33; 95% confidence interval (CI) 1.01-1.75 in training set and AOR, 1.59; 95% CI 1.01-2.52 in validation set] compared with HCC-free HBV-infected subjects and significantly increased the frequencies of HCC-related HBV mutations (A1762T/G1764A, T1753V, preS1 start codon mutation, and preS deletion); rs28362491 (Del/Del or Ins/Del + Del/Del versus Ins/Ins) significantly increased the frequency of A1762T/G1764A and reduced the frequency of preS2 start codon mutation. 2014 Annals of oncology Abstract HBV G1764A;G1764A;A1762T;A1762T;T1753V 422;591;584;415;430 428;597;590;421;436 PreS;PreS1;PreS2 470;438;627 474;443;632 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections;HBV infections 125;310;388;18;319 128;313;391;30;331 25223483 Effect of functional nuclear factor-kappaB genetic polymorphisms on hepatitis B virus persistence and their interactions with viral mutations on the risk of hepatocellular carcinoma. The interaction of rs2233406 variant genotypes (CT + TT versus CC) with A1762T/G1764A significantly increased HCC risk in genotype C HBV-infected subjects, with AOR of 2.61 (95% CI 1.09-6.26). 2014 Annals of oncology Abstract HBV G1764A;A1762T 79;72 85;78 Hepatocellular carcinoma;HBV infections 110;133 113;145 25243957 [Clinical significance of hepatitis B virus S gene mutation for recurrence of hepatitis B after liver transplantation]. One of the patients had T126I and G145A mutations, and the other had a M 133L mutation. 2014 Zhonghua gan zang bing za zhi Abstract HBV T126I;G145A;M133L 24;34;71 29;39;77 25244642 Hepatitis B virus depicts a high degree of conservation during the immune-tolerant phase in familiarly transmitted chronic hepatitis B infection: deep-sequencing and phylogenetic analysis. By deep-sequencing, the quantitative analysis of the dynamics of basal core promoter (BCP) (A1762T, G1764A; A1766C; T1773C; 8-bp deletion; and other) and precore (G1896A) variants among HBV isolates from family members exhibited differences during the follow-up. 2014 Journal of viral hepatitis Abstract HBV A1762T;G1764A;A1766C;T1773C;G1896A 92;100;108;116;163 98;106;114;122;169 BCP;BCP;Precore 65;86;154 84;89;161 25281206 Impacts of human leukocyte antigen DQ genetic polymorphisms and their interactions with hepatitis B virus mutations on the risks of viral persistence, liver cirrhosis, and hepatocellular carcinoma. rs2856718 variant genotypes were significantly associated with an increased frequency of HBV A1726C mutation, a LC-risk, HCC-protective mutation, in genotype C. 2014 Infection, genetics and evolution Abstract HBV A1726C 93 99 Hepatocellular carcinoma;Liver cirrhosis 121;112 124;114 25281206 Impacts of human leukocyte antigen DQ genetic polymorphisms and their interactions with hepatitis B virus mutations on the risks of viral persistence, liver cirrhosis, and hepatocellular carcinoma. The interaction of rs2856718 AG+GG genotype with T1753V, a HCC-risk mutation, significantly reduced LC risk, with an OR of 0.26 (95% CI, 0.09-0.78); whereas the interaction of rs2856718 AG genotype with C1673T, a LC-risk mutation, significantly increased HCC risk, with an OR of 2.80 (95% CI, 1.02-7.66) in genotype C HBV-infected subjects. 2014 Infection, genetics and evolution Abstract HBV T1753V;C1673T 49;203 55;209 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections;Liver cirrhosis;Liver cirrhosis 59;255;318;100;213 62;258;330;102;215 25283864 Significance of mutations in hepatitis B virus X gene for the pathogenesis of HB-associated glomerulonephritis. In control patients, missense nucleotide mutations of A1632C and A1635C were detected in 8% of subjects, both located in the non-functional region of the X gene. 2014 Acta virologica Abstract HBV A1632C;A1635C 54;65 60;71 X 154 155 25283864 Significance of mutations in hepatitis B virus X gene for the pathogenesis of HB-associated glomerulonephritis. In HBV-GN patients, missense nucleotide mutations of C1653T, A1726C, A1727T, C1730G, T1753C, A1762T, and G1764A were detected in 84% of subjects, all located in the trans-acting regulatory region of the X gene. 2014 Acta virologica Abstract HBV C1653T;A1726C;A1727T;C1730G;T1753C;A1762T;G1764A 53;61;69;77;85;93;105 59;67;75;83;91;99;111 X 203 204 HBV-associated glomerulonephritis 3 9 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The baseline mutation profiles, rtM204I (p=0.992), rtM204I/V (p=0.177), and rtL180M (p=0.051), were not correlated with the cumulative virological response, and the baseline HBV DNA level (p=0.032) was the only independent predictive factor for cumulative virological response. 2015 Gut and liver Abstract HBV M204I;M204I;M204V;L180M 34;53;53;78 39;60;60;83 RT;RT;RT 32;51;76 34;53;78 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The population of rtM204 mutants persisted or increased in 8 of 12 patients, and rtA181T mutants newly emerged as a minor population in four patients until 96 weeks. 2015 Gut and liver Abstract HBV A181T 83 88 RT;RT 18;81 20;83 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. CONCLUSION: The high rate of ADV resistance in patients with LMV-resistance might be attributable to preexisting rtA181V/T mutant virus. 2014 Antiviral research Abstract HBV A181V;A181T 115;115 122;122 RT 113 115 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. During ADV therapy, most rtM204V/I mutants were replaced by wild type in all 3 patients without the rtA181V/T mutation and in one patient with the rtA181V/T mutation. 2014 Antiviral research Abstract HBV M204V;M204I;A181V;A181T;A181V;A181T 27;27;102;102;149;149 34;34;109;109;156;156 RT;RT;RT 25;100;147 27;102;149 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. In patients with the rtA181V/T mutation (n = 6), the rtA181V/T mutant overtook the rtM204V/I mutant in 3 of 4 patients with ADV resistance. 2014 Antiviral research Abstract HBV A181V;A181T;A181V;A181T;M204V;M204I 23;23;55;55;85;85 30;30;62;62;92;92 RT;RT;RT 21;53;83 23;55;85 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. RESULTS: Before ADV therapy, rtA181V/T was observed in 30 of 680 clones (4.4%) from 7 patients with LMV resistance under dominant rt204V/I mutation and in one of 150 clones in treatment-naive patients. 2014 Antiviral research Abstract HBV A181V;A181T 31;31 38;38 RT;RT 29;130 31;132 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. Subsequently, wild type was replaced by the rtN236T and/or rtA181V/T mutant. 2014 Antiviral research Abstract HBV N236T;A181V;A181T 46;61;61 51;68;68 RT;RT 44;59 46;61 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. The majority of LMV-resistant mutants harbor the rtM204V/I mutation, while a minor fraction harbor the rtA181V/T mutation. 2014 Antiviral research Abstract HBV M204V;M204I;A181V;A181T 51;51;105;105 58;58;112;112 RT;RT 49;103 51;105 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. The rtA181V/T mutation was more frequently found in clones from LMV-resistant patients than in treatment-naive patients (p = 0.029). 2014 Antiviral research Abstract HBV A181V;A181T 6;6 13;13 RT 4 6 25303802 Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B. The rtN236T mutation was not observed in any clone. 2014 Antiviral research Abstract HBV N236T 6 11 RT 4 6 25318660 Incidence of natural resistance mutations in naive chronic hepatitis B patients: a systematic review and meta-analysis. Mutation rtM204V/I had the highest incidence of 4.89% (95%CI: 4.13-5.65%), and other primary mutations seldom spontaneously occurred. 2015 Journal of gastroenterology and hepatology Abstract HBV M204V;M204I 11;11 18;18 RT 9 11 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Functional analysis via transfection experiments indicate that the C139R and D144E mutations drastically reduced HBsAg antigenicity, while the Y225del mutation found in one interferon-treated patient impaired HBsAg secretion. 2014 Clinical and molecular hepatology Abstract HBV C139R;D144E;Y225del 67;77;143 72;82;150 S;S 113;209 118;214 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. The mutations include T123S, M125I/N, C139R, D144E, V177A, L192F, and W196L, some of which have not been reported before. 2014 Clinical and molecular hepatology Abstract HBV T123S;M125I;M125N;C139R;D144E;V177A;L192F;W196L 22;29;29;38;45;52;59;70 27;36;36;43;50;57;64;75 25323975 Prevalence of mutations in basal core promoter and precore region of hepatitis B virus in vaccinated and nonvaccinated individuals of the aboriginal Nicobarese tribe of Car Nicobar Island, India. Among the nonvaccinated subjects, 3 (4.5%) had an A1762T mutation, 8 (12.1%) had a G1764A mutation, 11 (16.7%) had a G1896A mutation and 4 (6.1%) had a G1899A mutation. 2014 Intervirology Abstract HBV A1762T;G1764A;G1896A;G1899A 50;83;117;152 56;89;123;158 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. BCP_T1753C, core_T147C, surface_L213I had contributed significantly in the disease progression to HCC (p < 0.05) in HBeAg positive patients whereas precore_T1858C, core_I116L, core_P130Q and preS1_S98T in HBeAg negative patients. 2014 PloS one Abstract HBV T1753C;T147C;L213I;T1858C;I116L;P130Q;S98T 3;16;31;155;168;180;197 10;22;37;162;174;186;201 BCP;C;C;C;C;C;Precore;PreS1;S 0;12;164;176;116;205;148;191;24 3;16;168;180;121;210;155;196;31 Hepatocellular carcinoma 98 101 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Beyond the classical mutations in basal core promoter (BCP) (A1762T/G1764A) and precore (G1862T), persistence of progressively accumulated mutations in enhancer-I, surface, HBx and core were showed significant association to liver disease progression. 2014 PloS one Abstract HBV G1764A;A1762T;G1862T 68;61;89 74;67;95 BCP;BCP;C;Enh I;X;Precore;S 34;55;181;152;173;80;164 53;58;185;162;176;87;171 Liver disease 225 238 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Furthermore, the effect of individual mutation was magnified by the combination with A1762T/G1764A in HCC pathogenesis. 2014 PloS one Abstract HBV G1764A;A1762T 92;85 98;91 Hepatocellular carcinoma 102 105 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Multivariate risk analysis had confirmed that core_P130Q [OR 20.71, 95% CI (1.64-261.77), p = 0.019] in B cell epitope and core_T147C [OR 14.58, 95% CI (1.17-181.76), p = 0.037] in CTL epitope were two independent predictors of HCC in HBeAg positive and negative patients respectively. 2014 PloS one Abstract HBV P130Q;T147C 50;127 56;133 C;C;C 46;123;235 50;127;240 Hepatocellular carcinoma 228 231 25351410 Single-nucleotide substitution of Hepatitis B virus in intrauterine infection. In contrast, the incidence of intrauterine HBV infection from mothers with mutation of T3205A was lower. 2015 Journal of viral hepatitis Abstract HBV T3205A 87 93 HBV infections 43 56 25351410 Single-nucleotide substitution of Hepatitis B virus in intrauterine infection. Most of the mutations were synonymous in pre-S1/S2/S region, while mutations of C2990T, T3205A, A167G, C407A, A667T and A680C resulted in amino acid substitution of A90V, S162T, T47A, P127T, L213F and I218L, respectively. 2015 Journal of viral hepatitis Abstract HBV C2990T;T3205A;A167G;C407A;A667T;A680C;A90V;S162T;T47A;P127T;L213F;I218L 80;88;96;103;110;120;165;171;178;184;191;201 86;94;101;108;115;125;169;176;182;189;196;206 S;PreS2;PreS1 51;47;41 52;50;46 25351410 Single-nucleotide substitution of Hepatitis B virus in intrauterine infection. The occurrence and location of mutations indicated that mutation of C2990T only existing in group NM may serve as an index for nonintrauterine infection. 2015 Journal of viral hepatitis Abstract HBV C2990T 68 74 25351410 Single-nucleotide substitution of Hepatitis B virus in intrauterine infection. Then, mutations of G403A, T670G, A673G, A167G, C407A, A667T and A680C may be closely related to intrauterine HBV infection. 2015 Journal of viral hepatitis Abstract HBV G403A;T670G;A673G;A167G;C407A;A667T;A680C 19;26;33;40;47;54;64 24;31;38;45;52;59;69 HBV infections 109 122 25374716 Death from Liver Failure despite Lamivudine Prophylaxis during R-CHOP Chemotherapy due to Rapid Emergence M204 Mutations. ALT 902 IU/L, HBeAg negative, HBV DNA 1.02E8 IU/mL, and genotyping confirmed L80I, M80V, and M204V/S mutations. 2013 Case reports in hepatology Abstract HBV L80I;M80V;M204V;M204S 77;83;93;93 81;87;100;100 C 14 19 25374716 Death from Liver Failure despite Lamivudine Prophylaxis during R-CHOP Chemotherapy due to Rapid Emergence M204 Mutations. Four months after chemotherapy, despite ongoing LAM of 7-month duration with confirmed adherence, severe asymptomatic hepatitis was noted during routine monitoring with ALT 1019 IU/L, HBeAg negative, HBV DNA 1.43E7 IU/mL, and genotyping confirmed L80I and M204I mutations. 2013 Case reports in hepatology Abstract HBV L80I;M204I 247;256 251;261 C 184 189 Hepatitis 118 127 25382636 A deep-sequencing method detects drug-resistant mutations in the hepatitis B virus in Indonesians. The proportions of the total number of reads containing mutations I169L/M, S202R, M204I/L or N236S were >1.0%. 2014 Intervirology Abstract HBV I169L;I169M;S202R;M204I;M204L;N236S 66;66;75;82;82;93 73;73;80;89;89;98 25418031 Hepatitis B surface antigen genetic elements critical for immune escape correlate with hepatitis B virus reactivation upon immunosuppression. Of the 13 HBsAg mutations found in these patients, 8 of 13 (M103I-L109I-T118K-P120A-Y134H-S143L-D144E-S171F) reside in a major hydrophilic loop (target of neutralizing antibodies [Abs]); some of them are already known to hamper HBsAg recognition by humoral response. 2015 Hepatology (Baltimore, Md.) Abstract HBV M103I;L109I;T118K;P120A;Y134H;S143L;D144E;S171F 60;66;72;78;84;90;96;102 65;71;77;83;89;95;101;107 S;S 10;228 15;233 25418031 Hepatitis B surface antigen genetic elements critical for immune escape correlate with hepatitis B virus reactivation upon immunosuppression. The remaining five (C48G-V96A-L175S-G185E-V190A) are localized in class I/II-restricted T-cell epitopes, suggesting a role in HBV escape from T-cell-mediated responses. 2015 Hepatology (Baltimore, Md.) Abstract HBV C48G;V96A;L175S;G185E;V190A 20;25;30;36;42 24;29;35;41;47 25449246 Genotyping and virological characteristics of hepatitis B virus in HIV-infected individuals in Sudan. The following mutations in the S region could account for the HBsAg negativity: sM133T, sE164G, sV168G, and sS174N. 2014 International journal of infectious diseases Abstract HBV M133T;E164G;V168G;S174N 80;88;96;108 86;94;102;114 S;S;S;S;S;S 62;31;80;88;96;108 67;32;81;89;97;109 25452041 Specific mutations in the C-terminus domain of HBV surface antigen significantly correlate with low level of serum HBV-DNA in patients with chronic HBV infection. In addition, in an in-vitro model Y206C + F220L determined a 2.8-3.3 fold-reduction of HBsAg-amount released in supernatants compared to single mutants and wt (Y206C + F220L = 5,679 IU/ml; Y206H = 16,305 IU/ml; F220L = 18,368 IU/ml; Y206C = 18,680 IU/ml; wt = 14,280 IU/ml, P < 0.05). 2015 The Journal of infection Abstract HBV Y206C;F220L;Y206C;F220L;Y206H;F220L;Y206C 34;42;160;168;189;211;233 39;47;165;173;194;216;238 S 87 92 25452041 Specific mutations in the C-terminus domain of HBV surface antigen significantly correlate with low level of serum HBV-DNA in patients with chronic HBV infection. RESULTS: Specific HBsAg-mutations (M197T,-S204N-Y206C/H-F220L) were significantly correlated with serum HBV-DNA <2000 IU/ml (posterior-probability>90%, P < 0.05). 2015 The Journal of infection Abstract HBV M197T;S204N;Y206C;Y206H;F220L 35;42;48;48;56 40;47;56;56;61 S 18 23 25452041 Specific mutations in the C-terminus domain of HBV surface antigen significantly correlate with low level of serum HBV-DNA in patients with chronic HBV infection. The co-occurrence of Y206C + F220L was found significant by cluster-analysis, (P = 0.02). 2015 The Journal of infection Abstract HBV Y206C;F220L 21;29 26;34 25452041 Specific mutations in the C-terminus domain of HBV surface antigen significantly correlate with low level of serum HBV-DNA in patients with chronic HBV infection. The presence of Y206C/H and/or F220L was also associated with lower median (IQR) HBsAg-levels and lower median (IQR) transaminases (for HBsAg:250[115-840] IU/ml for Y206C/H and/or F220L versus 4300[640-11,838] IU/ml for wild-type, P = 0.023; for ALT:28[21-40] IU/ml versus 53[34-90] IU/ml, P < 0.001). 2015 The Journal of infection Abstract HBV Y206C;Y206H;F220L;Y206C;Y206H;F220L 16;16;31;165;165;180 23;23;36;172;172;185 S;S 81;136 86;141 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. A C149R mutation, which may have resulted from failure in HBsAg detection, was found in one patient with OBI. 2014 PloS one Abstract HBV C149R 2 7 S 58 63 Occult Hepatitis B 105 108 25471066 Occult hepatitis B virus infection among blood donors in Colombia. The amino acid substitutions sY100H, sV184A, and sK141N were detected in ORF S and rtL108P, rtR110G, rtL180M, rtR192C, rtT150S, and rtL187V in ORF P. 2014 Virology journal Abstract HBV L108P;R110G;L180M;R192C;T150S;L187V;Y100H;V184A;K141N 85;94;103;112;121;134;29;37;49 90;99;108;117;126;139;35;43;55 P;RT;RT;RT;RT;RT;RT;S;S;S;S 147;83;92;101;110;119;132;29;37;49;77 148;85;94;103;112;121;134;30;38;50;78 25471066 Occult hepatitis B virus infection among blood donors in Colombia. The mutations rtL108P, rtR110G, rtR192C, rtT150S and rtI187V were characterized for the first time in these samples. 2014 Virology journal Abstract HBV L108P;R110G;R192C;T150S;I187V 16;25;34;43;55 21;30;39;48;60 RT;RT;RT;RT;RT 14;23;32;41;53 16;25;34;43;55 25475418 Genetic insights on host and hepatitis B virus in liver diseases. We have described common mutations in the HBV genome (G1896A, rtM204V, rtM204I) which modulate the pathogenesis and carcinogenesis of the liver. 2014 Mutation research. Reviews in mutation research Abstract HBV M204V;M204I;G1896A 64;73;54 69;78;60 RT;RT 62;71 64;73 Hepatocellular carcinoma 116 143 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. Basal core promoter (BCP) A1762T/G1764A and precore (PC) G1896A mutations were detected in these Romanian patients with chronic HBV infection. 2014 Hepatitis monthly Abstract HBV G1764A;A1762T;G1896A 33;26;57 39;32;63 BCP;BCP;Precore;Precore 0;21;53;44 19;24;55;51 Chronic HBV infection 120 141 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. BCP A1762T, G1764A and PC G1896A were significantly associated with HCC-tissue HBV sequencing (75.3%) (P < 0.001). 2014 Hepatitis monthly Abstract HBV A1762T;G1764A;G1896A 4;12;26 10;18;32 BCP;Precore 0;23 3;25 Hepatocellular carcinoma 68 71 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. PC G1896A alone was detected in HCC-serum HBV sequencing group (66.7%). 2014 Hepatitis monthly Abstract HBV G1896A 3 9 Precore 0 2 Hepatocellular carcinoma 32 35 25483515 Hepatitis B vaccination. Beside G145R, other S-gene mutations potentially able to evade neutralizing anti-HBs and infect vaccinated people have been described worldwide. 2015 Human vaccines & immunotherapeutics Abstract HBV G145R 7 12 S;S 81;20 84;21 25483515 Hepatitis B vaccination. Since the G145R substitution alters the projecting loop (aa 139-147) of the a determinant, the neutralizing antibodies induced by vaccination are no longer able to recognize the mutated epitope. 2015 Human vaccines & immunotherapeutics Abstract HBV G145R 10 15 S 76 89 25493022 Resistant mutants induced by adefovir dipivoxil in hepatitis B virus isolates. Patients with the rtA181T mutant were primarily infected with genotype C and e-antigen negative HBV, while patients with the rtN236T mutant were primarily infected by genotype B HBV (chi(2) = 6.004, 7.159; P = 0.023, 0.007). 2014 World journal of gastroenterology Abstract HBV A181T;N236T 20;127 25;132 C;RT;RT 77;18;125 86;20;127 25493022 Resistant mutants induced by adefovir dipivoxil in hepatitis B virus isolates. The most prevalent mutations were rtA181T, rtV214A, and rtN236T. 2014 World journal of gastroenterology Abstract HBV A181T;V214A;N236T 36;45;58 41;50;63 RT;RT;RT 34;43;56 36;45;58 25500663 Occult hepatitis B infection among individuals belonging to the aboriginal Nicobarese tribe of India. Single or multiple amino acids substitutions were found in 5 of 34 samples (14.7%) which includes I110T, P120T, P/T127I, A128P, M133L and G159V. 2014 Journal of infection in developing countries Abstract HBV T127I;P127I;I110T;P120T;A128P;M133L;G159V 112;112;98;105;121;128;138 119;119;103;110;126;133;143 25501679 Association between HBV Pre-S mutations and the intracellular HBV DNAs in HBsAg-positive hepatocellular carcinoma in China. Three Pre-S mutants (A2962G and C2964A in Pre-S1 and C105T in Pre-S2) were associated with higher tumor cccDNA levels (P < 0.05), and A2962G/C2964A mutants were associated with higher AFP levels. 2015 Clinical and experimental medicine Abstract HBV C2964A;A2962G;C2964A;C105T;A2962G 141;134;32;53;21 147;140;38;58;27 PreS;PreS1;PreS2 6;42;62 11;48;68 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Various mutations existed within the S gene; in five patients four known escape mutations including the common G145R and D144E were found. 2014 PloS one Abstract HBV G145R;D144E 111;121 116;126 S 37 38 25518716 Sensitivity of drug-resistant mutants of hepatitis B virus to poly-IC. Compared to the wt virus, the capacity of virus replication was reduced in most LAMr and ETVr mutants except those with mutations rtM(204V+L180M+V173L), and was similary in the ADVr mutants except rt(A121V+N236T). 2014 Acta virologica Abstract HBV L180M;V173L;A121V;N236T 139;145;200;206 144;150;205;211 RT 197 199 25521058 Seroepidemiology and occult hepatitis B virus infection in young adults in Banjarmasin, Indonesia. Thirteen amino acid substitutions were identified: T126S, P127S, Q129R, T131N, M133T, and Y161S in the HBsAg-positive group; P120T, T126I, G145S, Y161F, E164V, and V168F in the occult-HBV group; and T143S in both groups. 2015 Journal of medical virology Abstract HBV T126S;P127S;Q129R;T131N;M133T;Y161S;P120T;T126I;G145S;Y161F;E164V;V168F;T143S 51;58;65;72;79;90;125;132;139;146;153;164;199 56;63;70;77;84;95;130;137;144;151;158;169;204 S 103 108 25542480 Acute hepatitis B caused by a vaccine-escape HBV strain in vaccinated subject: sequence analysis and therapeutic strategy. Of all the substitutions found, Q129H, located in the "a" determinant region of HBsAg, can alter antigenicity, leading to mutants. 2015 Journal of clinical virology Abstract HBV Q129H 32 37 S 80 85 25566621 [Correlation study on Chinese medical syndrome types of chronic hepatitis B patients and HLA-DR13 gene, BCP mutation, and T-lymphocyte subsets]. The mutation of serum A1762T/G1764A was detected using PCR sequencing. 2014 Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi Abstract HBV G1764A;A1762T 29;22 35;28 25567052 Hepatitis B Virus Core Promoter A1762T/G1764A (TA)/T1753A/T1768A Mutations Contribute to Hepatocarcinogenesis by Deregulating Skp2 and P53. METHODS: A HBx combination (combo) mutant with changes in the CP region that corresponded to A1762T/G1764A (TA), T1753A, and T1768A was constructed and expressed in L-02 and Hep3B cells. 2015 Digestive diseases and sciences Abstract HBV G1764A;A1762T;T1753A;T1768A 100;93;113;125 106;99;119;131 Core promoter;X 62;11 64;14 25593470 Mutations of pre-core and basal core promoter before and after hepatitis B e antigen seroconversion. METHODS: The proportion of pre-core (G1896A) and basal core promoter (A1762T and G1764A) mutant viruses and serum levels of hepatitis B virus (HBV) DNA, hepatitis B surface antigen (HBsAg), and HB core-related antigen were analyzed in chronic hepatitis B patients before and after HBeAg seroconversion (n = 25), in those who were persistently HBeAg positive (n = 18), and in those who were persistently anti-HBe positive (n = 43). 2015 World journal of gastroenterology Abstract HBV G1896A;A1762T;G1764A 37;70;81 43;76;87 BCP;C;C;C;C;S;Precore;S 49;197;408;281;343;182;27;165 68;201;411;286;348;187;35;172 Chronic Hepatitis B 235 254 25596179 Tenofovir monotherapy versus tenofovir and entecavir combination therapy in patients with entecavir-resistant chronic hepatitis B with multiple drug failure: results of a randomised trial. All patients had at least one ETV-resistance mutation: rtT184A/C/F/G/I/L/S (n=49), rtS202G (n=43) and rtM250L/V (n=7), in addition to rtM204V/I (n=90). 2016 Gut Abstract HBV T184A;T184C;T184F;T184G;T184I;T184L;T184S;S202G;M250L;M250V;M204V;M204I 57;57;57;57;57;57;57;85;104;104;136;136 74;74;74;74;74;74;74;90;111;111;143;143 RT;RT;RT;RT 55;83;102;134 57;85;104;136 25612181 Spontaneous reactivation of hepatitis B virus (HBV) infection in patients with resolved or occult HBV infection. A precore G1896A variant with high quasispecies diversity was recovered from the patient. 2015 Journal of medical virology Abstract HBV G1896A 10 16 Precore 2 9 25625002 Clinical utility of complex mutations in the core promoter and proximal precore regions of the hepatitis B virus genome. We previously demonstrated that the accumulation of >= 6 mutations at eight key nucleotides located in these regions (G1613A, C1653T, T1753V, A1762T, G1764A, A1846T, G1896A, and G1899A) is a useful marker to predict the development of HCC regardless of advanced liver disease. 2015 World journal of hepatology Abstract HBV G1613A;C1653T;T1753V;A1762T;G1764A;A1846T;G1896A;G1899A 118;126;134;142;150;158;166;178 124;132;140;148;156;164;172;184 Hepatocellular carcinoma;Liver disease 235;262 238;275 25626648 Hepatitis B virus genotypes and mutations in the basal core promoter and pre-core/core in chronically infected patients in southern Brazil: a cross-sectional study of HBV genotypes and mutations in chronic carriers. Genotype A was associated with a higher prevalence of the G1862T mutation and the presence of a cytosine at position 1858. 2014 Revista da Sociedade Brasileira de Medicina Tropical Abstract HBV G1862T 58 64 25626648 Hepatitis B virus genotypes and mutations in the basal core promoter and pre-core/core in chronically infected patients in southern Brazil: a cross-sectional study of HBV genotypes and mutations in chronic carriers. Genotype D had a higher prevalence of the G1896A mutation and the presence of a thymine at position 1858. 2014 Revista da Sociedade Brasileira de Medicina Tropical Abstract HBV G1896A 42 48 25626648 Hepatitis B virus genotypes and mutations in the basal core promoter and pre-core/core in chronically infected patients in southern Brazil: a cross-sectional study of HBV genotypes and mutations in chronic carriers. The comparison between HBeAg status and the G1896A stop codon mutation in patients with genotype D revealed a relationship between HBV G1896A precore mutants and genotype D and hepatitis B e antigen (HBeAg) seroconversion. 2014 Revista da Sociedade Brasileira de Medicina Tropical Abstract HBV G1896A;G1896A 44;135 50;141 C;C;C;Precore 189;23;200;142 198;28;205;149 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. A critical role of interleukin (IL)-6 signaling in W4P-mediated tumorigenicity was tested by inhibition of Jak2. 2015 Molecular cancer Abstract HBV W4P 51 54 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. CONCLUSIONS: This study suggests that the W4P mutation during the natural course of chronic hepatitis B infection may contribute to HCC development, particularly in male patients, in an IL-6-dependent manner. 2015 Molecular cancer Abstract HBV W4P 42 45 Chronic HBV infection;Hepatocellular carcinoma 84;132 113;135 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. IL-6 levels of HCC patients with the W4P variant were significantly higher than those of patients with WT LHB. 2015 Molecular cancer Abstract HBV W4P 37 40 S 106 109 Hepatocellular carcinoma 15 18 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. IL-6, but not tumor necrosis factor-alpha, was elevated in male mice harboring W4P-induced tumor, and was reduced by estrogen. 2015 Molecular cancer Abstract HBV W4P 79 82 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. METHODS: LHB sequences from a carrier (wild type; WT) and W4P variant LHB sequence from an HCC patient were cloned and used to generate NIH3T3 and Huh7 cell lines. 2015 Molecular cancer Abstract HBV W4P 58 61 S;S 9;70 12;73 Hepatocellular carcinoma 91 94 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Recently, we reported a novel HCC-related W4P/R mutation in the large surface protein (LHB) of HBV genotype C, which was found exclusively in male HCC patients. 2015 Molecular cancer Abstract HBV W4P;W4R 42;42 47;47 S;S 64;87 77;90 Hepatocellular carcinoma;Hepatocellular carcinoma 30;147 33;150 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. RESULTS: Although both WT and W4P variant LHBs enhanced cell proliferation by regulating the cell cycle and facilitated cell colony formation, the W4P variant demonstrated significantly higher activity. 2015 Molecular cancer Abstract HBV W4P;W4P 30;147 33;150 S 42 46 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The ability to reduce cell proliferation and colony formation of W4P LHB was hampered by inhibition of IL-6 signaling. 2015 Molecular cancer Abstract HBV W4P 65 68 S 69 72 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. To confirm the effect of estrogen in W4P-mediated tumorigenicity, male mice were injected with estrogen and challenged with W4P-expressing cells. 2015 Molecular cancer Abstract HBV W4P;W4P 37;124 40;127 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P LHB induced higher production of IL-6 than WT LHB in cell lines, and the level was reduced by estrogen. 2015 Molecular cancer Abstract HBV W4P 0 3 S;S 4;50 7;53 25654280 [Relationship between hepatitis B virus polymerase gene mutation patterns of rtM204I/V and pre-core/basal core promoter mutations]. OBJECTIVE: To investigate the relationship between mutations of rtM204V/I (methionine to valine or isoleucine at position rt204 of reverse transcriptase domain) in the hepatitis B virus (HBV) polymerase gene and the G1896A and G1899A single mutations in the pre-eore (PC) region and the A1762T and G1764A double-mutations in the basal core promoter (BCP) region. 2014 Zhonghua gan zang bing za zhi Abstract HBV M204V;M204I;A1762T;G1896A;G1899A;G1764A 66;66;287;216;227;298 73;73;293;222;233;304 BCP;BCP;Precore;P;RT;RT;RT 329;350;268;192;131;64;122 348;353;270;202;152;66;124 25654280 [Relationship between hepatitis B virus polymerase gene mutation patterns of rtM204I/V and pre-core/basal core promoter mutations]. Of the 1543 strains (54.2%) with PC-BCP mutations, seven mutation patterns of G 1896A-G 1899A-G 1896A-G 1899A-A 1762T/G 1764A, A 1762T/G 1764AG 1896A, A 1762T/G 1764A-G 1899A, and A 1762T/G 1764A-G 1896A-G 1899A were identified. 2014 Zhonghua gan zang bing za zhi Abstract HBV G1764A;G1764A;G1764A;A1762T;A1762G;A1762T;A1762G;A1762T;A1762G;A1762T;A1762G;G1899A;G1896A;G1899A;G1899A;G1896A;G1899A;G1896A 118;159;188;110;110;151;151;127;127;180;180;86;94;102;167;196;204;78 125;166;195;117;117;158;158;134;134;187;187;93;101;109;174;203;211;85 BCP;Precore 36;33 39;35 25654280 [Relationship between hepatitis B virus polymerase gene mutation patterns of rtM204I/V and pre-core/basal core promoter mutations]. The three mutation patterns of G1896A-G1899A (P=0.000, OR=7.573), A1762T/G1764A-G1899A (P=0.000, OR=6.539) and A1762T/G1764A-G1896A-G1899A (P=0.000, OR=6.596) were associated with a greater risk of developing the YIDD mutation, according to binary logistic analysis. 2014 Zhonghua gan zang bing za zhi Abstract HBV G1764A;G1764A;G1896A;G1899A;G1899A;A1762T;G1896A;G1899A;A1762T 73;118;31;38;80;66;125;132;111 79;124;37;44;86;74;131;138;117 P 213 217 25654813 High incidence of lamivudine-resistance-associated vaccine-escape HBV mutants among HIV-coinfected patients on prolonged antiretroviral therapy. Three major patterns of mutations in HBV polymerase gene, namely single (rtM204V), double (rtL180M+rtM204V) and triple (rtV173L+rtL180M+rtM204V) mutations, are associated with 3TC-resistance; additionally, the triple mutation has vaccine-escape potential due to a corresponding change in overlapping surface gene. 2015 Antiviral therapy Abstract HBV M204V;L180M;M204V;V173L;L180M;M204V 75;93;101;122;130;138 80;98;106;127;135;143 P;RT;RT;RT;RT;RT;RT;S 41;73;91;99;120;128;136;300 51;75;93;101;122;130;138;307 25658544 Whole genome characterization of hepatitis B virus quasispecies with massively parallel pyrosequencing. Furthermore, quantitative comparison of mutation frequencies of each site between two groups resulted in a spectrum of substitutions associated with liver disease progression, and among which, C2288A/T, C2304A, and A/G2525C/T were novel candidates. 2015 Clinical microbiology and infection Abstract HBV C2288A;C2288T;C2304A;A2525C;A2525T;G2525C;G2525T 193;193;203;215;215;215;215 201;201;209;225;225;225;225 Liver disease 149 162 25692622 A new vaccine escape mutant of hepatitis B virus causes occult infection. The sequencing data of S coding regions shows that patient X has been infected by a new HBV variant with an A to C substitution at nt431, resulting in an Asp(GAC)to Ala(GCC) substitution at aa144 of major protein; CC to AA substitution at nt359 and nt360, resulting in an Pro(CCC) to Gln(CAA) substitution at aa120 of pre "a" epitope; A to G substitution at nt491, resulting in an Glu(GAG) to Gly(GGG) substitution at aa164 of post "a" epitope. 2015 Human vaccines & immunotherapeutics Abstract HBV A431C;A491G 108;335 136;363 S 23 24 25692622 A new vaccine escape mutant of hepatitis B virus causes occult infection. Three new mutations (S171F, S174N and Q181R) at the antigenic epitopes of HBV presented by HLA class I molecules are found. 2015 Human vaccines & immunotherapeutics Abstract HBV S171F;S174N;Q181R 21;28;38 26;33;43 25712861 Analysis of HBV genotype, drug resistant mutations, and pre-core/basal core promoter mutations in Korean patients with acute hepatitis B. No patient showed mutations that conferred resistance against lamivudine (L180M, M204V/I), adefovir (A181T, N236S), or entecavir (I169M, A184T/V, S202I/G, M250V/I/L). 2015 Journal of medical virology Abstract HBV L180M;M204V;M204I;A181T;N236S;I169M;A184T;A184V;S202I;S202G;M250V;M250I;M250L 74;81;81;101;108;130;137;137;146;146;155;155;155 79;88;88;106;113;135;144;144;153;153;164;164;164 25732900 New amino acid changes in drug resistance sites and HBsAg in hepatitis B virus genotype H. Classical lamivudine resistance mutations (rtM204V/rtL180M) were present in one naive-treatment patient infected with genotype G. 2015 Journal of medical virology Abstract HBV M204V;L180M 45;53 50;58 RT;RT 43;51 45;53 25732900 New amino acid changes in drug resistance sites and HBsAg in hepatitis B virus genotype H. Mutations at sites rt169, rt204, and rt215 resulted in the Y161C, I195M, and C206W mutations at HBsAg. 2015 Journal of medical virology Abstract HBV Y161C;I195M;C206W 59;66;77 64;71;82 S;RT;RT;RT 96;19;26;37 101;21;28;39 25732900 New amino acid changes in drug resistance sites and HBsAg in hepatitis B virus genotype H. New amino acid changes were identified in drug resistance sites in HBV strains from patients infected with genotype H; rtQ215E was present in two naive-NAs treatment patients and rtI169M was identified in a patient previously treated with lamivudine. 2015 Journal of medical virology Abstract HBV Q215E;I169M 121;181 126;186 RT;RT 119;179 121;181 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Additionally, several mutations were found in the BCP region with the following incidence rate; C1653 T (8.6%), A1752 G (10.8%),1762 AGG--TGA 1764 (26.9%), C1766T(2.2%),T1768 A (10.8%), C1858 T (64.5%), G1896 A (25.8%). 2014 Hepatitis monthly Abstract HBV C1653T;A1752G;C1766T;T1768A;C1858T;G1896A 96;112;156;169;186;203 103;119;162;176;193;210 BCP 50 53 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Mutation analysis in the S gene demonstrated two significant mutations which were W182 stop codon and deletion at open reading frame (ORF) of pre-S1 with the frequency occurrence of 2.2% (2/93) and 5.4% (5/93), respectively. 2014 Hepatitis monthly Abstract HBV W182X 82 91 PreS1;S 142;25 148;26 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The two patients with W182 stop codon were both male, infected with HBV genotype C and one showed progression of liver disease to hepatocellular carcinoma (HCC). 2014 Hepatitis monthly Abstract HBV W182X 22 31 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma 113;130;156 126;154;159 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. In addition, G1721A/A1775G/T1858C combined mutation was associated with higher viral load and lower age distribution. 2015 Hepatitis monthly Abstract HBV A1775G;T1858C;G1721A 20;27;13 26;33;19 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. Several combined mutations were obviously highly distributed in children with chronic HBV genotype C infection, such as G1721A/A1775G/T1858C triple mutation; a novel combined mutation type, exclusively detected in children with chronic HBV genotype C infection. 2015 Hepatitis monthly Abstract HBV A1775G;T1858C;G1721A 127;134;120 133;140;126 Chronic HBV infection;Chronic HBV infection 78;228 110;260 25742145 Clinical course of chronic hepatitis B patients receiving nucleos(t)ide analogues after virological breakthrough during monotherapy with lamivudine. The rt M204I mutation was observed more frequently. 2015 The new microbiologica Abstract HBV M204I 7 12 RT 4 6 25751379 [Clinical observation of telbivudine's antiviral efficacy and protection against mother-to-infant transmission of chronic hepatitis B during the first trimester of pregnancy]. RESULTS: The genetic variant rtM204I was detected in one of the women in the treatment group at 36 weeks of pregnancy. 2015 Zhonghua gan zang bing za zhi Abstract HBV M204I 31 36 RT 29 31 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. CONCLUSION: The HBV rtA181T mutation is closely associated with adefovir and lamivudine exposure.rtA181T may led to sW172*, culminating in suppression of HBsAg secretion.However, co-existence of the mutant with wild-type sequences was common among our patient population, suggesting that the mutation had little impact on serum HBsAg and HBV DNA levels across the clinical study population. 2015 Zhonghua gan zang bing za zhi Abstract HBV A181T;A181T;W172X 22;99;116 27;104;122 S;S;RT;RT;S 154;328;20;97;116 159;333;22;99;117 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. METHODS: Serum samples from 3, 013 patients who visited The 302 Hospital (Beijing, China) were investigated.HBV DNA was extracted and HBV mutations and genotypes were determined by direct sequencing.Recombinant plasmids harboring the rtA181T/sW172* mutant or wild type sequence were constructed and transfected into the HepG2 cell line. 2015 Zhonghua gan zang bing za zhi Abstract HBV W172X;A181T 242;236 248;241 RT;S 234;242 236;243 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. OBJECTIVE: To determine the mutational profile and clinical implications of the viral reverse-transcriptase (rt)A 181T mutation in hepatitis B virus (HBV) through population-based analysis of clinical samples. 2015 Zhonghua gan zang bing za zhi Abstract HBV A181T 111 118 RT;RT 86;109 107;111 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. RESULTS: The incidence of rtA181T across the study population was 4.1% (165/3, 013), and most of the rtAl 81T-positive patients had received adefovir and/or lamivudine.Forty percent (66/165) of the rtA 181T cases were single mutants and treatment responsive, 46.1% (76/165) included the adefovir-resistant mutation rtA 181 V/N236T, 12.1% (20/165) included the lamivudine-resistant mutation rtM204V/rtM2041, and 1.8% (3/165) included multidrug-resistant mutations.Interestingly, 73.9% (122/165) of the rtA181T-positive samples were detected with co-existing wild-type nucleotides at the site. 2015 Zhonghua gan zang bing za zhi Abstract HBV N236T;A181T;M204V;A181T;A181T;V236T 323;28;392;503;200;323 330;33;397;508;206;330 RT;RT;RT;RT 26;390;398;501 28;392;400;503 25751382 [Clinical emergence features and implications of hepatitis B virus rtA181T mutation]. The rates of HBV/C to HBV/B were 92.1% to 7.9% in the rtA181T-positive patients, but 82.1% to 17.9% in the rtA181T-negative paticnts (P less than 0.01).Almost all (98.2%; 129/165) of the rtA181T led to sW172*, while only 1.8% of the rtA181T (3/165) led to sW172L or sW172S.HBsAg secretion in vitro was reduced from the rtA181T/ sW172* strain, but there was no significant difference observed in the average serum HBsAg and HBV DNA levels of patients who carried or did not carry the mutant. 2015 Zhonghua gan zang bing za zhi Abstract HBV A181T;A181T;A181T;A181T;A181T;W172X;W172L;W172S;W172X 56;109;189;235;321;202;256;266;328 61;114;194;240;326;208;262;272;334 S;S;RT;RT;RT;RT;RT;S;S;S;S 273;413;54;107;187;233;319;202;256;266;328 278;418;56;109;189;235;321;203;257;267;329 25755318 Prevalence of Genotype D and Precore/Core Promoter Mutations in Hepatitis B Virus-infected Population of North India. Amplification and sequencing of the precore/core promoter region showed 1762(A-T) and 1764(G-A) mutations in 29% and 19% of the isolates, respectively. 2011 Journal of clinical and experimental hepatology Abstract HBV A1762T;G1764A 72;86 81;95 Core promoter;Precore 44;36 57;43 25786446 Hepatitis B e antigen and hepatitis B surface antigen seroclearance with the emergence of lamivudine-associated and core mutations following CD4 elevation in a patient with hepatitis B and HIV. A full-length HBV DNA analysis indicated that HBsAg had been lost after the development of the rtS143T mutation, which corresponded to the emergence of the sF134L and core mutations. 2015 Internal medicine (Tokyo, Japan) Abstract HBV S143T;F134L 97;156 102;162 C;S;RT;S 167;46;95;156 171;51;97;157 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. CONCLUSIONS: In this population with chronic HBeAg negative hepatitis B, an association was observed between the G1896A mutation in the Pre-core region of HBV and subsequent level of HBV DNA seven years later, which indicated that mutations in this region of HBV genome may contribute to disease progression in these patients and play an important role in HBV natural course of disease. 2015 Hepatitis monthly Abstract HBV G1896A 113 119 C;Precore 45;136 50;144 25800784 Tenofovir monotherapy versus tenofovir and entecavir combination therapy in adefovir-resistant chronic hepatitis B patients with multiple drug failure: results of a randomised trial. All patients had adefovir-resistant HBV mutations; rtA181V/T and/or rtN236T. 2016 Gut Abstract HBV A181V;A181T;N236T 53;53;70 60;60;75 RT;RT 51;68 53;70 25817219 Characterization of novel entecavir resistance mutations. CONCLUSIONS: VBT in this ETV-refractory patient is attributable to the novel ETV resistance mutations rtI163V and rtA186T. 2015 Journal of hepatology Abstract HBV I163V;A186T 104;116 109;121 RT;RT 102;114 104;116 25817219 Characterization of novel entecavir resistance mutations. Here, we characterized two novel mutations, rtI163V and rtA186T, associated with viral breakthrough (VBT) in an ETV-refractory patient. 2015 Journal of hepatology Abstract HBV I163V;A186T 46;58 51;63 RT;RT 44;56 46;58 25817219 Characterization of novel entecavir resistance mutations. Interestingly, the viral mutation pattern in the chimeric mice indicated dominant (or selective) proliferation of a clone containing rtI163V and rtA186T mutations plus LAMr under ETV treatment. 2015 Journal of hepatology Abstract HBV I163V;A186T 135;147 140;152 RT;RT 133;145 135;147 25817219 Characterization of novel entecavir resistance mutations. RESULTS: RtI163V and rtA186T mutations were detected together with LAMr (rtL180M and rtM204V) at VBT. 2015 Journal of hepatology Abstract HBV A186T;L180M;M204V 23;75;87 28;80;92 RT;RT;RT;RT 21;73;85;9 23;75;87;11 25817219 Characterization of novel entecavir resistance mutations. RtA186T plus LAMr reduced susceptibility to ETV more than 111.1-fold compared with the wild-type clone, while rtI163V plus LAMr resulted in a 20.4-fold reduction. 2015 Journal of hepatology Abstract HBV I163V;A186T 112;2 117;7 RT;RT 0;110 2;112 25817219 Characterization of novel entecavir resistance mutations. RtA186T significantly reduced viral replication efficacy, while the rtI163V mutation rescued it. 2015 Journal of hepatology Abstract HBV I163V;A186T 70;2 75;7 RT;RT 0;68 2;70 25817219 Characterization of novel entecavir resistance mutations. RtA186T was apparently responsible for ETV resistance but the selection of a clone with the double mutation plus LAMr suggests that rtI163V is required to sustain viral fitness. 2015 Journal of hepatology Abstract HBV I163V;A186T 134;2 139;7 RT;RT 132;0 134;2 25817219 Characterization of novel entecavir resistance mutations. RtI163V and rtA186T mutations were detected together with LAMr (rtL180M and rtM204V) at VBT. 2015 Journal of hepatology Abstract HBV I163V 2 7 RT;RT;RT;RT 0;12;64;76 2;14;66;78 25817219 Characterization of novel entecavir resistance mutations. Three-dimensional docking simulation indicated that rtA186T reduced the binding affinity of the HBV polymerase to ETV. 2015 Journal of hepatology Abstract HBV A186T 54 59 RT;P 52;100 54;110 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The frequencies of these HBeAg seroconversion-related mutations were significantly lower in HBeAg-negative children with CHB than in HBeAg-negative adults with CHB, especially for the mutation G1896A (41.1% vs 91.7%, P<0.001), and the average number of BCP/precore region mutations in samples from HBeAg-negative child patients was also obviously lower than in HBeAg-negative adult patients(3.62+-3.03 vs 4.89+-2.09, P<0.001), suggesting less impact of mutations in the BCP/precore region on HBeAg seroconversion in child patients than adult patients. 2015 PloS one Abstract HBV G1896A 193 199 BCP;BCP;C;C;C;C;C;C;Precore;Precore 253;470;25;92;133;298;361;492;257;474 256;473;30;97;138;303;366;497;264;481 Chronic Hepatitis B;Chronic Hepatitis B 121;160 124;163 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In anti-HBe positive chronic infections, sgF1b was more prone to have A1762T/G1764A mutation than sgA2, sgF4 and gD (75.0, 40.0, 33.3 and 31.8%, p<0.005), whereas in the pC region, gD and sgF4 were more likely to have G1896A than sgA2 and sgF1b (81.0, 72.7, 0.0 and 31.3%, p <0.001). 2015 PloS one Abstract HBV G1764A;A1762T;G1896A 77;70;218 83;76;224 C;Precore 8;170 11;172 Chronic HBV infection 21 39 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. The unexpected low frequency of the G1896A mutation in the sgF1b (despite carrying 1858T) prompted us to perform a further analysis in order to identify genotype-specific features that could justify the pattern mutations observed. 2015 PloS one Abstract HBV G1896A 36 42 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. CONCLUSIONS: This study indicates that the rate of G1896A mutation at the PC region among HBeAg negative patients, in the Golestan province of Iran, was similar to the average rate encountered in other parts of Iran. 2015 Jundishapur journal of microbiology Abstract HBV G1896A 51 57 C;Precore 90;74 95;76 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. Hepatitis B e antigen (HBeAg) negative chronic hepatitis B is frequently caused by a mutation (G1896A) in the hepatitis B virus (HBV) precore (PC) reading frame, which creates a stop codon, causing premature termination of the HBe protein. 2015 Jundishapur journal of microbiology Abstract HBV G1896A 95 101 C;C;C;Precore;Precore 12;227;23;143;134 21;230;28;145;141 Chronic Hepatitis B 39 58 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. OBJECTIVES: This study aimed to investigate the G1896A PC mutation and its effect on HBeAg detection in chronic HBV patients. 2015 Jundishapur journal of microbiology Abstract HBV G1896A 48 54 C;Precore 85;55 90;57 Chronic Hepatitis B 104 115 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. The comparison of nucleotide sequences with the reference sequence (Accession number: AB033559) in HBeAg negative patients showed that there was a high rate of mutations in G1896A (93.18%). 2015 Jundishapur journal of microbiology Abstract HBV G1896A 173 179 C 99 104 25828947 Upregulation of endoplasmic reticulum stress and reactive oxygen species by naturally occurring mutations in hepatitis B virus core antigen. Here, we found that the naturally occurring mutations P5T/H/L of the HBV core antigen induced ER stress. 2015 The Journal of general virology Abstract HBV P5T;P5H;P5L 54;54;54 61;61;61 C 73 77 25842192 Reactivation of resolved infection with the hepatitis B virus immune escape mutant G145R during dasatinib treatment for chronic myeloid leukemia. Here, we report the first case of reactivation of resolved infection with the HBV immune escape mutant G145R in a CML patient receiving dasatinib. 2015 International journal of hematology Abstract HBV G145R 103 108 Chronic myeloid leukemia 114 117 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. In summary, T216C and A2159G/C mutations were novel factors independently associated with ACLF. 2015 PloS one Abstract HBV T216C;A2159G;A2159C 12;22;22 17;30;30 Acute on chronic liver failure 90 94 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Multivariate analysis showed that T216C, G1896A, C1913A/G and A2159G/C were independent risk factors for ACLF. 2015 PloS one Abstract HBV T216C;G1896A;C1913A;C1913G;A2159G;A2159C 34;41;49;49;62;62 39;47;57;57;70;70 Acute on chronic liver failure 105 109 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. The results of Illumina sequencing showed that the mutations at 7 sites (T216C, G285A, A1846T, G1896A, C1913A/G, A2159G, and A2189C) of 12 ACLF patients were significantly higher than those of 12 controls. 2015 PloS one Abstract HBV T216C;G285A;A1846T;G1896A;C1913A;C1913G;A2189C;A2159G 73;80;87;95;103;103;125;113 78;85;93;101;111;111;131;119 Acute on chronic liver failure 139 143 25852125 Low risk of lamivudine-resistant HBV and hepatic flares in treated HIV-HBV-coinfected patients from Cote d'Ivoire. Among 11/127 (8.7%) patients with high-level persistent viraemia (last HBV VL: >=10(5) copies/ml), only two harboured incident LAM-resistance mutations at positions rtV173L+rtL180M+rtM204V with no patient exhibiting TDF/FTC-resistance. 2015 Antiviral therapy Abstract HBV V173L;L180M;M204V 167;175;183 172;180;188 RT;RT;RT 165;173;181 167;175;183 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. rs1234220 C allele was significantly associated with increased frequencies of HCC-risk A1652G, C1673T, and C1730G mutations in genotype B HBV-infected subjects. 2015 Chinese medical journal Abstract HBV A1652G;C1673T;C1730G 87;95;107 93;101;113 Hepatocellular carcinoma;HBV infections 78;138 81;150 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. The interaction of rs2299939 variant genotypes (GT+TT) with A3054T mutation significantly increased HCC risk (AOR = 2.41, 95% CI = 1.08-5.35); whereas its interaction with C3116T mutation significantly reduced HCC risk (AOR = 0.34, 95% CI = 0.18-0.66). 2015 Chinese medical journal Abstract HBV A3054T;C3116T 60;172 66;178 Hepatocellular carcinoma;Hepatocellular carcinoma 100;210 103;213 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. RESULTS: The mutated HBc particles in which R154 was replaced with glycine (G) residue (R154G) showed a drastic decrease in the ability to bind to the heparan sulphate proteoglycan and to avoid non-specific cellular uptake by several types of cancer cells. 2015 Journal of nanobiotechnology Abstract HBV R154G 88 93 C 21 24 25907725 [Analysis on genotype distribution and mutation of major hydroponic region of hepatitis B virus in Liaoning]. The mutation rate of T126I was highest (8.64%). 2015 Zhonghua liu xing bing xue za zhi Abstract HBV T126I 21 26 25910308 A case of entecavir resistance which is developed after complete viral suppression during entecavir treatment for nucleoside-naive chronic hepatitis B. The ETVr-related substitution (rtS202P) and lamivudine resistance-related substitutions (rtL180M+rtM204V) were detected by DNA sequencing analysis at week 145. 2014 The Turkish journal of gastroenterology Abstract HBV S202P;L180M;M204V 33;91;99 38;96;104 RT;RT;RT 31;89;97 33;91;99 25926495 Characterization of Full-Length Genomes of Hepatitis B Virus Quasispecies in Sera of Patients at Different Phases of Infection. A triple mutation (A1762T/G1764A/G1896A) was observed more frequently in genotype C than in genotype B. 2015 Journal of clinical microbiology Abstract HBV G1764A;G1896A;A1762T 26;33;19 32;39;25 25942596 The characteristic changes in hepatitis B virus x region for hepatocellular carcinoma: a comprehensive analysis based on global data. 3) Logistic regression showed that mutations A1383C (OR: 2.32, 95% CI: 1.34-4.01), R1479C/T (OR: 1.96, 95% CI: 1.05-3.64; OR: 5.15, 95% CI: 2.53-10.48), C1485T (OR: 2.40, 95% CI: 1.41-4.08), C1631T (OR: 4.09, 95% CI: 1.41-11.85), C1653T (OR: 2.58, 95% CI: 1.59-4.19), G1719T (OR: 2.11, 95% CI: 1.19-3.73), and T1800C (OR: 23.59, 95% CI: 2.25-247.65) were independent risk factors for genotype C HBV-related HCC, presenting different trends among individual disease phases. 2015 PloS one Abstract HBV A1383C;R1479C;R1479T;C1485T;C1631T;C1653T;G1719T;T1800C 45;83;83;153;191;230;268;310 51;91;91;159;197;236;274;316 Hepatocellular carcinoma 407 410 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. BACKGROUND: Hepatitis B virus (HBV) G1896A mutation was associated with HBeAg seronegativity and hepatitis B related acute-on-chronic liver failure. 2016 Journal of clinical laboratory analysis Abstract HBV G1896A 36 42 C 72 77 Acute on chronic liver failure 117 147 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. CONCLUSION: The proposed Taqman-ARMS real-time PCR method for the detection of G1896A mutation of HBV was rapid, simple, sensitive, specific, and applicable in the clinical setting. 2016 Journal of clinical laboratory analysis Abstract HBV G1896A 79 85 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. In this study, we developed Taqman amplification refractory mutation system (Taqman-ARMS) and established a strict control system to detect HBV G1896A mutant. 2016 Journal of clinical laboratory analysis Abstract HBV G1896A 144 150 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. RESULTS: The assay has the sensitivity of 1E+3 IU/ml G1896A template, and 0.1% weak population virus with G1896A could be found in mixtures. 2016 Journal of clinical laboratory analysis Abstract HBV G1896A;G1896A 53;106 59;112 25968238 Accurate Detection of Hepatitis B Virus G1896A Mutant by Developed Taqman-ARMS Followed a Strict Control System. Then, Taqman-ARMS was used to detect HBV G1896A mutant. 2016 Journal of clinical laboratory analysis Abstract HBV G1896A 41 47 25982306 Microarray-based genotyping and detection of drug-resistant HBV mutations from 620 Chinese patients with chronic HBV infection. Additionally, out of the 620 patient samples, 64.0% (397/620) were also detected with the precore stop-codon mutation (G1896A) by microarray assay. 2015 The Brazilian journal of infectious diseases Abstract HBV G1896A 119 125 Precore 90 97 25982306 Microarray-based genotyping and detection of drug-resistant HBV mutations from 620 Chinese patients with chronic HBV infection. Of these, nine and eight patients carried lamivudine (LAM)-/telbivudine (LdT)-resistance mutations (rtL180M, rtM204I/V) and adefovir (ADV)-resistance mutations (rtA181T/V, rtN236T), respectively. 2015 The Brazilian journal of infectious diseases Abstract HBV L180M;M204I;M204V;A181T;A181V;N236T 102;111;111;163;163;174 107;118;118;170;170;179 RT;RT;RT;RT 100;109;161;172 102;111;163;174 25989376 Impact of HBV genotypes A and D genetic variability on infection evolution. Mutations associated with immune-escape (T131N, D144A/E, G145K), amino acid polymorphisms in "a determinant" domain of S protein and mutations/deletions in preC/C region were found in isolates from acute and chronic hepatitis B cases. 2015 Infection, genetics and evolution Abstract HBV T131N;D144A;D144E;G145K 41;48;48;57 46;55;55;62 S;Precore;C;S 94;156;161;119 107;160;162;120 Chronic Hepatitis B 198 227 25997324 [The drug resistance mutation detection and relevant factors analysis of HBV P region in chronic hepatitis B patients in Weifang City, Shandong Province]. M204V/I mutation mostly existed in the form of joint L180M mutation, the mutation rate was age-related. 2015 Bing du xue bao Abstract HBV M204V;M204I;L180M 0;0;53 7;7;58 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. Moreover, no LAM-resistant rtM204I/V or ETV-resistant variants were detected during the 27-36 months of combination therapy. 2015 International journal of medical sciences Abstract HBV M204I;M204V 29;29 36;36 RT 27 29 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. Resistant rtA181V and rtN236T were undetectable after 21-24 months of combination therapy. 2015 International journal of medical sciences Abstract HBV A181V;N236T 12;24 17;29 RT;RT 10;22 12;24 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. RESULTS: HBV DNA decreased to the lowest level during ADV monotherapy at 6-18 months, with a decrease of 0.95-5.51 log10 copies/mL, whereas rtA181V or rtN236T gradually increased with extended therapy. 2015 International journal of medical sciences Abstract HBV A181V;N236T 142;153 147;158 RT;RT 140;151 142;153 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. A new amino acid substitution (rtD263E) was observed to develop in 60% of patients with viremia. 2015 Hepatitis monthly Abstract HBV D263E 33 38 RT 31 33 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. The rtD263E mutation might be associated with partial resistance to TDF. 2015 Hepatitis monthly Abstract HBV D263E 6 11 RT 4 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. CONCLUSIONS: The HBV basal core promoter/pre-core mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF. 2015 Virology journal Abstract HBV T1753V;A1762T;G1764A;C1766T;T1768A;A1846T;G1896A;G1899A 60;68;76;84;92;100;108;119 66;74;82;90;98;106;114;125 BCP;C;Precore 21;134;41 40;139;49 Acute on chronic liver failure 192 200 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Several mutations were significantly correlated with ACLF: T1753V (1.889, 95 % confidence interval (CI) [1.357-2.631]), A1762T (2.696 [2.265-3.207]), G1764A (3.005 [2.077-4.347]), A1762T/G1764A (2.379 [1.519-3.727]), C1766T (1.849 [1.403-2.437]), T1768A (2.440 [1.405-3.494]), A1846T (3.163 [2.157-4.639]), G1896A (2.181 [1.800-2.642]), G1899A (3.569 [2.906-4.385]) and G1896A/A1762T/G1764A (1.575 [1.172-2.116]). 2015 Virology journal Abstract HBV G1764A;A1762T;G1764A;A1762T;G1896A;T1753V;G1764A;C1766T;T1768A;A1846T;G1899A;A1762T;G1896A 187;377;384;180;370;59;150;217;247;277;337;120;307 193;383;390;186;376;65;156;223;253;283;343;126;313 Acute on chronic liver failure 53 57 26074702 Precore/basal core promoter mutants quantification throughout phases of hepatitis B virus infection by Simpleprobe. In five HBeAg-negative cases, we detected double mutation G1896A/G1899A. 2015 World journal of gastroenterology Abstract HBV G1899A;G1896A 65;58 71;64 C 8 13 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. BACKGROUND: The study aimed to clarify whether the rtI233V substitution affects adefovir (ADV) resistance. 2016 Antiviral therapy Abstract HBV I233V 53 58 RT 51 53 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. CONCLUSIONS: rtI233V usually emerged in ADV-treated patients with little impact on ADV susceptibility but it effectively restored replication capacity of the rtN236T mutant, suggesting that rtI233V may partly serve as a compensatory mutation associated with ADV resistance. 2016 Antiviral therapy Abstract HBV I233V;N236T;I233V 15;160;192 20;165;197 RT;RT;RT 13;158;190 15;160;192 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. Eight patients with rtI233V +- rtA181V/rtN236T had virological breakthrough in the clinical course of ADV treatment. 2016 Antiviral therapy Abstract HBV I233V;A181V;N236T 22;33;41 27;38;46 RT;RT;RT 20;31;39 22;33;41 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. Phenotypic analysis showed that rtI233V mutants from patient 1 and patient 2 exhibited 1.57-fold and 1.51-fold decreased susceptibility to ADV, respectively, compared to wild-type virus; by contrast, rtN236T and rtI233V+N236T mutants from patient 1 had 6.82-fold and 5.28-fold decreased susceptibility to ADV. 2016 Antiviral therapy Abstract HBV I233V;N236T;I233V;N236T 34;202;214;220 39;207;219;225 RT;RT;RT 32;200;212 34;202;214 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. RESULTS: The rtI233V substitution was detected in 38/5,344 (0.71%) ADV-treated patients and in 8/13,075 patients without receiving ADV (P<0.001). 2016 Antiviral therapy Abstract HBV I233V 15 20 RT 13 15 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. rtI233V, rtN236T and rtI233V+N236T mutants had 97.5%, 30.2% and 69.7% of replication capacity compared to wild-type virus in the absence of antivirals and all remained susceptible to lamivudine, entecavir and tenofovir. 2016 Antiviral therapy Abstract HBV I233V;N236T;I233V;N236T 2;11;23;29 7;16;28;34 RT;RT;RT 0;9;21 2;11;23 26079809 Increased occurrence of mutant rtI233V of HBV in patients receiving adefovir therapy. Viral replication capacity correspondingly decreased after eliminating rtI233V from rtI233V+N236T mutant and was restored after introducing rtI233V into rtN236T mutant. 2016 Antiviral therapy Abstract HBV I233V;I233V;N236T;I233V;N236T 73;142;155;86;92 78;147;160;91;97 RT;RT;RT;RT 71;84;140;153 73;86;142;155 26081397 [Occult hepatitis B virus infection in normal population, Xiamen]. 3 types of amino acid (AA) mutation (M133T, T140I, G145R) that influence "a" epitope conformation were observed in 9 subjects with occult HBV infection. 2015 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV M133T;T140I;G145R 37;44;51 42;49;56 HBV infections 138 151 26100402 Genetic variability of hepatitis B virus in Uruguay: D/F, A/F genotype recombinants. The following mutations were detected: a G1896A substitution, a 33-nucleotide deletion from position 2896 to 2928 in the Pre-S1 region involving Pre-S1 residues 3-13, a 33-nt deletion in the Pre-S1 region involving nt 2913-2945 and Pre-S1 residues 9-19. 2015 Archives of virology Abstract HBV G1896A 41 47 PreS1;PreS1;PreS1;PreS1 121;145;191;232 127;151;197;238 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. A mutation at nucleotide 1896 (G1896A) is the most common cause for the loss of HBeAg. 2015 Virology Abstract HBV G1896A 31 37 C 80 85 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. Differences between the wild-type and the G1896A mutant in early steps of HBV replication including the synthesis of pre-genomic RNA and transcripts have not been investigated. 2015 Virology Abstract HBV G1896A 42 48 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. In contrast to clinical data, cell culture studies report a high-replicating phenotype for the G1896A mutant. 2015 Virology Abstract HBV G1896A 95 101 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. In sum, our findings highlight the role of HBeAg in regulating hepatitis B virus replication fitness and transcription efficiency and new insights on the early steps of replication in the G1896A mutant. 2015 Virology Abstract HBV G1896A 188 194 C 43 48 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. Interestingly, trans-complementation of the G1896A mutant with HBeAg lowers the replication fitness and transcriptionefficiency to levels comparable to that of the wild-type. 2015 Virology Abstract HBV G1896A 44 50 C 63 68 26119876 Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro. The G1896A mutant is associated with higher replication fitness, transcription efficiency and higher levels of secreted HBsAg than the wild-type. 2015 Virology Abstract HBV G1896A 4 10 S 120 125 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. Once-daily peroral administration of CAdA reduced HBVETV-RL180M/S202G/M204V viremia (P = 0.0005) in human-liver-chimeric/ HBVETV-RL180M/S202G/M204V-infected mice, whereas ETV completely failed to reduce HBVETV-RL180M/S202G/M204V viremia. 2015 Hepatology (Baltimore, Md.) Abstract HBV S202G;S202G;M204V;M204V;S202G;M204V;L180M;L180M;L180M 136;64;70;142;217;223;57;210;129 141;71;75;147;222;228;63;216;135 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. Southern analysis using Huh-7 cells transfected with HBV-containing plasmids demonstrated that CAdA was potent against both wild-type (IC50= 7.2 nM) and ETV-resistant HBV (IC50= 69.6 nM for HBVETV-RL180M/S202G/M204V), whereas ETV failed to reduce HBVETV-RL180M/S202G/M204V DNA even at 1 muM. 2015 Hepatology (Baltimore, Md.) Abstract HBV S202G;S202G;M204V;M204V;L180M;L180M 261;204;210;267;197;254 266;209;215;272;203;260 26136470 Combined Analysis of the Prevalence of Drug-Resistant Hepatitis B Virus in Antiviral Therapy-Experienced Patients in Europe (CAPRE). The most frequently encountered primary mutation was M204V/I (48.7%), followed by A181T/V (3.8%) and N236T (2.6%). 2016 The Journal of infectious diseases Abstract HBV M204V;M204I;A181T;A181V;N236T 53;53;82;82;101 60;60;89;89;106 26136564 An Aptamer against the Matrix Binding Domain on the Hepatitis B Virus Capsid Impairs Virion Formation. A small domain (matrix domain [MD]) in the large surface protein L and a narrow region (matrix binding domain [MBD]) including isoleucine 126 on the capsid surface have been mapped, in which point mutations such as core I126A specifically blocked nucleocapsid envelopment. 2015 Journal of virology Abstract HBV I126A 220 225 Capsid;C;S;S 149;215;43;156 155;219;56;163 26136564 An Aptamer against the Matrix Binding Domain on the Hepatitis B Virus Capsid Impairs Virion Formation. By the systematic evolution of ligands by exponential enrichment (SELEX) method, we evolved DNA aptamers from an oligonucleotide library binding to purified recombinant capsids but not binding to the corresponding I126A mutant capsids. 2015 Journal of virology Abstract HBV I126A 214 219 Capsid;Capsid 169;227 176;234 26136564 An Aptamer against the Matrix Binding Domain on the Hepatitis B Virus Capsid Impairs Virion Formation. Its Kd for I126A capsids was 1,306 +- 503 nM. 2015 Journal of virology Abstract HBV I126A 11 16 Capsid 17 24 26165271 Biological characteristics of the A1762T/G1764A mutant strain of hepatitis B virus in vivo. The double nucleotide, A1762T and G1764A exchange (TA mutation), in the hepatitis B virus (HBV) genome basal core promoter (BCP) region is a common viral mutation in patients with chronic HBV infection. 2015 Molecular medicine reports Abstract HBV A1762T;G1764A 23;34 29;40 BCP;BCP 103;124 122;127 Chronic HBV infection 180 201 26194746 Outcomes including liver histology after liver transplantation for chronic hepatitis B using oral antiviral therapy alone. Seven patients had evidence of virological rebound, of whom 6 had evidence of rtM204V/I mutation and 1 had recurrence of hepatocellular carcinoma with low-level rebound and wild-type virus. 2015 Liver transplantation Abstract HBV M204V;M204I 80;80 87;87 RT 78 80 Hepatocellular carcinoma 121 145 26201521 Naturally occurring core immune-escape and carboxy-terminal mutations\truncations in patients with e antigen negative chronic hepatitis B. CONCLUSION: Core immune-escape mutations cT12S, cS21T, cT67P, cE113D, and cP130T/Q are significantly higher in decompensated liver disease patients and could influence the severity of liver disease in HBeAg -ve CHB patients. 2012 Hepatology international Abstract HBV T12S;S21T;T67P;E113D;P130T;P130Q 41;48;55;62;74;74 46;53;60;68;82;82 C;C;C;C;C;C;C 41;48;55;62;74;12;201 42;49;56;63;75;16;206 Liver disease;Chronic Hepatitis B 184;211 197;214 26201521 Naturally occurring core immune-escape and carboxy-terminal mutations\truncations in patients with e antigen negative chronic hepatitis B. Three core immune escape mutations were significantly higher in patients with coexisting precore stop codon compared with patients without precore stop codon mutation, cT12S (43 vs. 8%, p < 0.001), cS21T (16 vs. 3.4%, p < 0.026), and cE77D (30 vs. 4.5%, p < 0.002). 2012 Hepatology international Abstract HBV S21T;E77D;T12S 198;234;168 203;239;173 C;C;C;C;Precore;Precore 168;198;234;6;89;139 169;199;235;10;96;146 26201521 Naturally occurring core immune-escape and carboxy-terminal mutations\truncations in patients with e antigen negative chronic hepatitis B. When frequency of core immune escape mutations was compared among CHB and decompensated patients, and cT12S: (27 vs. 10%, p < 0.05), cS21T (16 vs. 1.35%, p < 0.01), cT67P/N: (20 vs. 4%, p < 0.001), cE113D (11.37 vs. 1.35%, p < 0.05), and cP130T/Q (7 vs. 0%, p < 0.001) mutations were found to be significantly higher in decompensated patients. 2012 Hepatology international Abstract HBV S21T;E113D;T67P;T67N;P130T;P130Q;T12S 133;198;165;165;238;238;102 138;204;172;172;246;246;107 C;C;C;C;C;C 102;133;165;198;238;18 103;134;166;199;239;22 Chronic Hepatitis B 66 69 26201776 Hepatitis B virus genotype C encoding resistance mutations that emerge during adefovir dipivoxil therapy: in vitro replication phenotype. CONCLUSIONS: The identification of secretion-defective HBV in the setting of ADV therapy for HBV genotype C, and to a lesser extent HBV genotype B, has major implications for the diagnosis and treatment of HBV in the Asia-Pacific region, as it is likely that quantitative HBsAg and viral load testing of serum from patients infected with HBV encoding rtA181T and rtN236T substitutions may not accurately reflect the level of replication within hepatocytes. 2013 Hepatology international Abstract HBV A181T;N236T 353;365 358;370 S;RT;RT 272;351;363 277;353;365 26201776 Hepatitis B virus genotype C encoding resistance mutations that emerge during adefovir dipivoxil therapy: in vitro replication phenotype. Importantly, less HBsAg was detected in the cells transfected with the rtA181T resistance mutants, and the overlapping sW172stop mutation ablated secretion of HBsAg into cell culture supernatants. 2013 Hepatology international Abstract HBV A181T;W172X 73;119 78;128 S;S;RT;S 18;159;71;119 23;164;73;120 26201776 Hepatitis B virus genotype C encoding resistance mutations that emerge during adefovir dipivoxil therapy: in vitro replication phenotype. We have recently shown that for HBV genotype D, the rtA181T/sW172stop substitution conferring resistance to adefovir dipivoxil (ADV) alters secretion of HBsAg and exerts a dominant-negative effect on wild-type virion secretion. 2013 Hepatology international Abstract HBV W172X;A181T 60;54 69;59 S;RT;S 153;52;60 158;54;61 26202027 HBsAg, HBeAg and HBV DNA level changes and precore/basal core promoter mutations in the natural history of chronic hepatitis B in Indonesian patients. We studied the changes in hepatitis B surface antigen (HBsAg), hepatitis B 'e' antigen (HBeAg) and HBV DNA levels, considering the implications of HBV genotype, basal core promoter (BCP) A1762T/G1764A and precore G1896A mutations in CHB. 2013 Hepatology international Abstract HBV G1764A;A1762T;G1896A 194;187;213 200;193;219 BCP;BCP;C;S;Precore;S 161;182;88;55;205;38 180;185;93;60;212;45 Chronic Hepatitis B 233 236 26202119 Ultradeep Sequencing for Detection of Quasispecies Variants in the Major Hydrophilic Region of Hepatitis B Virus in Indonesian Patients. The major population of MHR variants causing impaired of HBsAg secretion (e.g., G119R, Q129R, T140I, and G145R) was detected only in advanced liver disease patients. 2015 Journal of clinical microbiology Abstract HBV G119R;Q129R;T140I;G145R 80;87;94;105 85;92;99;110 S 57 62 Liver disease 142 155 26202119 Ultradeep Sequencing for Detection of Quasispecies Variants in the Major Hydrophilic Region of Hepatitis B Virus in Indonesian Patients. The most frequent MHR variants related to immune evasion in the major and intermediate populations were P120Q/T, T123A, P127T, Q129H/R, M133L/T, and G145R. 2015 Journal of clinical microbiology Abstract HBV P120Q;P120T;T123A;P127T;Q129H;Q129R;M133L;M133T;G145R 104;104;113;120;127;127;136;136;149 111;111;118;125;134;134;143;143;154 26202756 Hepatitis B virus genotype B and mutations in basal core promoter and pre-core/core genes associated with acute-on-chronic liver failure: a multicenter cross-sectional study in China. A multivariate analysis showed that factors such as HBV genotype B, age >=40 years and A1762T/G1764A, A1846T and G1896A mutations were independently associated with the development of HB-ACLF. 2014 Hepatology international Abstract HBV G1764A;A1762T;A1846T;G1896A 94;87;102;113 100;93;108;119 Acute on chronic liver failure 184 191 26202756 Hepatitis B virus genotype B and mutations in basal core promoter and pre-core/core genes associated with acute-on-chronic liver failure: a multicenter cross-sectional study in China. Comparing with CHB-S, the A1762T/G1764A mutation in genotype B and the A2159G mutation in genotype C were significantly more common in HB-ACLF patients. 2014 Hepatology international Abstract HBV G1764A;A1762T;A2159G 33;26;71 39;32;77 Acute on chronic liver failure;Chronic Hepatitis B 135;15 142;18 26202756 Hepatitis B virus genotype B and mutations in basal core promoter and pre-core/core genes associated with acute-on-chronic liver failure: a multicenter cross-sectional study in China. CONCLUSION: Chronic HBV infection with genotype B, A1762T/G1764A, A1846T and G1896A mutations has a higher possibility to develop HB-ACLF. 2014 Hepatology international Abstract HBV G1764A;A1762T;A1846T;G1896A 58;51;66;77 64;57;72;83 Acute on chronic liver failure 130 137 26202756 Hepatitis B virus genotype B and mutations in basal core promoter and pre-core/core genes associated with acute-on-chronic liver failure: a multicenter cross-sectional study in China. The A1762T/G1764A, A1846T and G1896A mutations were significantly more common in HB-ACLF patients infected with either genotype B or C as compared with CHB-M, whereas the C1913A/G and A2159G mutations were more associated with HB-ACLF in genotype C patients. 2014 Hepatology international Abstract HBV G1764A;A1762T;A1846T;G1896A;C1913A;C1913G;A2159G 11;4;19;30;171;171;184 17;10;25;36;179;179;190 Acute on chronic liver failure;Chronic Hepatitis B;Acute on chronic liver failure 227;152;81 234;155;88 26209374 Performance of HBsAg point-of-care tests for detection of diagnostic escape-variants in clinical samples. The only false-negative result occurred using the Quick Profileassay with a virus harboring a D144A mutation. 2015 Journal of clinical virology Abstract HBV D144A 94 99 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. METHODS: HBV harboring LMV-resistant mutations (rtM204I, rtM204V, and rtM204S) in the P gene at the YMDD ((203)tyrosine-methionine-aspartate-aspartate(206)) reverse transcriptase (RT) active site were generated and their sensitivity to Phyllanthus urinaria koreanis extract examined. 2015 BMC complementary and alternative medicine Abstract HBV M204I;M204V;M204S 50;59;72 55;64;77 P;RT;RT;RT;RT;RT;P;P 86;157;48;57;70;180;111;100 87;178;50;59;72;182;150;104 26260331 HBsAg sT123N mutation induces stronger antibody responses to HBsAg and HBcAg and accelerates in vivo HBsAg clearance. In the present study, 1.3-fold-overlength HBV genomes containing the sT123N substitution were digested from the pHBV1.3-sT123N construct and subcloned into the pAAV vector to generate pAAV1.3-sT123N for hydrodynamic injection (HI) in mice. 2015 Virus research Abstract HBV T123N;T123N;T123N 69;120;192 75;126;198 S;S;S 69;120;192 70;121;193 26260331 HBsAg sT123N mutation induces stronger antibody responses to HBsAg and HBcAg and accelerates in vivo HBsAg clearance. The results demonstrated that sT123N substitution impaired virion secretion, resulting in intracellular retention of HBcAg. 2015 Virus research Abstract HBV T123N 30 36 C;S 117;30 122;31 26260331 HBsAg sT123N mutation induces stronger antibody responses to HBsAg and HBcAg and accelerates in vivo HBsAg clearance. We have previously showed that sT123N substitution could generate additional N-glycosylated forms of HBsAg. 2015 Virus research Abstract HBV T123N 31 37 S;S 101;31 106;32 26283552 Detection and circulation of hepatitis B virus immune escape mutants among asymptomatic community dwellers in Ibadan, southwestern Nigeria. Eleven of which were subtyped as ayw4 while the remaining two could not be subtyped due to sR122Q/P substitutions. 2015 International journal of infectious diseases Abstract HBV R122Q;R122P 91;91 99;99 S 91 92 26288490 Distribution of hepatitis B virus genotype and cancer predicting precore and basal core promoter mutations. The total Double mutations of BCP at A1762T/G1764A nucleotide positions, and PC mutation at G1896A nucleotide position were seen in 29.3% and 21.3%, respectively. 2015 Medical journal, Armed Forces India Abstract HBV G1764A;A1762T;G1896A 44;37;92 50;43;98 BCP;Precore 30;77 33;79 26288490 Distribution of hepatitis B virus genotype and cancer predicting precore and basal core promoter mutations. Viral factors that may increase the risk for HCC development include HBV DNA level, genotypes, and naturally occurring mutations such as hepatitis B virus precore (PC) (G1896A) and basal core promoter (BCP) A1762T/G1764A double mutations. 2015 Medical journal, Armed Forces India Abstract HBV G1764A;A1762T;G1896A 214;207;169 220;213;175 BCP;BCP;Precore;Precore 181;202;164;155 200;205;166;162 Hepatocellular carcinoma 45 48 26290395 Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study. In control patients carrying A1762T/G1764A, addition of C1653T and/or T1753V significantly increased HCC risk (HR, 1.57; P = 0.038); combo mutations with C1653T, T1753V, and A1762T/G1764A improved the validity of HCC prediction by age, male, and cirrhosis (P = 0.002). 2015 Cancer prevention research (Philadelphia, Pa.) Abstract HBV G1764A;G1764A;A1762T;A1762T;C1653T;T1753V;C1653T;T1753V 36;181;174;29;56;70;154;162 42;187;180;35;62;76;160;168 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 101;213;246 104;216;255 26290395 Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study. In summary, HBV mutation A1762T/G1764A, C1653T, and T1753V in combination improve HCC prediction in HBV-infected patients. 2015 Cancer prevention research (Philadelphia, Pa.) Abstract HBV G1764A;A1762T;C1653T;T1753V 32;25;40;52 38;31;46;58 Hepatocellular carcinoma;HBV infections 82;100 85;112 26290395 Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study. Multivariate Cox regression analyses, including baseline characteristics of 2,114 patients, showed that age, male, cirrhosis, and HBV mutations (C1653T, T1753V, and A1762T/G1764A) independently increased HCC risk. 2015 Cancer prevention research (Philadelphia, Pa.) Abstract HBV G1764A;A1762T;C1653T;T1753V 172;165;145;153 178;171;151;159 Liver cirrhosis;Hepatocellular carcinoma 115;204 124;207 26290395 Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study. NA treatment for >=60 months was required for the prophylaxis of HCC in cirrhotic patients (P = 0.03); antiviral treatment reduced HCC risk in patients carrying A1762T/G1764A (HR, 0.40; P = 0.002) or C1653T (HR, 0.45; P = 0.04) and in those without T1753V (HR, 0.42; P = 0.005), but could not reduce HCC risk in patients without A1762T/G1764A or C1653T and in those with T1753V. 2015 Cancer prevention research (Philadelphia, Pa.) Abstract HBV G1764A;G1764A;A1762T;A1762T;C1653T;T1753V;C1653T;T1753V 168;336;329;161;200;249;346;371 174;342;335;167;206;255;352;377 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 65;131;300;72 68;134;303;81 26290395 Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study. To prevent HCC, patients infected with HBV carrying A1762T/G1764A or C1653T, but not T1753V, should be given priority of receiving antiviral treatments. 2015 Cancer prevention research (Philadelphia, Pa.) Abstract HBV G1764A;A1762T;C1653T;T1753V 59;52;69;85 65;58;75;91 Hepatocellular carcinoma 11 14 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. CONCLUSIONS: Although the patients carrying M204I mutation were more likely to show lack of responses to LAM therapy, LAM replacing by other nucleoside/tide analogs plus HBIG maybe still effective in decreasing hepatitis B recurrence after liver transplantation. 2015 Hepatitis monthly Abstract HBV M204I 44 49 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. Critical M204I mutation, as a proof for resistance to LAM, was detected among 46% of the subjects and natural entecavir resistance (S202I) was also distinguished in one subject. 2015 Hepatitis monthly Abstract HBV M204I;S202I 9;132 14;137 26309637 Detection and analysis of resistance mutations of hepatitis B virus. L180M, M204I and M204V were associated with the resistance to lamivudine and telbivudine; L180M, M204I, M204V and V173L were associated with the resistance to entecavir; A181T, N236T and N/H238T were related to the resistance to adefovir. 2015 International journal of clinical and experimental medicine Abstract HBV L180M;M204I;M204V;L180M;M204I;M204V;V173L;A181T;N236T;N238T;H238T 0;7;17;90;97;104;114;170;177;187;187 5;12;22;95;102;109;119;175;182;194;194 26309637 Detection and analysis of resistance mutations of hepatitis B virus. Of multi-base mutations, L180M combined M204V had a high prevalence and were frequently found in patients with resistance to lamivudine and telbivudine. 2015 International journal of clinical and experimental medicine Abstract HBV L180M;M204V 25;40 30;45 26309637 Detection and analysis of resistance mutations of hepatitis B virus. Of single base mutation, L180M, M204I, M204V and V173L had higher prevalence, and the incidence of L180M was closely related to the genotype of HBV. 2015 International journal of clinical and experimental medicine Abstract HBV L180M;M204I;M204V;V173L;L180M 25;32;39;49;99 30;37;44;54;104 26313279 [Characterization of basal core promoter/precore gene mutations in chronically infected patients with hepatitis B virus genotype D in Mersin Province, Turkey]. G1896A mutation was more common in HBeAg negative samples than in HBeAg positive samples (73.5% vs. 2015 Mikrobiyoloji bulteni Abstract HBV G1896A 0 6 C;C 35;66 40;71 26313279 [Characterization of basal core promoter/precore gene mutations in chronically infected patients with hepatitis B virus genotype D in Mersin Province, Turkey]. G1896A stop codon mutation in precore region seems to have a significant role in the loss of HBeAg in our patients. 2015 Mikrobiyoloji bulteni Abstract HBV G1896A 0 6 C;Precore 93;30 98;37 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Molecular modeling studies suggested that the rtL269I substitution affects template binding, which may eventually lead to the enhanced activity of rtI269-HBV polymerase in both WT virus and YMDD mutant. 2015 PloS one Abstract HBV L269I 48 53 P;RT;RT;P 158;46;147;190 168;48;149;194 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The clinical relevance of the rtL269I substitution was validated by its emergence in association with YMDD mutation in chronic hepatitis B (CHB) patients with sub-optimal response or treatment failure to LMV or CLV. 2015 PloS one Abstract HBV L269I 32 37 RT;YMDD 30;102 32;106 Chronic Hepatitis B;Chronic Hepatitis B 119;140 138;143 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtL269I substitution alone did not confer resistance to LMV, ETV, adefovir (ADV), or tenofovir (TDF). 2015 PloS one Abstract HBV L269I 6 11 RT 4 6 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtL269I substitution conferred 2- to 7-fold higher replication capacity in the wild-type (WT) or YMDD mutation backbone, regardless of drug treatment. 2015 PloS one Abstract HBV L269I 6 11 RT;P 4;101 6;105 26336997 Mechanism of Adefovir, Tenofovir and Entecavir Resistance: Molecular Modeling Studies of How A Novel Anti-HBV Agent (FMCA) Can Overcome the Drug Resistance. In this regard, homology modeled structure of HBV polymerase was used for minimization, conformational search and Glide XP docking followed by binding energy calculation on wild-type as well as on mutant HBV-polymerases (N236T, L180M+M204V+S202G & A194T). 2015 Current medicinal chemistry Abstract HBV N236T;L180M;M204V;S202G;A194T 221;228;234;240;248 226;233;239;245;253 P;P 50;208 60;219 26339047 Modification of Asparagine-Linked Glycan Density for the Design of Hepatitis B Virus Virus-Like Particles with Enhanced Immunogenicity. For the generation of hypoglycosylated VLPs, the wild-type (WT) HBsAgS N146 glycosylation site was converted to N146Q; for constructing hyperglycosylated VLPs, potential glycosylation sites were introduced in the HBsAgS external loop region at positions T116 and G130 in addition to the WT site. 2015 Journal of virology Abstract HBV N146Q 112 117 S;S 64;213 69;218 26339047 Modification of Asparagine-Linked Glycan Density for the Design of Hepatitis B Virus Virus-Like Particles with Enhanced Immunogenicity. The introduced T116N and G130N sites were utilized as glycosylation anchors resulting in the formation of hyperglycosylated VLPs. 2015 Journal of virology Abstract HBV T116N;G130N 15;25 20;30 26339047 Modification of Asparagine-Linked Glycan Density for the Design of Hepatitis B Virus Virus-Like Particles with Enhanced Immunogenicity. The T116N VLPs induced earlier and longer-lasting antibody responses than did the hypoglycosylated and WT VLPs. 2015 Journal of virology Abstract HBV T116N 4 9 26349829 A novel pyridazinone derivative inhibits hepatitis B virus replication by inducing genome-free capsid formation. A Cp V124W mutant, which strengthens capsid interdimer interactions, recapitulated the effect of 3711 on capsid assembly. 2015 Antimicrobial agents and chemotherapy Abstract HBV V124W 5 10 Capsid;Capsid;C 37;105;2 43;111;4 26349829 A novel pyridazinone derivative inhibits hepatitis B virus replication by inducing genome-free capsid formation. Both the 3TC/ETV dually resistant L180M/M204I mutant and the adefovir (ADV)-resistant A181T/N236T mutant were as susceptible to 3711 as wild-type HBV. 2015 Antimicrobial agents and chemotherapy Abstract HBV M204I;N236T;L180M;A181T 40;92;34;86 45;97;39;91 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. Consistent with previous studies, mutation rtM204I was found to be highly resistant to LDT. 2015 The Journal of general virology Abstract HBV M204I 45 50 RT 43 45 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. Furthermore, double mutations rtL80I/M204I and rtL80V/M204V had replication efficiency similar to that of rtL80I and rtL80V, respectively. 2015 The Journal of general virology Abstract HBV M204V;M204I;L80I;L80V;L80V;L80I 54;37;108;119;49;32 59;42;112;123;53;36 RT;RT;RT;RT 30;47;106;117 32;49;108;119 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. However, in contrast with their sensitivity to lamivudine, rtL80I and rtL80V were moderately resistant to LDT. 2015 The Journal of general virology Abstract HBV L80I;L80V 61;72 65;76 RT;RT 59;70 61;72 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. In vitro replication efficiency analyses showed that the RT mutations had different impacts on HBV replication, with a tendency of rtM204I>rtL80V>rtL80I. 2015 The Journal of general virology Abstract HBV M204I;L80V;L80I 133;141;148 138;145;152 RT;RT;RT;RT 57;131;139;146 59;133;141;148 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. Mutations rtM204I, rtL80I and rtL80V were detected in at least three of the four viral breakthrough patients, indicating the significant roles of the mutations in resistance to LDT. 2015 The Journal of general virology Abstract HBV M204I;L80I;L80V 12;21;32 17;25;36 RT;RT;RT 10;19;30 12;21;32 26382925 Resistant mutations and quasispecies complexity of hepatitis B virus during telbivudine treatment. Our results indicated that rtL80I and rtL80V may not only serve as replication complementary mutations to rtM204I, but also directly contribute to the LDT resistance. 2015 The Journal of general virology Abstract HBV L80I;L80V;M204I 29;40;108 33;44;113 RT;RT;RT 27;38;106 29;40;108 26384943 Occult hepatitis B virus infection and S gene escape mutants in HIV-infected patients after hepatitis B virus vaccination. Glycine to arginine mutation at residue 145 (G145R) within the 'a' region of the S gene was detected in one of the occult HBV infection cases who was in the non-responder group. 2016 International journal of STD & AIDS Abstract HBV G145R;G145R 45;0 50;43 S 81 82 HBV infections 122 135 26386408 Epidemiology of HBV infection in a cohort of Ugandan HIV-infected patients and rate and pattern of lamivudine-resistant HBV infection in patients receiving antiretroviral therapy. Of the 23 patients in whom HBV-DNA sequencing was successful, 17 had lamivudine-resistant HBV strains harbouring rtM204V/I mutations accompanied by secondary/compensatory mutations. 2015 Transactions of the Royal Society of Tropical Medicine and Hygiene Abstract HBV M204V;M204I 115;115 122;122 RT 113 115 26389515 Predictors of hepatitis B e antigen-negative hepatitis in chronic hepatitis B virus-infected patients from childhood to adulthood. HBeAg-negative hepatitis subjects carried more A1762T/G1764A, C2063A, and A2131C HBV gene mutations than those without HBeAg-negative hepatitis. 2016 Hepatology (Baltimore, Md.) Abstract HBV G1764A;A1762T;C2063A;A2131C 54;47;62;74 60;53;68;80 C;C 0;119 5;124 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. In the CD4+ and CD56+ subset of 2 HBV monoinfected cases on tenofovir therapy, mutations at residues associated with drug resistance and/or immune escape (i.e., G145R) were detected in a minor percentage of the population. 2015 PloS one Abstract HBV G145R 161 166 26419862 High Burden of HBV-Infection and Atypical HBV Strains among HIV-infected Cameroonians. Of note, one HBV variant carried the vaccine-escape mutation G145R that hinders HBsAg neutralization by antibodies. 2016 Current HIV research Abstract HBV G145R 61 66 S 80 85 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Amino acid escape mutation T125M was detected in only 2 samples of the occult infection group and in none of the overt group (P = 0.01). 2015 Virology journal Abstract HBV T125M 27 32 Occult Hepatitis B 71 87 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Different amino acid substitutions were identified in overt infection group: S143L/T (16.2 %, 12/74) and P120T/S (2.7 %, 2/74). 2015 Virology journal Abstract HBV S143L;S143T;P120T;P120S 77;77;105;105 84;84;112;112 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Q129R was significantly more frequent in cases with occult HBV infection (40 %, 4/10) than overt group (6.8 %, 5/74) (P = 0.01). 2015 Virology journal Abstract HBV Q129R 0 5 HBV infections 59 72 26447624 [Associations between hepatitis B virus x gene mutations and hepatocellular carcinoma]. CONCLUSION: Incidence of the T1674C mutation in the X region and of the T1753C mutation and the A1762T/G1764A double mutation in the BCP region was higher for patients with HBV-related HCC; the T1753C mutation and the A1762T/G1764A double mutation may inhibit the formation of HBeAg. 2015 Zhonghua gan zang bing za zhi Abstract HBV G1764A;G1764A;A1762T;A1762T;T1674C;T1753C;T1753C 103;225;218;96;29;72;194 109;231;224;102;35;78;200 BCP;C;X 133;277;52 136;282;53 Hepatocellular carcinoma 185 188 26447624 [Associations between hepatitis B virus x gene mutations and hepatocellular carcinoma]. Prevalence of the T1753C mutation and the A1762T/G1764A double mutation in the BCP region was significantly higher in the HCC group than in the chronic HBV infection group (P<0.05) and in the group of patients with hepatitis B e antigen (HBeAg)-negative status compared to the patients with HBeAg-positive status (P<0.05). 2015 Zhonghua gan zang bing za zhi Abstract HBV G1764A;A1762T;T1753C 49;42;18 55;48;24 BCP;C;C;C 79;227;238;291 82;236;243;296 Hepatocellular carcinoma;HBV infections 122;144 125;165 26447624 [Associations between hepatitis B virus x gene mutations and hepatocellular carcinoma]. RESULTS: Mutations of G1467C, G/C1479A, C1485T and C1653T in the X region were found, but did not show any significant difference in occurrence between the HCC group and the chronic HBV infection group (P>0.05). 2015 Zhonghua gan zang bing za zhi Abstract HBV G1467C;G1479A;C1479A;C1485T;C1653T 22;30;30;40;51 28;38;38;46;57 X 65 66 Hepatocellular carcinoma;HBV infections 156;174 159;195 26447624 [Associations between hepatitis B virus x gene mutations and hepatocellular carcinoma]. The T1674C mutation in the X region, however, occurred more frequently in the HCC group (29.27% vs.6.67%, P<0.05). 2015 Zhonghua gan zang bing za zhi Abstract HBV T1674C 4 10 X 27 28 Hepatocellular carcinoma 78 81 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. The surface gene from the child and his father had the same amino acid substitution pattern (T118K, T123N and G145A). 2015 PloS one Abstract HBV T118K;T123N;G145A 93;100;110 98;105;115 S 4 11 26478663 Hepatitis B virus infection in Indonesia. Pre-S2 mutations and mutations at C1638T and T1753V in HBV/B3 have been associated with advanced liver diseases including HCC. 2015 World journal of gastroenterology Abstract HBV C1638T;T1753V 34;45 40;51 PreS2 0 6 Liver disease;Hepatocellular carcinoma 97;122 111;125 26505028 A Nanoscale Mutation-Sensitive On/Off Switch Based Assays for the Detection of Hepatitis B Virus Lamivudine-Resistant Mutations. The purpose of this study was to develop methods for detecting the mutations of YMDD, rtL180M, and rtV173L by nanoscale mutation-sensitive switch consisting of high fidelity polymerase and phosphorothioate-modified allele specific primers. 2015 Journal of nanoscience and nanotechnology Abstract HBV L180M;V173L 88;101 93;106 P;RT;RT;P 174;86;99;80 184;88;101;84 26515673 Effect of tenofovir disoproxil fumarate on drug-resistant HBV clones. However, lamivudine plus adefovir-resistant clones (rtA181T/N236T) acquired tolerance to TDF, and the rtN236T mutation was considered to be a causal substitution for TDF resistance. 2016 The Journal of infection Abstract HBV N236T;N236T;A181T 60;104;54 65;109;59 RT;RT 52;102 54;104 26515673 Effect of tenofovir disoproxil fumarate on drug-resistant HBV clones. RESULTS: TDF susceptibilities of lamivudine-resistant clones (rtL180M/M204V) and lamivudine plus entecavir-resistant clones (rtL180M/S202G/M204V) were similar to wild type clones in vitro. 2016 The Journal of infection Abstract HBV M204V;S202G;M204V;L180M;L180M 70;133;139;64;127 75;138;144;69;132 RT;RT 62;125 64;127 26524917 [Variability of Reverse Transcriptase Gene and S Gene in Lamivudine-treated Chronic Hepatitis B Patients]. rtL180M coexisted with rtM204V (5/5, 100%). 2015 Bing du xue bao Abstract HBV L180M;M204V 2;25 7;30 RT;RT 0;23 2;25 26524917 [Variability of Reverse Transcriptase Gene and S Gene in Lamivudine-treated Chronic Hepatitis B Patients]. rtL80I was present in most of the patients with rtM204I (14/20, 70%). 2015 Bing du xue bao Abstract HBV L80I;M204I 2;50 6;55 RT;RT 0;48 2;50 26524917 [Variability of Reverse Transcriptase Gene and S Gene in Lamivudine-treated Chronic Hepatitis B Patients]. sM133L and sG145R variants were also present in patients with the YMDD mutation. 2015 Bing du xue bao Abstract HBV M133L;G145R 0;11 6;17 S;S;YMDD 0;11;66 1;12;70 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Although the structure of HIV-1 RT Q151M superimposes well onto that of HIV-1 RT in a closed conformation, a slight movement of the beta-strands (beta2-beta3) that partially create the dNTP-binding pocket was observed. 2015 Acta crystallographica. Section F, Structural biology communications Abstract HBV Q151M 35 40 RT;RT 32;78 34;80 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Here, the crystal structure of HIV-1 RT Q151M, determined at 2.6 A resolution, in a new crystal form with space group P321 is presented. 2015 Acta crystallographica. Section F, Structural biology communications Abstract HBV Q151M 40 45 RT 37 39 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The Q151M mutation in HIV-1 RT, located at the dNTP-binding site, confers resistance to various NRTIs, while maintaining sensitivity to tenofovir and lamivudine. 2015 Acta crystallographica. Section F, Structural biology communications Abstract HBV Q151M 4 9 RT 28 30 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The structure also highlighted the possibility that the hydrogen-bonding network among amino acids and NRTIs is rearranged by the Q151M mutation, leading to a difference in the affinity of NRTIs for HIV-1 RT and HBV Pol. 2015 Acta crystallographica. Section F, Structural biology communications Abstract HBV Q151M 130 135 P;RT 216;205 219;207 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Therefore, the structure of the dNTP-binding pocket of the HIV-1 RT Q151M mutant may reflect that of HBV Pol. 2015 Acta crystallographica. Section F, Structural biology communications Abstract HBV Q151M 68 73 P;RT 105;65 108;67 26541316 New broadly reactive neutralizing antibodies against hepatitis B virus surface antigen. Certain aa residues at position 122 (either R or K) define different HBV serotypes (either d or y), therefore, the affinity of the MAb HB1 for the epitope with R122K substitution was determined to evaluate its diagnostic potential. 2016 Virus research Abstract HBV R122K 160 165 26543337 Quantitative evaluation of hepatitis B virus mutations and hepatocellular carcinoma risk: a meta-analysis of prospective studies. C1653T in Enhancer II was significantly associated with HCC risk (pooled-RR=1.83; 95% CI: 1.21-2.76). 2015 Chinese journal of cancer research Abstract HBV C1653T 0 6 Enh II 10 21 Hepatocellular carcinoma 56 59 26543337 Quantitative evaluation of hepatitis B virus mutations and hepatocellular carcinoma risk: a meta-analysis of prospective studies. CONCLUSIONS: This study demonstrated that PreS mutations, C1653T, T1753V, and A1762T/G1764A, were associated with an increased risk of HCC. 2015 Chinese journal of cancer research Abstract HBV G1764A;A1762T;C1653T;T1753V 85;78;58;66 91;84;64;72 PreS 42 46 Hepatocellular carcinoma 135 138 26543337 Quantitative evaluation of hepatitis B virus mutations and hepatocellular carcinoma risk: a meta-analysis of prospective studies. For mutations in BCP, statistically significant pooled-RRs of HCC were obtained for T1753V (pooled-RR=2.09; 95% CI: 1.49-2.94) and A1762T/G1764A double mutations (pooled-RR=3.11; 95% CI: 2.08-4.64). 2015 Chinese journal of cancer research Abstract HBV G1764A;A1762T;T1753V 138;131;84 144;137;90 BCP 17 20 Hepatocellular carcinoma 62 65 26543337 Quantitative evaluation of hepatitis B virus mutations and hepatocellular carcinoma risk: a meta-analysis of prospective studies. No statistically significant association with HCC risk was observed for G1896A in the precore region (pooled-RR=0.77; 95% CI: 0.47-1.26). 2015 Chinese journal of cancer research Abstract HBV G1896A 72 78 Precore 86 93 Hepatocellular carcinoma 46 49 26564702 [Relationship between hepatitis B virus genotype, BCP/Pre-C region mutations and risk of hepatocellular carcinoma in Guangxi Zhuang Autonomous Region]. A1775G is the protective factor in the development of HCC (OR = 0.192, 95% CI: 0.059-0.622, P = 0.006). 2015 Zhonghua liu xing bing xue za zhi Abstract HBV A1775G 0 6 Hepatocellular carcinoma 54 57 26564702 [Relationship between hepatitis B virus genotype, BCP/Pre-C region mutations and risk of hepatocellular carcinoma in Guangxi Zhuang Autonomous Region]. CONCLUSION: The present investigation showed that BCP A1762T/G1764A, A1775G and Pre-C T1858C mutations are correlated with the incidence of HCC in Fusui county of Guangxi. 2015 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T;A1775G;T1858C 61;54;69;86 67;60;75;92 BCP;Precore 50;80 53;85 Hepatocellular carcinoma 140 143 26564702 [Relationship between hepatitis B virus genotype, BCP/Pre-C region mutations and risk of hepatocellular carcinoma in Guangxi Zhuang Autonomous Region]. Multiple logistic regression analysis indicated that A1762T/G1764A and T1858C mutations are the risk factors for the development of HCC (OR = 5.459, 95% CI: 1.397-21.332, P = 0.015; OR = 3.881, 95% CI: 1.462-10.305, P = 0.006). 2015 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T;T1858C 60;53;71 66;59;77 Hepatocellular carcinoma 132 135 26564702 [Relationship between hepatitis B virus genotype, BCP/Pre-C region mutations and risk of hepatocellular carcinoma in Guangxi Zhuang Autonomous Region]. RESULTS: The mutation rates of the A1762T/G1764A in the BCP region and the T1858C in the Pre-C region of HBV were significantly higher in HCC group than in control group (94.3% vs. 2015 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T;T1858C 42;35;75 48;41;81 BCP;Precore 56;89 59;94 Hepatocellular carcinoma 138 141 26564702 [Relationship between hepatitis B virus genotype, BCP/Pre-C region mutations and risk of hepatocellular carcinoma in Guangxi Zhuang Autonomous Region]. The mutation rate of A1775G was significantly higher in control group (28.6%) than in HCC group (13.2%) (P = 0.041). 2015 Zhonghua liu xing bing xue za zhi Abstract HBV A1775G 21 27 Hepatocellular carcinoma 86 89 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. Full-length HBV wild type (wt) and HBV rtA181T/sW172* expression plasmids were transfected into HepG2 cell lines or were injected into C57BL/6 mice. 2016 Japanese journal of infectious diseases Abstract HBV W172X;A181T 47;41 53;46 RT;S 39;47 41;48 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. Furthermore, GRP78 mRNA expression was increased 72 h post-transfection in HBV rtA181T/sW172* cells relative to HBV wt cells (P = 0.0154). 2016 Japanese journal of infectious diseases Abstract HBV W172X;A181T 87;81 93;86 RT;S 79;87 81;88 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. HBsAg levels were significantly higher in both supernatant of cells transfected with HBV wt and serum of mice injected with HBV wt, compared with that of HBV rtA181T/sW172* mutant. 2016 Japanese journal of infectious diseases Abstract HBV W172X;A181T 166;160 172;165 S;RT;S 0;158;166 5;160;167 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. HBV rtA181T/sW172* truncated surface proteins showed a more aggregated cytoplasmic pattern which were also localized to the ER in comparison with HBV wt. 2016 Japanese journal of infectious diseases Abstract HBV W172X;A181T 12;6 18;11 RT;S;S 4;12;29 6;13;36 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. The HBV sW172* truncation variant has a defect on HBsAg secretion which can lead to surface protein retention in the ER, where it may contribute to hepatocarcinogenesis through activating the ER stress signaling pathway. 2016 Japanese journal of infectious diseases Abstract HBV W172X 8 14 S;S;S 50;8;84 55;9;91 26567840 Possible Involvement of Multidrug-Resistant Hepatitis B Virus sW172* Truncation Variant in the ER Stress Signaling Pathway during Hepatocarcinogenesis. We investigated the biological effect of hepatitis B virus (HBV) rtA181T/sW172* point mutation on HBsAg secretion and the potential mechanisms involved in hepatocarcinogenesis. 2016 Japanese journal of infectious diseases Abstract HBV W172X;A181T 73;67 79;72 RT;S;S 65;73;98 67;74;103 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. Through stepwise regression analysis, HBV genotype, the 11 mutations, HLA-DQ/DR SNPs, and the interaction of rs9272105 with mutation A1752G were all entered into the HCC prediction model, and the area under the curve for the panel including the HLA-DQ/DR SNPs, HBV genotype and mutations was 0.840. 2015 Scientific reports Abstract HBV A1752G 133 139 Hepatocellular carcinoma 166 169 26571304 Chronic hepatitis B in pregnant women: is hepatitis B surface antigen quantification useful for viral load prediction? Two-thirds of HBeAg-negative subjects with high HBV DNA levels harboured BCP (A1762T/G1764A) and/or PC (G1896A) variants. 2015 International journal of infectious diseases Abstract HBV G1764A;A1762T;G1896A 85;78;104 91;84;110 BCP;C;Precore 73;14;100 76;19;102 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Additionally, among all substitutions, the A1762T and G1764A BCP mutations were the strongest indicators of chronicity. 2015 PloS one Abstract HBV A1762T;G1764A 43;54 49;60 BCP 61 64 26577140 Hepatitis B virus basal core promoter/precore mutants and association with liver cirrhosis in children with chronic hepatitis B virus infection. Among all the patients with genotype B viruses, those with LC had lower HBV DNA levels and higher G1899A mutation frequency than patients with CHB. 2016 Clinical microbiology and infection Abstract HBV G1899A 98 104 Chronic Hepatitis B;Liver cirrhosis 143;59 146;61 26577140 Hepatitis B virus basal core promoter/precore mutants and association with liver cirrhosis in children with chronic hepatitis B virus infection. Among all the patients with genotype C viruses, the patients with LC had higher prevalence of C1653T, A1762T/G1764A and G1896A mutation frequency, higher hepatitis B e antigen (HBeAg) -negative rates, lower viral load, lower elevated alanine aminotransferase and lower anti-HBe positive rates than CHB patients. 2016 Clinical microbiology and infection Abstract HBV G1764A;A1762T;C1653T;G1896A 109;102;94;120 115;108;100;126 C;C;C 166;274;177 175;277;182 Chronic Hepatitis B;Liver cirrhosis 298;66 301;68 26577140 Hepatitis B virus basal core promoter/precore mutants and association with liver cirrhosis in children with chronic hepatitis B virus infection. Patients with HBV genotype C viruses, high viral load and C1653T, A1762T/G1764A, G1896A mutant viruses, were more susceptible to developing LC. 2016 Clinical microbiology and infection Abstract HBV G1764A;A1762T;C1653T;G1896A 73;66;58;81 79;72;64;87 Liver cirrhosis 140 142 26577140 Hepatitis B virus basal core promoter/precore mutants and association with liver cirrhosis in children with chronic hepatitis B virus infection. The C1653T, T1753C, A1762T/G1764A and G1896A mutations had a significantly higher prevalence in patients with LC. 2016 Clinical microbiology and infection Abstract HBV G1764A;A1762T;C1653T;T1753C;G1896A 27;20;4;12;38 33;26;10;18;44 Liver cirrhosis 110 112 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Double (rtM204V+rtL180M) or triple (rtM204V+rtL180M+rtV173L) lamivudine-resistant mutations were introduced into HBV expression vector, followed by hydrodynamic injection into tail vein of NOD/SCID mice. 2014 Acta pharmaceutica Sinica. B Abstract HBV M204V;L180M;M204V;L180M;V173L 10;18;38;46;54 15;23;43;51;59 RT;RT;RT;RT;RT 8;16;36;44;52 10;18;38;46;54 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Primary resistance mutation (rtM204V) contributes to lamivudine (LAM)-resistance, and compensatory mutations (rtL180M and rtV173L) restore viral fitness and increase replication efficiency. 2014 Acta pharmaceutica Sinica. B Abstract HBV M204V;L180M;V173L 31;112;124 36;117;129 RT;RT;RT 29;110;122 31;112;124 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. BACKGROUND: Precore stop codon (G1896A) mutation is one of the commonest mutations found in patients with chronic hepatitis B. 2015 Hepatitis monthly Abstract HBV G1896A 32 38 Precore 12 19 Chronic Hepatitis B 106 125 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Clinical association revealed that subjects with G1896A mutations were mainly detected in asymptomatic chronic hepatitis B (58.3%) and liver cirrhosis (41.7%). 2015 Hepatitis monthly Abstract HBV G1896A 49 55 Chronic Hepatitis B;Liver cirrhosis 103;135 122;150 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. CONCLUSIONS: Our data suggested an intermediate prevalence of G1896A mutation among Malaysian hepatitis B carriers. 2015 Hepatitis monthly Abstract HBV G1896A 62 68 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. No significant association was observed between G1896A mutation and HBeAg-negativity. 2015 Hepatitis monthly Abstract HBV G1896A 48 54 C 68 73 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Nonetheless, G1896A was highly prevalent among HBV genotype B. 2015 Hepatitis monthly Abstract HBV G1896A 13 19 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. OBJECTIVES: We therefore investigated the presence of G1896A mutation in Malaysian population and its association with HBeAg status, clinical stage, hepatitis B virus (HBV) genotype and e-seroconversion rate. 2015 Hepatitis monthly Abstract HBV G1896A 54 60 C 119 124 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. RESULTS: The most commonly observed mutation in the precore region was C1858T with 64.5% prevalence. 2015 Hepatitis monthly Abstract HBV C1858T 71 77 Precore 52 59 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The basal core promoter mutations detected were A1762T-G1764A (26.9%), C1653T (8.6%), A1752G (10.8%) and C1766T (2.2%). 2015 Hepatitis monthly Abstract HBV A1762T;G1764A;C1653T;A1752G;C1766T 48;55;71;86;105 53;61;77;92;111 BCP 4 23 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The precore mutation of interest (G1896A) was identified in 25.8% of isolates. 2015 Hepatitis monthly Abstract HBV G1896A 34 40 Precore 4 11 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. Moreover, we observed three mutations in S region, including T127P, P153L, and F170S, which caused OBI. 2015 Jundishapur journal of microbiology Abstract HBV T127P;P153L;F170S 61;68;79 66;73;84 S 41 42 Occult Hepatitis B 99 102 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. There were three amino acid substitutions in the S region (T127P, P153L, and F170S) and one substitution in the RT region (Y135S). 2015 Jundishapur journal of microbiology Abstract HBV T127P;P153L;F170S;Y135S 59;66;77;123 64;71;82;128 RT;S 112;49 114;50 26598112 Clearance of HBV DNA in immunized children born to HBsAg-positive mothers, years after being diagnosed with occult HBV infection. The only still OBI-positive patient had an HBV DNA level of 50 copy/mL, carried the G145R mutation when tested in 2009 and again in 2013 in the 'a' determinant region of the surface protein. 2016 Journal of viral hepatitis Abstract HBV G145R 84 89 S;S 145;174 159;181 Occult Hepatitis B 15 18 26598693 High-resolution crystal structure of a hepatitis B virus replication inhibitor bound to the viral core protein. The compound NVR-010-001-E2 can induce assembly of the HBV core wild-type and Y132A mutant proteins and thermostabilize the proteins with a Tm increase of more than 10 C. 2015 Proc Natl Acad Sci U S A Abstract HBV Y132A 78 83 C 59 63 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. However, in the absence of rtM204I mutants, synergistic growth of the drug-resistant rtA181T mutants with the wild-type quasispecies could drive the composition of the viral population into a state of partial virological response. 2015 Scientific reports Abstract HBV M204I;A181T 29;87 34;92 RT;RT 27;85 29;87 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In particular, rtM204I mutants compete against other quasispecies, which eventually leads to virological breakthrough. 2015 Scientific reports Abstract HBV M204I 17 22 RT 15 17 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The phylogenies of the quasispecies revealed the independent origins of two critical quasispecies, i.e., the rtA181T and rtM204I mutants. 2015 Scientific reports Abstract HBV A181T;M204I 111;123 116;128 RT;RT 109;121 111;123 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Genotype C isolates had higher rates of rtA181T/V than genotype B . 2015 Scientific reports Abstract HBV A181T;A181V 42;42 49;49 RT 40 42 26613893 Mutations in the S gene and in the overlapping reverse transcriptase region in chronic hepatitis B Chinese patients with coexistence of HBsAg and anti-HBs. Mutation sI126S/T within the "a" determinant was the most frequent change, and only patients from group I had the sQ129R, sG130N, sF134I, sG145R amino acid changes, which are known to alter immunogenicity. 2016 The Brazilian journal of infectious diseases Abstract HBV I126S;I126T;Q129R;G130N;F134I;G145R 9;9;114;122;130;138 17;17;120;128;136;144 S;S;S;S;S 9;114;122;130;138 10;115;123;131;139 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. ALT levels were higher in patients with PC G1896A mutant percentage greater than 10%. 2015 Scientific reports Abstract HBV G1896A 43 49 Precore 40 42 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. BCP A1762T/G1764A double mutants were generally accompanied with PC 1896 wild type or lower PC G1896A mutant percentage. 2015 Scientific reports Abstract HBV G1764A;A1762T;G1896A 11;4;95 17;10;101 BCP;Precore;Precore 0;65;92 3;67;94 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. G1719T, T1753V, A1762T and G1764A were genotype C related. 2015 Scientific reports Abstract HBV G1719T;T1753V;G1764A;A1762T 0;8;27;16 6;14;33;22 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. Lower serum HBeAg and HBsAg levels were associated with higher BCP A1762T/G1764A mutant percentages (>= 50%). 2015 Scientific reports Abstract HBV G1764A;A1762T 74;67 80;73 BCP;C;S 63;12;22 66;17;27 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Treatment with lamivudine resulted in an increased rate of the viral mutations, rtM204V/I, rtL180M and rtL80I. 2016 Molecular medicine reports Abstract HBV M204V;M204I;L180M;L80I 82;82;93;105 89;89;98;109 RT;RT;RT 80;91;103 82;93;105 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Virological breakthrough was accompanied by significant rtM204I/V substitutions in eight of the patients. 2016 Molecular medicine reports Abstract HBV M204I;M204V 58;58 65;65 RT 56 58 26715821 Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. AIM: To develop a Fok-I nested polymerase chain reaction (PCR)-restriction fragment length polymorphism analysis (PRA) method for the detection of hepatitis B virus X region (HBx) V5M mutation. 2015 World journal of gastroenterology Abstract HBV V5M 180 183 X;X 175;165 178;166 26715821 Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. CONCLUSION: The Fok-I nested PRA developed in this study is a reliable and cost-effective method to detect HBxAg V5M mutation in chronic patients with genotype C2 infection. 2015 World journal of gastroenterology Abstract HBV V5M 113 116 26715821 Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. Our data also showed that V5M prevalence in HCC patients was significantly higher than in carrier patients (47.8%, 22/46 patients vs 0%, 0/23 patients, P < 0.001), suggesting that HBxAg V5M mutation may play a pivotal role in HCC generation in chronic patients with genotype C infections. 2015 World journal of gastroenterology Abstract HBV V5M;V5M 26;186 29;189 Hepatocellular carcinoma;Hepatocellular carcinoma 44;226 47;229 26715821 Development of Fok-I based nested polymerase chain reaction-restriction fragment length polymorphism analysis for detection of hepatitis B virus X region V5M mutation. To identify V5M mutants, digestion of nested PCR amplicons by the restriction enzyme Fok-I (GGA TGN9 ) was done. 2015 World journal of gastroenterology Abstract HBV V5M 12 15 26727850 GENOMIC ANALYSIS OF HEPATITIS B VIRUS STRAINS INFECTING ROMANIAN PATIENTS. All samples harbored sA105P substitution, usually found in HBIg therapy escape isolates. 2015 Roumanian archives of microbiology and immunology Abstract HBV A105P 21 27 S 21 22 26727850 GENOMIC ANALYSIS OF HEPATITIS B VIRUS STRAINS INFECTING ROMANIAN PATIENTS. An HBV isolate displaying a lamivudine complex resistance pattern, rtM204I in conjunction with rtL180M and rtA200V, was found in a lamivudine naive patient. 2015 Roumanian archives of microbiology and immunology Abstract HBV M204I;L180M;A200V 69;97;109 74;102;114 RT;RT;RT 67;95;107 69;97;109 26727850 GENOMIC ANALYSIS OF HEPATITIS B VIRUS STRAINS INFECTING ROMANIAN PATIENTS. Two patients treated with lamivudine were found to carry isolates harboring rtM204V lamivudine resistance mutation. 2015 Roumanian archives of microbiology and immunology Abstract HBV M204V 78 83 RT 76 78 26742490 Characterization of hepatitis B virus surface antigen variability and impact on HBs antigen clearance under nucleos(t)ide analogue therapy. In our hands, a lower ELISA reactivity of HBV-vaccinated mice sera was observed against the sT125M mutant. 2016 Journal of viral hepatitis Abstract HBV T125M 92 98 S 92 93 26742490 Characterization of hepatitis B virus surface antigen variability and impact on HBs antigen clearance under nucleos(t)ide analogue therapy. The sT125M+sP127T combination was observed in four nonresolvers of six, corroborated by aa covariance analysis, associated with a lower predicted antigenicity than sT125T+sP127P. 2016 Journal of viral hepatitis Abstract HBV T125M;P127T;T125T;P127P 4;11;164;171 10;17;170;177 S;S;S;S 4;11;164;171 5;12;165;172 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. The mutation M204V/I conferring resistance to 3TC was more common in HBV/A (47.4%) than in HBV/E isolates (0%) (P = .04). 2016 PloS one Abstract HBV M204V;M204I 13;13 20;20 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In addition to the common substitutions, unknown amino acid substitutions, such as rtL145 M/S, rtF151Y/L, rtR153Q, rtI224 V, rtN248H, rtS223A, rtS256C, need to be further verified. 2016 Medicine Abstract HBV L145M;L145S;F151Y;F151L;R153Q;I224V;N248H;S223A;S256C 85;85;97;97;108;117;127;136;145 93;93;104;104;113;123;132;141;150 RT;RT;RT;RT;RT;RT;RT 83;95;106;115;125;134;143 85;97;108;117;127;136;145 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. One patient developed virological breakthrough while bearing single, double, and triple (rtL180 M, rtM204 V, rtS202G) substitutions. 2016 Medicine Abstract HBV L180M;M204V;S202G 91;101;111 97;107;116 RT;RT;RT 89;99;109 91;101;111 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. BACKGROUND/AIMS: Hepatitis B virus (HBV) rtA181V/T mutants developed by long-term nucleos(t) ide analogue therapy are known to present cross-resistance for other nucleos (t) ide analogues, except entecavir (ETV). 2016 Saudi journal of gastroenterology Abstract HBV A181V;A181T 43;43 50;50 RT 41 43 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. CONCLUSIONS: ETV monotherapy and ETV plus ADV therapy were clinically effective and comparable as rescue therapy for HBV rtA181V/T mutants alone. 2016 Saudi journal of gastroenterology Abstract HBV A181V;A181T 123;123 130;130 RT 121 123 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Some studies reported that HBV rtA181V/T mutants could induce cross-resistance to ETV and showed incomplete response as well as persistence of HBV DNA, despite rescue therapy by ETV. 2016 Saudi journal of gastroenterology Abstract HBV A181V;A181T 33;33 40;40 RT 31 33 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. This study aimed to investigate the antiviral efficacy of ETV monotherapy and ETV plus adefovir (ADV) as rescue therapy for HBV rtA181V/T single mutation. 2016 Saudi journal of gastroenterology Abstract HBV A181V;A181T 130;130 137;137 RT 128 130 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Basal core promoter (BCP) A1762T/G1764A dual mutations in hepatocarcinogenesis remain controversial. 2016 Oncotarget Abstract HBV G1764A;A1762T 33;26 39;32 BCP;BCP 0;21 19;24 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Chronic HBV-infected patients and HCC patients with genotype B had a significantly lower risk of A1762T/G1764A dual mutations compared with patients with genotype C (OR = 0.30, P < 0.0001 and OR = 0.34, P = 0.04, respectively). 2016 Oncotarget Abstract HBV G1764A;A1762T 104;97 110;103 Hepatocellular carcinoma;HBV infections 34;8 37;20 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. HCC patients had a higher frequency of BCP A1762T/G1764A dual mutations compared with asymptomatic HBsAg carriers (ASC) and patients with chronic hepatitis B (CHB) and liver cirrhosis (LC) (OR = 5.59, P < 0.00001; OR = 2.87, P < 0.00001; OR = 1.55, P = 0.02, respectively). 2016 Oncotarget Abstract HBV G1764A;A1762T 50;43 56;49 BCP;S 39;99 42;104 Hepatocellular carcinoma;Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 0;138;159;168;185 3;157;162;183;187 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In conclusion, A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma, particularly in an HBV genotype C population, even without progression to cirrhosis. 2016 Oncotarget Abstract HBV G1764A;A1762T 22;15 28;21 Hepatocellular carcinoma;Liver cirrhosis 65;177 101;186 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In HBV genotype C subjects, A1762T/G1764A dual mutations contributed to significantly higher risk for HCC developing compared with non-mutation ones (OR = 3.47, P < 0.00001). 2016 Oncotarget Abstract HBV G1764A;A1762T 35;28 41;34 Hepatocellular carcinoma 102 105 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. No statistically significant difference was observed in the frequency of A1762T/G1764A dual mutations in cirrhotic HCC versus non-cirrhotic HCC patients (OR = 2.06, P = 0.05). 2016 Oncotarget Abstract HBV G1764A;A1762T 80;73 86;79 Liver cirrhosis;Liver cirrhosis 105;130 118;139 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Published studies up to June 1, 2015 investigating the frequency of A1762T/G1764A dual mutations from chronic hepatitis B virus (HBV) infection, including hepatocellular carcinoma (HCC), were systematically identified. 2016 Oncotarget Abstract HBV G1764A;A1762T 75;68 81;74 Chronic HBV infection;Hepatocellular carcinoma;Hepatocellular carcinoma 102;155;181 143;179;184 26873737 The Thr to Met substitution of amino acid 118 in hepatitis B virus surface antigen escapes from immune-assay-based screening of blood donors. A mutagenesis assay indicated that the Thr to Met substitution at aa 118 was the determinant for escape from HBsAg ELISA detection. 2016 The Journal of general virology Abstract HBV T118M 39 72 S 109 114 26873737 The Thr to Met substitution of amino acid 118 in hepatitis B virus surface antigen escapes from immune-assay-based screening of blood donors. DNA sequencing discovered two mutations at nt 353 (A to T) and nt 349 (T to A), leading to Thr to Met and Ser to Thr substitutions at aa 118 and 117 of HBsAg, respectively. 2016 The Journal of general virology Abstract HBV T349A 66 78 S 152 157 26876337 Prevalence of mutations in HBV DNA polymerase gene associated with nucleos(t)ide resistance in treatment-naive patients with Chronic Hepatitis B in Central China. Mutations in HBV DNA polymerase were detected in 24 patients (8.9%) including rtM204I/V (n=6), rtN236T (n=5), rtM250V (n=2), rtL180M (n=2), rtT184G (n=1), rtM207I (n=1), rtS202I (n=1), rtM204V/I & rtL180M (n=5), and rtM204I & rtM250V (n=1). 2016 The Brazilian journal of infectious diseases Abstract HBV M204I;M204V;N236T;M250V;L180M;T184G;M207I;S202I;M204V;M204I;L180M;M204I;M250V 80;80;97;112;127;142;157;172;187;187;199;218;228 87;87;102;117;132;147;162;177;194;194;204;223;233 P;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 21;78;95;110;125;140;155;170;185;197;216;226 31;80;97;112;127;142;157;172;187;199;218;228 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. Clonal analysis further revealed that the rtS202G or rtT184F was in all cases co-localized with rtL180M and rtM204V in any single virus isolate clone. 2016 Experimental and therapeutic medicine Abstract HBV S202G;T184F;L180M;M204V 44;55;98;110 49;60;103;115 RT;RT;RT;RT 42;53;96;108 44;55;98;110 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. In addition, rtT184F was present in ~20% of the viral population during virological breakthrough, at month 24. 2016 Experimental and therapeutic medicine Abstract HBV T184F 15 20 RT 13 15 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. In patient A, the rtL180M, rtS202G and rtM204V mutant variants were detected using pyrosequencing prior to virological breakthrough. 2016 Experimental and therapeutic medicine Abstract HBV L180M;S202G;M204V 20;29;41 25;34;46 RT;RT;RT 18;27;39 20;29;41 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. In patient B, the rtL180M, rtM204I and rtM204V mutants were present in ~70, 30 and 10% of the viral populations, respectively, at the time of study entry. 2016 Experimental and therapeutic medicine Abstract HBV L180M;M204I;M204V 20;29;41 25;34;46 RT;RT;RT 18;27;39 20;29;41 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. The rtL180M, rtT184F and rtM204V were predominant during the combination treatment. 2016 Experimental and therapeutic medicine Abstract HBV L180M;T184F;M204V 6;15;27 11;20;32 RT;RT;RT 4;13;25 6;15;27 26890489 Complete genome analysis of hepatitis B virus in human immunodeficiency virus infected and uninfected South Africans. In the core region, mutation G1888A was identified in four of the subgenotype A1 sequences. 2016 Journal of medical virology Abstract HBV G1888A 29 35 C 7 11 26890489 Complete genome analysis of hepatitis B virus in human immunodeficiency virus infected and uninfected South Africans. No drug resistance mutations were identified in the P ORF, while the L217R mutation was identified in one subgenotype A2 sequence. 2016 Journal of medical virology Abstract HBV L217R 69 74 P 52 53 26890489 Complete genome analysis of hepatitis B virus in human immunodeficiency virus infected and uninfected South Africans. The double (A1762T/G1764A) and triple (T1753C/A1762T/G1764A) mutations in the Basal core promoter were identified in four and two sequences, respectively. 2016 Journal of medical virology Abstract HBV G1764A;A1762T;G1764A;T1753C;A1762T 19;46;53;39;12 25;52;59;45;18 BCP 78 97 26899956 Molecular characterization of hepatitis B virus from chronically-infected patients in Niamey, Niger. Amino acid substitutions found in HBV sequences obtained here included P120T, S143L, G145A and A194T. 2016 International journal of infectious diseases Abstract HBV P120T;S143L;G145A;A194T 71;78;85;95 76;83;90;100 26899956 Molecular characterization of hepatitis B virus from chronically-infected patients in Niamey, Niger. These substitutions were characterized as being associated with modified antigenicity and, notably, with impaired serological detection of HBsAg, while the A194T variant was found to have a controversial role in reduced susceptibility to tenofovir. 2016 International journal of infectious diseases Abstract HBV A194T 156 161 S 139 144 26901602 Investigation by the Method of INNO-LiPA of Primary Resistance to Lamivudine in Patients with Chronic Hepatitis B Who Have Not Used Antiviral Therapy. The rtM204V and L180M mutation motif was found in one patient with HBeAg positivity. 2015 The West Indian medical journal Abstract HBV M204V;L180M 6;16 11;21 C;RT 67;4 72;6 26919858 Reactivation of resolved hepatitis B virus infection with immune escape mutations after long-term corticosteroid therapy. Full-genome HBV sequence analysis using serial serum samples revealed that the patient was infected with HBV subgenotype C2, which had the G1896R mixed mutation in the precore region. 2016 Clinical journal of gastroenterology Abstract HBV G1896R 139 145 Precore 168 175 26919858 Reactivation of resolved hepatitis B virus infection with immune escape mutations after long-term corticosteroid therapy. Interestingly, it had the immune escape mutations P120A and G145R in the S gene. 2016 Clinical journal of gastroenterology Abstract HBV P120A;G145R 50;60 55;65 S 73 74 2693611 Mutations that change the immunological subtype of hepatitis B virus surface antigen and distinguish between antigenic and immunogenic determination. When combined with substitution of serine 113 by threonine, replacement of arginine 122 by lysine or of tyrosine 134 by phenylalanine, or both of these changes, altered the antigenic subtype of HBsAg from y+d- to y+d. 1989 Journal of medical virology Abstract HBV S113T 35 58 26983387 [Drug-resistant mutations in hepatitis B virus found in chronic HBV carriers using PCR sequencing technology]. Each of the NAs had dominant drug-resistant mutational profiles, with rtM204I+rtL180M+-rtL80I (30.9%) for LAM, rtA181T/N (21.3%), rtS213T/N (21.3%) and rtV214A (21.3%) for ADV, rtl180M (48%) for ETV, rtM204I for LdT, and rtA194T for tenofovir disoproxil fumarate (TDF). 2016 Zhonghua gan zang bing za zhi Abstract HBV M204I;L180M;L80I;A181T;A181N;S213T;S213N;V214A;M204I;A194T 72;80;89;113;113;132;132;154;202;223 77;85;93;120;120;139;139;159;207;228 RT;RT;RT;RT;RT;RT;RT;RT;RT 70;78;87;111;130;152;177;200;221 72;80;89;113;132;154;179;202;223 26983387 [Drug-resistant mutations in hepatitis B virus found in chronic HBV carriers using PCR sequencing technology]. In addition, the data confirmed the preexisting TDF mutation rtA194T. 2016 Zhonghua gan zang bing za zhi Abstract HBV A194T 63 68 RT 61 63 26983387 [Drug-resistant mutations in hepatitis B virus found in chronic HBV carriers using PCR sequencing technology]. Two TDF drug-resistant mutations rtA194T were detected. 2016 Zhonghua gan zang bing za zhi Abstract HBV A194T 35 40 RT 33 35 26984835 Association between hepatitis B virus basal core promoter/precore region mutations and the risk of hepatitis B-related acute-on-chronic liver failure in the Chinese population: an updated meta-analysis. CONCLUSIONS: HBV T1753V, A1762T/G1764A, A1846T, G1896A, and G1899A mutations are correlated with an increase in the risk of HB-ACLF. 2016 Hepatology international Abstract HBV G1764A;T1753V;A1762T;A1846T;G1896A;G1899A 32;17;25;40;48;60 38;23;31;46;54;66 Acute on chronic liver failure 124 131 26984835 Association between hepatitis B virus basal core promoter/precore region mutations and the risk of hepatitis B-related acute-on-chronic liver failure in the Chinese population: an updated meta-analysis. In sensitivity, specificity, and accuracy analysis, A1762T/G1764A had the highest sensitivity (67.43 %); A1762T/G1764A + G1896A triple mutations had the highest specificity (93.70 %); and T1753V + A1762T + G1764A mutation had the highest accuracy (65.42 %). 2016 Hepatology international Abstract HBV G1764A;G1764A;A1762T;A1762T;G1896A;T1753V;A1762T;G1764A 59;112;52;105;121;188;197;206 65;118;58;111;127;194;203;212 26984835 Association between hepatitis B virus basal core promoter/precore region mutations and the risk of hepatitis B-related acute-on-chronic liver failure in the Chinese population: an updated meta-analysis. Statistically significant summary ORs for HB-ACLF were obtained for T1753V (1.99; 95 % confidence interval 1.30-3.02) and A1762T/G1764A (2.11; 95 %, 1.75-2.54) in the BCP region and for A1846T (3.33; 95 %, 2.23-4.97), G1896A (2.78; 95 %, 2.07-3.74), and G1899A (3.09; 95 %, 1.82-5.25) in the PC region. 2016 Hepatology international Abstract HBV G1764A;T1753V;A1762T;A1846T;G1896A;G1899A 129;68;122;186;218;254 135;74;128;192;224;260 BCP;Precore 167;292 170;294 Acute on chronic liver failure 42 49 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. CONCLUSIONS: Patients with the A1762T/G1764A mutation have a higher risk of severe fibrosis. 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T 38;31 44;37 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. Interestingly, the association of the G1899A mutation with the double A1762T/G1764A mutant significantly counteracted the deleterious effect of the sole double A1762T/G1764A mutant (odds ratio [OR] = 0.28 vs. 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;G1764A;A1762T;A1762T;G1899A 77;167;160;70;38 83;173;166;76;44 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. METHODS: Direct sequencing of the precore/core gene was used to detect A1762T/G1764A and G1757A mutations in the BCP and G1896A and G1899A mutations in the PC region. 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T;G1757A;G1896A;G1899A 78;71;89;121;132 84;77;95;127;138 BCP;C;Precore;Precore 113;42;156;34 116;46;158;41 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. RESULTS: The prevalences of A1762T/G1764A, G1757A, G1896A, and G1899A mutations were 34.1%, 38.7%, 54.9%, and 29.3% (P < 0.001), respectively. 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T;G1757A;G1896A;G1899A 35;28;43;51;63 41;34;49;57;69 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. The G1899A mutation is a protective factor against severe fibrosis that counteracted the deleterious effect of the A1762T/G1764A mutation. 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T;G1899A 122;115;4 128;121;10 26992056 Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity. The independent predictors of severe fibrosis (>=F3 Metavir) were older age (P < 0.001), male gender (P = 0.012), elevated alanine aminotransferase (P < 0.001), and the double A1762T/G1764A mutant with no other mutations (P = 0.011). 2016 Journal of gastroenterology and hepatology Abstract HBV G1764A;A1762T 183;176 189;182 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. Two amino acid changes were recorded in "a" determinant, including F130L and S135F with no evidence of the vaccine escape mutant G145R in any of the samples. 2016 Saudi journal of gastroenterology Abstract HBV F130L;S135F;G145R 67;77;129 72;82;134 27006281 Higher detection rates of amino acid substitutions in HBV reverse transcriptase/surface protein overlapping sequence is correlated with lower serum HBV DNA and HBsAg levels in HBeAg-positive chronic hepatitis B patients with subgenotype B2. In addition, two patients harboring drug resistance mutations rtL80V+rtM204I and rtL180M+rtM204V were found. 2016 Infection, genetics and evolution Abstract HBV L80V;M204I;L180M;M204V 64;71;83;91 68;76;88;96 RT;RT;RT;RT 62;69;81;89 64;71;83;91 27006281 Higher detection rates of amino acid substitutions in HBV reverse transcriptase/surface protein overlapping sequence is correlated with lower serum HBV DNA and HBsAg levels in HBeAg-positive chronic hepatitis B patients with subgenotype B2. The most frequently detected substitutions were rtN134D/S (44/143, 30.8%) and sT126A/S (22/143, 15.4%), which were located in the RT A-B interdomain region and the corresponding antigenicity determinant region of S protein, respectively. 2016 Infection, genetics and evolution Abstract HBV N134D;N134S;T126A;T126S 50;50;78;78 57;57;86;86 RT;RT;S;S 48;130;78;213 50;132;79;214 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. Stable overexpression of the naturally occurring HBx-DeltaC mutants, HBx-Delta14 or HBx-Delta35, in HCC cells Huh7 and immortalized normal liver cells MIHA resulted in a significant increase in the cells ability to self-renew, resist chemotherapy and targeted therapy, migrate and induce angiogenesis. 2016 Oncotarget Abstract HBV del 35 88 95 X;X;X 49;69;84 52;72;87 Hepatocellular carcinoma 100 103 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. After stable transfection of the HBV constructs into HepG2-off23 cells, cell lines with robust and tetracycline-inducible replications of wild-type HBV (HepG2-tetHBV-WT) and rtE218G-mutated HBV (HepG2-tetHBV-E218G) were selected. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G;E218G 176;208 181;213 RT 174 176 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. CONCLUSION: Wild-type and the rtE218G HBV mutant could be expressed and efficiently regulated by tetracycline in the established new cell lines. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 32 37 RT 30 32 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. HBV mutant with rtE218G could independently confer resistance to adefovir in vitro. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 18 23 RT 16 18 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. IC50 for HBV rtE218G mutant of adefovir was (6.49+-0.09) mumol/L, which was significantly higher than that for wild type virus (2.49+-0.05) mumol/L. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 15 20 RT 13 15 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. METHODS: Tetracycline transactivator (tTA) was stably transfected into human liver cell line HepG2.1.2 folds of full-length of wild-type or rtE218G-mutated HBV genomes were cloned into the pTRE vector and cotransfected into the tTA-expressing cells with a linear selection marker for hygromycin, respectively. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 142 147 RT 140 142 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. OBJECTIVE: To establish cell lines with inducible replications of wild-type or rtE218G, an adefovir-dipivoxil-resistant HBV mutant. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 81 86 RT 79 81 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. PTRE-based plasmids carrying wild-type HBV (pTRE-HBV-WT) or rtE218G mutant (pTRE-HBV-E218GHBV) were constructed. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 62 67 RT 60 62 27029368 [Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells]. The obtained cell lines were further used to evaluate the in vitro sensitivity of rtE218G mutant to adefovir-dipivoxil. 2016 Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] Abstract HBV E218G 84 89 RT 82 84 27031988 Functional analysis of 'a' determinant mutations associated with occult HBV in HIV-positive South Africans. Of the seven mutations analysed, four (S132P, C138Y, N146D and C147Y) resulted in decreased HBsAg expression in one viral background but not in the second viral background. 2016 The Journal of general virology Abstract HBV S132P;C138Y;N146D;C147Y 39;46;53;63 44;51;58;68 S 92 97 27031988 Functional analysis of 'a' determinant mutations associated with occult HBV in HIV-positive South Africans. One mutation (N146D) led to a decrease in HBsAg detected as compared to HA-tag, indicating that this mutation compromises the ability of the ELISA to detect HBsAg. 2016 The Journal of general virology Abstract HBV N146D 14 19 S;S 42;157 47;162 27055927 Prevalence of mutations within major hydrophilic region of hepatitis B virus and their correlation with genotypes among chronically infected patients in Egypt. The first loop comprised four patients with three mutations (P127S, P127T and Y134F). 2016 Arab journal of gastroenterology Abstract HBV P127S;P127T;Y134F 61;68;78 66;73;83 27055927 Prevalence of mutations within major hydrophilic region of hepatitis B virus and their correlation with genotypes among chronically infected patients in Egypt. The second loop contained six patients, all with one mutation, S143L, which was most frequently encountered in this study (6.8%). 2016 Arab journal of gastroenterology Abstract HBV S143L 63 68 27061406 Overt and occult hepatitis B virus infection among treatment-naive HIV-infected patients in Brazil. One patient had the M204I and L180M drug-resistance mutations (polymerase). 2016 Journal of medical virology Abstract HBV M204I;L180M 20;30 25;35 P 63 73 27061406 Overt and occult hepatitis B virus infection among treatment-naive HIV-infected patients in Brazil. Sequencing of the S gene revealed Y100C, T131N, and D144A mutations. 2016 Journal of medical virology Abstract HBV Y100C;T131N;D144A 34;41;52 39;46;57 S 18 19 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. We also detected borderline significant associations of PTPN12 eQTL rs11489585 with HBV mutations (P = 0.05 for G1799C). 2016 Cancer medicine Abstract HBV G1799C 112 118 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Specifically, we found one rtM204I+rtL180 M+rtM250 V+rtA181 V clone among 23 clones from patient 1 (4.35 %), one rtM204 V+vrtL180 M +rtM250 V+rtA181 V clone among 24 clones from patient 2 (4.17 %), and 2 clones harboring rtM204 V+rtL180 M+rtM250 V+rtA181 V and rtM204 V+rtL180 M+rtI169 V+rtA181 V among 20 clones from patient 3 (10.0 %). 2016 Annals of clinical microbiology and antimicrobials Abstract HBV M204I;L180M;M250V;A181V;M204V;M250V;A181V;M204V;L180M;M250V;A181V;M204V;L180M;I169V;A181V 29;37;46;55;115;135;144;223;232;241;250;263;272;281;290 34;43;52;61;121;141;150;229;238;247;256;269;278;287;296 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 27;35;44;53;113;133;142;221;230;239;248;261;270;279;288 29;37;46;55;115;135;144;223;232;241;250;263;272;281;290 27131009 Serologic and molecular characteristics of hepatitis B virus infection in vaccinated schizophrenia patients in China. Moreover, one HBV strain in the schizophrenia group presented I126S vaccine escape mutation (5.88%), while three HBV isolates showed Q129H, M133L, and G145R vaccine escape mutations in the control group (6.81%). 2016 Journal of infection in developing countries Abstract HBV I126S;Q129H;M133L;G145R 62;133;140;151 67;138;145;156 Schizophrenia 32 45 27132039 Hepatitis B virus basal core promoter mutations show lower replication fitness associated with cccDNA acetylation status. HBV monomers bearing BCP mutations A1762T/G1764A and A1762T/G1764A/C1766T, and precore mutations G1896A, G1899A and G1896A/G1899A, were transfected into HepG2 cells using a plasmid-free approach. 2016 Virus research Abstract HBV G1764A;G1899A;A1762T;G1764A;C1766T;G1896A;A1762T;G1899A;G1896A 42;123;35;60;67;97;53;105;116 48;129;41;66;73;103;59;111;122 BCP;Precore 21;79 24;86 27133305 Discordant diagnostic results due to a hepatitis B virus T123A HBsAg mutant. Such discordance has been observed repeatedly in Canada with samples having a mutation at HBsAg codon 123 (sT123A). 2016 Diagnostic microbiology and infectious disease Abstract HBV T123A 107 113 S;S 107;90 108;95 27133305 Discordant diagnostic results due to a hepatitis B virus T123A HBsAg mutant. The sT123A mutation leads to loss of detection by immunoassays commonly used in Canadian diagnostic laboratories, which may produce misleading results and diagnoses. 2016 Diagnostic microbiology and infectious disease Abstract HBV T123A 4 10 S 4 5 27144395 Betaine Inhibits Hepatitis B Virus with an Advantage of Decreasing Resistance to Lamivudine and Interferon alpha. BET suppressed HBV DNA rebound produced by the resistance of HBV to lamivudine and decreased the resistance mutation (rtM204V/I) of HBV DNA. 2016 Journal of agricultural and food chemistry Abstract HBV M204V;M204I 120;120 127;127 RT 118 120 27158197 Precore/core region mutations of hepatitis B virus related to clinical severity. Certain mutations, including preC G1896A, are also significantly related to HBeAg-negative chronic infection. 2016 World journal of gastroenterology Abstract HBV G1896A 34 40 C;Precore 76;29 81;33 27165167 Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations. Here, we present a case of fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A double mutations in the core promoter region. 2016 Clinical journal of gastroenterology Abstract HBV T1768A;C1766T 123;116 129;122 Core promoter 154 167 Fulminant Hepatitis B 33 52 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. The 3TC resistance mutations rtL180M and rtM204V were observed in 10 (47.6%) of the 21 patients, while 5 patients (23.8%) had rtV173L, rtL180M and rtM204V mutations. 2017 Antiviral therapy Abstract HBV L180M;M204V;V173L;L180M;M204V 31;43;128;137;149 36;48;133;142;154 RT;RT;RT;RT;RT 29;41;126;135;147 31;43;128;137;149 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. Additional N-glycosylation-associated mutations, sQ129N and s131-133TSM NST, but not s126-127 "RPCMNCTI," greatly attenuated anti-HBs binding to HBsAg. 2016 PloS one Abstract HBV Q129N 49 55 S;S;S;S;S 130;145;49;60;85 133;150;50;61;86 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. RESULTS: Twenty-one preS/S-gene mutants were cloned from four sequential serum samples, including 13 mutants that were not previously documented: (1) sI/T126V+sG145R; (2) preS1 nt 3014-3198 deletion; (3) preS1 nt 3046-3177 deletion; (4) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion; (5) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion+sG145R; (6) preS1 nt 3115-3123 deletion+sQ129N; (7) preS1 nt 3115-3123 deletion+s126-127 "RPCMNCTI" insertion; (8) s115-116 "INGTST" insertion; (9) s115-116 "INGTST" insertion+sG145R; (10) s126-127 "RPCMNCTI" insertion; (11) preS1 nt 2848-2862 deletion+preS2 initiation codon M I; (12) s122-123 "KSTGLCK" insertion+sQ129N; and (13) preS2 initiation codon M I+s131-133TSM NST. 2016 PloS one Abstract HBV T126V;I126V;G145R;G145R;Q129N;G145R;Q129N 153;150;159;355;395;531;670 158;158;165;360;400;536;675 PreS;S;PreS1;PreS1;PreS1;PreS1;PreS1;PreS1;PreS1;PreS2;PreS2;S;S;S;S;S;S;S;S;S;S;S;S;S;S 20;25;171;204;237;298;366;406;579;607;686;150;159;265;326;354;394;434;469;502;530;543;640;669;713 24;26;176;209;242;303;371;411;584;612;691;151;160;266;327;355;395;435;470;503;531;544;641;670;714 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Mutation site analysis of the both groups' mothers demonstrated 108 different mutation sites in the HBV pre-S/S gene, with 105 silent mutations and 5 missense mutations including ntA826G, ntC531T, ntT667C, ntC512T and ntC546A. 2016 Hepatitis monthly Abstract HBV A826G;C531T;T667C;C512T;C546A 180;189;198;207;219 186;195;204;213;225 PreS;S 104;110 109;111 27245734 Hepatitis B infection in HIV-1-infected patients receiving highly active antiretroviral therapy in Lome, Togo: Prevalence and molecular consequences. The detected resistance mutations were rtL180M (14/15 patients) and rtM204V/I (15/15). 2016 South African medical journal Abstract HBV L180M;M204V;M204I 41;70;70 46;77;77 RT;RT 39;68 41;70 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. Only in 3% (2/63) the mutations were within the a-determinant of HBsAg (M133T and G145S, one case each). 2016 PloS one Abstract HBV M133T;G145S 72;82 77;87 S 65 70 27303803 Hepatitis B Virus Core Promoter Double Mutations (A1762T, G1764A) Are Associated with Lower Levels of Serum Dihydrolipoyl Dehydrogenase. OBJECTIVES: The aim of this study was to identify serum proteins with differential concentrations between hepatocellular carcinoma (HCC) patients and HBsAg asymptomatic carriers among individuals infected with hepatitis B virus (HBV) with basal core promoter (BCP) double mutations (A1762T, G1764A). 2016 Intervirology Abstract HBV A1762T;G1764A 283;291 289;297 BCP;BCP;S 239;260;150 258;263;155 Hepatocellular carcinoma;Hepatocellular carcinoma 106;132 130;135 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. At the initiation of sequential monotherapy with ADV, LAM-resistant variants (rtM204V/I and rtL180M) were detected in the three patients. 2016 Experimental and therapeutic medicine Abstract HBV M204V;M204I;L180M 80;80;94 87;87;99 RT;RT 78;92 80;94 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. During 30-41 months of ADV-ETV combination therapy, viral load reduction was 2.59-3.28 log10 copies/ml; ADV-resistant variants rtA181T/V and rtN236T were undetectable following 11-24 months of combination therapy; and rtL180M and rtM204I/V remained dominant in the viral population. 2016 Experimental and therapeutic medicine Abstract HBV A181T;A181V;N236T;L180M;M204I;M204V 129;129;143;220;232;232 136;136;148;225;239;239 RT;RT;RT;RT 127;141;218;230 129;143;220;232 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. During ADV sequential monotherapy, LAM-resistant variants were gradually decreased, whereas ADV-resistant rtA181V/T and rtN236T variants gradually increased in the viral population. 2016 Experimental and therapeutic medicine Abstract HBV A181V;A181T;N236T 108;108;122 115;115;127 RT;RT 106;120 108;122 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In conclusion, the results of the present study suggested that, in patients with LAM and ADV-resistant variants that developed during LAM-ADV sequential monotherapy, ETV-ADV combination therapy may partially inhibit the replication of HBV DNA; however, LAM-resistant rtL180M and rtM204I/V variants remained predominant following 30-41 months combination therapy. 2016 Experimental and therapeutic medicine Abstract HBV L180M;M204I;M204V 269;281;281 274;288;288 RT;RT 267;279 269;281 27328656 Intergenotype recombinant analysis of full-length hepatitis B virus genomes from 516 Chinese patients with different illness categories. Difference in basal core promoter A1762T/G1764A mutations and precore G1896A mutation incidences was not significant between B/C recombinant and genotypes B or C virus, although the significance was there between genotypes B and C viruses. 2017 Journal of medical virology Abstract HBV G1764A;A1762T;G1896A 41;34;70 47;40;76 BCP;Precore 14;62 33;69 27329484 A case of acute hepatitis B in a chronic hepatitis C patient after daclatasvir and asunaprevir combination therapy: hepatitis B virus reactivation or acute self-limited hepatitis? T118 K mutation at the S region as an immune escape mutant was identified. 2016 Clinical journal of gastroenterology Abstract HBV T118K 0 6 S 23 24 27340355 Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma. CONCLUSION: The presence of T1753V mutation in HBV X-gene significantly increases the risk of HCC development in patients chronically infected with genotype C HBV. 2016 World journal of gastroenterology Abstract HBV T1753V 28 34 X 51 52 Hepatocellular carcinoma 94 97 27340355 Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma. Out of 240 CHB patients, 25 (10%) had C1653T and 33 (14%) had T1753V mutation in X region; 157 (65%) had A1762T/G1764A mutations in BCP region, 50 (21%) had G1896A mutation in precore region and 67 (28%) had pre-S deletions. 2016 World journal of gastroenterology Abstract HBV G1764A;A1762T;C1653T;T1753V;G1896A 112;105;38;62;157 118;111;44;68;163 BCP;Precore;PreS;X 132;176;208;81 135;183;213;82 Chronic Hepatitis B 11 14 27340355 Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma. The cumulative occurrence rates of HCC were 5% and 19% at 10 and 15 years, respectively, in patients with T1753V mutant, which were significantly higher than 1% and 1% in those with wild type HBV (P < 0.001). 2016 World journal of gastroenterology Abstract HBV T1753V 106 112 Hepatocellular carcinoma 35 38 27340355 Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma. The prevalence of T1753V mutation was significantly higher in patients who developed HCC than in those without HCC. 2016 World journal of gastroenterology Abstract HBV T1753V 18 24 Hepatocellular carcinoma;Hepatocellular carcinoma 85;111 88;114 27354181 HIV therapy with unknown HBV status is responsible for higher rate of HBV genome variability in Ethiopia. Despite the finding that rtL180M and rtM204V/I were higher among ART-experienced individuals, the overall prevalence of DRMs (48.0% versus 36.4%) showed no significance difference among antiretroviral therapy (ART) status. 2017 Antiviral therapy Abstract HBV M204V;M204I;L180M 39;39;27 46;46;32 RT;RT 25;37 27;39 27354181 HIV therapy with unknown HBV status is responsible for higher rate of HBV genome variability in Ethiopia. In particular, the 'a' determinant surface gene mutations (sT125S, sA128V, sQ129H/R, sT131I, sC137S, sT143M, sD144D/E, sG145R, sT148P) and the majority of clustered/multiple as well as drug selected immune escape HBsAg mutations were more prevalent in HBV-HIV-coinfected individuals. 2017 Antiviral therapy Abstract HBV T125S;A128V;Q129H;Q129R;T131I;C137S;T143M;D144D;D144E;G145R;T148P 59;67;75;75;85;93;101;109;109;119;127 65;73;83;83;91;99;107;117;117;125;133 S;S;S;S;S;S;S;S;S;S;S;S 20;213;59;67;75;85;93;101;109;119;127;35 34;218;60;68;76;86;94;102;110;120;128;42 HBV-HIV coinfections 252 270 27354181 HIV therapy with unknown HBV status is responsible for higher rate of HBV genome variability in Ethiopia. Lamivudine selected DRMs, that is, rtL180M (29.3%) and rtM204V/I (29.3%) and rtV173L (15.5%) were more prevalent in HBV-HIV-coinfected individuals but absent in HBV-monoinfected individuals. 2017 Antiviral therapy Abstract HBV L180M;M204V;M204I;V173L 37;57;57;79 42;64;64;84 RT;RT;RT 35;55;77 37;57;79 HBV infections;HBV-HIV coinfections 161;116 177;134 27354181 HIV therapy with unknown HBV status is responsible for higher rate of HBV genome variability in Ethiopia. RESULTS: In 34 out of 161 study subjects (21.1%) HBV drug resistance mutations (DRMs) were detected with a frequency of 3.1% rtL80F/I, 0.6% rtA181V, 1.2% rtT184S, 6.2% rtV173L, 10.6% rtL180M, 10.6% rtM204V/I and 8.1% rtI233V. 2017 Antiviral therapy Abstract HBV L80F;L80I;A181V;T184S;V173L;L180M;M204V;M204I;I233V 127;127;142;156;170;185;200;200;219 133;133;147;161;175;190;207;207;224 RT;RT;RT;RT;RT;RT;RT 125;140;154;168;183;198;217 127;142;156;170;185;200;219 27381922 HBsAg mutations related to occult hepatitis B virus infection in HIV-positive patients result in a reduced secretion and conformational changes of HBsAg. We generated a series of expression constructs of variant HBsAg with "a" determinant amino acid substitutions including P127L, P127T, S136Y, and P127T + S136Y using site-directed mutagenesis. 2017 Journal of medical virology Abstract HBV P127L;P127T;S136Y;P127T;S136Y 120;127;134;145;153 125;132;139;150;158 S 58 63 27382800 Genetic diversity of hepatitis B virus and mutations associated to hepatocellular carcinoma in patients from Venezuela, with different stages of liver disease. Additionally, mutations were more common in early stages of liver disease in HBV subgenotype F2-infected patients, and a significant association between this subgenotype and the emergence of T 1753C, A1762T, A1762T/G1764A (p=0.04) and C1773T (p=0.001) mutations in chronic patients was found, when compared to the HBV subgenotype F3. 2016 Investigacion clinica Abstract HBV G1764A;T1753C;A1762T;A1762T;C1773T 215;191;200;208;235 221;198;206;214;241 Liver disease 60 73 27382800 Genetic diversity of hepatitis B virus and mutations associated to hepatocellular carcinoma in patients from Venezuela, with different stages of liver disease. By comparing F2 with all other HBV subgenotypes, a positive association for the three basal core promoter (BCP) mutants (A1762T, A1762T/G1764A p=0.01, G1764A p=0.04) was found. 2016 Investigacion clinica Abstract HBV G1764A;A1762T;A1762T;G1764A 136;121;129;151 142;127;135;157 BCP;BCP 86;107 105;110 27382800 Genetic diversity of hepatitis B virus and mutations associated to hepatocellular carcinoma in patients from Venezuela, with different stages of liver disease. The A1762T mutation was significantly associated with the advanced stage of liver disease (p=0.008). 2016 Investigacion clinica Abstract HBV A1762T 4 10 Liver disease 76 89 27386641 [Effect of Telbivudine Tablet Combined Jianpi Bushen Recipe on HBV Specific Cytotoxic T Lymphocyte and HBeAg Seroconversion in Patients with HBeAg Positive Chronic Hepatitis B]. rtM204I variation occurred in 1 case (2.22%) of the treatment group and 2 cases (4.44%) in the control group. 2016 Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi Abstract HBV M204I 2 7 RT 0 2 27402524 Hepatitis B Virus Infection in Indonesia 15 Years After Adoption of a Universal Infant Vaccination Program: Possible Impacts of Low Birth Dose Coverage and a Vaccine-Escape Mutant. Six samples (11.5%) had an amino acid substitution within the a determinant of the S gene region, and one sample had T140I that was suggested as a vaccine-escape mutant type. 2016 The American journal of tropical medicine and hygiene Abstract HBV T140I 117 122 S;S 62;83 75;84 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. HBx mutations (T1753V, A1762T, G1764A, and T1768A) are frequently observed in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). 2016 Cancer science Abstract HBV T1753V;A1762T;G1764A;T1768A 15;23;31;43 21;29;37;49 X 0 3 Hepatocellular carcinoma;Hepatocellular carcinoma 110;136 134;139 27422771 The relationship between HBcrAg and HBV reinfection in HBV related post-liver transplantation patients. Two HBV re-infected patients without HCC recurrence had HBs gene mutations G145R and G145A, respectively. 2017 Journal of gastroenterology Abstract HBV G145R;G145A 75;85 80;90 S 56 59 Hepatocellular carcinoma 37 40 27439498 Localization of immunodominant epitopes within the "a" determinant of hepatitis B surface antigen using monoclonal antibodies. The T123N mutation had the largest impact on antibody binding to HBsAg. 2016 Archives of virology Abstract HBV T123N 4 9 S 65 70 27446286 Association between clinical features and YMDD mutations in patients with chronic hepatitis B following lamivudine therapy. The turn of secondary protein structure of P gene changed to beta sheet when a rtM204V mutation occurred, and no change of secondary protein structure was associated with the rtL180M mutation. 2016 Experimental and therapeutic medicine Abstract HBV M204V;L180M 81;177 86;182 P;RT;RT 43;79;175 44;81;177 27446286 Association between clinical features and YMDD mutations in patients with chronic hepatitis B following lamivudine therapy. Two patients with rtM204V + rtL180M belonged to genotype C and another patient with rtL180M alone belonged to genotype D. 2016 Experimental and therapeutic medicine Abstract HBV M204V;L180M;L180M 20;30;86 25;35;91 RT;RT;RT 18;28;84 20;30;86 27458715 Molecular epidemiology of co-infection with hepatitis B virus and human immunodeficiency virus (HIV) among adult patients in Harare, Zimbabwe. PreS deletion mutants and small S antigen variants M133I/T and D144G were identified. 2017 Journal of medical virology Abstract HBV M133I;M133T;D144G 51;51;63 58;58;68 PreS;S 0;26 4;33 27473751 Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. However, in comparison to three other variants (FH_T1766C, FH_A1768T and FH_T1766C/A1768T) with wild-type nucleotide(s) at 1766 and/or 1768, the FH genome exhibited a 2.5-5-fold enhancement of viral replication by heightened pregenomic RNA synthesis and a 1.5-2.5-fold reduction in the hepatitis B e antigen (HBeAg) synthesis by the downregulation of the precore mRNA level. 2016 The Journal of general virology Abstract HBV A1768T;A1768T;T1766C 83;61;75 89;68;82 C;C;Precore 298;309;355 307;314;362 Fulminant Hepatitis B 145 147 27473751 Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. The present study demonstrates that the C1766T/T1768A mutations in the BCP region of genotype A HBV enhance viral replication, downregulate HBeAg expression and are responsible for the predominant localization of the core protein in the cytoplasm, which are likely associated with the development of fulminant hepatitis. 2016 The Journal of general virology Abstract HBV T1768A;C1766T 47;40 53;46 BCP;C;C 71;217;140 74;221;145 Fulminant Hepatitis B 300 319 27473751 Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. There were no discernible differences between FH and two variants (FH_A1742G and FH_C1809T) with regard to viral replication and protein expression. 2016 The Journal of general virology Abstract HBV A1742G;C1809T 69;83 76;90 Fulminant Hepatitis B 46 48 27473751 Enhanced pregenomic RNA levels and lowered precore mRNA transcription efficiency in a genotype A hepatitis B virus genome with C1766T and T1768A mutations obtained from a fulminant hepatitis patient. We recently found four unique mutations [G to A at nucleotide 1742 (G1742A), C1766T, T1768A and T1809C] in the basal core promoter (BCP) region of a genotype A hepatitis B virus (HBV) strain (FH) obtained from a 53-year-old man with fatal fulminant hepatitis. 2016 The Journal of general virology Abstract HBV G1742A;G1742A;T1768A;T1809C;C1766T 41;68;85;96;77 66;74;91;102;83 BCP;BCP 111;132 130;135 Fulminant Hepatitis B;Fulminant Hepatitis B 239;192 258;194 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. The pre-S1, pre-S2 and S region sequences in HCC tissue showed amino acid (AA) substitutions (F19L, P24L, S59F, T131I, Q129H) and deletions (in positions 4,8, 17 and 86) in the S region, AA substitutions (T40S, P124K, L54P, G76A, N222T and I273L) in pre-S1 region and AA substitutions in pre-S2 region (P41H and P66L). 2016 Oncotarget Abstract HBV F19L;P24L;S59F;T131I;Q129H;T40S;P124K;L54P;G76A;N222T;I273L;P41H;P66L 94;100;106;112;119;205;211;218;224;230;240;303;312 98;104;110;117;124;209;216;222;228;235;245;307;316 PreS1;PreS1;PreS2;PreS2;S;S 4;250;12;288;23;177 10;256;18;294;24;178 Hepatocellular carcinoma 45 48 27492206 Different Variants in Reverse Transcriptase Domain Determined by Ultra-deep Sequencing in Treatment-naive and Treated Indonesian Patients Infected with Hepatitis B Virus. The known rtM204I mutation was the most frequent in both groups. 2016 The Kobe journal of medical sciences Abstract HBV M204I 12 17 RT 10 12 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. T54N, L80I/V, I91L/V, L180M, M204I/V, Q215P/S, and F221Y/S showed the highest number of mutations in all groups with different frequencies. 2016 Electronic physician Abstract HBV T54N;L80I;L80V;I91L;I91V;L180M;M204I;M204V;Q215P;Q215S;F221Y;F221S 0;6;6;14;14;22;29;29;38;38;51;51 4;12;12;20;20;27;36;36;45;45;58;58 27525840 Identification of a mutation in Hepatitis B virus surface antigen capable of evading ELISA screening. DNA sequencing of the HBsAg region of this HBV mutant revealed two novel mutation sites that resulted in a Thr-to-Met substitution at amino acid (aa) position 118 and a Lys to Asn substitution at aa position 122 of HBsAg. 2016 Genetics and molecular research Abstract HBV K122N 169 211 S;S 22;215 27;220 27535046 DDB1 Stimulates Viral Transcription of Hepatitis B Virus via HBx-Independent Mechanisms. To gain further insight into the DDB1-HBx interaction, we generated HBx mutants deficient for DDB1 binding (i.e., R96A, L98A, and G99A) and examined whether they support HBx-stimulated viral DNA replication. 2016 Journal of virology Abstract HBV R96A;L98A;G99A 114;120;130 118;124;134 X;X;X 38;68;170 41;71;173 27535686 Detection of Anti-Hepatitis B Virus Drug Resistance Mutations Based on Multicolor Melting Curve Analysis. The two-reaction assay had a limit of detection of 5 copies per reaction and could detect a minor mutant population (5% of the total population) with the reverse transcriptase M204V amino acid mutation in the presence of the major wild-type population when the overall concentration was 104 copies/mul. 2016 Journal of clinical microbiology Abstract HBV M204V 176 181 RT 154 175 27538443 Management of Clevudine-Resistant Chronic Hepatitis B: A Multicenter Cohort Study. METHODS: Patients with CLV-resistant CHB were enrolled in the cohort, and all patients developed virologic breakthrough during CLV therapy and had confirmed-genotypic resistance to CLV (rtM204I mutation) before enrollment. 2017 Gut and liver Abstract HBV M204I 188 193 RT 186 188 27544241 Naturally Occurring Surface Antigen Variants of Hepatitis B Virus in Tunisian Patients. The global prevalence of the major hydrophilic region variants was 12.1%, with substitution S143L/T as the most frequent (4%). 2016 Intervirology Abstract HBV S143L;S143T 92;92 99;99 27581951 HBV/4DR 9G test and its comparison with INNO-LiPA HBV multi-DR test for the detection of drug-resistant Hepatitis B virus. The rtA181V, rtM204V/I, rtN236T and, rtM250V are high prevalent mutations found in the drug-resistant HBV strains. 2016 Journal of virological methods Abstract HBV A181V;M204V;M204I;N236T;M250V 6;15;15;26;39 11;22;22;31;44 RT;RT;RT;RT 4;13;24;37 6;15;26;39 27583985 Small surface antigen variants of HBV associated with responses to telbivudine treatment in chronic hepatitis B patients. CONCLUSIONS: Our findings suggest that the decrease in viral population heterogeneity at an early stage of LdT treatment was associated with the subsequent optimal virological response, and the early appearance of some specific mutations, such as sG44E, sW172* and sW182*, is a potential indicator of a partial virological response in continuing therapy. 2017 Antiviral therapy Abstract HBV G44E;W172X;W182X 247;254;265 252;260;271 S;S;S 247;254;265 248;255;266 27583985 Small surface antigen variants of HBV associated with responses to telbivudine treatment in chronic hepatitis B patients. RESULTS: Sequencing results revealed different dynamics of non-synonymous mutations, such as sL9P, sN40S, sG44E, sW172*, sW182* and sS187F, between patients with a complete virological response and those with a partial virological response. 2017 Antiviral therapy Abstract HBV L9P;N40S;G44E;W172X;W182X;S187F 93;99;106;113;121;132 97;104;111;119;127;138 S;S;S;S;S;S 93;99;106;113;121;132 94;100;107;114;122;133 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. The data showed different compensatory changes followed by the rtM204I/V. 2016 SpringerPlus Abstract HBV M204I;M204V 65;65 72;72 RT 63 65 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. and two patients (NOs.4 and 8) carrying the rtA181T resistance mutations increasingly showed high levels of rtN236T. 2016 Oncotarget Abstract HBV A181T;N236T 46;110 51;115 RT;RT 44;108 46;110 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. During treatment, the rtA181T resistance-associated site appeared with increasing frequency in six of eight patients (NOs. 2016 Oncotarget Abstract HBV A181T 24 29 RT 22 24 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In addition to the common substitutions, some previously unknown amino acid substitutions, such as rtD134N, rtL145M/S, rtF151Y/L, rtR153Q, and rtS223A, should be further studied. 2016 Oncotarget Abstract HBV D134N;L145M;L145S;F151Y;F151L;R153Q;S223A 101;110;110;121;121;132;145 106;117;117;128;128;137;150 RT;RT;RT;RT;RT 99;108;119;130;143 101;110;121;132;145 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Other known pre-existing mutations showed no dynamic fluctuations, including in rtA194T, rtP177G, rtF249A, and rtD263E. 2016 Oncotarget Abstract HBV A194T;P177G;F249A;D263E 82;91;100;113 87;96;105;118 RT;RT;RT;RT 80;89;98;111 82;91;100;113 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. RESULTS: At baseline, all 46 treatment-naive patients harbored rtA181V/T substitutions (1.2%-4.6%) and rtN236T substitutions (1.6%-6.1%). 2016 Oncotarget Abstract HBV A181V;A181T;N236T 65;65;105 72;72;110 RT;RT 63;103 65;105 27613286 Low prevalence of hepatitis B vaccine escape mutants among individuals born after the initiation of a nationwide vaccination program in Iran. An I195M mutation within the S gene was detected in two of the three HBV-DNA-positive cases. 2016 Archives of virology Abstract HBV I195M 3 8 S 29 30 27613286 Low prevalence of hepatitis B vaccine escape mutants among individuals born after the initiation of a nationwide vaccination program in Iran. The I195M mutation found in the surface gene could have been induced by immune pressure. 2016 Archives of virology Abstract HBV I195M 4 9 S 32 39 27624502 Hepatitis B virus infection in children of HBV-related chronic liver disease patients: a study of intra-familial HBV transmission. Recognized mutations associated with HBsAg detection and/or vaccination failure, T140I, T143S/M, G145R, and Y161F, were identified in 20 subjects; while mutations linked to HBeAg-defective variants, PC G1896A and BCP A1762T/G1764A, were found in 7 and 11 subjects, respectively. 2017 Hepatology international Abstract HBV G1764A;T140I;T143S;T143M;G145R;Y161F;G1896A;A1762T 224;81;88;88;97;108;202;217 230;86;95;95;102;113;208;223 BCP;C;S;Precore 213;173;37;199 216;178;42;201 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. After quantitative evaluations, the effects of the G145R mutation on the secondary and 3D structures of the HBsAg were investigated. 2016 Hepatitis monthly Abstract HBV G145R 51 56 S 108 113 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. It is now well established that the common G145R mutation is highly capable of escaping from HBsAg immune recognition. 2016 Hepatitis monthly Abstract HBV G145R 43 48 S 93 98 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. MATERIALS AND METHODS: Three-dimensional (3D) structure of HBsAg for both the wild-type and G145R mutant were predicted and refined using several web tools. 2016 Hepatitis monthly Abstract HBV G145R 92 97 S 59 64 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. OBJECTIVES: The present study analyzed the effects of the G145R mutation on the structure and immunogenic activity of the HBsAg. 2016 Hepatitis monthly Abstract HBV G145R 58 63 S 122 127 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. RESULTS: The G145R mutation causes a considerable reduction in the immunogenic activity of the HBsAg through a conformational change in the HBsAg antigenic loops. 2016 Hepatitis monthly Abstract HBV G145R 13 18 S;S 95;140 100;145 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The G145R mutation also increased the compactness and stability of the HBsAg by enhancing the rigidity of the "a" determinant. 2016 Hepatitis monthly Abstract HBV G145R 4 9 S 71 76 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Some mutations (e.g., sE2G, sL21S, sR24K, sT47A/K, sC69stop (sC69*), sL95W, sL98V, and sG145R) negatively correlated with serum HBsAg levels. 2017 Journal of hepatology Abstract HBV E2G;L21S;R24K;T47A;T47K;C69X;C69X;L95W;L98V;G145R 22;28;35;42;42;51;61;69;76;87 26;33;40;49;49;59;66;74;81;93 S;S;S;S;S;S;S;S;S;S 128;22;28;35;42;51;61;69;76;87 133;23;29;36;43;52;62;70;77;88 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Virion secretion could be rescued for sE2G, sC69*, and sG145R by co-expression of wild-type HBsAg. 2017 Journal of hepatology Abstract HBV E2G;C69X;G145R 38;44;55 42;49;61 S;S;S;S 92;38;44;55 97;39;45;56 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The most prevalent amino acids substitutions were R38K found in 14 (17.1 %) sequences, following by H44L in 11 (13.4 %), K13E in 8 (9.8 %), N29K in 8 (9.8 %), A35E in 8 (9.8 %), V80I in 7 (8.5 %) and in 6 (7.3 %) sequences for S90T. 2016 Infectious agents and cancer Abstract HBV H44L;R38K;K13E;N29K;A35E;V80I;S90T 100;50;121;140;159;178;227 104;54;125;144;163;182;231 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. A significant number of mutations (Thr118Val, Thr125Met, Thr126Ile, Pro127Thr, Ala128Val, Thr131Asn/Ser, Thr/Ser143Leu/Met) were found in 'a' determinant region which may admit resistance to the available vaccines and failure of HBsAg detection. 2016 SpringerPlus Abstract HBV T143L;T143M;S143L;S143M;T118V;T125M;T126I;P127T;A128V;T131N;T131S 105;105;105;105;35;46;57;68;79;90;90 122;122;122;122;44;55;66;77;88;103;103 S;S 139;229 153;234 27694733 Monitoring of genotypic resistance profile in chronic hepatitis B patients receiving nucleos(t)ide analogues in Huzhou, China. Among patients who harbored rtM204 combination mutations, rtM204I and rtM204V were significantly associated with rtL80I/V and rtL180M, respectively. 2016 Journal of infection in developing countries Abstract HBV M204I;M204V;L80I;L80V;L180M 60;72;115;115;128 65;77;121;121;133 RT;RT;RT;RT;RT 28;58;70;113;126 30;60;72;115;128 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. A total of 10 mutations (including pre-S2 start codon mutation and pre-S deletion in pre-S gene, G1613A, C1653T, A1762T, and G1764A mutations in X gene, A2159G, A2189Y, G2203W, and C2288R mutations in C gene) showed an increased risk of HCC. 2016 International journal of molecular sciences Abstract HBV A1762T;G1613A;C1653T;G1764A;A2159G;A2189Y;G2203W;C2288R 113;97;105;125;153;161;169;181 119;103;111;131;159;167;175;187 C;PreS;PreS;PreS2;X 201;67;85;35;145 202;72;90;41;146 Hepatocellular carcinoma 237 240 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. In the validation study, pre-S deletion, C1653T, A1762T/G1764A, A2159G, A2189Y, G2203W, and C2288R mutations were associated with increased HCC risk in univariate analysis. 2016 International journal of molecular sciences Abstract HBV G1764A;A1762T;C1653T;A2159G;A2189Y;G2203W;C2288R 56;49;41;64;72;80;92 62;55;47;70;78;86;98 PreS 25 30 Hepatocellular carcinoma 140 143 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Multivariate analysis indicated that pre-S deletion, A1762T/G1764A, A2159G, and A2189Y mutations were independently related with HCC development. 2016 International journal of molecular sciences Abstract HBV G1764A;A1762T;A2159G;A2189Y 60;53;68;80 66;59;74;86 PreS 37 42 Hepatocellular carcinoma 129 132 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. Escape mutations associated with failure of diagnosis (Y100C, R122K and Q129H) and with vaccine escape (Q129R and T131N) were detected in varying frequencies in the population. 2016 Virology journal Abstract HBV Y100C;R122K;Q129H;Q129R;T131N 55;62;72;104;114 60;67;77;109;119 27779207 HBV core promoter mutations and AKT upregulate S-phase kinase-associated protein 2 to promote postoperative hepatocellular carcinoma progression. Results showed double mutation A1762T/G1764A (TA) combined with other mutation(s) (TACO) in HBV genome and phosphorylated AKT (pAKT) were more common in PHCC than BHCC. 2016 Scientific reports Abstract HBV G1764A;A1762T 38;31 44;37 Hepatocellular carcinoma 163 167 27787680 Identification of a new hepatitis B virus recombinant D2/D3 in the city of Sao Paulo, Brazil. The precore/core mutations A1762T + G1764A (40.9%) were found mostly in genotypes A and D, and G1896A (29.55%) was more frequent in genotype D than in genotype A. 2017 Archives of virology Abstract HBV A1762T;G1764A;G1896A 27;36;95 33;42;101 C;Precore 12;4 16;11 27792585 Comparison of Detection Rate and Mutational Pattern of Drug-Resistant Mutations Between a Large Cohort of Genotype B and Genotype C Hepatitis B Virus-Infected Patients in North China. For adefovir-resistant mutations, HBV/C-infected patients had a higher detection rate of rtA181 V (HBV/C 5.29% vs. HBV/B 1.36%, p < 0.01) and a lower detection rate of rtN236T (2.70% vs. 6.54%, p < 0.01). 2017 Microbial drug resistance (Larchmont, N.Y.) Abstract HBV A181V;N236T 91;170 97;175 RT;RT 89;168 91;170 27792585 Comparison of Detection Rate and Mutational Pattern of Drug-Resistant Mutations Between a Large Cohort of Genotype B and Genotype C Hepatitis B Virus-Infected Patients in North China. For entecavir-resistant mutations, HBV/C-infected patients had a higher detection rate of rtM204 V/I+T184 substitution or S202G/C (3.66% vs. 2017 Microbial drug resistance (Larchmont, N.Y.) Abstract HBV S202G;S202C 122;122 129;129 RT 90 92 27792585 Comparison of Detection Rate and Mutational Pattern of Drug-Resistant Mutations Between a Large Cohort of Genotype B and Genotype C Hepatitis B Virus-Infected Patients in North China. For entecavir-resistant mutations, HBV/C-infected patients had a higher detection rate of rtM204 V/I+T184 substitution or S202G/C (3.66% vs. 2.16%, p < 0.01) and a lower detection rate of rtM204 V/I+M250 V/I/L substitution (0.67% vs. 1.46%, p < 0.01). 2017 Microbial drug resistance (Larchmont, N.Y.) Abstract HBV M204V;M204I;M204V;M204I;M250V;M250I;M250L 190;190;92;92;199;199;199 198;198;100;100;209;209;209 27808472 A novel hepatitis B virus subgenotype D10 circulating in Ethiopia. In addition, 63% genotype A and 33% genotype D strains had the basal core promoter mutations, A1762T/G1764A. 2017 Journal of viral hepatitis Abstract HBV G1764A;A1762T 101;94 107;100 BCP 63 82 27808472 A novel hepatitis B virus subgenotype D10 circulating in Ethiopia. Seventy-two per cent of the genotype D strains had the precore premature stop codon G1896A. 2017 Journal of viral hepatitis Abstract HBV G1896A 84 90 Precore 55 62 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. G145R was detected in one-fourth of the children with immunoprophylaxis failure. 2016 PloS one Abstract HBV G145R 0 5 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. HBeAg-positive patients were prone to have the G145R mutant as a minor population. 2016 PloS one Abstract HBV G145R 47 52 C 0 5 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, the pre-existence of the G145R mutant as a minor population in pregnant women does not always cause breakthrough infection in infants. 2016 PloS one Abstract HBV G145R 34 39 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In the breakthrough cohort, the frequency of the G145R mutant ranged from 0.54% to 6.58%. 2016 PloS one Abstract HBV G145R 49 54 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In the control cohort, the frequency of the G145R mutant ranged from 0.42% to 4.1%. 2016 PloS one Abstract HBV G145R 44 49 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The minor strain as well as the major strain of the G145R mutant were evaluated in three cohorts using a locked nucleic acid probe-based real-time PCR. 2016 PloS one Abstract HBV G145R 52 57 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The role of the hepatitis B virus (HBV) mutant G145R, with a single change in amino acid 145 of the surface protein, as a minor population remains unknown in mother-to-child transmission. 2016 PloS one Abstract HBV G145R 47 52 S 100 107 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Three babies born to 3 pregnant women with the G145R mutant were evaluated. 2016 PloS one Abstract HBV G145R 47 52 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. Nucleotide substitution rates were also higher within the medium/low MBL2 production group in all positions described to have an influence in liver cancer development, except for A1499G. 2016 Aging Abstract HBV A1499G 179 185 Hepatocellular carcinoma 142 154 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S-escape mutant, G145R, was not discovered. 2016 PloS one Abstract HBV G145R 17 22 S 0 1 27871021 Stop codons in the hepatitis B surface proteins are enriched during antiviral therapy and are associated with host cell apoptosis. Cell lines were transfected with infectious HBV clones encoding surface stop codons rtM204I/sW196*, rtA181T/sW172*, rtV191I/sW182*, and a panel of substitutions in the surface proteins. 2017 Virology Abstract HBV W196X;W172X;W182X;M204I;A181T;V191I 92;108;124;86;102;118 98;114;130;91;107;123 RT;RT;RT;S;S;S;S;S 84;100;116;92;108;124;64;168 86;102;118;93;109;125;71;175 27871021 Stop codons in the hepatitis B surface proteins are enriched during antiviral therapy and are associated with host cell apoptosis. The most cytopathic variant was rtM204I/sW196*. 2017 Virology Abstract HBV W196X;M204I 40;34 46;39 RT;S 32;40 34;41 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. METHODS: This study was based on the analysis of the specific observation of HBV subgenotype A1 in the serum/plasma, while subgenotype A2 with G145R mutation in the peripheral blood leukocytes (PBLs). 2016 World journal of virology Abstract HBV G145R 143 148 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. In the RT gene, Q149K was the most frequently identified amino acid substitution (9.83%), followed by L122F (8.19%), N118D/T (6.55%), L157M (4.91%), and H124Y (3.27%). 2016 Hepatitis monthly Abstract HBV Q149K;L122F;N118D;N118T;L157M;H124Y 16;102;117;117;134;153 21;107;124;124;139;158 RT 7 9 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The most amino acid substitutions of surface protein were Q129H (34.42%) and A168V (8.2%), other escape mutants observed in this study were P127L/T, S117G, T125M, S143L, D144E and E164D. 2016 Hepatitis monthly Abstract HBV Q129H;A168V;P127L;P127T;S117G;T125M;S143L;D144E;E164D 58;77;140;140;149;156;163;170;180 63;82;147;147;154;161;168;175;185 S 37 44 27882070 Serological Patterns and Molecular Characterization of Occult Hepatitis B Virus Infection among Blood Donors. Mutations in the S region of HBV DNA included S114T, G119R, P120S, T125M, C139Y, T140I, C147W, T148A, A159V/G, E164D, V168A, and R169C. 2016 Hepatitis monthly Abstract HBV S114T;G119R;P120S;T125M;C139Y;T140I;C147W;T148A;A159V;A159G;E164D;V168A;R169C 46;53;60;67;74;81;88;95;102;102;111;118;129 51;58;65;72;79;86;93;100;109;109;116;123;134 S 17 18 27894395 Relationship between hepatitis B virus reverse transcriptase 181 mutation and S gene mutation in hepatitis B virus chronically infected patients. Among 25 containing rtA181T/V mutation patients, 7 rtA181T mutation cases with sW172L, 6 rtA181T mutation cases with sW172*, 12 rtA181Vmutation cases with sL173F. 2016 Cellular and molecular biology (Noisy-le-Grand, France) Abstract HBV A181T;A181T;A181V;A181T;A181V;W172L;W172X;L173F 91;22;22;53;130;79;117;155 96;29;29;58;135;85;123;161 RT;RT;RT;RT;S;S;S 20;51;89;128;79;117;155 22;53;91;130;80;118;156 27894395 Relationship between hepatitis B virus reverse transcriptase 181 mutation and S gene mutation in hepatitis B virus chronically infected patients. Mutation sites of pre-existing and adefovir dipivoxil induced resistance were different (adefovir dipivoxil induced resistance mode is rtA181T/V, and pre-existing mode is the other). 2016 Cellular and molecular biology (Noisy-le-Grand, France) Abstract HBV A181T;A181V 137;137 144;144 RT 135 137 27894395 Relationship between hepatitis B virus reverse transcriptase 181 mutation and S gene mutation in hepatitis B virus chronically infected patients. rtA181T mutation was accompanied with not only sW172 * mutation, but also sW172L mutation, rtA181V mutation was accompanied with sL173F mutation or Pre-S2 initiation codon to termination mutation. 2016 Cellular and molecular biology (Noisy-le-Grand, France) Abstract HBV A181T;A181V;W172X;W172L;L173F 2;93;47;74;129 7;98;54;80;135 PreS2;RT;RT;S;S;S 148;0;91;47;74;129 154;2;93;48;75;130 27908829 Exploring the binding mechanism of Heteroaryldihydropyrimidines and Hepatitis B Virus capsid combined 3D-QSAR and molecular dynamics. The computational results disclose that the non-polar contribution is the major driving force and Y132A mutation enhances the binding affinity for inhibitor 2 bound to HBV. 2017 Antiviral research Abstract HBV Y132A 98 103 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Combined analysis of complimentary DNA microarray and microRNA array identified microRNA-873-mediated reduced expression of the CUB and Sushi multiple domains 3 (CSMD3) protein, a putative tumor suppressor, in TgSW172* mice. 2016 Oncogenesis Abstract HBV W172X 212 218 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Hepatitis B virus (HBV) carrying the rtA181T/sW172* mutation conferred cross-resistance to adefovir and lamivudine. 2016 Oncogenesis Abstract HBV W172X;A181T 45;39 51;44 RT;S 37;45 39;46 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Higher proportion of apoptotic cells was found in TgSW172*-H mice, accompanied by increased cyclin E levels, suggesting increased hepatocyte turnover. 2016 Oncogenesis Abstract HBV W172X 52 58 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Molecular analysis of liver tissues revealed significantly increased expression of glucose-regulated protein 78 and phosphorylated extracellular signal-regulated kinases 1 in TgSW172* mice, and decreased expression of B-cell lymphoma-extra large in TgSW172*-H mice. 2016 Oncogenesis Abstract HBV W172X;W172X 177;251 183;257 B cell lymphoma 218 233 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Our transgenic mice experiments confirmed that HBV pre-S/S gene carrying the sW172* mutation had an increased oncogenic potential. 2016 Oncogenesis Abstract HBV W172X 77 83 PreS;S;S 51;57;77 56;58;78 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. The other two carried the sW172* mutation with high and low intrahepatic expression levels (TgSW172*-H and L). 2016 Oncogenesis Abstract HBV W172X;W172X 26;94 32;100 S 26 27 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. When sacrificed 18 months after birth, none of the TgWT mice developed hepatocellular carcinoma (HCC), whereas 6/26 (23.1%) TgSW172*-H and 2/24 (8.3%) TgSW172*-L mice developed HCC (TgWT vs TgSW172*; P=0.0021). 2016 Oncogenesis Abstract HBV W172X;W172X;W172X 126;153;192 132;159;198 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 71;97;177 95;100;180 27919846 Nucleos(t)ide analogues causes HBV S gene mutations and carcinogenesis. DATA SOURCES: PubMed and Web of Science were searched using terms: "hepatitis B virus", "HBV drug resistance mutation", "HBV surface protein", "HBV truncation", "hepatocellular carcinoma", "rtA181T/sW172*", "rtM204I/sW196*", "rtV191I/sW182*", and relevant articles published in English in the past decades were reviewed. 2016 Hepatobiliary & pancreatic diseases international Abstract HBV W172X;W196X;W182X;A181T;M204I;V191I 198;216;234;192;210;228 204;222;240;197;215;233 RT;RT;RT;S;S;S;S 190;208;226;198;216;234;125 192;210;228;199;217;235;132 Hepatocellular carcinoma 162 186 27919846 Nucleos(t)ide analogues causes HBV S gene mutations and carcinogenesis. RESULTS: The rtA181T/sW172* and rtV191I/sW182* mutants occurred more frequently than the rtM204I/sW196* mutant both in chronic hepatitis B patients and the HBV-related hepatocellular carcinoma tissues. 2016 Hepatobiliary & pancreatic diseases international Abstract HBV W172X;W182X;W196X;A181T;V191I;M204I 21;40;97;15;34;91 27;46;103;20;39;96 RT;RT;RT;S;S;S 13;32;89;21;40;97 15;34;91;22;41;98 Chronic Hepatitis B;Hepatocellular carcinoma 119;168 138;192 27919846 Nucleos(t)ide analogues causes HBV S gene mutations and carcinogenesis. The rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182* are the most frequently reported drug-resistant mutations with C-terminal truncation, these mutations have oncogenic potential. 2016 Hepatobiliary & pancreatic diseases international Abstract HBV W172X;W196X;W182X;A181T;M204I;V191I 12;28;47;6;22;41 18;34;53;11;27;46 RT;RT;RT;S;S;S 4;20;39;12;28;47 6;22;41;13;29;48 27920641 Severe de novo Hepatitis B Recovered from Late-Onset Liver Insufficiency with Prolonged Ascites and Hypoalbuminemia due to Hepatitis B Virus Genotype Bj with Precore Mutation. An immediate and sufficient suppression of virus replication with potent antiviral therapy is critical, particularly in patients infected with HBV precore mutation (G1896A) and/or Bj genotype, which may have a high viral replication and direct hepatocellular damage. 2016 Case reports in gastroenterology Abstract HBV G1896A 165 171 Precore 147 154 27920641 Severe de novo Hepatitis B Recovered from Late-Onset Liver Insufficiency with Prolonged Ascites and Hypoalbuminemia due to Hepatitis B Virus Genotype Bj with Precore Mutation. Hepatitis B virus (HBV) isolated from the patient was of genotype Bj, with a precore mutation (G1896A) exhibiting an extremely high viral load at the onset of hepatitis. 2016 Case reports in gastroenterology Abstract HBV G1896A 95 101 Precore 77 84 Hepatitis 159 168 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As the polymerase gene completely overlaps with the envelope (S) gene, HBV rtA181T mutation also carries sW172 mutations. 2016 Scientific reports Abstract HBV A181T 77 82 S;P;RT;S;S 52;7;75;62;105 60;17;77;63;106 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Compared with wild-type strains, there were intracellular accumulations of HBsAg and HBcAg in rtA181/sW172* but none in rtA181/sW172L mutant strains. 2016 Scientific reports Abstract HBV W172X;W172L 101;127 107;133 C;S;RT;RT;S;S 85;75;94;120;101;127 90;80;96;122;102;128 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In animal experiments, we were amazed to find that viral replication in rtA181T/sW172* mutant increased and maintained significantly longer than that in rtA181T/sW172L mutant, while no significant difference was observed between rtA181T/sW172L and wild-type strains. 2016 Scientific reports Abstract HBV W172X;W172L;W172L;A181T;A181T;A181T 80;161;237;74;155;231 86;167;243;79;160;236 RT;RT;RT;S;S;S 72;153;229;80;161;237 74;155;231;81;162;238 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In cell experiments, a slight decline of viral replication was observed in both two mutants as compared to wild-type strains, but the levels of supernatant HBsAg and HBV DNA in rtA181T/sW172* were significantly lower than those in rtA181T/sW172L transfected cells. 2016 Scientific reports Abstract HBV W172X;W172L;A181T;A181T 185;239;179;233 191;245;184;238 S;RT;RT;S;S 156;177;231;185;239 161;179;233;186;240 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In summary, the characteristics of above two rtA181T mutants mentioned above were significantly different, and it is necessary and important for us to distinguish sW172* truncated mutation from sW172L substituted mutation. 2016 Scientific reports Abstract HBV A181T;W172X;W172L 47;163;194 52;169;200 RT;S;S 45;163;194 47;164;195 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In this study, we investigated whether there were biological differences between rtA181T/sW172* (coding truncated HBsAg) and rtA181T/sW172L (coding substituted HBsAg) mutants. 2016 Scientific reports Abstract HBV W172X;W172L;A181T;A181T 89;133;83;127 95;139;88;132 S;S;RT;RT;S;S 114;160;81;125;89;133 119;165;83;127;90;134 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The hepatitis B virus(HBV) polymerase rtA181T mutation is selected during long-term antiviral therapy. 2016 Scientific reports Abstract HBV A181T 40 45 RT;P 38;27 40;37 27998385 Hepatitis B Immunoprophylactic Failure and Characteristics of the Hepatitis B Virus Gene in Mother-Infant Pairs in Parts of China. The frequency of amino acid mutation of the 'a' determinant region was 16.67% (5/30), including that of Q129H, F134Y, S136Y, and G145E. 2016 Biomedical and environmental sciences Abstract HBV Q129H;F134Y;S136Y;G145E 104;111;118;129 109;116;123;134 S 45 59 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. CONCLUSIONS: In patients with CHB, measurement of I97L and additional mutation P79Q would be useful for predicting persistent low HBV DNA, normal ALT, and HBsAg clearance. 2017 Clinical microbiology and infection Abstract HBV I97L;P79Q 50;79 54;83 S 155 160 Chronic Hepatitis B 30 33 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. Cumulative incidences of persistent low HBV DNA and HBsAg clearance were significantly higher in patients with I97L than in those with wild-type I97 (p = 0.003 and p = 0.016, respectively), and even higher in those with P79Q. 2017 Clinical microbiology and infection Abstract HBV I97L;P79Q 111;220 115;224 S 52 57 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. RESULTS: Incidence of Core mutation I97L differed significantly among groups: A, 30% (3/10); B, 36.4% (4/11); C, 83.3% (10/12) (p = 0.021). 2017 Clinical microbiology and infection Abstract HBV I97L 36 40 C 22 26 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. Subsequently, 82 patients with CHB were evaluated for the I97L mutation and the additional mutation P79Q. 2017 Clinical microbiology and infection Abstract HBV I97L;P79Q 58;100 62;104 Chronic Hepatitis B 31 34 27998820 Core I97L mutation in conjunction with P79Q is associated with persistent low HBV DNA and HBs antigen clearance in patients with chronic hepatitis B. We compared cumulative incidences of persistent low HBV DNA and HBsAg clearance in patients with or without I97L and P79Q by the Kaplan-Meier method. 2017 Clinical microbiology and infection Abstract HBV I97L;P79Q 108;117 112;121 S 64 69 28017671 Analysis of the prevalence of drug-resistant hepatitis B virus in patients with antiviral therapy failure in a Chinese tertiary referral liver centre (2010-2014). and genotype C isolates had a significantly higher A181V/T incidence than genotype B (54.9% vs. 2017 Journal of global antimicrobial resistance Abstract HBV A181V;A181T 51;51 58;58 28017671 Analysis of the prevalence of drug-resistant hepatitis B virus in patients with antiviral therapy failure in a Chinese tertiary referral liver centre (2010-2014). M204I, N236T and L180M+M204V+V173L/S202G were the most common substitutions for l-nucleoside (3TC and LdT), ADV and ETV genotypic resistant phenotypes, respectively. 2017 Journal of global antimicrobial resistance Abstract HBV S202G;M204I;N236T;L180M;M204V;V173L 35;0;7;17;23;29 40;5;12;22;28;34 28017671 Analysis of the prevalence of drug-resistant hepatitis B virus in patients with antiviral therapy failure in a Chinese tertiary referral liver centre (2010-2014). N236T incidence in genotype B was significantly higher than in genotype C (43.2% vs. 2017 Journal of global antimicrobial resistance Abstract HBV N236T 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. In addition, ELISA revealed reduced HBs antigenicity of two mutants, W1S N146G and W1S Q129R/G145R. 2017 PloS one Abstract HBV G145R;N146G;Q129R;W1S;W1S 93;73;87;69;83 98;78;92;72;86 S 36 39 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. On the other hand, the single mutants of W1S, P120K and T123D, significantly impaired the reactivity, while W1S-aW3S and the double mutant of W1S, P120K/T123D, resulted in a complete loss of antigenicity. 2017 PloS one Abstract HBV T123D;T123D;P120K;W1S;P120K;W1S;W1S 153;56;147;41;46;108;142 158;61;152;44;51;111;145 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Using the same commercial immunoassay kit, we found that the single mutants, K120P and D123T, were marginally reactive, whereas W3S-aW1S and the double mutant, K120P/D123T, exhibited antigenicity roughly equivalent to the wild-type wako1S. 2017 PloS one Abstract HBV D123T;D123T;K120P;K120P;W3S 166;87;160;77;128 171;92;165;82;131 28088502 The nucleotide changes within HBV core promoter/precore during the first 12weeks of nucleos(t)ide treatment might be associated with a better virological response. The mutation rates of A1762T/G1764A and G1896A were found to decrease from 46.2% (24/52) at baseline to 36.5% (19/52) at week 12 (P=0.426) and from 28.8% (15/52) to 21.2% (11/52) (P=0.497), respectively. 2017 Infection, genetics and evolution Abstract HBV G1764A;A1762T;G1896A 29;22;40 35;28;46 28103819 Telbivudine versus entecavir in patients with undetectable hepatitis B virus DNA: a randomized trial. Seven patients (14.9%) exhibited genotypic resistance mutations (M204I +/- L180M) during the virologic breakthrough. 2017 BMC gastroenterology Abstract HBV M204I;L180M 65;75 70;80 28124958 [Atypical serological profiles in hepatitis B infections: investigation of S gene mutations in cases with concurrently positive for HBsAg and anti-HBs]. Sequence analysis of seven samples showed S gene mutations in two samples, one was sS143L with sS193L, a HBV vaccine escape mutation, and the other was sP120R, a HBV immune escape mutation. 2016 Mikrobiyoloji bulteni Abstract HBV S143L;S193L;P120R 83;95;152 89;101;158 S;S;S;S 42;83;95;152 43;84;96;153 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. Mutations: rtM204V (39.3%), M204V+L180M (10.7%) while rtA181V (8.1%) and rtN236T (8.3%) were observed with LAM and ADV regimen, respectively. 2016 The Indian journal of medical research Abstract HBV M204V;A181V;N236T;M204V;L180M 13;56;75;28;34 18;61;80;33;39 RT;RT;RT 11;54;73 13;56;75 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Additionally, S210R increased the percentage of cells in G2/M-phase (26+-8% for wt versus 33+-6% for S210R, P <0.001). 2017 Oncotarget Abstract HBV S210R;S210R 14;101 19;106 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Furthermore, P203Q and P203Q+S210R increased the percentage of cells in S-phase compared to wt, indicating cell-cycle progression (P203Q:26+-13%; P203Q+S210R:29+-14%; wt:18%+-9, P <0.01. 2017 Oncotarget Abstract HBV P203Q;P203Q;S210R;P203Q;P203Q;S210R 13;23;29;131;146;152 18;28;34;136;151;157 S 72 73 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In in-vitro experiments, P203Q, S210R and P203Q+S210R significantly reduced the ratio [secreted/intracellular HBsAg] compared to wt at each time-point analysed (P <0.05), supporting an impaired HBsAg-secretion. 2017 Oncotarget Abstract HBV P203Q;S210R;P203Q;S210R 25;32;42;48 30;37;47;53 S;S 110;194 115;199 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. RESULTS: Two HBsAg mutations significantly correlated with HCC: P203Q (17.4% [4/23] in HCC vs 1.0% [1/105] in non-HCC, P=0.004); S210R (34.8% [8/23] in HCC vs 3.8% [4/105] in non-HCC, P <0.001); P203Q+S210R (17.4% [4/23] in HCC vs 0% [0/110] in non-HCC, P=0.001). 2017 Oncotarget Abstract HBV P203Q;S210R;P203Q;S210R 64;129;195;201 69;134;200;206 S 13 18 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 59;87;152;224;114;179;249 62;90;155;227;117;182;252 28198078 Mutation in the S gene of hepatitis B virus and anti-HBs subtype-nonspecificity contributed to the co-existence of HBsAg and anti-HBs in patients with chronic hepatitis B virus infection. Besides, some HBsAg variations in group I patients, sG145R mutation, inserted mutations, and continuous aa mutations within the major hydrophilic region (MHR), decreased the neutralized capacity of anti-HBs from HBV vaccinated persons. 2017 Journal of medical virology Abstract HBV G145R 52 58 S;S;S 203;14;52 206;19;53 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. In contrast, mutations at positions in close contact with HAP-specific groups (P25A, P25S, or V124F) only reduce susceptibility to HAP_R01, but not to SBA_R01. 2017 Scientific reports Abstract HBV P25A;P25S;V124F 79;85;94 83;89;99 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Interestingly, two reference compounds HAP_R01 and SBA_R01 bind to the same pocket at the dimer-dimer interface in the crystal structures of core protein Y132A hexamer. 2017 Scientific reports Abstract HBV Y132A 154 159 C 141 145 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Notably, P25S and V124F substitutions exist in low-abundance quasispecies in treatment-naive patients, suggesting potential clinical relevance. 2017 Scientific reports Abstract HBV P25S;V124F 9;18 13;23 28236303 Characterization of hepatitis B virus (HBV) preS/S gene mutations in blood donors with occult HBV infection in the Baoji area of North China. Specifically, the incidence of five OBI-related major hydrophilic region mutations (sS117T, sT118K, sT131N, sT134Y/L, and sD144E) was significantly higher in blood donors with OBI than in controls. 2017 Transfusion Abstract HBV S117T;T118K;T131N;T134Y;T134L;D144E 84;92;100;108;108;122 90;98;106;116;116;128 S;S;S;S;S 84;92;100;108;122 85;93;101;109;123 Occult Hepatitis B;Occult Hepatitis B 36;176 39;179 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. G1896A nonsense mutation promoted more efficient core protein expression than mutated precore ATG, while a +1 frameshift mutation was ineffective. 2017 Virology Abstract HBV G1896A 0 6 C;Precore 49;86 53;93 28300730 The enrichment of HBV immune-escape mutations during nucleoside/nucleotide analogue therapy. Except for the combination of sP120T+sA128V, other double combinations (n=11) were only detected in the NA treatment group, and nine of these combinations in the treatment group were detected in HBV variants without antiviral resistance mutations. 2017 Antiviral therapy Abstract HBV P120T;A128V 30;37 36;43 S;S 30;37 31;38 28300730 The enrichment of HBV immune-escape mutations during nucleoside/nucleotide analogue therapy. RESULTS: A total of 97 patients in the NA treatment group had resistance mutations, with rtM204I/V/S being the most common substitution (78 of 97), while no resistance mutations were detected in the treatment-naive group. 2017 Antiviral therapy Abstract HBV M204I;M204V;M204S 91;91;91 100;100;100 RT 89 91 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Significantly high frequencies of 6 S-substitutions and one novel RT-substitution, rtH124N with 6.5-fold-reduced susceptibility to TDF in vitro, were noted at baseline in TDF non-responders than responders. 2017 Scientific reports Abstract HBV H124N 85 90 RT;RT 66;83 68;85 28316253 Predominance of Hepatitis B Virus Genotype A Among Treated HIV Infected Patients Experiencing High Hepatitis B Virus Drug Resistance in Nairobi, Kenya. Five subjects had rtV173L, rtL180M, and rtM204V and one with rtL180M and rtM204V major mutations. 2017 AIDS research and human retroviruses Abstract HBV V173L;L180M;M204V;L180M;M204V 20;29;42;63;75 25;34;47;68;80 RT;RT;RT;RT;RT 18;27;40;61;73 20;29;42;63;75 28322924 Evolutionary trends of resistance mutational patterns of HBV reverse transcriptase over years (2002-2012) of different treatment regimens: The legacy of lamivudine/adefovir combination treatment. Furthermore, the study allows a better understanding of how viral genotype (A vs D) conditions specific mutational pathways to resistance against lamivudine and entecavir, and demonstrates that the use of adefovir in lamivudine experienced patients is associated to peculiar mutational patterns, in particular A181V + F/Y221L. 2017 Antiviral research Abstract HBV Y221L;F221L;A181V 318;318;310 325;325;315 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Amino-acid (aa) substitution from glycine to arginine at aa 145 (G145R), in the major hydrophilic region, has been reported in patients with HBsAg and anti-HBs coexistence. 2017 Emerging microbes & infections Abstract HBV G145R;G145R 34;65 63;70 S;S 156;141 159;146 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. However, there is limited knowledge about the clinical features and viral quasispecies characteristics associated with G145R mutant hepatitis B virus (HBV) infection. 2017 Emerging microbes & infections Abstract HBV G145R 119 124 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Moreover, the frequencies of mutations (L173P, Q181R and A184V) in cytotoxic T lymphocyte epitopes increased before entecavir treatment. 2017 Emerging microbes & infections Abstract HBV L173P;Q181R;A184V 40;47;57 45;52;62 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. The quasispecies characteristics of the G145R mutant HBV were investigated via ultra-deep sequencing. 2017 Emerging microbes & infections Abstract HBV G145R 40 45 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. We herein describe the dynamic changes in the serological and virological markers in a case of hepatitis B with coexisting HBsAg and anti-HBs, caused by a G145R immune escape mutant (genotype C). 2017 Emerging microbes & infections Abstract HBV G145R 155 160 S;S 138;123 141;128 28332360 Entecavir to Telbivudine Switch Therapy in Entecavir-Treated Patients with Undetectable Hepatitis B Viral DNA. All subjects with virological rebound (n=5) showed drug-resistant mutation: three had mutation rtM204I, and two had mutation rtM204V. 2017 Yonsei medical journal Abstract HBV M204I;M204V 97;127 102;132 RT;RT 95;125 97;127 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. A mutation on D114E was simultaneously detected. 2017 Yonsei medical journal Abstract HBV D114E 14 19 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Among them, three mutations, S114T, P127S/T, M133T, were detected in common. 2017 Yonsei medical journal Abstract HBV S114T;P127S;P127T;M133T 29;36;36;45 34;43;43;50 28339094 F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. As a result, rtF221Y was identified as a risk factor for poor prognosis and may be a potential viral marker for predicting prognosis in HCC. 2017 Molecular medicine reports Abstract HBV F221Y 15 20 RT 13 15 Hepatocellular carcinoma 136 139 28339094 F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. rtF221Y was also an independent risk factor for poor overall survival rates (HR=2.557; 95% CI, 1.344-4.866; P=0.004). 2017 Molecular medicine reports Abstract HBV F221Y 2 7 RT 0 2 28339094 F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. The mutation of R122 K in the HBV S protein was closely associated with tumor recurrence (P<0.001). 2017 Molecular medicine reports Abstract HBV R122K 16 22 S 34 35 28339094 F221Y mutation in hepatitis B virus reverse transcriptase is associated with hepatocellular carcinoma prognosis following liver resection. The rtF221Y variation and a tumor size >8 cm were found to be independent risk factors for the postoperative recurrence of HCC, with hazard ratios of 2.345 (95% CI, 1.391-3.953; P=0.001) and 1.838 (95% CI, 1.069-3.161; P=0.028), respectively. 2017 Molecular medicine reports Abstract HBV F221Y 6 11 RT 4 6 Hepatocellular carcinoma 123 126 28339215 Discovery and Pre-Clinical Characterization of Third-Generation 4-H Heteroaryldihydropyrimidine (HAP) Analogues as Hepatitis B Virus (HBV) Capsid Inhibitors. X-ray crystallographic study of analogue 12 (HAP_R01) with Cp149 Y132A mutant hexamer clearly elucidated the role of C6 carboxyl group played for the increased binding affinity, which formed strong hydrogen bonding interactions with capsid protein and coordinated waters. 2017 Journal of medicinal chemistry Abstract HBV Y132A 65 70 Capsid;C 233;59 239;61 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. While A1762T/G1764A core promoter mutations were highly prevalent in both groups, the G1896A precore mutation to abolish hepatitis B e antigen (HBeAg) expression was more common in HCC clones (55% vs. 2017 Virus research Abstract HBV G1764A;A1762T;G1896A 13;6;86 19;12;92 Core promoter;C;C;Precore 20;133;144;93 33;142;149;100 Hepatocellular carcinoma 181 184 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. We identified BCP A1762T/G1764A in 15/35 (43%), PC G1896A in 20/35 (57%), 'a' determinant mutations in 12/45 (26.7%) and preS2 deletions in 6/16 (37.5%). 2017 Tropical medicine & international health Abstract HBV G1764A;A1762T;G1896A 25;18;51 31;24;57 S;BCP;Precore;PreS2 75;14;48;121 89;17;50;126 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. CONCLUSIONS: The results of the present study suggested that ETV is efficient in rescuing rtA181T/V mutation CHB patients. 2017 Virology journal Abstract HBV A181T;A181V 92;92 99;99 RT 90 92 Chronic Hepatitis B 109 112 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Data is limited on the efficacy of entecavir (ETV) rescuing chronic hepatitis B (CHB) patients with rtA181T/V mutation. 2017 Virology journal Abstract HBV A181T;A181V 102;102 109;109 RT 100 102 Chronic Hepatitis B;Chronic Hepatitis B 60;81 79;84 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. METHODS: Thirty-one patients with rtA181T/V mutation and 25 patients with rtA181T/V and rtN236T mutation were enrolled. 2017 Virology journal Abstract HBV A181T;A181V;A181T;A181V;N236T 36;36;76;76;90 43;43;83;83;95 RT;RT;RT 34;74;88 36;76;90 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. No significant difference in baseline characteristics was observed between the rtA181T/V group and rtA181T/V + rtN236T group. 2017 Virology journal Abstract HBV A181T;A181V;A181T;A181V;N236T 81;81;101;101;113 88;88;108;108;118 RT;RT;RT 79;99;111 81;101;113 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. RESULTS: After emergence of rtA181T/V mutant, serum HBV DNA levels increased over 4 log10 IU/mL, but the total bilirubin, alanine aminotransferase (ALT) levels raised moderately. 2017 Virology journal Abstract HBV A181T;A181V 30;30 37;37 RT 28 30 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. The mean HBV DNA reduction, HBsAg and ALT levels were also similar between different rtA181T/sW172 mutations (P > 0.05). 2017 Virology journal Abstract HBV A181T 87 92 S;RT;S 28;85;93 33;87;94 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Virological, serological and biochemical outcomes of ETV rescue therapy over 12 months in CHB patients with rtA181T/V mutation strains were investigated. 2017 Virology journal Abstract HBV A181T;A181V 110;110 117;117 RT 108 110 Chronic Hepatitis B 90 93 28381384 Novel HBV mutations and their value in predicting efficacy of conventional interferon. CONCLUSIONS: PC-P159T (ntC2288A), BCP-N118T (ntA1726C), BCP-L134L (ntA1775C/G/T), PC-G182C (ntG2357T) and PC-S64A/T (ntT2003G/A) were novel identified mutations that impacted IFN therapeutic efficacy. 2017 Hepatobiliary & pancreatic diseases international Abstract HBV C2288A;A1726C;A1775C;A1775G;A1775T;G2357T;T2003G;T2003A;P159T;N118T;L134L;G182C;S64A;S64T 24;46;68;68;68;93;118;118;16;38;60;85;109;109 31;53;79;79;79;100;127;127;21;43;65;90;115;115 BCP;BCP;Precore;Precore;Precore 34;56;13;82;106 37;59;15;84;108 28381384 Novel HBV mutations and their value in predicting efficacy of conventional interferon. Multivariate logistic regression analysis showed that baseline DNA, PC-P159T (ntC2288A), BCP-N118T (ntA1726C) and BCP-L134L (ntA1775C/G/T) influenced VR independently. 2017 Hepatobiliary & pancreatic diseases international Abstract HBV C2288A;A1726C;A1775C;A1775G;A1775T;P159T;N118T;L134L 79;101;126;126;126;71;93;118 86;108;137;137;137;76;98;123 BCP;BCP;Precore 89;114;68 92;117;70 28381384 Novel HBV mutations and their value in predicting efficacy of conventional interferon. PC-G182C (ntG2357T), PC-S64A/T (ntT2003G/A) and BMI were independent influence factors for HBeAg clearance, HBeAg seroconversion and BR, respectively. 2017 Hepatobiliary & pancreatic diseases international Abstract HBV G2357T;T2003G;T2003A;G182C;S64A;S64T 11;33;33;3;24;24 18;42;42;8;30;30 C;C;Precore;Precore 91;108;0;21 96;113;2;23 28381384 Novel HBV mutations and their value in predicting efficacy of conventional interferon. PC-W28STOP (ntG1896A) was significantly higher in the combined response (CR) group than that in the no CR group (91.7% vs 39.7%, P=0.001). 2017 Hepatobiliary & pancreatic diseases international Abstract HBV W28X;G1896A 3;13 10;20 Precore 0 2 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. CONCLUSIONS: The rtS78T/sC69* HBV mutation, associated with enhanced replication and insufficient response to antiviral treatment, may favor long-term persistence of these isolates. 2017 Journal of hepatology Abstract HBV C69X;S78T 24;19 29;23 RT;S 17;24 19;25 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Functional analyses of the mutations in vitro revealed that the rtS78T/sC69* mutation, but not the preS1/S2 deletion, significantly enhanced viral replication and conferred reduced susceptibility to ETV and TDF. 2017 Journal of hepatology Abstract HBV C69X;S78T 71;66 76;70 PreS1;PreS2;RT;S 99;99;64;71 104;105;66;72 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Molecular analyses identified a distinct mutation, rtS78T/sC69*, that abolishes HBsAg detection, enhances replication, sustains exosome-mediated virion secretion and decreases susceptibility to antivirals, thereby representing a potentially high-risk mutation for HBV-infected individuals. 2017 Journal of hepatology Abstract HBV C69X;S78T 58;53 63;57 S;RT;S 80;51;58 85;53;59 HBV infections 264 276 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. RESULTS: Sequencing analyses revealed the selection of the rtS78T HBV polymerase mutation in both cases that simultaneously creates a premature stop codon at sC69 and thereby deletes almost the entire small HBV surface protein. 2017 Journal of hepatology Abstract HBV S78T 61 65 RT;S;P;S 59;158;70;211 61;159;80;218 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The sC69* mutation caused truncation of HBs protein, leading to impaired detection by commercial HBsAg assay, without causing intracellular HBsAg retention or affecting HBV secretion. 2017 Journal of hepatology Abstract HBV C69X 4 9 S;S;S;S 40;97;140;4 43;102;145;5 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. CONCLUSION: Occult HBV infection is common in patients with hematological malignancies and associated with P120T and S143L mutations. 2017 World journal of hepatology Abstract HBV P120T;S143L 107;117 112;122 Hematologic Neoplasms 60 86 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. The complete HBV genome was retrieved from 6 occult HBV patients, and P120T and S143L were detected in 3 and 2 cases, respectively. 2017 World journal of hepatology Abstract HBV P120T;S143L 70;80 75;85 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. The in vitro analyses revealed that a lower level of extracellular HBsAg was detected by chemiluminescence enzyme immunoassay (CLEIA) with the clone containing T120 mutation, compared with the wild type or the clone with S143L mutation despite the similar levels of extracellular and intracellular HBsAg detected by Western blot. 2017 World journal of hepatology Abstract HBV S143L 221 226 S;S 67;298 72;303 28401569 Influences on viral replication and sensitivity to GLS4, a HAP compound, of naturally occurring T109/V124 mutations in hepatitis B virus core protein. In vitro infection assay showed T109N and all V124 mutants failed to synthesize cccDNA and following viral proteins. 2017 Journal of medical virology Abstract HBV T109N 32 37 28401569 Influences on viral replication and sensitivity to GLS4, a HAP compound, of naturally occurring T109/V124 mutations in hepatitis B virus core protein. Specially, T109N and all V124 mutants caused severe deficiencies in viral plus-strand DNA synthesis. 2017 Journal of medical virology Abstract HBV T109N 11 16 28401569 Influences on viral replication and sensitivity to GLS4, a HAP compound, of naturally occurring T109/V124 mutations in hepatitis B virus core protein. T109I showed modestly decreased sensitivities with IC50 3.3- to 6.8-folds higher than wild-type virus. 2017 Journal of medical virology Abstract HBV T109I 0 5 28401569 Influences on viral replication and sensitivity to GLS4, a HAP compound, of naturally occurring T109/V124 mutations in hepatitis B virus core protein. T109I single mutation and all T109S/M/C/N mutations impaired HBeAg secretion. 2017 Journal of medical virology Abstract HBV T109I;T109S;T109M;T109C;T109N 0;30;30;30;30 5;41;41;41;41 C 61 66 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. Over time, we observed substantial decreases in the prevalence of HBV e antigen (HBeAg) and increasing prevalence of the precore G1899A mutation and HBV-DNA levels in HBeAg-positive patients. 2017 Emerging infectious diseases Abstract HBV G1899A 129 135 C;C;C;Precore 70;81;167;121 79;86;172;128 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. CONCLUSIONS: We identified a new HBV RT substitution of rtH55R in genotype-C-infected CHB patients. 2018 Antiviral therapy Abstract HBV H55R 58 62 RT;RT 37;56 39;58 Chronic Hepatitis B 86 89 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. In vitro studies showed that rtH55R had a similar HBV DNA level compared to wild type. 2018 Antiviral therapy Abstract HBV H55R 31 35 RT 29 31 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. In vitro studies suggest that it might play some replication compensatory role in rtM204I mutants under lamivudine treatment. 2018 Antiviral therapy Abstract HBV M204I 84 89 RT 82 84 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. It is frequently found in combination with rtM204I/V substitution under NUC treatment. 2018 Antiviral therapy Abstract HBV M204I;M204V 45;45 52;52 RT 43 45 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. RESULTS: Among 261 NUC-treated CHB patients, we found a high detection rate of rtM204I/V substitution (30.7% [80/261]). 2018 Antiviral therapy Abstract HBV M204I;M204V 81;81 88;88 RT 79 81 Chronic Hepatitis B 31 34 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. The replication capacity of the rtM204I clone was found to significantly decrease under lamivudine treatment, but this was not found in the rtH55R+rtM204I clone. 2018 Antiviral therapy Abstract HBV M204I;H55R;M204I 34;142;149 39;146;154 RT;RT;RT 32;140;147 34;142;149 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. The rtH55R+rtM204I clone had a significantly better replication capacity than the rtM204I clone without NUCs (P<0.05). 2018 Antiviral therapy Abstract HBV H55R;M204I;M204I 6;13;84 10;18;89 RT;RT;RT 4;11;82 6;13;84 28440785 Impacts of HBV rtH55R polymerase substitution on viral replication and rtM204I/V resistance to nucleoside/nucleotide antiviral drugs. We identified a new substitution of rtH55R, and its detection rate had a significantly increasing trend from 3.8% (9/240) in the untreated group to 7.2% (13/181) or 33.8% (27/80) in the treated group with rtM204 or with rtM204I/V substitutions (P<0.0001). 2018 Antiviral therapy Abstract HBV H55R;M204I;M204V 38;222;222 42;229;229 RT;RT;RT 36;205;220 38;207;222 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. In CHB, HBV DNA from the serum samples of patients with poor response or virological breakthrough can be hybridized to probes containing the M204I mutation to visualize fluorescence under fluorescence microscopy, where fluorescence intensity is related to the virus load, in our method. 2017 Sensors (Basel, Switzerland) Abstract HBV M204I 141 146 Chronic Hepatitis B 3 6 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. These results show that QDs can be used as fluorescent probes to detect viral HBV DNA polymerase gene variation, and is a simple readout system without complex and expensive instruments, which provides an attractive platform for the detection of HBV M204I mutation. 2017 Sensors (Basel, Switzerland) Abstract HBV M204I 250 255 P 86 96 28460156 Genetic and phylogenic characterization of hepatitis B virus in the eastern part of the Democratic Republic of Congo. Only the I169T nucleotide substitution was observed in two genotype A samples. 2018 Journal of medical virology Abstract HBV I169T 9 14 28472081 HBV DNA genome co-transfection procedure for the evaluation of relative fitness. In the seroconversion experiment, subgenotype D1 (sgtD1) deletion (1763-1770) had significantly lower fitness comparing with both sgtD1 wild type and sgtD1mut G1896A, while, in the case of occupation of ecological niche experiment, the results showed the same relative fitness between all of the genotype combinations, except F1b-F4. 2017 PloS one Abstract HBV G1896A 159 165 28478205 Complete genome sequencing and clinical analysis of intrahepatic hepatitis B virus cccDNA from HCC. Additionally, in vitro analysis revealed that T1719G mutation reduced viral replication efficacy. 2017 Microbial pathogenesis Abstract HBV T1719G 46 52 28478205 Complete genome sequencing and clinical analysis of intrahepatic hepatitis B virus cccDNA from HCC. Finally, significantly higher levels of preoperative alpha-fetoprotein were observed in patients harboring the G1078T, C1653T, G1727A, C1913A, T1978C, or C3116T mutations at the cccDNA level. 2017 Microbial pathogenesis Abstract HBV G1078T;C1653T;G1727A;C1913A;T1978C;C3116T 111;119;127;135;143;154 117;125;133;141;149;160 28478205 Complete genome sequencing and clinical analysis of intrahepatic hepatitis B virus cccDNA from HCC. RESULTS: High frequencies of C1653T, T1753V, and A1762T/G1764A cccDNA mutations were observed in both tumor and non-tumor tissues. 2017 Microbial pathogenesis Abstract HBV G1764A;A1762T;C1653T;T1753V 56;49;29;37 62;55;35;43 28478205 Complete genome sequencing and clinical analysis of intrahepatic hepatitis B virus cccDNA from HCC. T1719G, C1329A, and T3098C mutations were related to the overall survival of HCC patients. 2017 Microbial pathogenesis Abstract HBV T1719G;C1329A;T3098C 0;8;20 6;14;26 Hepatocellular carcinoma 77 80 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. A meta-analysis of pooled results from case-control studies examined the association between mutations G1896A, A1762T, G1764A, and A1762T/G1764A and the risk of HCC. 2017 Medicine Abstract HBV G1764A;A1762T;A1762T;G1896A;G1764A 138;131;111;103;119 144;137;117;109;125 Hepatocellular carcinoma 161 164 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. CONCLUSION: In summary, we found that G1896A, A1762T, G1764A, and A1762T/G1764A are associated with an increased risk of HCC. 2017 Medicine Abstract HBV G1764A;A1762T;G1896A;A1762T;G1764A 73;66;38;46;54 79;72;44;52;60 Hepatocellular carcinoma 121 124 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. RESULTS: We included 29 articles for analysis and found that G1896A (summary odds ratios [OR] = 2.04, 95% confidence interval [CI] = 1.41-2.95), A1762T (summary OR = 3.96, 95% CI = 1.98-7.92), G1764A (summary OR = 3.48, 95% CI = 1.99-6.09), and A1762T/G1764A (summary OR = 3.96, 95% CI = 2.77-5.65) are each associated with a statistically significant increase in the risk of HCC. 2017 Medicine Abstract HBV G1764A;A1762T;G1896A;A1762T;G1764A 252;245;61;145;193 258;251;67;151;199 Hepatocellular carcinoma 376 379 28500726 Mutations associated with drug resistance and prevalence of vaccine escape mutations in patients with chronic hepatitis B infection. In addition, four mutations in gene S (three cases with the sI195M mutation and one with the W196L mutation), were detected, corresponding to a rate of 6% of vaccine escape mutations. 2017 Journal of medical virology Abstract HBV W196L;I195M 93;60 98;66 S;S 36;60 37;61 28500726 Mutations associated with drug resistance and prevalence of vaccine escape mutations in patients with chronic hepatitis B infection. Six patients (7%) exhibited resistance mutations to LAM, ETV, and TDF: two with patterns L180M + M204V and four with other different patterns: L80I + L180M + M204I; L80V + L180M + M204V; M204I; A194T. 2017 Journal of medical virology Abstract HBV L180M;M204V;L80I;L180M;M204I;L80V;L180M;M204V;M204I;A194T 89;97;143;150;158;165;172;180;187;194 94;102;147;155;163;169;177;185;192;199 28566379 Discovery and Mechanistic Study of Benzamide Derivatives That Modulate Hepatitis B Virus Capsid Assembly. However, unlike SBAs, BA compounds uniquely induced the formation of empty capsids that migrated more slowly in native agarose gel electrophoresis from A36V mutant than from the wild-type core protein. 2017 Journal of virology Abstract HBV A36V 152 156 Capsid;C 75;188 82;192 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. Mutations at HBsAg amino acid positions 143-145 are the most common (46%) with the mutation serine 143 to leucine the most frequently occurring change (28%). 2017 PloS one Abstract HBV S143L 92 113 S 13 18 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The majority (~90%) of occult D1 sequences had the sQ129R mutation in the surface gene. 2017 PloS one Abstract HBV Q129R 51 57 S;S 51;74 52;81 28600703 Prevalence of S gene mutations within the major hydrophilic region of hepatitis B virus in patients in Dongguan, southern China. Furthermore, the mutations sY100C, sQ101R/K, sS114A, sP120T, sT/I126A/N/S, sQ129R, sM133L/T/S and sG145R/A were prevalent in at least one genotype, with a frequency higher than 1%, which indicated that these mutations were relatively common. 2017 Archives of virology Abstract HBV T126A;T126N;T126S;I126A;I126N;I126S;Y100C;Q101R;Q101K;S114A;P120T;Q129R;M133L;M133T;M133S;G145R;G145A 61;61;61;61;61;61;27;35;35;45;53;75;83;83;83;98;98 73;73;73;73;73;73;33;43;43;51;59;81;93;93;93;106;106 S;S;S;S;S;S;S;S 27;35;45;53;61;75;83;98 28;36;46;54;62;76;84;99 28600703 Prevalence of S gene mutations within the major hydrophilic region of hepatitis B virus in patients in Dongguan, southern China. In addition, sQ101K/R was found only in genotype C isolates (P < 0.05), and sT126A was only discovered in genotype B isolates (P = 0.047), indicating that such mutations were genotype-associated mutations. 2017 Archives of virology Abstract HBV Q101K;Q101R;T126A 13;13;76 21;21;82 S;S 13;76 14;77 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. A total of 49 patients with chronic hepatitis B were included in the study, and the HBV A1762T/G1764A double mutant strain was detected in four samples (8.16%) by polymerase chain reaction followed by restriction fragment length analysis (PCR-RFLP). 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 95;88 101;94 Chronic Hepatitis B 28 47 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. In this study, 75% of the samples with the HBV A1762T/G1764A double mutation were HBeAg negative and anti-HBe positive, reflecting seroconversion even though they still displayed high viral loads. 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 54;47 60;53 C;C 106;82 109;87 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. Mutant HBV strains, such as the HBV A1762T/G1764A double mutant, have been associated with poor prognosis and higher risk of the patient for developing cirrhosis and/or hepatocellular carcinoma. 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 43;36 49;42 Liver cirrhosis;Hepatocellular carcinoma 152;169 161;193 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. On the other hand, carriers of the HBV A1762T/G1764A double mutant had higher levels of ALT (p=0.0028), while AST levels did not differ between groups (p=0.051). 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 46;39 52;45 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. Our study has shown that the HBV A1762T/G1764A double mutant strain circulates in Brazilian patients, and is associated with elevated levels of ALT and HBeAg seroconversion. 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 40;33 46;39 C 152 157 28606415 Identification of hepatitis B virus A1762T/G1764A double mutant strain in patients in Southern Brazil. This study analyzed the presence of the HBV A1762T/G1764A double mutant in patients with chronic HBV and its association with clinical parameters such as viral load, aminotransferases, and HBV antigens. 2017 The Brazilian journal of infectious diseases Abstract HBV G1764A;A1762T 51;44 57;50 Chronic Hepatitis B 89 100 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. RESULTS: A total of 62 patients (34.1%) had precore mutation (A1896G), and genotype D was the predominant genotype in these patients, which was followed by an unknown genotype that was suspected for genotype B. 2017 Electronic physician Abstract HBV A1896G 62 68 Precore 44 51 28647474 Antiviral profiling of the capsid assembly modulator BAY41-4109 on full-length HBV genotype A-H clinical isolates and core site-directed mutants in vitro. Combined analyses of clinical isolates and SDMs identified aa changes at positions 29, 33 and 118 led to reduced antiviral activity of BAY41-4109 with fold changes in EC50 values of 6, 46, and 9 for D29G, T33N, and Y118F, respectively. 2017 Antiviral research Abstract HBV D29G;T33N;Y118F 199;205;215 203;209;220 28654219 A comparative study of hepatitis B virus X protein mutants K130M, V131I and KV130/131MI to investigate their roles in fibrosis, cirrhosis and hepatocellular carcinoma. Furthermore, these might be the possible reasons for higher occurrence of AG1762/1764TA as compared to A1762T and G1764A in cirrhosis and HCC patients. 2017 Journal of viral hepatitis Abstract HBV A1762T;G1764A 103;114 109;120 Liver cirrhosis;Hepatocellular carcinoma 124;138 133;141 28654219 A comparative study of hepatitis B virus X protein mutants K130M, V131I and KV130/131MI to investigate their roles in fibrosis, cirrhosis and hepatocellular carcinoma. Hepatitis B virus (HBV) genomic mutations A1762T, G1764A and AG1762/1764TA cause production of HBV X protein (HBx) mutants, namely K130M, V131I and KV130/131MI. 2017 Journal of viral hepatitis Abstract HBV A1762T;G1764A;K130M;V131I 42;50;131;138 48;56;136;143 X;X 110;99 113;100 28658511 Occult hepatitis B virus infection in immunized children born to carrier mothers. Her HBV genome had a G145R mutation in the S gene that might have been induced by HBIG treatment. 2017 Pediatrics international Abstract HBV G145R 21 26 S 43 44 28673869 Impact of deletions and mutations in Hepatitis B virus envelope proteins on serological profile and clinical evolution. CD8+/CD4+ T-cell epitopes and B-cell epitopes in the major hydrophilic region (MHR), such as sI126N and sG145R possibly involved in the rare coexisting Hepatitis B surface Antigen (HBsAg)/anti-HBs serological pattern. 2017 Virus research Abstract HBV I126N;G145R 93;104 99;110 S;S;S;S;S 193;181;93;104;164 196;186;94;105;171 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. Cells transfected with the G1862T subgenotype A1 plasmid showed decreased expression of intracellular HBcAg and of nuclear preC/C/HBeAg and extracellular HBeAg, when compared to cells transfected with its wild-type counterpart as a result of the accumulation of the mutant protein in the endoplasmic reticulum (ER) and ER-Golgi intermediate compartment (ERGIC) . 2017 The Journal of general virology Abstract HBV G1862T 27 33 C;C;C;Precore;C 102;130;154;123;128 107;135;159;127;129 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. Huh7 cells were transfected with subgenotype A1 replication-competent plasmids, with and without G1862T. 2017 The Journal of general virology Abstract HBV G1862T 97 103 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. Increase in ER stress can result in liver damage, which has been shown to be a contributing factor to hepatocarcinogenesis and may explain why G1862T is frequently found in subgenotype A1 from liver disease patients. 2017 The Journal of general virology Abstract HBV G1862T 143 149 Liver disease;Liver disease 36;193 48;206 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. The G1862T mutation, which occurs most frequently in subgenotype A1 of the hepatitis B virus (HBV), results in a valine to phenylalanine substitution at the -3 position of the signal peptide cleavage site at the amino end of the precore/core (preC/C) precursor protein. 2017 The Journal of general virology Abstract HBV G1862T 4 10 C;Precore;C;Precore 237;243;248;229 241;247;249;236 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. The introduction of G1862T did not affect HBsAg expression. 2017 The Journal of general virology Abstract HBV G1862T 20 26 S 42 47 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. The objective of this study was to functionally characterize the G1862T mutation relative to its wild-type counterpart in subgenotype A1. 2017 The Journal of general virology Abstract HBV G1862T 65 71 28678685 Expression of wild-type or G1862T mutant HBe antigen of subgenotype A1 of hepatitis B virus and the unfolded protein response in Huh7 cells. Therefore, it is evident that the presence of G1862T in subgenotype A1 does not completely abolish HBeAg expression, but affects the rate of HBeAg maturation, its passage through the secretory pathway and activation of the UPR. 2017 The Journal of general virology Abstract HBV G1862T 46 52 C;C 99;141 104;146 28687901 Virological and Clinical Characteristics of Hepatitis B Virus Genotype A. Regarding virological factors, the G1896A precore mutation is rarely observed in genotype A as it would disrupt an essential stem-loop structure in the epsilon signal essential for pregenomic RNA packaging. 2018 Journal of gastroenterology Abstract HBV G1896A 35 41 Precore 42 49 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The mutations were rtA194T, rtL180M + rtM204V, rtS202I, rtM204I, and rtA181S. 2017 Infection and drug resistance Abstract HBV A194T;L180M;M204V;S202I;M204I;A181S 21;30;40;49;58;71 26;35;45;54;63;76 RT;RT;RT;RT;RT;RT 19;28;38;47;56;69 21;30;40;49;58;71 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Secondary substitutions (rtL80V and rtV173G/A/L) occurred more frequently than primary NUCr substitutions (rtI169L; rtA181G; T184A/S; rtS202T/R; rtM204L and rtM250K). 2017 Viruses Abstract HBV L80V;V173G;V173A;V173L;I169L;A181G;S202T;S202R;M204L;M250K;T184A;T184S 27;38;38;38;109;118;136;136;147;159;125;125 31;47;47;47;114;123;143;143;152;164;132;132 RT;RT;RT;RT;RT;RT;RT 25;36;107;116;134;145;157 27;38;109;118;136;147;159 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Typical amino acid substitutions associated with NUCr were of rtL80V, rtV173L and rtT184A/S. 2017 Viruses Abstract HBV T184A;T184S;L80V;V173L 84;84;64;72 91;91;68;77 RT;RT;RT 62;70;82 64;72;84 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. The hottest mutation position was aa126 (I126S/N and T126A, 29.63%), and aa 145 (G145R/A, 25.93%). 2017 Scientific reports Abstract HBV I126S;I126N;T126A;G145R;G145A 41;41;53;81;81 48;48;58;88;88 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. Moreover, the HBV genotype B4 isolates were found not only to be recombinants of genotype C, which results in a high cancer risk, but also to have other risk of HCC, pre-S deletions, the G1613A mutation, and X region insertions corresponding to the promoter. 2017 PloS one Abstract HBV G1613A 187 193 PreS;X 166;208 171;209 Hepatocellular carcinoma 161 164 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. The promoter mutation G1613A was found in 13.6% of cases, and a 24 bp insertion from nt1673 in the X region was found in 6.3% of cases. 2017 PloS one Abstract HBV G1613A 22 28 X 99 100 28774406 Natural history of acute and chronic hepatitis B: The role of HBV genotypes and mutants. In chronic hepatitis B patients, genotype C and D have a higher frequency of basal core promoter A1762T/G1764A mutations than genotype A and B. 2017 Best practice & research. Clinical gastroenterology Abstract HBV G1764A;A1762T 104;97 110;103 BCP 77 96 Chronic Hepatitis B 3 22 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. The genotypic analysis of the HBV strain identified T127P, F170FL and S204R mutations of HbsAg, which can hinder HBsAg recognition in a diagnostic assay. 2017 BMC infectious diseases Abstract HBV T127P;S204R 52;70 57;75 S;S 89;113 94;118 28822954 The variability of hepatitis B envelope is associated with HBs antigen persistence in either chronic or acute HBV genotype A infection. Interestingly, the mutation sY161F found in 3/8 non-resolvers was associated with a decrease in predicted antigenicity (28%; AnTheProt). 2017 Journal of clinical virology Abstract HBV Y161F 28 34 S 28 29 28859616 Molecular characterization of hepatitis B virus in Vietnam. A G1896A mutation in the precore gene was present in 30.6% of genotype B isolates. 2017 BMC infectious diseases Abstract HBV G1896A 2 8 Precore 25 32 28859616 Molecular characterization of hepatitis B virus in Vietnam. A1762T and G1764 T mutations and a double mutation (A1762T and G1764 T) in the BCP region were significantly more frequent in genotype C1 isolates (p < 0.001). 2017 BMC infectious diseases Abstract HBV A1762T;G1764T;A1762T;G1764T 0;11;52;63 6;18;58;70 BCP 79 82 28870397 Eradicating hepatitis B virus: The critical role of preventing perinatal transmission. Most late infections with sG145R were in vaccine non-responders, suggesting escape from HBIG rather than from vaccine-induced antibody. 2017 Biologicals Abstract HBV G145R 26 32 S 26 27 28870397 Eradicating hepatitis B virus: The critical role of preventing perinatal transmission. New analyses of our data from US trials of HBIG and HBV vaccine in high-risk infants revealed better efficacy with yeast-recombinant vaccine than plasma-derived vaccine, especially in preventing late onset infections, with evidence that vaccine prevented transmission of maternal HBV infection with the glycine to arginine mutation in surface antigen codon 145 (sG145R). 2017 Biologicals Abstract HBV G145R 362 368 S;S 362;335 363;342 HBV infections 280 293 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1485T-HBxTg mice were more susceptible to diethylnitrosamine-induced hepatocarcinogenesis than WT-HBxTg mice and control non-Tg mice. 2017 Scientific reports Abstract HBV C1485T 0 6 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The promotion of hepatocarcinogenesis in C1485T-HBxTg mice was accompanied by the activation of beta-catenin and Jun N-terminal kinase (JNK) signaling pathways as well as the production of reactive oxygen species, whereas the activation of nuclear factor-kappa B in the livers of C1485T-HBxTg mice was attenuated. 2017 Scientific reports Abstract HBV C1485T;C1485T 41;280 47;286 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. These results demonstrate that the HBx C1485T mutation contributes to human and murine hepatocarcinogenesis. 2017 Scientific reports Abstract HBV C1485T 39 45 X 35 38 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We generated transgenic mice expressing wild-type (WT-HBxTg) and mutant (C1485T-HBxTg) HBx to assess the carcinogenic potential of mutated HBx. 2017 Scientific reports Abstract HBV C1485T 73 79 X;X 87;139 90;142 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We herein identified C1485T and C1653T mutations in the HBx gene as independent risk of HCC for HBV through the analysis using serum from chronic hepatitis B patients. 2017 Scientific reports Abstract HBV C1485T;C1653T 21;32 27;38 X 56 59 Hepatocellular carcinoma;Chronic Hepatitis B 88;138 91;157 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The A1762T/G1764A variant was identified in 36.7% of the patients with grade 1 and 2 liver fibrosis (29/79) and in 81.8% of the patients with grade 3 and 4 liver fibrosis (9/11) (p < 0.01); in 76.9% of the patients with cirrhosis (10/13) and in 38.1% of the patients without cirrhosis (40/105) (p = 0.01); and in 77.8% of the patients with hepatocellular carcinoma (HCC) (7/9) and in 39.4% of the patients without HCC (43/109) (p = 0.03). 2017 Memorias do Instituto Oswaldo Cruz Abstract HBV G1764A;A1762T 11;4 17;10 Liver fibrosis;Liver fibrosis;Liver cirrhosis;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 85;156;220;275;340;366;414 99;170;229;284;364;369;417 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The A1762T/G1764A variant was independently associated with advanced forms of liver fibrosis, hepatic cirrhosis, and HCC. 2017 Memorias do Instituto Oswaldo Cruz Abstract HBV G1764A;A1762T 11;4 17;10 Liver fibrosis;Liver cirrhosis;Hepatocellular carcinoma 78;94;117 92;111;120 28939157 Molecular evolution of hepatitis B vaccine escape variants in China, during 2000-2016. Four sites (A5T/S, L21S, T/A126S and T/N131I/A) and 13 sites (N3S, T5A, G10Q/R/E, L21S, T47K/A/V, L98V/P, I/S126N/V/T, Q129H/R/L, T131P/I/N/A, G145A/R, L175S/F, L213I/S, V224A/G) were found to be under positive selection in genotype B and C HBV vaccine escape strains, respectively. 2017 Vaccine Abstract HBV L21S;T126S;A126S;T131I;T131A;N131I;N131A;T5A;G10Q;G10R;G10E;L21S;T47K;T47A;T47V;L98V;L98P;I126N;I126V;I126T;S126N;S126V;S126T;Q129H;Q129R;Q129L;T131P;T131I;T131N;T131A;G145A;G145R;L175S;L175F;L213I;L213S;V224A;V224G;A5T;A5S;N3S 19;25;25;37;37;37;37;67;72;72;72;82;88;88;88;98;98;106;106;106;106;106;106;119;119;119;130;130;130;130;143;143;152;152;161;161;170;170;12;12;62 23;32;32;46;46;46;46;70;80;80;80;86;96;96;96;104;104;117;117;117;117;117;117;128;128;128;141;141;141;141;150;150;159;159;168;168;177;177;17;17;65 28939157 Molecular evolution of hepatitis B vaccine escape variants in China, during 2000-2016. More importantly, N3S, L21S, T47K, L98V, I/S126T and L213I mutations were detected in 1 (2.5%), 1 (2.5%), 1 (2.5%), 3 (7.5%), 1 (2.5%), 1 (2.5%) genotype C HBV infected Chinese younger with neonatal HBV vaccination, respectively. 2017 Vaccine Abstract HBV L21S;T47K;L98V;I126T;S126T;L213I;N3S 23;29;35;41;41;53;18 27;33;39;48;48;58;21 HBV infections 156 168 28971485 Evolution of the serologic and virologic course of occult HBV infection in therapy experienced HIV co-infected patients. While the HBsAg gene sequences isolated from chronic HBV infection were genetically stable over time, OBI-associated variants (sP111R, sT127P, sY161F) were neither stable nor predominant during the course of infection. 2018 Journal of medical virology Abstract HBV P111R;T127P;Y161F 127;135;143 133;141;149 S;S;S;S 10;127;135;143 15;128;136;144 HBV infections;Occult Hepatitis B 45;102 66;105 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Other mutations were found, L109R and G130E, located in critical positions of the HBsAg sequence. 2017 PloS one Abstract HBV L109R;G130E 28;38 33;43 S 82 87 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Two HBV escape mutants were identified, G145R, reported worldwide, and W156*; this stop codon was identified in a child with occult HBV infection. 2017 PloS one Abstract HBV G145R;W156X 40;71 45;76 HBV infections 132 145 29039614 Substitutions of rtL228 and/or L229 are involved in the regulation of replication and HBsAg secretion in hepatitis B virus, and do not affect susceptibility to nucleos(t)ide analogs. Decreased HBsAg secretion in the supernatant and production in the cell lysate wasobserved with single rtL229W or in combination with rtL228W, while there was no significant difference between wild-type and mutant HBV with regard to the level of HBeAg in the supernatant and susceptibility to commonly-used NAs. 2017 Molecular medicine reports Abstract HBV L229W;L228W 105;136 110;141 C;S;RT;RT 246;10;103;134 251;15;105;136 29039614 Substitutions of rtL228 and/or L229 are involved in the regulation of replication and HBsAg secretion in hepatitis B virus, and do not affect susceptibility to nucleos(t)ide analogs. Mutations including rtL228C/W, rtL229W and rtL228W/L229W were introduced into a HBV replication competent plasmid by fusion polymerase chain reaction. 2017 Molecular medicine reports Abstract HBV L229W;L228C;L228W;L229W;L228W 51;22;22;33;45 56;29;29;38;50 RT;RT;RT 20;31;43 22;33;45 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. Additionally, a significantly higher frequency of G1896A and A1762T/G1764A mutations were found in HBeAg negative than in ACLF patients (p < 0.0001). 2017 Virology journal Abstract HBV G1764A;G1896A;A1762T 68;50;61 74;56;67 C 99 104 Acute on chronic liver failure 122 126 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. Clonal sequencing of PCR-amplified HBV P/S and BCP/PC gene fragments was done and HBV diversity, frequency of immune escape (IE) and drug resistance (DR) mutations and mutations in BCP/PC gene (G1896A and A1762T/G1764A), were compared between each group. 2017 Virology journal Abstract HBV G1764A;A1762T;G1896A 212;205;194 218;211;200 BCP;BCP;Precore;Precore 47;181;51;185 50;184;53;187 29096158 Human hepatocytes apoptosis induced by replication of hepatitis B virus subgenotypes F1b and F4: Role of basal core promoter and preCore mutations. The BCPdm (A1762T/G1764A) and preCore (G1896A) mutants induced higher levels of apoptosis than the wt virus. 2018 Virology Abstract HBV G1764A;A1762T;G1896A 18;11;39 24;17;45 Precore 30 37 29119303 Evolution of drug-resistant mutations in HBV genomes in patients with treatment failure during the past seven years (2010-2016). Among the primary NA-resistant mutations, rtM204I (13.44%, 545/4055) occurred more frequently, followed by rtM204V, rtN236T, rtA181T, and rtA181V. 2018 Virus genes Abstract HBV M204I;M204V;N236T;A181T;A181V 44;109;118;127;140 49;114;123;132;145 RT;RT;RT;RT;RT 42;107;116;125;138 44;109;118;127;140 29119303 Evolution of drug-resistant mutations in HBV genomes in patients with treatment failure during the past seven years (2010-2016). For single-base mutations, rtL180M and rtA181V increased gradually during the past seven years, while rtM204I/V and rtN236T decreased after 2015. 2018 Virus genes Abstract HBV L180M;A181V;M204I;M204V;N236T 29;41;104;104;118 34;46;111;111;123 RT;RT;RT;RT 27;39;102;116 29;41;104;118 29119303 Evolution of drug-resistant mutations in HBV genomes in patients with treatment failure during the past seven years (2010-2016). Frequencies of rtL180M and rtA181T/V increased gradually in the past seven years, to which we should pay more attention. 2018 Virus genes Abstract HBV L180M;A181T;A181V 17;29;29 22;36;36 RT;RT 15;27 17;29 29119303 Evolution of drug-resistant mutations in HBV genomes in patients with treatment failure during the past seven years (2010-2016). Moreover, single-base mutation rtA181V and multi-base mutations (rtL180M + M204I and rtL180M + M204V + M204I) were more common in HBV genotype C than those in genotype B (1.94% vs. 2018 Virus genes Abstract HBV A181V;L180M;L180M;M204I;M204V;M204I 33;67;87;75;95;103 38;72;92;80;100;108 RT;RT;RT 31;65;85 33;67;87 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. At baseline, 47 of 162 (29.0%) patients had the pcW28* mutation and were more frequently HBeAg-negative (adjusted-OR = 4.37, 95%CI = 1.76-10.86) and had non-A HBV genotypes (adjusted-OR = 9.14, 95%CI = 4.05-20.66). 2018 Antiviral research Abstract HBV W28X 49 54 C;Precore 89;48 94;50 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. In 114 patients without baseline mutation and available data, four developed incident pcW28* mutation by the end of follow-up (cumulative 3.5%, 95%CI = 1.3-9.1%). 2018 Antiviral research Abstract HBV W28X 87 92 Precore 86 88 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. In a three-year prospective cohort of 165 HIV-HBV co-infected patients, pcW28* mutation was determined via DNA-chip during yearly sampling. 2018 Antiviral research Abstract HBV W28X 73 78 Precore 72 74 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. In conclusion, the pcW28* mutation infrequently appeared in this co-infected study population with increased use of potent antivirals and suppressed levels of circulating virus. 2018 Antiviral research Abstract HBV W28X 20 25 Precore 19 21 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. In the 32 patients with liver biopsies, 10 (31.3%) patients harboring the pcW28* mutation had significantly lower adjusted mean cccDNA (0.05 versus without = 0.43 copies/cell, p < 0.001) and total IH-DNA levels (2.31 versus without = 18.59 copies/cell, p = 0.006). 2018 Antiviral research Abstract HBV W28X 75 80 Precore 74 76 29169914 Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients. The precore (pc) W28* mutation arises from immune-selective pressures during the hepatitis B "e" antigen (HBeAg)-positive phase of chronic hepatitis B virus (HBV) infection and has been linked to severe liver-related morbidity. 2018 Antiviral research Abstract HBV W28X 17 21 C;Precore;Precore 106;13;4 111;15;11 Chronic HBV infection 131 172 29212929 Nucleic Acid Polymers Are Active against Hepatitis Delta Virus Infection In Vitro. NAP antiviral activity was effective against HDV virions bearing the main hepatitis B virus (HBV) immune escape substitutions (D144A and G145R) and was pangenomic with regard to HBV envelope proteins. 2018 Journal of virology Abstract HBV D144A;G145R 127;137 132;142 S 182 190 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. DNA sequencing analysis of the HBV genome revealed triple mutations (A1762T, G1764A, and T1753V) in the BCP region, which could further enhance the ability of HBV replication. 2017 Medical science monitor Abstract HBV A1762T;G1764A;T1753V 69;77;89 75;83;95 BCP 104 107 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Recent studies have shown that the uncommon serological pattern of coexistent circulating HBV surface antigen (HBsAg) and its antibody (anti-HBs) was associated with double mutations (A1762T/G1764A) in the basal core promoter (BCP) region of the HBV genome, which is critical for HBV replication. 2017 Medical science monitor Abstract HBV G1764A;A1762T 191;184 197;190 BCP;BCP;S;S;S 206;227;141;111;94 225;230;144;116;101 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. All HIV/HBV positive cases were on ART with anti-HBV activity (i.e., 3TC) and 3TC associated HBV DRMs (i.e., rtV173L, rtL180M, and rtM204V) were detected in 7/13 (53.8%) subjects. 2017 PloS one Abstract HBV V173L;L180M;M204V 111;120;133 116;125;138 RT;RT;RT 109;118;131 111;120;133 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. H94Y and K130M mutations were also significantly associated with severe liver disease. 2017 Oncotarget Abstract HBV H94Y;K130M 0;9 4;14 Liver disease 72 85 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. I127T, V131I, and F132Y/I/R mutations showed a significant increasing trend associated with the disease progression to HCC. 2017 Oncotarget Abstract HBV I127T;V131I;F132Y;F132I;F132R 0;7;18;18;18 5;12;27;27;27 Hepatocellular carcinoma 119 122 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. One double mutation (K130M+V131I) and two triple mutations (I127T+K130M+V131L and K130M+V131I+F132Y) were observed, with significant rising prevalence through progressive clinical phases of liver disease to HCC. 2017 Oncotarget Abstract HBV K130M;V131I;I127T;K130M;V131L;K130M;V131I;F132Y 21;27;60;66;72;82;88;94 26;32;65;71;77;87;93;99 Liver disease;Hepatocellular carcinoma 190;207 203;210 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. The mutations at the 31 (Ser314Pro), 529 (Asp480Asn), and 1078 (Ser663Ala) sites all resulted in amino acid changes in hepatitis B virus polymerase and were associated with shortened life-span. 2017 PloS one Abstract HBV S314P;D480N;S663A 25;42;64 34;51;73 P 137 147 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. The percentage of resistance to Lamivudine was high (40%) and varied according to the M204V/I motif. 2018 PloS one Abstract HBV M204V;M204I 86;86 93;93 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. A1846T mutation is significantly associated with poor prognosis of ACLF. 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T 0 6 Acute on chronic liver failure 67 71 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. A1846T was significantly associated with the mortality of ACLF patients within six months after the disease onset (OR 1.704, p = .041). 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T 0 6 Acute on chronic liver failure 58 62 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. CONCLUSION: Occurrence of A1846T and C1913A is positively associated with clinical presentations of severe liver disease. 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T;C1913A 26;37 32;43 Liver disease 107 120 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. In vitro experiment revealed that A1846T mutant resulted in 3.20-fold and 1.85-fold increase of replication capacity and promoter activity, respectively compared with wild type counterpart (p < .001), while C1913A led to a significant decrease of core protein expression (p < .05). 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T;C1913A 34;207 40;213 C 247 251 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. Replicons containing A1846T, C1913A or other mutant sequences, or the wild-type counterparts were constructed respectively, and then transfected into HepG2 cells for phenotype analysis. 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T;C1913A 21;29 27;35 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. RESULTS: There was significant difference in the detection rates of A1846T (30.82%, 40.41% and 55.48%, respectively) and C1913A/G (15.52%, 28.77%, and 35.62%, respectively) among patients with CHB-M, those with CHB-S, and those with ACLF (p < .01). 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T;C1913A;C1913G 68;121;121 74;129;129 S 215 216 Acute on chronic liver failure;Chronic Hepatitis B;Chronic Hepatitis B 233;193;211 237;196;214 29322851 Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases. This study aimed to observe the clinical and virological implications of the A1846T and C1913A/G mutations of HBV genome in the development and treatment outcome of severe liver diseases, which has not been previously determined. 2018 Scandinavian journal of gastroenterology Abstract HBV A1846T;C1913A;C1913G 77;88;88 83;96;96 Liver disease 172 186 29326804 Occult Hepatitis B Virus Infection and Associated Genotypes among HBsAg-negative Subjects in Burkina Faso. A single "false OBI" strain had the characteristic mutation G145R. 2018 Mediterranean journal of hematology and infectious diseases Abstract HBV G145R 60 65 Occult Hepatitis B 16 19 29339154 A new hepatitis B virus e antigen-negative strain gene used as a reference sequence in an animal model. The G1896A variant resulted in a premature stop codon and abolished HBeAg expression. 2018 Biochemical and biophysical research communications Abstract HBV G1896A 4 10 C 68 73 29339154 A new hepatitis B virus e antigen-negative strain gene used as a reference sequence in an animal model. The main four point variants including A1762T, G1764A, G1896A, and G1899A were detected in the full-length genome. 2018 Biochemical and biophysical research communications Abstract HBV A1762T;G1764A;G1896A;G1899A 39;47;55;67 45;53;61;73 29339154 A new hepatitis B virus e antigen-negative strain gene used as a reference sequence in an animal model. The strain will increase viral replication and infection for mutations A1762T and G1764A in the basal core promoter region, and mutations G1896A and G1899A in the pre-core region. 2018 Biochemical and biophysical research communications Abstract HBV A1762T;G1764A;G1896A;G1899A 71;82;138;149 77;88;144;155 BCP;Precore 96;163 115;171 29353073 Serum HBV DNA plus RNA shows superiority in reflecting the activity of intrahepatic cccDNA in treatment-naive HBV-infected individuals. Moreover, high-frequency R193M and P196A mutations were found in the RT region of HBV polymerase leading to lower serum HBV DNA and higher serum HBV RNA levels in HBeAg-negative chronic HBV infection phase. 2018 Journal of clinical virology Abstract HBV R193M;P196A 25;35 30;40 C;P;RT 163;86;69 168;96;71 Chronic HBV infection 178 199 29393485 Early changes in quasispecies variant after antiviral therapy for chronic hepatitis B. Furthermore, several mutation patterns, such as cI97L and cP130T showed alterations in the secondary structure and predicted antigenicity of HBV protein. 2018 Molecular medicine reports Abstract HBV I97L;P130T 48;58 53;64 C;C 48;58 49;59 29406612 2'-Fluoro-6'-methylene carbocyclic adenosine and its phosphoramidate prodrug: A novel anti-HBV agent, active against drug-resistant HBV mutants. In vitro, these molecules have demonstrated significant activity against LMV/entecavir (ETV) triple mutants (L180M + S202G + M204V). 2018 Medicinal research reviews Abstract HBV L180M;S202G;M204V 109;117;125 114;122;130 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. However, HBV mono-infected blood donors and CLD patients who had no any drug resistance gene variants developed comparable G1862T (60.6% vs. 65.1%) and G1896A (24.2% vs. 11.6%) PC gene mutations. 2018 PloS one Abstract HBV G1896A;G1862T 152;123 158;129 Precore 177 179 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. RESULTS: Among the major mutant variants detected, double BCP mutations (A1762T/G1764A) (25.9%), Kozak sequences mutations (nt1809-1812) (51.7%) and the classical PC mutations such as A1814C/C1816T (15.4%), G1896A (25.2%) and G1862T (44.8%) were predominant mutant variants. 2018 PloS one Abstract HBV G1764A;C1816T;A1762T;A1814C;G1896A;G1862T 80;191;73;184;207;226 86;197;79;190;213;232 BCP;Precore 58;163 61;165 29411271 Molecular characterization of hepatitis B virus X gene in HIV-positive South Africans. The basal core promoter mutations T1753C, A1762T, and G1764A were identified in the majority of sequences. 2018 Virus genes Abstract HBV T1753C;A1762T;G1764A 34;42;54 40;48;60 BCP 4 23 29414186 Substantial variation in the hepatitis B surface antigen (HBsAg) in hepatitis B virus (HBV)-positive patients from South Africa: Reliable detection of HBV by the Elecsys HBsAg II assay. All occult HBV infection-associated Y100C and common diagnostic and vaccine-escape-associated P120T, G145R, K122R, M133L, M133T, Q129H, G130N, and T126S mutations were reliably detected by the assay, which consistently detected the presence of HBsAg in all 179 samples including samples with 11 novel mutations. 2018 Journal of clinical virology Abstract HBV Y100C;P120T;G145R;K122R;M133L;M133T;Q129H;G130N;T126S 36;94;101;108;115;122;129;136;147 41;99;106;113;120;127;134;141;152 S 244 249 HBV infections 11 24 29414186 Substantial variation in the hepatitis B surface antigen (HBsAg) in hepatitis B virus (HBV)-positive patients from South Africa: Reliable detection of HBV by the Elecsys HBsAg II assay. Frequency of occult HBV infection-associated Y100C mutations was also determined. 2018 Journal of clinical virology Abstract HBV Y100C 45 50 HBV infections 20 33 29414186 Substantial variation in the hepatitis B surface antigen (HBsAg) in hepatitis B virus (HBV)-positive patients from South Africa: Reliable detection of HBV by the Elecsys HBsAg II assay. The major vaccine-induced escape mutation G145R was observed in two samples. 2018 Journal of clinical virology Abstract HBV G145R 42 47 29424069 Development of a fibrosis index including hepatitis B virus basal core promoter A1762T mutation for pretherapeutic evaluation. A fibrosis score including Anti-hepatitis B e antibody, Basal core promoter (BCP) A1762T mutation, and Platelet count Index (named ABPI) was derived from the modeling cohort. 2018 Journal of gastroenterology and hepatology Abstract HBV A1762T 82 88 BCP;BCP 56;77 75;80 29424069 Development of a fibrosis index including hepatitis B virus basal core promoter A1762T mutation for pretherapeutic evaluation. CONCLUSIONS: We developed a transaminase-free fibrosis score (ABPI) utilizing basal core promoter A1762T data, which outperformed APRI and FIB-4. 2018 Journal of gastroenterology and hepatology Abstract HBV A1762T 98 104 BCP 78 97 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. The minor populations of variants harbouring the W4R, L30S, Q118R/Stop, N123D and S124F/P mutations in the pre-S region and the L21F/S and L42F/S mutations in the S region were detected more frequently in OBI-related HCC than in HBsAg-positive HCC. 2018 Infectious agents and cancer Abstract HBV L30S;Q118R;Q118X;N123D;S124F;S124P;L21F;L21S;L42F;L42S;W4R 54;60;60;72;82;82;128;128;139;139;49 58;70;70;77;89;89;134;134;145;145;52 S;PreS;S 229;107;163 234;112;164 Hepatocellular carcinoma;Hepatocellular carcinoma;Occult Hepatitis B 217;244;205 220;247;208 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. A series of novel PLC-related mutations including A2159G, A2189C and G2203W at the C gene, A799G, A987G and T1055A at the P gene of HBV genome were identified by using samples from the cohort. 2018 Hepatoma research Abstract HBV A2159G;A2189C;G2203W;A799G;A987G;T1055A 50;58;69;91;98;108 56;64;75;96;103;114 C;P 83;122 84;123 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Additionally, our transgenic mouse model that expresses full HBV genome with the W4P mutation in preS1 could be effectively used for the studies of the progression of liver diseases, including HCC. 2018 World journal of gastroenterology Abstract HBV W4P 81 84 PreS1 97 102 Liver disease;Hepatocellular carcinoma 167;193 181;196 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. AIM: To study sex disparity in susceptibility to hepatocellular carcinoma (HCC), we created a transgenic mouse model that expressed the full hepatitis B virus (HBV) genome with the W4P mutation. 2018 World journal of gastroenterology Abstract HBV W4P 181 184 Hepatocellular carcinoma;Hepatocellular carcinoma 49;75 73;78 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. CONCLUSION: Together, our data indicate that the W4P mutation in preS1 may contribute to sex disparity in susceptibility to HCC by causing increased HBV virion replication and enhanced IL-6-mediated inflammation in male individuals. 2018 World journal of gastroenterology Abstract HBV W4P 49 52 PreS1 65 70 Hepatocellular carcinoma 124 127 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. RESULTS: W4P TG males exhibited more pronounced hepatomegaly, significantly increased granule generation in liver tissue, elevated HBsAg expression in the liver and serum, and higher serum ALT and IL-6 levels compared to W4P TG females or littermate control groups. 2018 World journal of gastroenterology Abstract HBV W4P;W4P 9;221 12;224 S 131 136 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. We compared serum levels of hepatitis B surface antigen (HBsAg), interleukin (IL)-6, and the liver enzymes alanine aminotransferase (ALT) and aspartate transaminase (AST), as well as liver histopathological features in male and female transgenic (W4P TG) mice and in nontransgenic littermates of 10 mo of age. 2018 World journal of gastroenterology Abstract HBV W4P 247 250 S;S 57;40 62;47 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. RT sequence analysis showed the presence of a number of immune escape mutations: strains from all of the patients had a serine at HBsAg position 140; 3 also had T116N, Y100C, and P142L+S143L substitutions; and 1 had a G112R substitution. 2018 PloS one Abstract HBV T116N;Y100C;P142L;S143L;G112R 161;168;179;185;218 166;173;184;190;223 S;RT 130;0 135;2 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. An M133T mutation creating a novel glycosylation site at N131could rescue virion secretion of N146Q mutant (loss of original glycosylation site) and immune escape mutants such as G145R. 2018 Virology Abstract HBV M133T;N146Q;G145R 3;94;179 8;99;184 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Both G145R and N146Q mutations impaired virion secretion through the S protein. 2018 Virology Abstract HBV G145R;N146Q 5;15 10;20 S 69 70 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Here we demonstrate that other novel N-linked glycosylation sites could rescue virion secretion of the G145R and N146Q mutants to variable extents. 2018 Virology Abstract HBV G145R;N146Q 103;113 108;118 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation restored virion secretion through the S protein, and could work in trans. 2018 Virology Abstract HBV M133T 4 9 S 57 58 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. BACKGROUND: It has been reported that the emergence of HBV rtA181T/sW172* mutant could result in a dominant secretion defect of HBsAg and increase the risk of HCC development. 2018 Virology journal Abstract HBV W172X;A181T 67;61 73;66 RT;S;S 59;67;128 61;68;133 Hepatocellular carcinoma 159 162 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. CONCLUSIONS: The emergence of sW172* mutant may increase the tumorigenesis of HBV, and its mechanism may be associated with down-regulated expression of TGFBI in TGF-beta/Smad signaling pathway. 2018 Virology journal Abstract HBV W172X 30 36 S 30 31 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. This study was designed to reveal the role and possible pathogenic mechanism of truncated mutant HBsAg in tumorigenesis of HBV rtA181T/sW172* mutant. 2018 Virology journal Abstract HBV W172X;A181T 135;129 141;134 RT;S;S 127;135;97 129;136;102 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Conclusion: HBV DNA genomic mutations in A1762T/G1764A and Pre S deletion were associated with worse prognoses and early recurrence for HBV-HCC patients after surgery. 2018 Cancer management and research Abstract HBV G1764A;A1762T 48;41 54;47 PreS 59 64 Hepatocellular carcinoma 140 143 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Multivariate analysis with Cox proportional hazards model revealed that both A1762T/G1764A mutation and Pre S deletion were independent prognostic factors for OS (hazard ratio [HR]=3.701, 95% CI=1.390-9.855, p=0.009, and HR=4.816, 95% CI=2.311-10.032, p<0.001, respectively) and DFS (HR=3.245, 95% CI=1.400-7.521, p=0.006, and HR=2.437, 95% CI=1.311-4.530, p<0.001, respectively), and patients with dual mutations were found to have the worst OS and DFS (p<0.001 and p<0.001, respectively). 2018 Cancer management and research Abstract HBV G1764A;A1762T 84;77 90;83 PreS 104 109 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Patients with A1762T/G1764A mutation or Pre S deletion were more likely to have early recurrence (p=0.042 and p=0.019, respectively). 2018 Cancer management and research Abstract HBV G1764A;A1762T 21;14 27;20 PreS 40 45 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Results: Both A1762T/G1764A mutation and Pre S deletion related to worse overall survival (OS, p=0.040 and p<0.001, respectively) and disease-free survival (DFS, p=0.040 and p<0.001, respectively), G1899A mutation related to worse OS (p=0.030), A1762T/G1764A mutation correlated with tumor size (r=0.204, p=0.019), G1899A mutation correlated with vascular invasion (r=0.332, p<0.001), and Pre S deletion correlated with alpha-fetoprotein (AFP; r=0.254, p=0.003) positively. 2018 Cancer management and research Abstract HBV G1764A;G1764A;A1762T;G1899A;A1762T;G1899A 21;252;14;198;245;315 27;258;20;204;251;321 PreS;PreS 41;389 46;394 29629487 Quasispecies characters of hepatitis B virus in immunoprophylaxis failure infants. In our data, the substitution rate of amino acid located at a determinant is relatively low (< 10%), I/T126A, C124S, F134Y, K141Q, Q129H, D144A, G145V, and N146K, which showed no statistical difference to their mothers, proving that these vaccine escape mutants preexist maternally as minor variants. 2018 European journal of clinical microbiology & infectious diseases Abstract HBV I126A;T126A;C124S;F134Y;K141Q;Q129H;D144A;G145V;N146K 101;101;110;117;124;131;138;145;156 108;108;115;122;129;136;143;150;161 S 60 73 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. 3.69-fold in half maximal effective concentration of wild-type strain); rtA181T/sW172L + rtS202G + rtM204V strain exhibited higher HBV DNA production and entecavir resistance fold than that of rtA181T/sW172* + rtS202G + rtM204V strain (50.98% vs. 2018 Antiviral research Abstract HBV W172L;W172X;S202G;A181T;M204V;A181T;S202G;M204V 80;201;91;74;101;195;212;222 86;207;96;79;106;200;217;227 RT;S;RT;RT;RT;S;RT;RT 72;80;89;99;193;201;210;220 74;81;91;101;195;202;212;222 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. 44.33% (524/1182) rtA181T-positive samples were detected with signature drug-resistant mutations, including 325 with adefovir-resistant mutation rtA181V/N236T, 57 with lamivudine-resistant mutation rtM204V/I, 99 with entecavir-resistant mutation rtM204V/I plus rt184/202/250 substitution(s), and 43 with multidrug-resistant mutation rtA181V/N236T + rtM204V/I +- rt184/202/250 substitution(s). 2018 Antiviral research Abstract HBV N236T;N236T;A181T;A181V;M204V;M204I;M204V;M204I;A181V;M204V;M204I 153;341;20;147;200;200;248;248;335;351;351 158;346;25;152;207;207;255;255;340;358;358 RT;RT;RT;RT;RT;RT;RT;RT 18;145;198;246;261;333;349;362 20;147;200;248;263;335;351;364 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. In conclusion, rtA181T/sW172non-stop mutation may increase resistance fold of adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation and might influence clinical presentation of NAs-treated patients. 2018 Antiviral research Abstract HBV W172X;A181T;A181T 140;17;134 146;22;139 RT;RT;S;S 15;132;23;140 17;134;24;141 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. rtA181T/sW172S + rtN236T and rtA181T/sW172L + rtN236T mutants exhibited higher HBV DNA production and adefovir resistance fold than that of rtA181T/sW172* + rtN236T mutant (98.02% and 85.5% vs. 2018 Antiviral research Abstract HBV W172S;W172L;W172X;A181T;N236T;A181T;N236T;A181T;N236T 8;37;148;2;19;31;48;142;159 14;43;154;7;24;36;53;147;164 RT;S;RT;RT;S;RT;RT;S;RT 0;8;17;29;37;46;140;148;157 2;9;19;31;38;48;142;149;159 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. The patients with rtA181T/sW172non-stop mutants had a higher HBV DNA level compared to those with rtA181T/sW172* mutants. 2018 Antiviral research Abstract HBV W172X;A181T;A181T 106;20;100 112;25;105 RT;S;RT;S 18;26;98;106 20;27;100;107 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. The rtA181T mutation was detected in 5.37% (1182/22,009) of the patients' samples. 2018 Antiviral research Abstract HBV A181T 6 11 RT 4 6 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. The rtA181T-causative sW172*, sW172non-stop (sW172 L/S), and mixed sW172*/non-stop mutations occupied 82.91%, 7.70%, and 9.39%, respectively. 2018 Antiviral research Abstract HBV A181T;W172X;W172L;W172S;W172X 6;22;45;45;67 11;28;54;54;82 RT;S;S;S;S 4;22;30;45;67 6;23;31;46;68 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. The rtA181T/sW172non-stop mutation had a higher ratio of coexistence with adefovir-resistant mutation compared to rtA181T/sW172* mutation (42.86% vs. 2018 Antiviral research Abstract HBV W172X;A181T;A181T 122;6;116 128;11;121 RT;S;RT;S 4;12;114;122 6;13;116;123 29630974 Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation. The study aimed to characterize rtA181T/sW172stop (*) and rtA181T/sW172non-stop mutations of hepatitis B virus (HBV). 2018 Antiviral research Abstract HBV W172X;A181T;A181T 40;34;60 49;39;65 RT;S;RT;S 32;40;58;66 34;41;60;67 29642827 [Analysis of hepatitis B virus (HBV) preS1, preS2 and S gene regions from patient groups infected with HBV genotype D]. The amino acid variants were as follows; PreS1: A33T, A39T, P41K, D44del, D50N, T51P, D54N, L65P/M, F67L, W77T, A81S, Q82E, I84T, L85I/M, Q86H/T, L88S, A90T/V, N91K/del, A95P, S96A, T97I/A, N98K, Q100K, S101T, S109T, P110S, N114D/E, PreS2: M1V, Q2R, S5H, F8S, H9Q, Q13L, D14N, R16K, R18K, G19S/D, F22L/S, S28T, G30E, N33T, V39A, P41H/L, I42T/L, I45T, F46Y, S47L, R48K, I49T, D51V/G, P52L, A53V, L54R/G, N55K; S gene: E2D, I4F, F8L, G10A, V14A, F20S, L22del, R24K, P29L, Q30K, N40S, F41del, G44E, T45L, T46P, V47A, L49R, Q54R, P56L, S64F, P70A, M75I, C76Y, R79H, I81T, F83C, L88P, L94S, Y100F, Q101H/R, M103L, L104F, L109I/M, I110L, G112S/R, S113N/P, S114A/del, T115I, T116N, T118A/K, P120A/T, T123A, in "a" determinant; T126I, Q129H/R, T131N, M133T, Y134N, S136Y, S143L/M/T, D144E, G145A/R. 2018 Mikrobiyoloji bulteni Abstract HBV A33T;A39T;P41K;D44del;D50N;T51P;D54N;L65P;L65M;F67L;W77T;A81S;Q82E;I84T;L85I;L85M;Q86H;Q86T;L88S;A90T;A90V;N91K;A95P;S96A;T97I;T97A;N98K;Q100K;S101T;S109T;P110S;N114D;N114E;S5H;H9Q;Q13L;D14N;R16K;R18K;G19S;G19D;F22L;F22S;S28T;G30E;N33T;V39A;P41H;P41L;I42T;I42L;I45T;F46Y;S47L;R48K;I49T;D51V;D51G;P52L;A53V;L54R;L54G;N55K;F8L;G10A;V14A;F20S;L22del;R24K;P29L;Q30K;N40S;F41del;G44E;T45L;T46P;V47A;L49R;Q54R;P56L;S64F;P70A;M75I;C76Y;R79H;I81T;F83C;L88P;L94S;Y100F;Q101H;Q101R;M103L;L104F;L109I;L109M;I110L;G112S;G112R;S113N;S113P;S114A;T115I;T116N;T118A;T118K;P120A;P120T;T123A;T126I;Q129H;Q129R;T131N;M133T;Y134N;S136Y;S143L;S143M;S143T;D144E;G145A;G145R;M1V;Q2R;F8S;E2D;I4F 48;54;60;66;74;80;86;92;92;100;106;112;118;124;130;130;138;138;146;152;152;160;170;176;182;182;190;196;203;210;217;224;224;250;260;265;271;277;283;289;289;297;297;305;311;317;323;329;329;337;337;345;351;357;363;369;375;375;383;389;395;395;403;427;432;438;444;450;458;464;470;476;482;490;496;502;508;514;520;526;532;538;544;550;556;562;568;574;580;586;593;593;602;609;616;616;625;632;632;641;641;650;661;668;675;675;684;684;693;720;727;727;736;743;750;757;764;764;764;775;782;782;240;245;255;417;422 52;58;64;72;78;84;90;98;98;104;110;116;122;128;136;136;144;144;150;158;158;168;174;180;188;188;194;201;208;215;222;231;231;253;263;269;275;281;287;295;295;303;303;309;315;321;327;335;335;343;343;349;355;361;367;373;381;381;387;393;401;401;407;430;436;442;448;456;462;468;474;480;488;494;500;506;512;518;524;530;536;542;548;554;560;566;572;578;584;591;600;600;607;614;623;623;630;639;639;648;648;659;666;673;682;682;691;691;698;725;734;734;741;748;755;762;773;773;773;780;789;789;243;248;258;420;425 PreS1;PreS2;S 41;233;409 46;238;410 29652648 Pre-S2 Start Codon Mutation of Hepatitis B Virus Subgenotype B3 Effects on NF-kappaB Expression and Activation in Huh7 Cell Lines. A cross-sectional study on hepatitis B patients in Indonesia showed association of pre-S2 start codon mutation (M120 V) with cirrhosis and hepatocellular carcinoma (HCC), which was dissimilar from studies from other populations where pre-S2 deletion mutation was more prevalent. 2018 Viral immunology Abstract HBV M120V 112 118 PreS2;PreS2 83;234 89;240 Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma 125;139;165 134;163;168 29652648 Pre-S2 Start Codon Mutation of Hepatitis B Virus Subgenotype B3 Effects on NF-kappaB Expression and Activation in Huh7 Cell Lines. HBV subgenotypes B3, each carrying wild-type (wt) HBs, M120 V, and pre-S2 deletion mutation were isolated from three HCC patients. 2018 Viral immunology Abstract HBV M120V 55 61 S;PreS2 50;67 53;73 Hepatocellular carcinoma 117 120 29652648 Pre-S2 Start Codon Mutation of Hepatitis B Virus Subgenotype B3 Effects on NF-kappaB Expression and Activation in Huh7 Cell Lines. However, M120 V mutation may utilize a different pathway in liver disease progression that involves high expression of NF-kappaB subunit, p50. 2018 Viral immunology Abstract HBV M120V 9 15 Liver disease 60 73 29652648 Pre-S2 Start Codon Mutation of Hepatitis B Virus Subgenotype B3 Effects on NF-kappaB Expression and Activation in Huh7 Cell Lines. M120 V mutant had a significantly higher mRNA level compared with wt and pre-S2 deletion mutant; however, there were no significant differences in HBs protein expressions. 2018 Viral immunology Abstract HBV M120V 0 6 S;PreS2 147;73 150;79 29652648 Pre-S2 Start Codon Mutation of Hepatitis B Virus Subgenotype B3 Effects on NF-kappaB Expression and Activation in Huh7 Cell Lines. The transcription level of p50 was higher in M120 V mutation compared with HBs wild-type and pre-S2 deletion mutant. 2018 Viral immunology Abstract HBV M120V 45 51 S;PreS2 75;93 78;99 29654894 Trends in hepatitis B virus resistance to nucleoside/nucleotide analogues in North China from 2009-2016: A retrospective study. Despite >50% of M204I/V+-L180M among all HBV resistance cases annually and extensive exposure of patients to lamivudine (LAM), telbivudine (LdT) and adefovir dipivoxil (ADV), ETV resistance also showed a dramatically increased incidence, which rose to 17.1% in 2016. 2018 International journal of antimicrobial agents Abstract HBV M204I;M204V;L180M 16;16;25 23;23;30 29654894 Trends in hepatitis B virus resistance to nucleoside/nucleotide analogues in North China from 2009-2016: A retrospective study. Moreover, A181T/V, ETV resistance mutations and multidrug resistance mutations were found more frequently in HBV genotype C compared with genotype B (21.2% vs. 2018 International journal of antimicrobial agents Abstract HBV A181T;A181V 10;10 17;17 29654894 Trends in hepatitis B virus resistance to nucleoside/nucleotide analogues in North China from 2009-2016: A retrospective study. whereas M204I and N236T were more predominant in genotype B than genotype C (40.3% vs. 2018 International journal of antimicrobial agents Abstract HBV M204I;N236T 8;18 13;23 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. Association of the pcG1896A mutation with time to undetectable HBV-DNA, hepatitis B "e" antigen (HBeAg) seroclearance (in HBeAg-positive patients), and hepatitis B surface antigen (HBsAg) seroclearance was evaluated using Cox proportional hazards regression. 2018 Journal of viral hepatitis Abstract HBV G1896A 20 27 C;C;S;Precore;S 97;122;181;19;164 102;127;186;21;171 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. Baseline pcG1896A mutation was identified in 51 (59.3%) patients, who were more commonly HBeAg-negative (P < .001) and had basal core promotor A1762T/G1764A mutations (P < .001). 2018 Journal of viral hepatitis Abstract HBV G1764A;G1896A;A1762T 150;10;143 156;17;149 BCP;C;Precore 123;89;9 142;94;11 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. Cumulative proportion of undetectable HBV-DNA was significantly higher in patients with baseline mutation (pcG1896A = 86.6% vs no pcG1896A = 66.9%, P = .04), but not after adjusting for baseline HBV-DNA levels and anti-HBV agent (P = .2). 2018 Journal of viral hepatitis Abstract HBV G1896A;G1896A 108;131 115;138 Precore;Precore 107;130 109;132 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. In conclusion, lacking the pcG1896A mutation before ARV initiation appeared to increase HBsAg seroclearance rates during treatment. 2018 Journal of viral hepatitis Abstract HBV G1896A 28 35 S;Precore 88;27 93;29 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. No difference in cumulative proportion of HBeAg seroclearance was observed between mutation groups (pcG1896A = 57.1% vs no pcG1896A = 54.3%, P = .7). 2018 Journal of viral hepatitis Abstract HBV G1896A;G1896A 101;124 108;131 C;Precore;Precore 42;100;123 47;102;125 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. Significantly higher cumulative proportion of HBsAg seroclearance was observed in patients without this mutation (pcG1896A = 0% vs no pcG1896A = 36.9%, P < .001), even after adjusting for baseline HBsAg quantification and anti-HBV agent (P < .001). 2018 Journal of viral hepatitis Abstract HBV G1896A;G1896A 115;135 122;142 S;S;Precore;Precore 46;197;114;134 51;202;116;136 29660214 Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa. The nucleotide substitution G1896A on the precore (pc) region has been implicated in virological and serological responses during treatment in hepatitis B virus (HBV)-infected patients. 2018 Journal of viral hepatitis Abstract HBV G1896A 28 34 Precore;Precore 51;42 53;49 HBV infections 143 175 29663445 Mutations within the major hydrophilic region (MHR) of Hepatitis B virus from individuals with simultaneous HBsAg and anti-HBs in Guangzhou, Southern China. In addition, sQ101 K, sT131N, and sM133L were more frequently discovered in group I with significant difference (P < 0.05). 2018 Journal of medical virology Abstract HBV Q101K;T131N;M133L 13;22;34 20;28;40 S;S;S 13;22;34 14;23;35 29669831 Hepatitis B Virus Core Protein Dephosphorylation Occurs during Pregenomic RNA Encapsidation. Moreover, core proteins with point mutations at the wall of the HAP pocket, V124A and V124W, assembled empty capsids and nucleocapsids with altered phosphorylation status. 2018 Journal of virology Abstract HBV V124A;V124W 76;86 81;91 Capsid;C 109;10 116;14 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Eight mutations in RT (rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V, and rtM309K) are significantly associated with HCC progression. 2018 World journal of gastroenterology Abstract HBV L80I;D134N;N139K;N139T;N139H;Y141F;M204I;M204V;F221Y;I224V;M309K 25;33;42;42;42;55;64;64;75;84;97 29;38;51;51;51;60;71;71;80;89;102 RT;RT;RT;RT;RT;RT;RT;RT;RT 19;23;31;40;53;62;73;82;95 21;25;33;42;55;64;75;84;97 Hepatocellular carcinoma 138 141 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. CONCLUSIONS: preliminary selection of recombinant HBsAg containing G145R mutation with antigenic and immunogenic properties similar to the native analogue creates the basis for development of a specifc component of hepatitis B vaccine with escape mutation G145R in HBsAg. 2017 Voprosy virusologii Abstract HBV G145R;G145R 67;256 72;261 S;S 50;265 55;270 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. METHODS: antigenic properties of recombinant HBsAg with G145R mutation were compared with each other and with native mutants by serological fngerprinting method. 2017 Voprosy virusologii Abstract HBV G145R 56 61 S 45 50 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. Mutant G145R also differs from a wild type HBsAg by its immunogenic properties. 2017 Voprosy virusologii Abstract HBV G145R 7 12 S 43 48 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. OBJECTIVES: a comparative study of antigenic and immunogenic properties of native and recombinant G145R mutants and an estimation of possibility for developing antigenic component of hepatitis B vaccine with G145R mutation in HBsAg. 2017 Voprosy virusologii Abstract HBV G145R;G145R 98;208 103;213 S 226 231 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. Prevalent G145R mutation in S-gene leads to the most expressed changes of serological properties of HBV. 2017 Voprosy virusologii Abstract HBV G145R 10 15 S 28 29 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. RESULTS: it was found that not all the recombinant HBsAg variants with G145R substitution have the same antigenic properties as native HBsAg with similar mutation. 2017 Voprosy virusologii Abstract HBV G145R 71 76 S;S 51;135 56;140 29733168 [A comparative characteristic of antigenic properties of recombinant and native hbs-antigens with G145R mutation and evaluation of their immunogenicity]. Titers of antibodies specifc to wild type or mutant G145R type of HBsAg in sera of immunized animals were measured. 2017 Voprosy virusologii Abstract HBV G145R 52 57 S 66 71 29739114 Mutations in Core Gene Region of Hepatitis B Virus in Patients with Chronic Hepatitis B. Some types of mutations (V27I, R47H, Y132I, R174STOP, S181P, Q182K) were only detected in subjects with liver cirrhosis. 2018 Clinical laboratory Abstract HBV V27I;R47H;Y132I;R174X;S181P;Q182K 25;31;37;44;54;61 29;35;42;52;59;66 Liver cirrhosis 104 119 29804376 [Monitoring by high-sensitivity HBV DNA assay during treatment in chronic hepatitis B e antigen negative patients]. After treatment, the detection rate of the above mutation sites decreased, but C1653T, C1673T and G1899A were not detected. 2018 Zhonghua gan zang bing za zhi Abstract HBV C1653T;C1673T;G1899A 79;87;98 85;93;104 29804376 [Monitoring by high-sensitivity HBV DNA assay during treatment in chronic hepatitis B e antigen negative patients]. For 49 cases of HBeAg-negative patients, HBV B, C, B and C were mixed before tenofovir dipivoxil treatment, and C1653T, A1762T and G1764A mutation sites were detected in patients with D genotype. 2018 Zhonghua gan zang bing za zhi Abstract HBV C1653T;A1762T;G1764A 112;120;131 118;126;137 C 16 21 29804376 [Monitoring by high-sensitivity HBV DNA assay during treatment in chronic hepatitis B e antigen negative patients]. New mutation sites such as G1915A / C, L180M, M204V, V207I / L, T184A and V173L were detected, Low resistance rate (25%). 2018 Zhonghua gan zang bing za zhi Abstract HBV G1915A;V207I;V207L;G1915A;G1915C;L180M;M204V;V207I;T184A;V173L 27;53;53;27;27;39;46;53;64;74 33;62;62;37;37;44;51;58;69;79 29804376 [Monitoring by high-sensitivity HBV DNA assay during treatment in chronic hepatitis B e antigen negative patients]. Patients C, B, C, B, and C were examined for C1673T, G1896, G1858, G1899A. 2018 Zhonghua gan zang bing za zhi Abstract HBV C1673T;G1899A 45;67 51;73 29843851 Fulminant hepatitis B virus (HBV) infection in an infant following mother-to-child transmission of an e-minus HBV mutant: Time to relook at HBV prophylaxis in South African infants. Genetic analysis of virus from mother and infant showed that both had the G1896A mutation in the preC/C gene, which truncates hepatitis e antigen (HBeAg) during translation, causing an HBeAg-negative phenotype. 2018 South African medical journal Abstract HBV G1896A 74 80 C;C;C;Precore;C 136;147;185;97;102 145;152;190;101;103 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Strong correlation was observed between sP120T and rtM204I/V (P < 0.001), and their co-presence determined an increased HBV-DNA. 2018 BMC infectious diseases Abstract HBV M204I;M204V;P120T 53;53;40 60;60;46 RT;S 51;40 53;41 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. The immune-associated escape mutations and the NA-induced immune-escape mutations sI195M, sI196S, and sE164D (resulting from drug-resistance mutation rtM204 V, rtM204I, and rtV173L) were retrieved from literature and examined. 2018 BMC infectious diseases Abstract HBV M204V;M204I;V173L;I195M;I196S;E164D 152;162;175;82;90;102 158;167;180;88;96;108 RT;RT;RT;S;S;S 150;160;173;82;90;102 152;162;175;83;91;103 29859540 Applications of next-generation sequencing analysis for the detection of hepatocellular carcinoma-associated hepatitis B virus mutations. All the 12 HCC-associated SNVs proved by meta-analysis were confirmed by NGS analysis, except for C1766T and T1768A which were mainly expressed in genotypes A and D, but including the subgroup analysis of A1762T. 2018 Journal of biomedical science Abstract HBV C1766T;T1768A;A1762T 98;109;205 104;115;211 Hepatocellular carcinoma 11 14 29893492 An Association Between Core Mutations in Hepatitis B Virus Genotype F1b and Hepatocellular Carcinoma in Alaskan Native People. Clones containing the A2051C mutation replicated more efficiently than the wild type in association with enhanced stability of core protein dimerization. 2019 Hepatology (Baltimore, Md.) Abstract HBV A2051C 22 28 C 127 131 29893492 An Association Between Core Mutations in Hepatitis B Virus Genotype F1b and Hepatocellular Carcinoma in Alaskan Native People. In the HCC patients, T1938C and A2051C mutations in the core region had accumulated significantly with A1762T/G1764A mutations in the basal core promoter (BCP) region and G1896A mutation in the precore (PC) region. 2019 Hepatology (Baltimore, Md.) Abstract HBV G1764A;T1938C;A2051C;A1762T;G1896A 110;21;32;103;171 116;27;38;109;177 BCP;BCP;C;Precore;Precore 134;155;56;203;194 153;158;60;205;201 Hepatocellular carcinoma 7 10 29912972 Characterisation of the hepatitis B virus cross-species transmission pattern via Na+/taurocholate co-transporting polypeptides from 11 New World and Old World primate species. An exchange from arginine to glycine (as present in humans and great apes) at this position (R158G) alone was sufficient to achieve full transport-competing HBV myr-preS1-peptide binding and susceptibility for HBV/HDV infection. 2018 PloS one Abstract HBV R158G 93 98 PreS1 165 170 HBV-HDV coinfections 210 227 29948380 BCP/PC mutation prevalence and their association with HBV replication in HIV/HBV co-infected patients. A1762T, G1764A and G1896A mutations were common mutations identified in the BCP/PC region. 2018 Archives of virology Abstract HBV A1762T;G1764A;G1896A 0;8;19 6;14;25 BCP;Precore 76;80 79;82 29948380 BCP/PC mutation prevalence and their association with HBV replication in HIV/HBV co-infected patients. However, the prevalence of the G1896A mutation was significantly high among the HBeAg negative HIV/HBV co-infected patients, and may be associated with high HBV replication. 2018 Archives of virology Abstract HBV G1896A 31 37 C 80 85 HBV-HIV coinfections 95 114 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. CDDO-me exerted cytotoxic activity against W4P-LHB-expressing NIH3T3 cells, HepG2 cells, and Huh7 cells, and induced apoptotic cell death in a dose-dependent manner, demonstrating its anti-cancer activity against HCC. 2018 Pharmacology Abstract HBV W4P 43 46 S 47 50 Hepatocellular carcinoma 213 216 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. Furthermore, -CDDO-me administration significantly suppressed tumor growth induced by W4P-LHB-expressing NIH3T3 cells in nude mice, confirming its anti-cancer activity. 2018 Pharmacology Abstract HBV W4P 86 89 S 90 93 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. In addition, CDDO-me treatment resulted in decreased cell migration and colony formation in in vitro assays using W4P-LHB-NIH3T3, HepG2, or Huh7 cell lines, supporting its anti-cancer activity through STAT3 inhibition. 2018 Pharmacology Abstract HBV W4P 114 117 S 118 121 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. Previously, we showed that hepatitis B virus (HBV) large surface protein (LHB) variant W4P promotes carcinogenesis and tumor progression through STAT3 activation. 2018 Pharmacology Abstract HBV W4P 87 90 S;S 51;74 64;77 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. Sublethal concentrations of CDDO-me suppressed STAT3 activation by W4P-LHB ectopic expression and interleukin-6 treatment in W4P-LHB-NIH3T3 and Huh7 cells respectively. 2018 Pharmacology Abstract HBV W4P;W4P 67;125 70;128 S;S 71;129 74;132 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. The suppression of STAT3 activation by CDDO-me in W4P-LHB-NIH3T3 cells was further confirmed by decreased cyclin D1 protein levels and increased p21 and p53 mRNA synthesis. 2018 Pharmacology Abstract HBV W4P 50 53 S 54 57 29953997 Bardoxolone Methyl Suppresses Hepatitis B Virus Large Surface Protein Variant W4P-Related Carcinogenesis and Hepatocellular Carcinoma Cell Proliferation Via the Inhibition of Signal Transducer and Activator of Transcription 3 Signaling. Thus, we examined the anti-cancer activity of CDDO-me against HCC using W4P-LHB-expressing NIH3T3 cells and HepG2 and Huh7 HCC cell lines. 2018 Pharmacology Abstract HBV W4P 72 75 S 76 79 Hepatocellular carcinoma;Hepatocellular carcinoma 62;123 65;126 30040979 Identification of a novel tri-genotypic recombinant Hepatitis B virus in Bangladesh. Additionally, the complete genome has a frameshift deletion of nine nucleotides from overlapping Surface and Polymerase genes, and a vaccine escape mutation, A128 V, in the surface protein. 2018 Virus research Abstract HBV A128V 158 164 P;S;S 109;97;173 119;104;180 30043328 Clinical implication and viral mutation in basal core promoter/pre-core of hepatitis B virus C/D recombinant. but a lower frequency of G1896A stop mutation (33.6 vs. 76.5%, p < 0.001) was observed in patients with the C/D recombinant than in patients with genotype C2. 2018 Hepatology international Abstract HBV G1896A 25 31 30043328 Clinical implication and viral mutation in basal core promoter/pre-core of hepatitis B virus C/D recombinant. Significantly higher levels of HBV DNA (6.7 卤 1.6 vs. 5.9 卤 1.5, p = 0.014), HBeAg (263.5 vs. 20.0, p = 0.013) and A1762T/G1764A double-mutations (81.0 vs. 61.8%, p = 0.018) 2018 Hepatology international Abstract HBV G1764A;A1762T 122;115 129;121 30043328 Clinical implication and viral mutation in basal core promoter/pre-core of hepatitis B virus C/D recombinant. The clonal frequencies of A1762T, G1764A, G1896A and A1846T were lower in patients with C/D than C2. 2018 Hepatology international Abstract HBV A1762T;G1764A;G1896A;A1846T 26;34;42;53 32;40;48;59 30075160 Comparison of replication competence of wild-type and lamivudine-resistant hepatitis B virus isolates from a chronic hepatitis B patient. Sequencing reverse transcriptase region of HBV revealed that the patient developed lamivudine-resistant mutations (rtV173 L, rtL180 M, and rtM204 V) 36 months after the start of lamivudine therapy, and lamivudine-resistant mutants reversed to wild-type after the treatment was stopped for 8 months. 2018 Virus research Abstract HBV V173L;L180M;M204V 117;127;141 123;133;147 RT;RT;RT;RT 11;115;125;139 32;117;127;141 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. The reactivated virus was HBV genotype F3 with vaccine escape mutations G145R, P120Q, and Q129P. 2018 World journal of hepatology Abstract HBV G145R;P120Q;Q129P 72;79;90 77;84;95 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. The commonest RAM was rtM204I/V, either alone or in combination with associated mutations, and identified in both reportedly treatment-naive and treatment-experienced adults. 2018 PLoS neglected tropical diseases Abstract HBV M204I;M204V 24;24 31;31 RT 22 24 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. We also identified the suite of mutations rtM204V/I + rtL180M + rtV173L, that has been associated with vaccine escape, in over 1/3 of cohorts. 2018 PLoS neglected tropical diseases Abstract HBV M204V;M204I;L180M;V173L 44;44;56;66 51;51;61;71 RT;RT;RT 42;54;64 44;56;66 30089690 Assembly Properties of Hepatitis B Virus Core Protein Mutants Correlate with Their Resistance to Assembly-Directed Antivirals. We examined the effects of two closely related CpAMs, HAP12 and HAP13, which differ by a single atom but have drastically different antiviral activities, on the assembly of wild-type Cp and three T109 mutants (T109M, T109I, and T109S) that display a range of resistances. 2018 Journal of virology Abstract HBV T109M;T109I;T109S 210;217;228 215;222;233 C 183 185 30092176 HBV epidemiology and genetic diversity in an area of high prevalence of hepatitis B in southern Brazil. LAM-resistant mutation (rtM204I) and ADV-resistant mutations (rtA181V) were detected in only one patient each. 2018 The Brazilian journal of infectious diseases Abstract HBV M204I;A181V 26;64 31;69 RT;RT 24;62 26;64 30095435 Association of characteristics of HBV quasispecies with hepatitis B surface antigen seroconversion after pegylated interferon-alpha-2a treatment in child patients. The baseline mutations A1762T/G1764A, C1913A, and T2003A/G or C2004T were correlated with non-response to therapy (P=0.025, P=0.036, P=0.032, respectively). 2018 Antiviral therapy Abstract HBV G1764A;A1762T;C1913A;T2003A;T2003G;C2004T 30;23;38;50;50;62 36;29;44;58;58;68 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. With hepatitis B virus double mutation (HBVDM) and KRAS G12V point mutation as model double mutations, it is shown that PEPS was able to detect double-stranded HBVDM and KRAS with 70% detection efficiency or better at concentration as low as 10-19 M against single-stranded mutation detection at the same concentrations, which was validated by the following in situ fluorescent reporter microspheres (FRMs) detection as well as microscopic visualization of the FRMs bound to the captured mutant on the PEPS surface. 2018 Biosensors & bioelectronics Abstract HBV G12V 56 60 S 507 514 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. And vtHBsAg with Q129 N impaired HBV replication ability. 2018 Virus research Abstract HBV Q129N 17 23 S 6 11 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. Antigenicity of vtHBsAg of Q129 N and T131 N/M133 T was reduced compared with wild type (wt) HBsAg. 2018 Virus research Abstract HBV Q129N;T131N;M133T 27;38;45 33;44;51 S;S 18;93 23;98 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. Expression plasmids of vtHBsAg with aa substitutions Q129 L, T123 N, Q129 N and T131 N/M133 T were constructed. 2018 Virus research Abstract HBV Q129L;T123N;Q129N;T131N;M133T 53;61;69;80;87 59;67;75;86;93 S 25 30 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. Further, we discovered that vtHBsAg with Q129 N distinctly impaired HBV replication capacity, but vtHBsAg with T131 N/M133 T had no impact on viral replication. 2018 Virus research Abstract HBV Q129N;M133T 41;116 47;124 S;S 30;100 35;105 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. In addition, we discovered impaired ability to induce anti-HBs responses against wtHBsAg in mice immunized with plasmids pHBsAg- Q129 N and T131 N/M133 T. 2018 Virus research Abstract HBV Q129N;T131N;M133T 129;139;147 135;145;153 S;S 59;83 62;88 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. In our study, we aim to investigate biological significance of amino acid (aa) substitutions in HBsAg, Q129 N and T131 N/M133 T, for glycosylation, antigenicity and immunogenicity of variant HBsAg (vtHBsAg) and viral replication. 2018 Virus research Abstract HBV Q129N;T131N;M133T 103;113;121 109;119;127 S;S;S 96;191;200 101;196;205 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. Thus, we conclude that vtHBsAg with Q129 N or T131 N/M133 T creates new N-glycosylation and interferes with both the antigenicity and immunogenicity of vtHBsAg. 2018 Virus research Abstract HBV Q129N;T131N;M133T 36;45;53 42;51;59 S;S 25;154 30;159 30179704 Amino acid substitutions Q129N and T131N/M133T in hepatitis B surface antigen (HBsAg) interfere with the immunogenicity of the corresponding HBsAg or viral replication ability. vtHBsAg of Q129 N and T131 N/M133 T created new N-glycosylation and displayed perinuclear distribution by IF staining with the anti-HA. 2018 Virus research Abstract HBV Q129N;T131N;M133T 11;21;29 17;27;35 S 2 7 30184362 Genetic variability in coding regions of the surface antigen and reverse transcriptase domain of hepatitis B virus polymerase, Colombia, 2002-2014 A single escape mutation, P120Q, was identified in one more. 2018 Biomedica Abstract HBV P120Q 26 31 30184362 Genetic variability in coding regions of the surface antigen and reverse transcriptase domain of hepatitis B virus polymerase, Colombia, 2002-2014 The L180M and M204V resistance mutations were simultaneously identified in one sample, while the I169L resistance mutation was identified in another one. 2018 Biomedica Abstract HBV L180M;M204V;I169L 4;14;97 9;19;102 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Conclusion: An integrated genotypic analysis of HBV RT sequences from patients with chronic HBV treated with ETV led to the discovery of the novel ETVr substitution rtA181C. 2018 Hepatology communications Abstract HBV A181C 167 172 RT;RT 52;165 54;167 Chronic Hepatitis B 84 95 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV harboring the rtA181C substitution without LVDr substitutions rtL180M+rtM204V remained susceptible to inhibition by ETV, adefovir, and tenofovir, although cross-resistance to LVD and telbivudine was observed. 2018 Hepatology communications Abstract HBV A181C;L180M;M204V 20;68;76 25;73;81 RT;RT;RT 18;66;74 20;68;76 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One LVD-experienced patient-derived HBV RT harboring LVDr substitutions rtL180M+rtM204V with rtA181C displayed reduced ETV susceptibility (122-fold greater than wild-type HBV) and remained susceptible to adefovir and tenofovir. 2018 Hepatology communications Abstract HBV A181C;L180M;M204V 95;74;82 100;79;87 RT;RT;RT;RT 40;72;80;93 42;74;82;95 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous studies revealed that ETV-resistant (ETVr) HBV DNA resulted from substitutions in the HBV reverse transcriptase (RT) at positions rtT184, rtS202, or rtM250 in combination with lamivudine resistance (LVDr) substitutions rtM204I/V+-rtL180M. 2018 Hepatology communications Abstract HBV M204I;M204V;L180M 230;230;241 237;237;246 RT;RT;RT;RT;RT;RT;RT 99;122;139;147;158;228;239 120;124;141;149;160;230;241 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. This substitution was always detected in combination with LVDr substitutions rtL180M+rtM204V in ETV-treated patients. 2018 Hepatology communications Abstract HBV L180M;M204V 79;87 84;92 RT;RT 77;85 79;87 30229977 Clinical Outcome and Viral Genome Variability of Hepatitis B Virus-Induced Acute Liver Failure. Amino acid deletions (del; 16-22 and 20-22) in preS2 and SHB mutation L49R were exclusively detected in patients with ALF-NSR. 2019 Hepatology (Baltimore, Md.) Abstract HBV L49R 70 74 Small S;PreS2 57;47 60;52 Liver disease 118 121 30257068 Effect of hepatitis B virus (HBV) surface-gene variability on markers of replication during treated human immunodeficiency virus-HBV infection in Western Africa. Twelve S-gene MUPIQHs were identified among 21 patients (28.8%): sS140L (n = 4), sD144A (n = 1), sS167L (n = 2), sS174N (n = 6), sP178Q (n = 2), sG185L (n = 2), sW191L (n = 2), sP203Q/R (n = 2), sS204N/I/R/K/T/G (n = 7), sN207T (n = 2), sF212C (n = 1) and sV224A/Y (n = 7). 2019 Liver international Abstract HBV S140L;D144A;S167L;S174N;P178Q;G185L;W191L;P203Q;P203R;S204N;S204I;S204R;S204K;S204T;S204G;N207T;F212C;V224A;V224Y 65;81;97;113;129;145;161;177;177;195;195;195;195;195;195;221;237;256;256 71;87;103;119;135;151;167;185;185;211;211;211;211;211;211;227;243;264;264 S;S;S;S;S;S;S;S;S;S;S;S;S 7;65;81;97;113;129;145;161;177;195;221;237;256 8;66;82;98;114;130;146;162;178;196;222;238;257 30285571 Predictors of Therapeutic Outcome to Nucleotide Reverse Transcriptase Inhibitor in Hepatitis B Patients. Another mutation rtN248H observed in E motif considered to have effect on DNA primer grip, which forms part of binding pocket. 2018 Viral immunology Abstract HBV N248H 19 24 RT 17 19 30285571 Predictors of Therapeutic Outcome to Nucleotide Reverse Transcriptase Inhibitor in Hepatitis B Patients. The A-B motif interdomain rtL122F mutation was found in nonresponder patients in our study. 2018 Viral immunology Abstract HBV L122F 28 33 RT 26 28 30317788 [Correlation between serum HBV DNA level and HBsAg titer in HBeAg-positive pregnant women and impact of genomic variability of hepatitis B virus pre S/S regions on their correlations]. Compared with the control group, mutation sites A60V (100% vs. 15.38%,聽蠂(2) = 7.61,聽P聽< 0.01), V90A (100% vs. 30.77%,聽蠂(2) = 4.43,聽P聽< 0.05) and I161T of HBV preS/S region (80.00% vs. 0,聽蠂(2) = 9.14,聽P聽< 0.01) showed a significant decrease in HBsAg titer. 2018 Zhonghua gan zang bing za zhi Abstract HBV V90A;I161T;A60V 95;145;48 99;150;52 30317788 [Correlation between serum HBV DNA level and HBsAg titer in HBeAg-positive pregnant women and impact of genomic variability of hepatitis B virus pre S/S regions on their correlations]. Single or multiple amino acid mutations sites A60V, V90A, and I161T in preS/S region may be one of the reasons that lead to a significant drop in HBsAg titer and affect its correlation with HBV DNA levels. 2018 Zhonghua gan zang bing za zhi Abstract HBV A60V;V90A;I161T 46;52;62 50;56;67 S;PreS;S 146;71;76 151;75;77 30345529 Epidemiology, risk factors, and molecular characterization of occult hepatitis B infection among anti-hepatitis B core antigen alone subjects. Important mutations in surface protein and reverse transcriptase were sI92T, sQ129H, rtL80I, rtS85F, rtL91I. 2019 Journal of medical virology Abstract HBV L80I;S85F;L91I;I92T;Q129H 87;95;103;70;77 91;99;107;75;83 RT;RT;RT;RT;S;S;S 43;85;93;101;70;77;23 64;87;95;103;71;78;30 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. By performing Co-IP assay in HBV-free Huh7 cells expressing wild-type HBx, mutant HBx-S31A, or HBx-S31D (serine31 was mutated into alanine31 or aspartic acid31 ), we found that the phosphorylated serine31 with its near amino acid residues constituted a RPLphosphoS31 GP (R, arginine; P, proline; L, leucine; S, serine; G, glycine) motif in HBx for 14-3-3zeta docking. 2018 Cancer medicine Abstract HBV S31A;S31D 86;99 90;103 X;X;X;X;S 70;82;95;340;308 73;85;98;343;309 30368502 High Prevalence of HBV Lamivudine-Resistant Mutations in HBV/HIV Co-Infected Patients on Antiretroviral Therapy in the Area with the Highest Prevalence of HIV/HBV Co-Infection in China. The major pattern of lamivudine (3TC)-resistant mutations is L180M+M204I+L80I (35.7%). 2018 Intervirology Abstract HBV L180M;M204I;L80I 61;67;73 66;72;77 30377627 Hepatitis B Virus (HBV) Infection and Re-activation During Nucleos(t)ide Reverse Transcriptase Inhibitor-Sparing Antiretroviral Therapy in a High-HBV Endemicity Setting. In one case of reactivation, anti-HBs increased from 14 to >1000 IU/L; sequencing showed HBV genotype A3 and 3 escape mutations in surface (Y100C, K122R, Y161FY). 2018 Open forum infectious diseases Abstract HBV Y100C;K122R;Y161F;Y161Y 140;147;154;154 145;152;160;160 S;S 34;131 37;138 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. The escape mutations sP120L, sG130R, sY134H, and sD144A were identified predominantly among HBV isolates from blood donors. 2019 Virus genes Abstract HBV P120L;G130R;Y134H;D144A 21;29;37;49 27;35;43;55 S;S;S;S 21;29;37;49 22;30;38;50 30404796 Hepatitis B e Antigen Inhibits NF-kappaB Activity by Interrupting K63-Linked Ubiquitination of NEMO. It is reported that the hepatitis B e antigen (HBeAg) can interfere with NF-kappaB activity, which then leads to high viral loads, while HBV with the G1896A mutation remains infectious without the production of HBeAg but can induce more severe proinflammatory response and liver damage. 2019 Journal of virology Abstract HBV G1896A 150 156 C;C;C 36;47;211 45;52;216 Liver disease 273 285 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Multivariate risk analysis confirmed that the core mutations A80V and L116I were both independent predictors of HBV-associated liver disease progression. 2018 Frontiers in cellular and infection microbiology Abstract HBV A80V;L116I 61;70 65;75 C 46 50 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Six of the seven significant core mutations that were identified in this study were located within immuno-active epitopes; E77Q, A80I/T/V, and L116I were located within B-cell epitopes, and F24Y, E64D, and V91S/T were located within T-cell epitopes. 2018 Frontiers in cellular and infection microbiology Abstract HBV E77Q;A80I;A80T;A80V;L116I;F24Y;E64D;V91S;V91T 123;129;129;129;143;190;196;206;206 127;137;137;137;148;194;200;212;212 C 29 33 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Two precore mutations, W28* and G29D, and six core mutations, F24Y, E64D, E77Q, A80I/T/V, L116I, and E180A were significantly associated with the development of cirrhosis and HCC. 2018 Frontiers in cellular and infection microbiology Abstract HBV G29D;F24Y;E64D;E77Q;L116I;E180A;W28X;A80I;A80T;A80V 32;62;68;74;90;101;23;80;80;80 36;66;72;78;95;106;27;88;88;88 C;Precore 46;4 50;11 Liver cirrhosis;Hepatocellular carcinoma 161;175 170;178 30417200 Analysis of fitness differences of hepatitis B virus genotypes D and F using a cotransfection assay. Our results show that for the subgenotype (sgt) D1, which has an 8-nucleotide deletion (sgtD1del) and exhibits lower fitness, the levels of extracellular DNA and intracellular replicative intermediates were much lower than with sgtD1wt or sgtD1mut (G1896A), which had higher fitness. 2019 Archives of virology Abstract HBV G1896A 249 255 30421112 In Vitro Anti-hepatitis B Virus Activity of 2',3'-Dideoxyguanosine. Furthermore, using a transient transfection assay, DoG showed similar antiviral activity against HBV wild-type, 3TC-resistant rtA181V, and adefovir-resistant rtN236T mutants. 2018 Virologica Sinica Abstract HBV A181V;N236T 128;160 133;165 RT;RT 126;158 128;160 30462954 [Risk factors analysis and a new risk scoring system predicting hepatocarcinogenesis for chronic genotype C HBV infected patients]. In genotype C HBV infected patients, male gender, aged 40 years and over, and four DNA mutations (T1674CG, A1762T/G1764A, A3120T, and A2962G) can increase the risk of HCC (P<0.05); interferon therapy can reduce the risk of HCC (P<0.05). 2018 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T;A3120T;A2962G 114;107;122;134 120;113;128;140 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 167;223;14 170;226;26 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. CONCLUSIONS: F30V was closely correlated with HBV-induced HCC in vivo, reduced HBV replicative efficiency by affecting HBx-binding to cccDNA and increased anti-apoptotic HBx activity in vitro. 2019 Clinical microbiology and infection Abstract HBV F30V 13 17 X;X 119;170 122;173 Hepatocellular carcinoma 58 61 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. F30V also decreased the percentage of apoptotic cells compared with wild-type (14.8 +- 6.8% versus 19.1 +- 10.1%, p <0.01, without affecting cell-cycle progression) and increased the probability of HBx-Ser-31 being phosphorylated by PI3K-Akt kinase (known to promote anti-apoptotic activity). 2019 Clinical microbiology and infection Abstract HBV F30V 0 4 X 198 201 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. In vitro, F30V determined a 40% and 60% reduction in pgRNA and core-associated HBV-DNA compared with wild-type (p <0.05), in parallel with a significant decrease of HBx binding to cccDNA and decreased HBx stability. 2019 Clinical microbiology and infection Abstract HBV F30V 10 14 C;X;X 63;165;201 67;168;204 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. RESULTS: F30V was the only HBx mutation correlated with HCC (18.5% (5/27) in HCC patients versus 1.0% (1/96) in non-HCC patients, p 0.002); a result confirmed by multivariate analysis. 2019 Clinical microbiology and infection Abstract HBV F30V 9 13 X 27 30 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 56;77;116 59;80;119 30472417 The novel HBx mutation F30V correlates with hepatocellular carcinoma in vivo, reduces hepatitis B virus replicative efficiency and enhances anti-apoptotic activity of HBx N terminus in vitro. This suggests that F30V (although hampering HBV's replicative capacity) may promote hepatocyte survival, so potentially allowing persistent production of viral progeny and initiating HBV-driven hepatocarcinogenesis. 2019 Clinical microbiology and infection Abstract HBV F30V 19 23 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. It is of utmost importance to screen the G1896A precore mutation. 2018 Saudi journal of biological sciences Abstract HBV G1896A 41 47 Precore 48 55 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. LCR can be a suitable tool for screening of G1896A mutations. 2018 Saudi journal of biological sciences Abstract HBV G1896A 44 50 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Patients were screened for the presence or absence of precore G1896A mutation by PCR-LCR. 2018 Saudi journal of biological sciences Abstract HBV G1896A 62 68 Precore 54 61 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The exceptionally high prevalence of G1896A in FH and HCC demonstrates that the precore mutants are strongly associated with the progression of liver diseases in patients with HBeAg negative serology. 2018 Saudi journal of biological sciences Abstract HBV G1896A 37 43 C;Precore 176;80 181;87 Fulminant Hepatitis B;Hepatocellular carcinoma;Liver disease 47;54;144 49;57;158 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The findings are also suggestive of screening HBV precore G1896A mutation particularly in HBeAg negative cases. 2018 Saudi journal of biological sciences Abstract HBV G1896A 58 64 C;Precore 90;50 95;57 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation increases proportionately in severe form of liver diseases. 2018 Saudi journal of biological sciences Abstract HBV G1896A 12 18 Precore 4 11 Liver disease 72 86 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The serum ALT level was statistically significant between HBeAg negative WT and G1896A mutants in chronic hepatitis cases. 2018 Saudi journal of biological sciences Abstract HBV G1896A 80 86 C 58 63 Chronic Hepatitis B 98 115 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The study was designed to assess the impact of G1986A mutations in patients with different clinical spectra of the liver disease by PCR-LCR. 2018 Saudi journal of biological sciences Abstract HBV G1986A 47 53 Liver disease 115 128 30570771 Hepatitis B virus in Mar del Plata, Argentina: Genomic characterization and evolutionary analysis of subgenotype F1b. A unique D3 presented the G1896A substitution at the preC (HBeAg negative phenotype). 2019 Journal of medical virology Abstract HBV G1896A 26 32 C;Precore 59;53 64;57 30570771 Hepatitis B virus in Mar del Plata, Argentina: Genomic characterization and evolutionary analysis of subgenotype F1b. The double substitution G1764A/A1762T at the BCP (reduced HBeAg expression) was found in 20% F1b, 2% A2, 2% D1, and 2% D3 samples. 2019 Journal of medical virology Abstract HBV A1762T;G1764A 31;24 37;30 BCP;C 45;58 48;63 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Of these M184 V (12.5%), K70R (10.0%), K103 N (12.5%), Y181C (10.0%), M46 L (2.5%) and L90 M (2.5%) were most frequently identified, suggesting resistance to lamivudine, nevirapine, efavirenz and zidovudine. 2018 BMC pregnancy and childbirth Abstract HBV M184V;K70R;K103N;Y181C;M46L;L90M 9;25;39;55;70;87 15;29;45;60;75;92 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Furthermore, reactivated HBV in 11 of 16 (69%) non-HSCT cases possessed substitutions associated with impaired virion secretion, including E2G, L77R, L98V, T118K, and Q129H in the S region, and M1I/V in the PreS2 region. 2018 Scientific reports Abstract HBV L77R;L98V;T118K;Q129H;E2G;M1I;M1V 144;150;156;167;139;194;194 148;154;161;172;142;199;199 PreS2;S 207;180 212;181 Hematopoietic stem cell transplantation 51 55 30586543 Novel fluoronucleoside analog NCC inhibits lamivudine-resistant hepatitis B virus in a hepatocyte model. We generated a stable cell line encoding the major pattern of lamivudine-resistant mutations rtL180M/M204V and designated it "HepG2.RL1". 2018 The Brazilian journal of infectious diseases Abstract HBV M204V;L180M 101;95 106;100 RT 93 95 30589264 Synthesis of an Anti-hepatitis B Agent, 2'-Fluoro-6'-methylene-carbocyclic Adenosine (FMCA) and Its Phosphoramidate (FMCAP). 2'-Fluoro-6'-methylene-carbocyclic adenosine (FMCA, 12) and its phosphoramidate prodrug (FMCAP, 14) have been proven as a potential anti-HBV agent against both adefovir-resistant as well as lamivudine-resistant double (rtL180M/rtM204V) mutants. 2019 The Journal of organic chemistry Abstract HBV L180M;M204V 221;229 226;234 RT;RT 219;227 221;229 30589264 Synthesis of an Anti-hepatitis B Agent, 2'-Fluoro-6'-methylene-carbocyclic Adenosine (FMCA) and Its Phosphoramidate (FMCAP). Furthermore, in vitro, these agents have demonstrated significant activity against lamivudine/entecavir triple mutants (L180M + S202G + M204V). 2019 The Journal of organic chemistry Abstract HBV L180M;S202G;M204V 120;128;136 125;133;141 30600290 The Effect of ICOS Polymorphism Interactions with HBV Mutations on HBV Subtype Infection Outcomes. Additionally, the A1762T, G1764A and A1762T/G1764A mutations were associated with an increased risk of LC in the genotype C group. 2018 Annals of hepatology Abstract HBV G1764A;A1762T;A1762T;G1764A 44;18;37;26 50;24;43;32 Liver cirrhosis 103 105 30600290 The Effect of ICOS Polymorphism Interactions with HBV Mutations on HBV Subtype Infection Outcomes. Further study indicated that interactions between ICOS rs10932029 genotype "TC" and A1762T or A1762T/G1764A mutations significantly decreased the LC risk in the genotype C group. 2018 Annals of hepatology Abstract HBV G1764A;A1762T;A1762T 101;84;94 107;90;100 Liver cirrhosis 146 148 30600290 The Effect of ICOS Polymorphism Interactions with HBV Mutations on HBV Subtype Infection Outcomes. The interactions between the rs10932029 genotype "TC" and A1762T or A1762T/G1764A mutations could decrease the risk of LC. 2018 Annals of hepatology Abstract HBV G1764A;A1762T;A1762T 75;58;68 81;64;74 Liver cirrhosis 119 121 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. G120A mutation resulted in an increased HBV DNA level in vitro, consistent with the serological results in patients. 2019 Viruses Abstract HBV G120A 0 5 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. G82A, A115C and G120A mutants boosted the intracellular HBV total RNA level. 2019 Viruses Abstract HBV G82A;A115C;G120A 0;6;16 4;11;21 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. In vitro experiments in HepG2 cells showed that G82A, A115C and G120A mutants increased the hepatitis B surface antigen (HBsAg) levels, while C18T had an opposite effect. 2019 Viruses Abstract HBV G82A;A115C;G120A;C18T 48;54;64;142 52;59;69;146 S;S 121;104 126;111 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Luciferase assay revealed distinct promoter activities among SPII mutants; especially SPII of G120A mutant had a 15-fold higher activity than that of wild-type (p < 0.001). 2019 Viruses Abstract HBV G120A 94 99 S promoter II;S promoter II 61;86 65;90 30670420 CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus. CMCdG also reduced the level of HBVETV-R L180M/S202G/M204V viremia by ~1 log in HBVETV-R L180M/S202G/M204V-infected human liver-chimeric mice, while ETV (1 mg/kg/day q.d.) completely failed to reduce the viremia. 2019 Antimicrobial agents and chemotherapy Abstract HBV S202G;M204V;S202G;M204V;L180M;L180M 47;53;95;101;41;89 52;58;100;106;46;94 30670420 CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus. CMCdG potently inhibited HBV production in HepG2.2.15 cells (50% inhibitory concentration [IC50], ~30 nM) and HBVWT Ce plasmid-transfected Huh7 cells (IC50, 206 nM) and efficiently suppressed ETV-resistant HBVETV-R L180M/S202G/M204V (IC50, 2,657 nM), while it showed no or little cytotoxicity (50% cytotoxic concentration, >500 muM in most hepatocytic cells examined). 2019 Antimicrobial agents and chemotherapy Abstract HBV S202G;M204V;L180M 221;227;215 226;232;220 30670420 CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus. CMCdG's in vitro activity was determined using quantitative PCR and Southern blotting assays, and its cytotoxicity was determined with a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay, while its in vivo activity and safety were determined in human liver-chimeric mice infected with wild-type HBV genotype Ce (HBVWT Ce) and an entecavir (ETV)-resistant HBV variant containing the amino acid substitutions L180M, S202G, and M204V (HBVETV-R L180M/S202G/M204V). 2019 Antimicrobial agents and chemotherapy Abstract HBV S202G;M204V;L180M;S202G;M204V;L180M 468;474;428;435;446;462 473;479;433;440;451;467 30670420 CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus. However, CMCdG-TP retains good contacts with both the HBVWT Ce RT and HBVETV-R L180M/S202G/M204V RT complexes. 2019 Antimicrobial agents and chemotherapy Abstract HBV S202G;M204V;L180M 85;91;79 90;96;84 RT;RT 63;97 65;99 30670420 CMCdG, a Novel Nucleoside Analog with Favorable Safety Features, Exerts Potent Activity against Wild-Type and Entecavir-Resistant Hepatitis B Virus. Structural analyses using homology modeling, semiempirical quantum methods, and molecular dynamics revealed that although ETV triphosphate (TP) forms good van der Waals contacts with L180 and M204 of HBVWT Ce reverse transcriptase (RT), its contacts with the M180 substitution are totally lost in the HBVETV-R L180M/S202G/M204V RT complex. 2019 Antimicrobial agents and chemotherapy Abstract HBV S202G;M204V;L180M 316;322;310 321;327;315 RT;RT;RT 209;232;328 230;234;330 30702819 Analyses of the Genetic Diversities and Mutations of the Hepatitis B Virus Genome BCP/Pre C Region. Other mutations in descending order by mutation rate were a: A1762T/G1764A combined mutation (90. 48%); G1756C/T1803A/A(1757 ~ 1765)/A (1824 ~ 1832) combined mutation (80. 95%); T1753C/A1762T/ G1764A combined mutation (57. 14%); A1762T/G1764A/G1896A combined mutation (42. 86%); G1756C/螖(1757~176.5) combined mutation,(28. 57%); T1753C/A1762T/G1764A/G1896A combined mutation (23. 81%). 2017 Bing du xue bao Abstract HBV G1764A;T1803A;A (1757 ~ 1765);A (1824 ~ 1832);A1762T;G1764A;G1764A;G1896A;del 1757~1765;G1896A;G1756C;A1762T;T1753C;A1762T;G1756C;T1753C 68;111;118;133;185;192;236;243;286;350;104;61;178;229;279;329 74;117;132;148;191;198;242;249;299;356;110;67;184;235;285;335 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. And such reduction caused by T1719G mutation could be rescued by HBx protein. 2019 Journal of viral hepatitis Abstract HBV T1719G 29 35 X 65 68 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. In this study, we aimed to evaluate the function and mechanisms of the T1719G mutation on viral replication capacity. 2019 Journal of viral hepatitis Abstract HBV T1719G 71 77 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. It was repeatedly reported that the hepatitis B virus (HBV) T1719G mutation was very common and related to progression and malignancy of liver disease. 2019 Journal of viral hepatitis Abstract HBV T1719G 60 66 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. Our results show that the T1719G mutation decreases HBV viral replication capacity possibly by mutant HBx protein and altered Enh II activity. 2019 Journal of viral hepatitis Abstract HBV T1719G 26 32 Enh II;X 126;102 132;105 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. Our results showed that the T1719G mutation impaired viral replication efficacy compared with the wild type both by reducing Enh II activity and binding capacity of HNF3beta with Enh II. 2019 Journal of viral hepatitis Abstract HBV T1719G 28 34 Enh II;Enh II 125;179 131;185 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. Simultaneously, the HBx or HBx-mut (T1719G) plasmid was co-transfected to evaluate the effect of HBx on viral replication. 2019 Journal of viral hepatitis Abstract HBV T1719G 36 42 X;X;X 20;27;97 23;30;100 30706588 HBV T1719G mutation reduced HBV replication through mutant Enh II and HBx protein in vitro. Wild-type and T1719G mutation-bearing HBV1.2x plasmids were transfected into Huh7 and HepG2 cells, respectively, and HBV total RNA, 3.5 kb RNA and supernatant HBV DNA were assessed using real-time PCR, hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) levels were measured by time-resolved fluoroimmunoassay. 2019 Journal of viral hepatitis Abstract HBV T1719G 14 20 C;C;S;S 254;265;231;214 263;270;236;221 30771531 Diverse immune responses to HBV surface epitope variants after vaccine booster in adolescents immunized in infancy. Antibody affinity to sG145R and the IFN-gamma-secreting cell response to some epitope 16-33 variants were still impaired even after booster administration. 2019 Clinical microbiology and infection Abstract HBV G145R 21 27 S 21 22 30771531 Diverse immune responses to HBV surface epitope variants after vaccine booster in adolescents immunized in infancy. IFN-gamma-secreting T cells to epitope 16-33 containing R24K and the antibody affinity to sG145R were still significantly lower than to the wild type. 2019 Clinical microbiology and infection Abstract HBV R24K;G145R 56;90 60;96 S 90 91 30794889 Identification of a quadruple mutation that confers tenofovir resistance in chronic hepatitis B patients. RESULTS: Five mutations (rtS106C [C], rtH126Y [Y], rtD134E [E], rtM204I/V, and rtL269I [I]) were commonly found in viral isolates from 2 patients. 2019 Journal of hepatology Abstract HBV S106C;H126Y;D134E;M204I;M204V;L269I 27;40;53;66;66;81 32;45;58;73;73;86 C;RT;RT;RT;RT;RT 34;25;38;51;64;79 35;27;40;53;66;81 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. By contrast, the emergence of rtI163V was not related to ETV treatment. 2019 Antiviral research Abstract HBV I163V 32 37 RT 30 32 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. Classical ETV-resistance mutations rtT184/S202/M250substitution+rtM204V/I+-L180M (LAM-r), rtA186T, and rtI163V were detected in 1252 (5.69%), 14 (0.06%), and 230 (1.05%) of the 22,009 patients, respectively. 2019 Antiviral research Abstract HBV M204V;M204I;A186T;I163V;L180M 66;66;92;105;75 73;73;97;110;80 RT;RT;RT;RT 35;64;90;103 37;66;92;105 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. Compared to wild-type strain, two patient-derived mutants' rtL180M+A186T+M204V and rtL180M+T184S+A186T+M204V had 86.7% and 89.2% decreased replication capacity, 210- and 555-fold increased ETV resistance, respectively; and artificial elimination of rtA186T largely restored their ETV sensitivity. 2019 Antiviral research Abstract HBV L180M;L180M;A186T;A186T;M204V;T184S;A186T;M204V 61;85;251;67;73;91;97;103 66;90;256;72;78;96;102;108 RT;RT;RT 59;83;249 61;85;251 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. In conclusion, our study confirmed that rtA186T plus LAM-r is a novel ETV-resistance mutation pattern which conferred ETV resistance in multiple Chinese patients. 2019 Antiviral research Abstract HBV A186T 42 47 RT 40 42 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. Six rtA186T-positive patients were followed up longitudinally, showing that these patients all had received sequential adefovir and LAM monotherapies prior to ETV treatment. 2019 Antiviral research Abstract HBV A186T 6 11 RT 4 6 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. The 14 rtA186T-positive patients were all treated with LAM and ETV, and the emergence of the rtA186T+LAM-r was closely associated with virological breakthrough or inadequate virological response to ETV. 2019 Antiviral research Abstract HBV A186T;A186T 9;95 14;100 RT;RT 7;93 9;95 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. The rtA186T mutants remained sensitive to tenofovir. 2019 Antiviral research Abstract HBV A186T 6 11 RT 4 6 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. The rtA186T mutation always coexisted with LAM-r, but not with rtI163V. 2019 Antiviral research Abstract HBV A186T;I163V 6;65 11;70 RT;RT 4;63 6;65 30796932 Prevalence of the entecavir-resistance-inducing mutation rtA186T in a large cohort of Chinese hepatitis B virus patients. This study aimed to clarify whether rtA186T and rtI163V substitutions of hepatitis B virus (HBV) contributed to entecavir (ETV) resistance. 2019 Antiviral research Abstract HBV A186T;I163V 38;50 43;55 RT;RT 36;48 38;50 30835025 Pre-S/Surface and Core Promoter/Precore Mutations in Chronic Hepatitis B Patients with Severe Acute Exacerbation. Cox regression analysis showed that independent predictors for mortality at week 24 of treatment in SAE patients were higher international normalized ratio, the presence of ascites, and T1753C/A/G mutations. 2019 Digestive diseases and sciences Abstract HBV T1753C;T1753A;T1753G 186;186;186 196;196;196 Acute Hepatitis B 100 103 30835025 Pre-S/Surface and Core Promoter/Precore Mutations in Chronic Hepatitis B Patients with Severe Acute Exacerbation. Multivariate analysis showed that the independent factors for SAE were V14G/A and L21S in surface genes, codons 109-119 deletions in pre-S1 genes, M1V/T/I in pre-S2 genes, and C1766T/T1768A and C1913A/G mutations in BCP/PC genes. 2019 Digestive diseases and sciences Abstract HBV T1768A;V14G;V14A;L21S;C1766T;C1913A;C1913G;M1V;M1T;M1I 183;71;71;82;176;194;194;147;147;147 189;77;77;86;182;202;202;154;154;154 BCP;Precore;PreS1;PreS2;S 216;220;133;158;90 219;222;139;164;97 30835025 Pre-S/Surface and Core Promoter/Precore Mutations in Chronic Hepatitis B Patients with Severe Acute Exacerbation. The SAE patients with T1753C/A/G mutations had a higher rate of acute-on-chronic liver failure (P = 0.006) and higher MELD score (P = 0.018) than those without T1753C/A/G mutations. 2019 Digestive diseases and sciences Abstract HBV T1753C;T1753A;T1753G;T1753C;T1753A;T1753G 22;22;22;160;160;160 32;32;32;170;170;170 Acute on chronic liver failure 64 94 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Artificial elimination of rtA181C largely restored the rtL180M+A181C+M204V mutant's sensitivity to ETV. 2019 Emerging microbes & infections Abstract HBV L180M;A181C;A181C;M204V 57;28;63;69 62;33;68;74 RT;RT 26;55 28;57 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. BACKGROUND AND AIMS: Entecavir (ETV) resistance of hepatitis B virus (HBV) conventionally requires rt184, 202, or 250 mutations plus lamivudine-resistance mutation (rtM204V/I +- L180M). 2019 Emerging microbes & infections Abstract HBV M204V;M204I;L180M 167;167;178 174;174;183 RT;RT 99;165 101;167 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. CONCLUSIONS: Both clinical and experimental data support rtL180M+A181C+M204V as a novel non-classical ETV-resistance mutation pattern. 2019 Emerging microbes & infections Abstract HBV L180M;A181C;M204V 59;65;71 64;70;76 RT 57 59 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In clinical practice, undetectable serum HBV DNA was achieved in two of five longitudinally followed rtA181C-positive patients who received switching-to TDF therapy, but not in the other three who received add-on adefovir therapy during observation. 2019 Emerging microbes & infections Abstract HBV A181C 103 108 RT 101 103 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Molecular modelling of viral RT binding to ETV showed that the rtL180M+A181C+M204V mutant had a less stable conformation compared to rtL180M+M204V mutant. 2019 Emerging microbes & infections Abstract HBV L180M;L180M;A181C;M204V;M204V 65;135;71;77;141 70;140;76;82;146 RT;RT;RT 29;63;133 31;65;135 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Patient-derived representative rtA181C-containing mutants, rtL180M+A181C+M204V, rtL180M+A181C+M204V+M250V, and rtL180M+A181C+S202G+M204V, exhibited 45.7%, 25.9%, and 25.0% replication capacity and 85.6-, 356.1-, and 307.1-fold decreased susceptibility to ETV respectively compared to the wild-type strain, while the three mutants remained sensitive to tenofovir (TDF). 2019 Emerging microbes & infections Abstract HBV L180M;L180M;L180M;A181C;A181C;M204V;A181C;M204V;M250V;A181C;S202G;M204V 61;82;113;33;67;73;88;94;100;119;125;131 66;87;118;38;72;78;93;99;105;124;130;136 RT;RT;RT;RT 31;59;80;111 33;61;82;113 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtA181C mutation was detected with rtL180M+M204V mutations in 18 lamivudine-experienced ETV-treated patients, and the emergence of the mutations was associated with virological breakthrough or inadequate virological response to ETV. 2019 Emerging microbes & infections Abstract HBV L180M;A181C;M204V 41;6;47 46;11;52 RT;RT 4;39 6;41 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. This study aimed to clarify whether rtL180M+A181C+M204V mutations may contribute to HBV ETV resistance. 2019 Emerging microbes & infections Abstract HBV L180M;A181C;M204V 38;44;50 43;49;55 RT 36 38 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. RT mutations included: V173L, S202I, L180M, M204V and T184A. 2019 PeerJ Abstract HBV V173L;S202I;L180M;M204V;T184A 23;30;37;44;54 28;35;42;49;59 RT 0 2 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. These mutations included: L109R, Q129R, M133L, S143L and D144E with overall prevalence of 18.9% (95% CI [9.5-34.2]). 2019 PeerJ Abstract HBV L109R;Q129R;M133L;S143L;D144E 26;33;40;47;57 31;38;45;52;62 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Although the sW182* protein appeared not to be very stable in the cultured liver cells, we confirmed that the protein can be highly expressed and retained for a prolonged period of time in the hepatocytes in the mouse liver, indicating its stable nature in the physiological condition. 2019 PloS one Abstract HBV W182X 13 19 S 13 14 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Here, we expressed in a liver cell line Huh-7 a carboxy terminally truncated protein from a nonsense mutant of the LHBs gene, sW182* (stop codon at tryptophane-182). 2019 PloS one Abstract HBV W182X 126 132 S;S 115;126 119;127 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In the Huh-7 cells, the sW182* mutant downregulated tumor suppressors p53 and Smad4. 2019 PloS one Abstract HBV W182X 24 30 S 24 25 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. On the other hand, we found that c-Jun activation domain-binding protein 1 (Jab1) physically interacts with the sW182*, but not wild-type LHBs. 2019 PloS one Abstract HBV W182X 112 118 S;S 138;112 142;113 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The sW182* mutant inhibited the promoter activity of downstream target genes of the tumor suppressors. 2019 PloS one Abstract HBV W182X 4 10 S 4 5 30882363 Molecular cloning and phenotypic analysis of drug-resistance mutants with relevant S-region variants of HBV for a patient during 189-month anti-HBV treatment. Interestingly, the rtA181T-causative sW172stop to sW172non-stop mutation transition was observed at HBV DNA fluctuations. 2019 Antiviral therapy Abstract HBV A181T;W172X 21;37 26;46 RT;S;S 19;37;50 21;38;51 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Further mutagenesis study revealed that the P5T mutation of core protein plays an important role in the enhanced viral replication through increasing the levels of capsid formation and pregenomic RNA encapsidation. 2019 Antiviral research Abstract HBV P5T 44 47 C;Capsid 60;164 64;170 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Furthermore, although in the non-responder group the frequency of the LAM resistance-associated mutations (rtM204V/I) decreased at 6 months compared with the baseline, it did not disappear in any of the patients after six months of treatment. 2019 Experimental and therapeutic medicine Abstract HBV M204V;M204I 109;109 116;116 RT 107 109 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. In the present study, 16 CHB patients with the rtM204I/V mutation in the tyrosine-methionine-aspartate-aspartate motif of the C domain of the polymerase gene who switched to LAM/ADV treatment due to LAM resistance were assessed. 2019 Experimental and therapeutic medicine Abstract HBV M204I;M204V 49;49 56;56 P;RT;P 142;47;73 152;49;112 Chronic Hepatitis B 25 28 30908666 Molecular and serological characterization of occult hepatitis B virus infection among patients with hemophilia. sR73H, sI110L, sP120A, sP127T, sQ129H, sG130R, and sC137S were shown to be the most determinant escape mutation and OBI-relevant mutants. 2019 Journal of medical virology Abstract HBV R73H;I110L;P120A;P127T;Q129H;G130R;C137S 0;7;15;23;31;39;51 5;13;21;29;37;45;57 S;S;S;S;S;S;S 0;7;15;23;31;39;51 1;8;16;24;32;40;52 Occult Hepatitis B 116 119 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. Sequencing revealed multiple substitutions in preS1, preS2, and S regions for one panel including a rare D144N substitution associated with vaccine breakthrough that emerged with increasing frequency as the breakthrough infection developed. 2019 Virology journal Abstract HBV D144N 105 110 PreS1;PreS2;S 46;53;64 51;58;65 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. IMPLICATIONS: Our findings suggested that HBx-K130M/V131I-mutant variant promoted HCC progression by activating AKT/FOXO1 pathway and inducing stronger inflammation in liver via AA metabolism. 2019 Molecular cancer research Abstract HBV V131I;K130M 52;46 57;51 X 42 45 Hepatocellular carcinoma 82 85 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. Taken together, the increased rate of HCC observed in chronic hepatitis B patients with K130M/V131I-mutated X protein, may be due to changes in AA metabolism and AKT/FOXO1 signaling. 2019 Molecular cancer research Abstract HBV V131I;K130M 94;88 99;93 X 108 109 Hepatocellular carcinoma;Chronic Hepatitis B 38;54 41;73 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. To compare the potential tumorigenic effects of K130M/V131I (Mut) and wild-type (WT) HBx on HCC, the Sleeping Beauty (SB) transposon system was used to deliver HBx Mut and WT into the livers of fumarylacetoacetate hydrolase (Fah)-deficient mice and in the context of transformation related protein 53 (Trp53) deficiency. 2019 Molecular cancer research Abstract HBV V131I;K130M 54;48 59;53 X;X 85;160 88;163 Hepatocellular carcinoma 92 95 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Among those with a viral load <=5.0 log IU/ml, patients with the G2765A substitution showed a significantly lower HBV viral load than those with the wild-type sequence. 2019 Virology journal Abstract HBV G2765A 65 71 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. CONCLUSION: G2765A substitution in the pre-S1 promoter reduced the expression of L protein and resulted in a low viral load and less severe disease in chronic HBV infections. 2019 Virology journal Abstract HBV G2765A 12 18 Large S;S1 promoter 81;39 90;54 Chronic HBV infection 151 173 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Furthermore, the G2765A substitution greatly reduced the L protein expression level of vector-produced virus particles. 2019 Virology journal Abstract HBV G2765A 17 23 S 57 66 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. HepG2 cells transfected with the G2765A substitution vector showed reduced luciferase activity of the pre-S1 promoter, as well as reduced expression of pre-S1 mRNA and L protein. 2019 Virology journal Abstract HBV G2765A 33 39 S;PreS1;S1 promoter 168;152;102 177;158;117 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. RESULTS: In total, 35 patients were enrolled and 13 patients (37.1%) had a single base substitution in the pre-S1 promoter region; the most frequent substitution was a G-to-A substitution at the 2765th base (G2765A) in the Sp1 region. 2019 Virology journal Abstract HBV G2765A 208 214 S1 promoter;S1 promoter 107;223 122;226 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. The HBV viral load showed a negative correlation with the substitution ratio of the Sp1 region or G2765A (r = - 0.493 and - 0.473, respectively). 2019 Virology journal Abstract HBV G2765A 98 104 S1 promoter 84 87 31086664 Analysis of hepatitis B virus genotype and gene mutation in patients with advanced liver disease in East Kalimantan, Indonesia. The C1505A mutation in X region, T1753V and A1762T/G1764A mutations in the basal core promoter region and C1858T in precore (PC) region were frequent and only detected in patients with ALD (28.9, 40, 73.5 and 17.6%, respectively), whereas the G1896A mutation in the PC region was frequently detected in HBV carriers. 2019 Biomedical reports Abstract HBV G1764A;C1505A;T1753V;A1762T;C1858T;G1896A 51;4;33;44;106;243 57;10;39;50;112;249 BCP;Precore;Precore;Precore;X 75;125;266;116;23 94;127;268;123;24 Liver disease 185 188 31105017 Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients. A number of truncation-related mutations were higher in HCC/Cirrhotic group (P>0.001), albeit only C69* stop codon was statistically significant (P=0.003). 2019 Annals of hepatology Abstract HBV C69X 99 103 Hepatocellular carcinoma;Liver cirrhosis 56;60 59;69 31105017 Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients. CONCLUSION: The higher frequency of substitutions in MHR and immune epitopes at positions such as Y134 and P120 as well as stop codons such as C69* in HCC/cirrhotic group might candidate them as predictive factors for infection outcome. 2019 Annals of hepatology Abstract HBV C69X 143 147 Hepatocellular carcinoma;Liver cirrhosis 151;155 154;164 31105017 Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients. However, Y134N/F/L (P=0.04) and P120T/S (P=0.009) were significantly detected in MHR and B-cell epitope of HCC/Cirrhotic group. 2019 Annals of hepatology Abstract HBV Y134N;Y134F;Y134L;P120T;P120S 9;9;9;32;32 18;18;18;39;39 Hepatocellular carcinoma;Liver cirrhosis 107;111 110;120 31105017 Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients. In RT, some potentially resistant substitutions such as Q215S, V191I and V214A, were revealed. 2019 Annals of hepatology Abstract HBV Q215S;V191I;V214A 56;63;73 61;68;78 RT 3 5 31130119 [HBV pol/S gene mutations in chronic hepatitis B patients receiving nucleoside/nucleotide analogues treatment]. Because of the HBV pol/S gene overlapping, in 27 patients immun-selected amino acid substitutions (sI110L, sT127P, sS114A, sT123A), in nine patients HBIg selected escape mutants (sP120R, sT123N, sE164D, sY134F, sQ129H, sT118A, sP127K), in seven patients vaccine escape mutants (sT126I, sP120S, sG145A, s S193L) and in one patient misdiagnosis of HBsAg (sT131I) were detected. 2019 Mikrobiyoloji bulteni Abstract HBV S193L;I110L;T127P;S114A;T123A;P120R;T123N;E164D;Y134F;Q129H;T118A;P127K;T126I;P120S;G145A;T131I 304;99;107;115;123;179;187;195;203;211;219;227;278;286;294;353 309;105;113;121;129;185;193;201;209;217;225;233;284;292;300;359 S;P;P;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 346;19;23;99;107;115;123;179;187;195;203;211;219;227;278;286;294;302;353 351;22;24;100;108;116;124;180;188;196;204;212;220;228;279;287;295;303;354 31130119 [HBV pol/S gene mutations in chronic hepatitis B patients receiving nucleoside/nucleotide analogues treatment]. Primary/secondary drug mutations (rtM204I/V, rtI169S, rtL180M, rtT184L, rtA194V, rtM204I/rtL91I, rtQ149K, rtQ215H/S, rtN238D) were detected in 38 (45.2%) of the patients. 2019 Mikrobiyoloji bulteni Abstract HBV M204I;M204V;I169S;L180M;T184L;A194V;Q149K;Q215H;Q215S;N238D;M204I;L91I 36;36;47;56;65;74;99;108;108;119;83;91 43;43;52;61;70;79;104;115;115;124;88;95 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 34;45;54;63;72;81;89;97;106;117 36;47;56;65;74;83;91;99;108;119 31130120 [Determination of reverse transcriptase inhibitor nucleoside analogue resistance profile in pretreatment phase of patients with viral hepatitis B]. However, potential drug resistance mutations such as rtR164R, rtG165D/A, rtG172Q, rtS176N, rtF178V, rtA181G, rtS185N/G/C, rtV207M, rtQ215H/S, rtL231V, rtI233K, rtN238S, rtV253T, rtC256G/S and rtI266R/V were detected in untreated patient samples in B, C, D and D domains of reverse transcriptase region. 2019 Mikrobiyoloji bulteni Abstract HBV R164R;G165D;G165A;G172Q;S176N;F178V;A181G;S185N;S185G;S185C;V207M;Q215H;Q215S;L231V;I233K;N238S;V253T;C256G;C256S;I266R;I266V 55;64;64;75;84;93;102;111;111;111;124;133;133;144;153;162;171;180;180;194;194 60;71;71;80;89;98;107;120;120;120;129;140;140;149;158;167;176;187;187;201;201 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 273;53;62;73;82;91;100;109;122;131;142;151;160;169;178;192 294;55;64;75;84;93;102;111;124;133;144;153;162;171;180;194 31130120 [Determination of reverse transcriptase inhibitor nucleoside analogue resistance profile in pretreatment phase of patients with viral hepatitis B]. Primary drug resistance mutations such as rtI169T, rtA181T/V, rtT184A/C/F/G/I/L/M/S, rtA194T, rtS202C/G/I, rtM204I/V/S, rtN236T, rt M250I/L/V and rtV173L were not detected in any of the patient samples. 2019 Mikrobiyoloji bulteni Abstract HBV I169T;A181T;A181V;T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;A194T;S202C;S202G;S202I;M204I;M204V;M204S;N236T;V173L;M250I;M250L;M250V 44;53;53;64;64;64;64;64;64;64;64;87;96;96;96;109;109;109;122;148;132;132;132 49;60;60;83;83;83;83;83;83;83;83;92;105;105;105;118;118;118;127;153;141;141;141 RT;RT;RT;RT;RT;RT;RT;RT;RT 42;51;62;85;94;107;120;129;146 44;53;64;87;96;109;122;131;148 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Notably, 11 mutations at position 169, 202, 250, 173, 180, 200, 207, 214, 237, 242 and 245 coexisted with M204I or V. 2019 Scientific reports Abstract HBV M204I 106 111 31153830 Occult HBV infection in patients with autoimmune hepatitis: A virological and clinical study. In addition to those already reported OBI-associated AA substitutions (e.g., sG145R and sV184A), some new OBI-associated AA substitutions (e.g., sV106A, sC137* and sL176P) were found in AIH patients in our study. 2020 Journal of microbiology, immunology, and infection Abstract HBV G145R;V184A;V106A;C137X;L176P 77;88;145;153;164 83;94;151;159;170 S;S;S;S;S 77;88;145;153;164 78;89;146;154;165 Autoimmune Hepatitis B;Occult Hepatitis B;Occult Hepatitis B 186;38;106 189;41;109 31179360 Hepatitis B virus reverse transcriptase polymorphisms between treated and treatment-naive chronically infected patients. 13/98 (13.27%) of patients had M539I/V substitutions corresponding to YMDD motif. 2019 Virusdisease Abstract HBV M539I;M539V 31;31 38;38 YMDD 70 74 31179360 Hepatitis B virus reverse transcriptase polymorphisms between treated and treatment-naive chronically infected patients. Drug resistance conferring substitutions (DRCSs) were rtL180M (22/98), rtA194V (11/98), rtM204V (1/98), and rtM204I (11/98). 2019 Virusdisease Abstract HBV L180M;A194V;M204V;M204I 56;73;90;110 61;78;95;115 RT;RT;RT;RT 54;71;88;108 56;73;90;110 31179360 Hepatitis B virus reverse transcriptase polymorphisms between treated and treatment-naive chronically infected patients. Two substitutions N459Y and L515M were significantly correlated (R2 = 0.486 and R2 = 0.941 respectively) with FLLAQ motif variation. 2019 Virusdisease Abstract HBV N459Y;L515M 18;28 23;33 3118876 Site-directed mutagenesis of hepatitis B surface antigen sequence at codon 160 from arginine to lysine for conversion of subtypic determinant from r to w. These results indicate that a point mutation from G to A at nucleotide 479 in the S gene, changing codon 160 for arginine to that for lysine, can convert the subtypic determinant of hepatitis B surface antigen from r to its allelic determinant w. 1987 Biochemical and biophysical research communications Abstract HBV G479A 50 74 S;S 82;194 83;201 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Primary or secondary NA resistance (NAr) mutations were not found, except A181T in RT (rtA181T) by Sanger sequencing, but they were detected by next-generation sequencing. 2019 Journal of clinical microbiology Abstract HBV A181T;A181T 89;74 94;79 RT;RT 83;87 85;89 31218588 Complementation of Wild-Type and Drug-Resistant Hepatitis B Virus Genomes to Maintain Viral Replication and Rescue Virion Production under Nucleos(t)ide Analogs. In the present study, HBV genomes with frequently detected reverse transcriptase (RT)/surface truncation MTs, rtA181T/sW172*, rtV191I/sW182* and rtM204I/sW196*, were phenotypically characterized alone or together with their WT counterparts in different ratios by transient transfection in the absence or presence of NAs. 2019 Virologica Sinica Abstract HBV W172X;W182X;W196X;A181T;V191I;M204I 118;134;153;112;128;147 124;140;159;117;133;152 RT;RT;RT;RT;RT;S;S;S;S 59;82;110;126;145;118;134;153;86 80;84;112;128;147;119;135;154;93 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. None of the known tenofovir resistance mutations (M240V/I, L180M, A194T, V214A, N238T) were identified in any individuals. 2019 Viruses Abstract HBV M240V;M240I;L180M;A194T;V214A;N238T 50;50;59;66;73;80 57;57;64;71;78;85 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Functional studies showed that sC69* mutant was associated with lower viral spread, but could be rescued by coexisting with the WT. 2019 Frontiers in microbiology Abstract HBV C69X 31 36 S 31 32 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Here, a mutant of sC69* in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69* was 4.37% (19/435), most of which coexisted with the WT (78.95%, 15/19), indicating mixed viral populations. 2019 Frontiers in microbiology Abstract HBV C69X;C69X 18;138 23;143 S;S;S;S 18;138;62;45 19;139;66;52 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Our data provide information that sC69* coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host. 2019 Frontiers in microbiology Abstract HBV C69X 34 39 S 34 35 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The lower immune response was not caused by the lower replication of sC69* mutant. 2019 Frontiers in microbiology Abstract HBV C69X 69 74 S 69 70 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant showed to attenuate host innate immune response during infection and poly (I:C) treatment such as IL29, ISG15, and RIG-I (p < 0.05). 2019 Frontiers in microbiology Abstract HBV C69X 4 9 S 4 5 31267215 Impact of hepatitis B virus genotype F on in vitro diagnosis: detection efficiency of HBsAg from Amerindian subgenotypes F1b and F4. A phosphorylation site (target for protein kinase C) produced by the G145R substitution might prevent recognition by anti-HBs antibodies. 2019 Archives of virology Abstract HBV G145R 69 74 S 122 125 31267215 Impact of hepatitis B virus genotype F on in vitro diagnosis: detection efficiency of HBsAg from Amerindian subgenotypes F1b and F4. Prediction of the tertiary structure of subgenotypes F1b and F4 revealed changes inside and outside the major hydrophilic region (aa 101-160) of the HBsAg compared to genotype A and the G145R variant. 2019 Archives of virology Abstract HBV G145R 186 191 S 149 154 31267215 Impact of hepatitis B virus genotype F on in vitro diagnosis: detection efficiency of HBsAg from Amerindian subgenotypes F1b and F4. This study examined the effect of virus-like particles containing HBsAg from genotypes A and F (particularly, F1b and F4) produced in Pichia pastoris in relation to the anti-HBs antibodies used in the immunoassays for in vitro diagnosis and compared it with that exerted by the G145R S-escape mutant. 2019 Archives of virology Abstract HBV G145R 278 283 S;S;S 174;66;284 177;71;285 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Most OBI strains were wild-type HBV, but some substitutions V168A, S174 N, V177A, Q129R/L/H, G145A/R in S region of genotype B (OBIB) and T47K/V/A, P49H/L, Q101R/H/K, S174 N, L175S, V177A, T118 M/R/K, G145R/A/K/E, R160K/N in S region of genotype C (OBIC) strains were identified in high frequency. 2019 BMC infectious diseases Abstract HBV V168A;S174N;V177A;Q129R;Q129L;Q129H;G145A;G145R;T47K;T47V;T47A;P49H;P49L;Q101R;Q101H;Q101K;S174N;L175S;V177A;T118M;T118R;T118K;G145R;G145A;G145K;G145E;R160K;R160N 60;67;75;82;82;82;93;93;138;138;138;148;148;156;156;156;167;175;182;189;189;189;201;201;201;201;214;214 65;73;80;91;91;91;100;100;146;146;146;154;154;165;165;165;173;180;187;199;199;199;212;212;212;212;221;221 S;S 104;225 105;226 Occult Hepatitis B 5 8 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Conclusions: Our results showed common mutations within HBsAg, occurring in immune epitopes, a high rate of G1896A mutations in the PC region, and a negative correlation between the emergence of A1762T/G1764A mutation and the G1764T/C1766G mutant in the BCP region. 2019 Mediterranean journal of hematology and infectious diseases Abstract HBV G1764A;C1766G;G1896A;A1762T;G1764T 202;233;108;195;226 208;239;114;201;232 BCP;S;Precore 254;56;132 257;61;134 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. None of the strains with A1762T/G1764A mutation carried the G1764T/C1766G mutant. 2019 Mediterranean journal of hematology and infectious diseases Abstract HBV G1764A;C1766G;A1762T;G1764T 32;67;25;60 38;73;31;66 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The PC and BCP mutations were G1896A (61.0%), G1899A (23.0%), A1762T/G1764A (23.0%) and G1764T/C1766G (26.0%). 2019 Mediterranean journal of hematology and infectious diseases Abstract HBV G1764A;C1766G;G1896A;G1899A;A1762T;G1764T 69;95;30;46;62;88 75;101;36;52;68;94 BCP;Precore 11;4 14;6 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Furthermore, we identified novel variants that either independently or in combination with precore mutation G1896A were associated with the transition from HBeAg positive to the negative phase of infection. 2019 Scientific reports Abstract HBV G1896A 108 114 C;Precore 156;91 161;98 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Patients with viral variants C1817T and A1838G had viral loads nearly three orders of magnitude lower than patients without those variants. 2019 Scientific reports Abstract HBV C1817T;A1838G 29;40 35;46 31341154 Association Between HBx Variations and Development of Severe Liver Disease Among Indonesian Patients. However, the roles of two novel X gene mutations (A12S/T and L16F/P) on hepatocarcinogenesis are unclear relative to wild-type X gene. 2019 The Kobe journal of medical sciences Abstract HBV A12S;A12T;L16F;L16P 50;50;61;61 56;56;67;67 X;X 32;127 33;128 31341154 Association Between HBx Variations and Development of Severe Liver Disease Among Indonesian Patients. In addition, the double mutation K130M/V131I and the triple mutation N88V/K130M/V131I were associated with a 2.5 times higher risk of advanced liver disease. 2019 The Kobe journal of medical sciences Abstract HBV V131I;K130M;V131I;N88V;K130M 39;74;80;69;33 44;79;85;73;38 Liver disease 143 156 31341412 Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations. Background: The basal core promoter (BCP) double mutations (A1762T and G1764A) of hepatitis B virus (HBV) have been reported to be an aetiological factor of hepatocellular carcinoma (HCC). 2019 International journal of medical sciences Abstract HBV A1762T;G1764A 60;71 66;77 BCP;BCP 16;37 35;40 Hepatocellular carcinoma;Hepatocellular carcinoma 157;183 181;186 31359359 Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B. Based on NGS, the prevalence of T1753V (T1753C/A/G) and A1762T/G1764A variants were significantly lower in responders compared to non-responders (8.3% vs. 2019 Virus genes Abstract HBV G1764A;T1753V;T1753C;T1753A;T1753G;A1762T 63;32;40;40;40;56 69;38;50;50;50;62 31359359 Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B. No significant difference between groups was found regarding C1653T and G1896A mutants. 2019 Virus genes Abstract HBV C1653T;G1896A 61;72 67;78 31359359 Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B. The absence of T1753V and A1762T/G1764A mutations were factors associated with CR (OR 11.65, 95%CI 1.36-100.16, P = 0.025, and OR 4.36, 95%CI 1.08-17.63, P = 0.039, respectively). 2019 Virus genes Abstract HBV G1764A;T1753V;A1762T 33;15;26 39;21;32 31359359 Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B. The existence of pre-treatment T1753V, A1762T/G1764A mutations and their combination yielded negative predictive values of 94.7%, 85.7% and 93.8%, respectively. 2019 Virus genes Abstract HBV G1764A;T1753V;A1762T 46;31;39 52;37;45 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. All mutations simultaneously created a stop codon at sC69 (sC69*). 2019 Antiviral research Abstract HBV C69X 59 64 S;S 53;59 54;60 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. Artificial elimination of the rtS78T mutation had a limited effect on the drug susceptibilities. 2019 Antiviral research Abstract HBV S78T 32 36 RT 30 32 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. The data obtained in the present study suggested that the emergence of the rtS78T/sC69* mutation was not closely related to entecavir/tenofovir treatment and itself appeared insufficient to confer drug resistance unless it coexisted with signature drug-resistance mutations. 2019 Antiviral research Abstract HBV C69X;S78T 82;77 87;81 RT;S 75;82 77;83 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. The HBV DNA and RNA levels of the rtS78T/sC69* mutant were significantly increased compared to the wild-type; while the mutant had undetectable secreted and intracellular HBsAg, and its half maximal effective concentration to lamivudine, adefovir, entecavir, and tenofovir were 3.73-, 1.61-, 4.76-, and 3.71-fold of the wild-type, respectively. 2019 Antiviral research Abstract HBV C69X;S78T 41;36 46;40 S;RT;S 171;34;41 176;36;42 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. The prevalence of rtS78T/sC69* did not differ significantly between the patients with and without entecavir/tenofovir treatment. 2019 Antiviral research Abstract HBV C69X;S78T 25;20 30;24 RT;S 18;25 20;26 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. The rtS78T mutation was detected in 0.83% (182/22,009) of the patients' samples. 2019 Antiviral research Abstract HBV S78T 6 10 RT 4 6 31398372 Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment. This study aimed to investigate clinical occurrence and significance of the rtS78T/sC69* mutation of hepatitis B virus (HBV). 2019 Antiviral research Abstract HBV C69X;S78T 83;78 88;82 RT;S 76;83 78;84 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. Our epidemiological study showed HBeAg negative infections of rt269I infections were attributed to a higher frequency of preC mutations at 1896 (G to A). 2019 Frontiers in immunology Abstract HBV G1896A 139 152 C;Precore;RT 33;121;62 38;125;64 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Multiple mutations were confirmed in 24 Cambodian C1 isolates, especially double mutation at A1762T/G1764A in 18 isolates (75.0%), and combination mutation at C1653T and/or T1753V and A1762T/G1764A in 14 isolates (58.3%). 2019 Scientific reports Abstract HBV G1764A;G1764A;A1762T;C1653T;T1753V;A1762T 100;191;93;159;173;184 106;197;99;165;179;190 31442597 The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. Among different substitution types at sI126, the sI126T (N = 28) was found to be associated with significantly lower serum HBsAg level. 2019 Infection, genetics and evolution Abstract HBV I126T 49 55 S;S;S 123;38;49 128;39;50 31442597 The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. Clone sequencing revealed that sI126T-harboring SHBs sequences had varied genetic backbones with zero to nine additional AA substitutions. 2019 Infection, genetics and evolution Abstract HBV I126T 31 36 S;Small S 31;48 32;52 31442597 The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. Our findings suggest that the modulation of HBsAg level by sI126T is affected by additional AA substitution(s) in the S region of HBV. 2019 Infection, genetics and evolution Abstract HBV I126T 59 65 S;S;S 118;59;44 119;60;49 31442597 The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV. Thus, we constructed 24 HBsAg expression plasmids harboring sI126T without (plasmid 1, P1) or with (P2-P24) additional AA substitution(s) and studied them in the HepG2 cells. 2019 Infection, genetics and evolution Abstract HBV I126T 60 66 S;S 24;60 29;61 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Interestingly, both the wild-type and D2N/D4N mutant displayed identical assembly profiles when their charge densities matched each other. 2018 ACS omega Abstract HBV D4N;D2N 42;38 45;41 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The role of electrostatic interactions in the viral capsid assembly process was studied by comparing the assembly process of a truncated hepatitis B virus capsid protein Cp149 with its mutant protein D2N/D4N, which has the same conformational structure but four fewer charges per dimer. 2018 ACS omega Abstract HBV D4N;D2N 204;200 207;203 Capsid;Capsid;C 52;155;170 58;161;172 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Although mutant P130T also displayed a hypermaturation phenotype in vivo, it cannot efficiently rescue the immature virion secretion of mutant I97L. 2019 Journal of virology Abstract HBV P130T;I97L 16;143 21;147 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Although viral DNA of mutant I97L with immature genome is less persistent than wild-type HBV in time course experiments, viral DNA of mutant P130T with genome hypermaturation, surprisingly, is more persistent. 2019 Journal of virology Abstract HBV I97L;P130T 29;141 33;146 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Here, we demonstrated that mutant I97L can secrete immature genome in mice. 2019 Journal of virology Abstract HBV I97L 34 38 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, a frequent naturally occurring HBc variant, I97L, changing from an isoleucine to a leucine at amino acid 97, exhibited an immature secretion phenotype in culture, which preferentially secretes virions containing immature genomes. 2019 Journal of virology Abstract HBV I97L;I97L 53;76 57;116 C 40 43 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In contrast, mutant P130T, changing from a proline to a threonine at amino acid 130, exhibited a hypermaturation phenotype by accumulating an excessive amount of intracellular fully mature DNA genome. 2019 Journal of virology Abstract HBV P130T;P130T 20;43 25;83 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L in mice exhibited pleiotropic phenotypes: (i) excessive numbers of serum HBV virions containing immature genomes, (ii) significantly reduced numbers of intracellular relaxed-circle and single-stranded DNAs, and (iii) less persistent intrahepatic and secreted HBV DNAs than wild-type HBV. 2019 Journal of virology Abstract HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The most frequent naturally occurring mutation in HBV core protein occurs at amino acid 97, changing an isoleucine to leucine (I97L). 2019 Journal of virology Abstract HBV I97L 127 131 C 54 58 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Unexpectedly, the single mutant P130T exhibited in vivo a novel phenotype in prolonging the persistence of HBV genome in hepatocytes. 2019 Journal of virology Abstract HBV P130T 32 37 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Using a hydrodynamic delivery mouse model, we studied the in vivo behaviors of these two mutants, I97L and P130T. 2019 Journal of virology Abstract HBV I97L;P130T 98;107 102;112 31498528 Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance. CONCLUSION: An rtL180M/T184L/A200V/M204V mutant with moderate resistance to TDF monotherapy was selected during sequential nucleoside analogue (NA) treatment in a stepwise manner. 2020 Liver international Abstract HBV T184L;A200V;M204V;L180M 23;29;35;17 28;34;40;22 RT 15 17 31498528 Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance. In vitro phenotyping demonstrated that the rtL180M/T184L/A200V/M204V mutant had moderate resistance to TDF treatment, with a 4.52-fold higher half maximal effective concentration than that of wild-type virus. 2020 Liver international Abstract HBV T184L;A200V;M204V;L180M 51;57;63;45 56;62;68;50 RT 43 45 31498528 Entecavir resistance mutations rtL180M/T184L/M204V combined with rtA200V lead to tenofovir resistance. METHODS AND RESULTS: Here, we report viral rebound in a patient with chronic hepatitis B who underwent TDF monotherapy and harboured a quadruple mutant consisting of classic entecavir (ETV)-resistance mutations (rtL180M/T184L/M204V) together with an rtA200V mutation in the reverse transcriptase gene. 2020 Liver international Abstract HBV T184L;M204V;L180M;A200V 220;226;214;252 226;231;219;257 RT;RT;RT 274;212;250 295;214;252 Chronic Hepatitis B 69 88 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Conclusions: According to the results, point mutations such as L11Q, N37S, K38R and A49V, as well as certain deletions, may be associated with HBV infection outcome, among an HBV genotype D pure population. 2019 Clinical and experimental hepatology Abstract HBV L11Q;N37S;K38R;A49V 63;69;75;84 67;73;79;88 HBV infections 143 156 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. The rate of critical point mutations, including L11Q, N37S and K38R, was significantly higher in the ASC group, whereas the A49V substitution rate was significantly higher in the LC/HCC group (p < 0.05). 2019 Clinical and experimental hepatology Abstract HBV L11Q;N37S;K38R;A49V 48;54;63;124 52;58;67;128 Hepatocellular carcinoma;Liver cirrhosis 182;179 185;181 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Only mutations C85R, L87R, L88R, and C90R within TMD2 were associated with defective HBsAg production. 2019 Emerging microbes & infections Abstract HBV C85R;L87R;L88R;C90R 15;21;27;37 19;25;31;41 S 85 90 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. A mutation in C-region of HBsAg (L216*), was associated with reduced HBsAg production and secretion. 2019 Viruses Abstract HBV L216X 33 38 C;S;S 14;26;69 15;31;74 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. An HBsAg mutation (L216*) was found to be more frequent in ALF patients and was associated with reduced HBsAg production and secretion. 2019 Viruses Abstract HBV L216X 19 24 S;S 3;104 8;109 Liver disease 59 62 31542053 Hepatitis B virus reactivation sustained by a hepatitis B virus surface antigen immune-escape mutant isolate in a patient who was hepatitis B core antibody positive during treatment with sofosbuvir and velpatasvir for hepatitis C virus infection: a case report. Sequencing analysis revealed the hepatitis B virus genotype D3 and the presence of two relevant immune-escape mutations (P120S and T126I) in the major hydrophilic region by analyzing the S region. 2019 Journal of medical case reports Abstract HBV P120S;T126I 121;131 126;136 S 187 188 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. AIM: To investigate prevalence of the naturally occurring rtM204I mutations in treatment-naive CHB genotype C2 patients and their influence on antiviral therapy. 2019 World journal of gastroenterology Abstract HBV M204I 60 65 RT 58 60 Chronic Hepatitis B 95 98 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Almost patients receiving tenofovir achieved CVR at 12 mo of tenofovir, irrespective of pre-existence of naturally occurring rtM204I mutations (CVR rates: patients with rtM204I, 100%; patients without rtM204I, 96.6%), whereas, pre-existence of naturally-occurring rtM204I-mutations prior to NAs significantly affects CVR rates in patients receiving entecavir (at 12 mo: Patients with rtM204I, 16.7%; patients without rtM204I, 95.6%, P < 0.001). 2019 World journal of gastroenterology Abstract HBV M204I;M204I;M204I;M204I;M204I;M204I 127;171;203;266;386;419 132;176;208;271;391;424 RT;RT;RT;RT;RT;RT 125;169;201;264;384;417 127;171;203;266;386;419 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. CONCLUSION: The newly developed LNA-RT-PCR method could detect naturally occurring rtM204I mutations with high-sensitivity. 2019 World journal of gastroenterology Abstract HBV M204I 85 90 RT 83 85 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Multivariate analysis showed that naturally occurring rtM204I variants were more frequently detected in patients with significant fibrosis [odd-ratio (OR) 3.397, 95% confidence-interval (CI) 1.119-10.319, P = 0.031]. 2019 World journal of gastroenterology Abstract HBV M204I 56 61 RT 54 56 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Of 232 patients receiving NAs, multivariate analysis revealed that achievement of CVR was reversely associated with naturally occurring rtM204I variants prior to NAs treatment (OR 0.014, 95%CI 0.002-0.096, P < 0.001). 2019 World journal of gastroenterology Abstract HBV M204I 138 143 RT 136 138 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. RESULTS: The LNA-RT-PCR could discriminate rtM204I mutant-type (17 patients, 4.2%) from rtM204 wild-type (386 patients, 95.8%) in 403 of 410 patients (98.3% sensitivity). 2019 World journal of gastroenterology Abstract HBV M204I 45 50 RT;RT 43;88 45;90 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Tenofovir is a more suitable treatment than entecavir for CHB patients carrying the naturally occurring rtM204I mutations. 2019 World journal of gastroenterology Abstract HBV M204I 106 111 RT 104 106 Chronic Hepatitis B 58 61 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The rtM204I variants were analyzed by a newly developed locked nucleotide probe (LNA probe) based real-time PCR (LNA-RT-PCR) method. 2019 World journal of gastroenterology Abstract HBV M204I 6 11 RT 4 6 31550370 Virological Factors Associated With the Occurrence of Hepatitis B Virus (HBV) Reactivation in Patients With Resolved HBV Infection Analyzed Through Ultradeep Sequencing. The population of S3N amino acid substitution and nucleotide G1896A and G1899A mutations in each individual showed a similar percentage of occurrence. 2020 The Journal of infectious diseases Abstract HBV S3N;G1896A;G1899A 18;61;72 21;67;78 31550370 Virological Factors Associated With the Occurrence of Hepatitis B Virus (HBV) Reactivation in Patients With Resolved HBV Infection Analyzed Through Ultradeep Sequencing. The prevalence of the S3N amino acid substitution in the envelope protein and mutations at positions G1896A and G1899A in the precore region were significantly higher in the HBVr compared with AHB. 2020 The Journal of infectious diseases Abstract HBV S3N;G1896A;G1899A 22;101;112 25;107;118 S;Precore 57;126 65;133 Acute Hepatitis B 193 196 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. NAs resistant mutation occurrence patterns were multitudinous; single mutation patterns of rtM204I/V and rtL180M occurrences accounted for majority, followed by the combinational mutation pattern L180M + M204I/V. 2019 Scientific reports Abstract HBV M204I;M204V;L180M;L180M;M204I;M204V 93;93;107;196;204;204 100;100;112;201;211;211 RT;RT 91;105 93;107 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. Multinomial regression analysis revealed that the K130M/V131I mutations were correlated with CLD progression (OR, 7.629; 95% CI, 1.578-36.884). 2019 Biomedical reports Abstract HBV V131I;K130M 56;50 61;55 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. Significant differences in viral load were found in HBV-infected patients who had X gene mutations, such as R87W/G, I127L/T/N/S and K130M/V131I mutations (P<0.05). 2019 Biomedical reports Abstract HBV V131I;R87W;R87G;I127L;I127T;I127N;I127S;K130M 138;108;108;116;116;116;116;132 143;114;114;127;127;127;127;137 X 82 83 HBV infections 52 64 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The presence of K130M and V131I mutations may be predictive for the progression of HBV-associated CLD in Indonesia. 2019 Biomedical reports Abstract HBV K130M;V131I 16;26 21;31 31566576 High frequency of drug resistance mutations in the HBV genome in ART-experienced HIV-coinfected patients in southwestern Nigeria. HBV polymerase amino acid substitutions found included rtV173L, rtL180M, rtM204V, rtK212R, rtS213T, rtV214A, rtL229V and rtP237A/S. 2019 Antiviral therapy Abstract HBV V173L;L180M;M204V;K212R;S213T;V214A;L229V;P237A;P237S 57;66;75;84;93;102;111;123;123 62;71;80;89;98;107;116;130;130 P;RT;RT;RT;RT;RT;RT;RT;RT 4;55;64;73;82;91;100;109;121 14;57;66;75;84;93;102;111;123 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Between compartments, core gene variants revealed Arg94Leu, Glu86Arg and Ser41Thr while X gene variants revealed Phe73Val, Ala44Val, Ser146Ala and Ser147Pro. 2019 Scientific reports Abstract HBV R94L;E86R;S41T;F73V;A44V;S146A;S147P 50;60;73;113;123;133;147 58;68;81;121;131;142;156 C;X 22;88 26;89 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. In addition, a virus surface antigen mis-sense mutation resulting in M125T was detected in all the samples and could account for surface antigen negativity and occult HBV status. 2019 Scientific reports Abstract HBV M125T 69 74 S;S 21;129 28;136 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. In tumor compartments per se, several mis-sense mutations were detected, notably the classic T1762A/A1764G mutation in the basal core promoter. 2019 Scientific reports Abstract HBV A1764G;T1762A 100;93 106;99 BCP 123 142 31622056 [Identification and molecular-genetic characteristics of the hepatitis B virus among HIV-infected patients in Arkhangelsk.] Two HBV isolates with drug resistance mutations in the polymerase gene, leaded to amino acid substitutions (L180M, M204V) associated with the resistance development to lamivudine, entecavir, telbivudine and tenofovir were identifying. 2019 Voprosy virusologii Abstract HBV L180M;M204V 108;115 113;120 P 55 65 31624004 Characteristics of amino acid substitutions within the "a" determinant region of hepatitis B virus in chronically infected patients with coexisting HBsAg and anti-HBs. The most frequent amino acid substitution was located at position s126 and the predominant substitution was sI126T in HBsAg+/anti-HBs+ patients with genotype C. 2020 Clinics and research in hepatology and gastroenterology Abstract HBV I126T 108 114 S;S;S;S 130;118;66;108 133;123;67;109 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. Potential IEMs sY100C, sA128V, and sM133T, and several polymerase mutants were identified. 2020 International journal of infectious diseases Abstract HBV Y100C;A128V;M133T 15;23;35 21;29;41 P;S;S;S 55;15;23;35 65;16;24;36 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. A T126A mutant was also detected in the umbilical cord (9.2%) and serum (7.0%) of the first-born child of Family 1. 2019 BMC infectious diseases Abstract HBV T126A 2 7 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. In Family 1, deep sequencing detected a T143S mutant as a minor population (1.7-2.0%) in the umbilical cords and serum of all three children and in the serum of the mother. 2019 BMC infectious diseases Abstract HBV T143S 40 45 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. In Family 2, the deep sequencing showed no VEMs in the umbilical cords, but it detected D144A (2.5%) and G145A (11.2%) mutants in the serum of the 2nd-born child. 2019 BMC infectious diseases Abstract HBV D144A;G145A 88;105 93;110 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The direct sequencing showed that there were no VEMs in the serum of the children or mother of Family 1 and family 2, but it identified a G145A mutant in the nails of the mother of Family 2. 2019 BMC infectious diseases Abstract HBV G145A 138 143 31846615 The genetic variability of hepatitis B virus subgenotype F1b precore/core gene is related to the outcome of the acute infection. Mutations T1753C, A1762T, G1764A, C1766T, T1768A G1896A, G2092T and T2107C were associated with acute liver failure and progression to chronic hepatitis. 2020 Virus research Abstract HBV T1753C;A1762T;G1764A;C1766T;G2092T;T2107C;T1768A;G1896A 10;18;26;34;57;68;42;49 16;24;32;40;63;74;48;55 Liver disease;Chronic Hepatitis B 96;135 115;152 31877352 Occurrence of occult hepatitis B virus infection associated with envelope protein mutations according to anti-HBs carriage in blood donors. Mutations pre-s1T68I and sQ129R/L were found uniquely in 15-25% of anti-HBs(+) OBIB carriers and mutation pre-s1A54E was found preferentially in anti-HBs(+) OBIC, while 17 substitutions were found preferentially in 11-38% of anti-HBs(-) OBIB strains. 2020 International journal of infectious diseases Abstract HBV Q129R;Q129L 25;25 33;33 S;S;S;PreS1;PreS1;S 72;150;230;10;106;25 75;153;233;16;112;26 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. These data underscored that there is no concern for primary mutations in Northern Cyprus, however, we have identified a compensatory mutation (rtV173M) that may have primary mutation characteristics by combining with other mutation patterns. 2019 Polish journal of microbiology Abstract HBV V173M 145 150 RT 143 145 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. The most common NA resistance mutation was rtQ215H/P/S (16.67%), however, for S gene the misdiagnosis mutations were observed most frequently (9.25%). 2019 Polish journal of microbiology Abstract HBV Q215H;Q215P;Q215S 45;45;45 54;54;54 RT;S 43;78 45;79 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Clinically significant mutations, such as preS1 C2964A, reverse transcriptase domain I91L, and small HBsAg N3S, were identified. 2020 International journal of molecular sciences Abstract HBV C2964A;I91L;N3S 48;85;107 54;89;110 S;PreS1;RT 101;42;56 106;47;77 31954005 Analysis of Hepatitis B virus (HBV) mutations in patients from Western Saudi Arabia with chronic disease. Mutations at preS1-A2922C, X-A1624C and PC-G1887A were detected only in cases with either a high fibrosis score or hepatocellular carcinoma (HCC), while mutations at positions PC-C1982A, PC-G1951T, X-C1628T and X-A1630G were detected more frequently in HCC cases, without reaching statistical significance. 2018 Journal of infection in developing countries Abstract HBV A2922C;A1624C;G1887A;C1982A;G1951T;C1628T;A1630G 19;29;43;179;190;200;213 25;35;49;185;196;206;219 Precore;Precore;Precore;PreS1;X;X;X 40;176;187;13;27;198;211 42;178;189;18;28;199;212 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 115;141;253 139;144;256 31966550 Associations between serum HBX quasispecies and their integration in hepatocellular carcinoma. In these, the HBX-integrated groups had significantly higher mutation frequencies at C1497T, A1630G, G1721A, A1762T/G1764A and A1774G. 2017 International journal of clinical and experimental pathology Abstract HBV G1764A;C1497T;A1630G;G1721A;A1762T;A1774G 116;85;93;101;109;127 122;91;99;107;115;133 X 14 17 32003338 Hepatitis B virus X protein: The X factor in chronic hepatitis B virus disease progression. The frequency of aminoacid substitution in proapoptotic domain was higher in HBeAg negative participants including I127V (34%), K130M (34%), V131I (40%). 2019 Indian journal of medical microbiology Abstract HBV I127V;K130M;V131I 115;128;141 120;133;146 C 77 82 32003338 Hepatitis B virus X protein: The X factor in chronic hepatitis B virus disease progression. The frequency of double mutation (K130M+V131I) and triple mutation (I127V+K130M+V131I) were found to be higher (32% and 36%) in HBeAg negative participants. 2019 Indian journal of medical microbiology Abstract HBV V131I;I127V;K130M;V131I 40;68;74;80 45;73;79;85 C 128 133 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. Additionally, we experimentally simulated previously reported ETV/3TC resistance for HBV using HIVY115F/F116Y/Q151M with F160M/M184V (L180M/M204V in HBV RT) substituted. 2020 Scientific reports Abstract HBV M204V;L180M 140;134 145;139 RT 153 155 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. GST pull-down assay and co-immunoprecipitation analysis demonstrated that Pin1 associated with phosphorylated HBc at the Thr160-Pro and Ser162-Pro motifs. 2020 Frontiers in cell and developmental biology Abstract HBV T160P;S162P 121;136 131;146 C 110 113 32084506 7-Deaza-7-fluoro modification confers on 4'-cyano-nucleosides potent activity against entecavir/adefovir-resistant HBV variants and favorable safety. Southern blot analysis using wild-type HBV (HBVWT)-encoding-plasmid-transfected HepG2 cells revealed that CdFA efficiently suppresses the production of HBVWT (IC50 = 153.7 nM), entecavir (ETV)-resistant HBV carrying L180M/S202G/M204V substitutions (HBVETVR; IC50 = 373.2 nM), and adefovir dipivoxil (ADV)-resistant HBV carrying A181T/N236T substitutions (HBVADVR; IC50=192.6 nM), whereas ETV and ADV were less potent against HBVETVR and HBVADVR (IC50: >1,000 and 4,022.5 nM, respectively). 2020 Antiviral research Abstract HBV N236T;S202G;M204V;L180M;A181T 334;222;228;216;328 339;227;233;221;333 32087080 Mutations in reverse transcriptase region of HBV affect Hepatitis B surface antigen titers and its correlation with HBV DNA. For patients with A181T/V or N236T mutation, HBsAg was positively correlated with HBV DNA in older patients (>= 40 years), but not in younger patients (< 40 years). 2019 Journal of infection in developing countries Abstract HBV A181T;A181V;N236T 18;18;29 25;25;34 S 45 50 32087080 Mutations in reverse transcriptase region of HBV affect Hepatitis B surface antigen titers and its correlation with HBV DNA. HBsAg was positively correlated with HBV DNA levels in the wild-type group (r = 0.322, p < 0.01), as well as in the M204I/V, L180M+M204I/V, A181T/V, and N236T subgroups, while no correlation was found in the A181T/V+N236T subgroup (r = 0.159, p = 0.217). 2019 Journal of infection in developing countries Abstract HBV M204I;M204V;A181T;A181V;M204I;M204V;L180M;A181T;A181V;N236T;N236T 131;131;208;208;116;116;125;140;140;153;216 138;138;215;215;123;123;130;147;147;158;221 S 0 5 32087080 Mutations in reverse transcriptase region of HBV affect Hepatitis B surface antigen titers and its correlation with HBV DNA. Moreover, for patients with N236T mutation, HBsAg was positively correlated with HBV DNA level in the HBeAg negative group (r = 0.435, p = 0.016), but not in the HBeAg positive group (r = 0.105, p = 0.594). 2019 Journal of infection in developing countries Abstract HBV N236T 28 33 C;C;S 102;162;44 107;167;49 32087080 Mutations in reverse transcriptase region of HBV affect Hepatitis B surface antigen titers and its correlation with HBV DNA. RESULTS: HBsAg was lower in the wild-type and A181T/V+N236T groups as compared to the M204I/V, L180M+M204I/V and N236T groups. 2019 Journal of infection in developing countries Abstract HBV A181T;A181V;M204I;M204V;N236T;M204I;M204V;L180M;N236T 46;46;101;101;54;86;86;95;113 53;53;108;108;59;93;93;100;118 S 9 14 32087080 Mutations in reverse transcriptase region of HBV affect Hepatitis B surface antigen titers and its correlation with HBV DNA. Then, the patients were divided into five sub-groups, including M204I/V, L180M+M204I/V, A181T/V, N236T and A181T/V+N236T according to the mutation spectra. 2019 Journal of infection in developing countries Abstract HBV M204I;M204V;A181T;A181V;M204I;M204V;L180M;A181T;A181V;N236T;N236T 79;79;107;107;64;64;73;88;88;97;115 86;86;114;114;71;71;78;95;95;102;120 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. These NLGSs are located in the major hydrophilic region of HBsAg (known to be the target of antibodies) and resulted from the single mutation T115N, T117N, T123N, N114ins, and from the triple mutant S113N+T131N+M133T. 2020 Viruses Abstract HBV T115N;T117N;T123N;S113N;T131N;M133T;N114ins 142;149;156;199;205;211;163 147;154;161;204;210;216;170 S 59 64 32155009 [The prevalence clinically significant virus mutations among patients with chronic viral hepatitis B.] Another 12.5% of the isolates are characterized by mutations that are independently associated with the liver cirrhosis and hepatocellular carcinoma development, including 21, 24, 27 nucleotides deletions in the Pre-S2 region and the S11F mutation in the PreCore region. 2020 Klinicheskaia laboratornaia diagnostika Abstract HBV S11F 234 238 Precore;PreS2 255;212 262;218 Liver cirrhosis;Hepatocellular carcinoma 104;124 119;148 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. APPROACH AND RESULTS: In this study, we retrospectively monitored the emergence and reversion of the rtM204I/V mutant, a signature lamivudine resistance (LAMR ) mutation serving as a biomarker of cccDNA turnover in liver biopsies and longitudinal serum samples from two clinical trials. 2021 Hepatology (Baltimore, Md.) Abstract HBV M204I;M204V 103;103 110;110 RT 101 103 32216026 Entecavir-resistant hepatitis B virus decreases surface antigenicity: A full genome and functional characterization. Additionally, the ETV resistance mutations rtT184A/L, rtS202G and rtM250V were found among three patients. 2020 Liver international Abstract HBV T184A;T184L;S202G;M250V 45;45;56;68 52;52;61;73 RT;RT;RT 43;54;66 45;56;68 32216026 Entecavir-resistant hepatitis B virus decreases surface antigenicity: A full genome and functional characterization. More importantly, the rtI169T mutation in the RT domain, led to the sF161L mutation in the overlapping S gene, which decreased in surface antigenicity. 2020 Liver international Abstract HBV I169T;F161L 24;68 29;74 RT;RT;S;S;S 22;46;68;103;130 24;48;69;104;137 32216026 Entecavir-resistant hepatitis B virus decreases surface antigenicity: A full genome and functional characterization. RESULTS: The rtL180M + rtM204V mutations were common among all the clones analysed. 2020 Liver international Abstract HBV L180M;M204V 15;25 20;30 RT;RT 13;23 15;25 32283837 In silico Analysis of Genetic Diversity of Human Hepatitis B Virus in Southeast Asia, Australia and New Zealand. The three HBV variants identified most frequently were p.V5L, c.1896G>A and double mutation c.1762A>T/c.1764G>A, while genotypes B and C had the widest range of mutation types. 2020 Viruses Abstract HBV V5L;G1896A;A1762T;G1764A 57;64;94;104 60;71;101;111 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Results confirmed by multivariable analysis correcting for patients'demographics, HBV-DNA, ALT and infection-status.In genotype-D, specific C-terminus mutations (V190A-S204N-Y206C-Y206F-S210N) significantly correlate with HBsAg<1000IU/ml(P-value from <0.001 to 0.04). 2020 Emerging microbes & infections Abstract HBV V190A;S204N;Y206C;Y206F;S210N 162;168;174;180;186 167;173;179;185;191 S 222 227 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. These mutations lie in divergent pathways involving other HBsAg C-terminus mutations: V190A + F220L (Phi = 0.41, P = 0.003), S204N + L205P (Phi = 0.36, P = 0.005), Y206F + S210R (Phi = 0.47, P < 0.001) and S210N + F220L (Phi = 0.40, P = 0.006). 2020 Emerging microbes & infections Abstract HBV V190A;F220L;S204N;L205P;Y206F;S210R;S210N;F220L 86;94;125;133;164;172;206;214 91;99;130;138;169;177;211;219 S 58 63 32336003 Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection. E2G might cause HBsAg secretion impairment that results in intracellular accumulation and a decrease in HBsAg secretion. 2020 Journal of viral hepatitis Abstract HBV E2G 0 3 S;S 16;104 21;109 32336003 Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection. Five of the ten mutations (E2G, D144E, G145R, V168A and S174N) strongly decreased extracellular HBsAg level (P < .05) in the transfection system. 2020 Journal of viral hepatitis Abstract HBV D144E;G145R;V168A;S174N;E2G 32;39;46;56;27 37;44;51;61;30 S 96 101 32336003 Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection. Hence, ten mutations were associated with genotype B occult HBV infection; E2G and V168A were novel mutations which we confirmed significantly affect HBsAg detection. 2020 Journal of viral hepatitis Abstract HBV E2G;V168A 75;83 78;88 S 150 155 HBV infections 60 73 32336003 Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection. Notably, the E2G mutation had the most significant impact on the ratio of extracellular HBsAg (3.8% vs pHBV1.3B) and intracellular HBsAg (239.3% vs pHBV1.3B) (P < .05), and the fluorescence density of E2G mutant HBsAg was significantly higher than that of pHBV1.3B (P < .0001). 2020 Journal of viral hepatitis Abstract HBV E2G;E2G 13;201 16;204 S;S;S 88;131;212 93;136;217 32336003 Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection. Ten occult infection-related mutations (E2G, Q101R, K122R, M133T, D144E, G145R, V168A, S174N, L175S and I226S) were significantly more frequent in the occult infection group (P < .05). 2020 Journal of viral hepatitis Abstract HBV Q101R;K122R;M133T;D144E;G145R;V168A;S174N;L175S;I226S;E2G 45;52;59;66;73;80;87;94;104;40 50;57;64;71;78;85;92;99;109;43 Occult Hepatitis B 151 167 32417895 Anti-HBV activity of the HBV capsid assembly modulator JNJ-56136379 across full-length genotype A-H clinical isolates and core site-directed mutants in vitro. Core amino acid substitutions in the CAM-binding pocket, when tested as SDMs at positions 23, 25, 30, 33, 37, 106, 110, 118, 124, 127 and 128, reduced JNJ-56136379 anti-HBV activity; EC50 fold increases ranged from 3.0 (S106T) to 85 (T33N). 2020 The Journal of antimicrobial chemotherapy Abstract HBV S106T;T33N 220;234 225;238 C 0 4 32504396 Molecular characterization of hepatitis B virus isolated from Black South African cancer patients, with and without hepatocellular carcinoma. The following mutations were significantly more frequent in HCC cases than in controls (p < 0.05): in the BCP/PC 1753C/G (22.5% vs. 0%), 1764A (69.4% vs. 38.1%), and T64C (51.5% vs. 20%) in the preS2, which results in a F22L substitution. 2020 Archives of virology Abstract HBV T64C;F22L 166;220 170;224 BCP;Precore;PreS2 106;110;194 109;112;199 Hepatocellular carcinoma 60 63 32519312 Spontaneous reactivation of hepatitis B virus with S gene mutations in an elderly patient with diabetic nephropathy. Full-genome HBV sequence analysis revealed that the patient was infected with HBV of subgenotype B1 and it had an "a" determinant mutation M133L in the S gene coding HBsAg. 2020 Clinical journal of gastroenterology Abstract HBV M133L 139 144 S;S 166;152 171;153 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Clinical prognosis-related genetic variations such as nucleotide mutation T1762/A1764 (27.93%), A2189C (12.85%), G1613A (8.94%), T1753C (8.38%), T53C (4.47%) T3098C (1.68%) and PreS deletion (2.23%) were detected in CD recombinants. 2020 Virology journal Abstract HBV A2189C;G1613A;T1753C;T53C;T3098C 96;113;129;145;158 102;119;135;149;164 PreS 177 181 32542478 Analysis of HBsAg mutations in the 25 years after the implementation of the hepatitis B vaccination plan in China. HBV strains with internal stop codons of HBsAg (e.g., sC69*) and additional N-glycosylation (e.g., sG130N) mutations should be studied extensively to prevent them from becoming dominant circulating strains. 2020 Virus genes Abstract HBV C69X;G130N 54;99 59;105 S;S;S 41;54;99 46;55;100 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. Several lamivudine-associated HBV resistance mutations, including L180M, A181T, M204I, and M204V, were observed. 2020 Viruses Abstract HBV L180M;A181T;M204I;M204V 66;73;80;91 71;78;85;96 32564557 [Relationship between mutations of HBV basal core promoter region in HBsAg-positive mothers and intrauterine transmission]. Conclusion: A1762T/G1764A double mutations of HBV DNA from the genotype C of those HBsAg-positive mothers could reduced the risk of HBV intrauterine transmission during pregnancy. 2020 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T 19;12 25;18 S 83 88 32564557 [Relationship between mutations of HBV basal core promoter region in HBsAg-positive mothers and intrauterine transmission]. Maternal A1762T/G1764A double mutations appeared to be possibly associated with neonatal HBeAg (P=0.050). 2020 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T 16;9 22;15 C 89 94 32564557 [Relationship between mutations of HBV basal core promoter region in HBsAg-positive mothers and intrauterine transmission]. Rates of A1762T/G1764A double mutations were significantly different between the intrauterine transmission group and the control group (7.53% vs. 2020 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T 16;9 22;15 32564557 [Relationship between mutations of HBV basal core promoter region in HBsAg-positive mothers and intrauterine transmission]. Results from the multivariate analysis showed that the A1762T/G1764A double mutations had reduced the risk of intrauterine transmission (aOR=0.065, 95%CI: 0.006-0.746, P=0.028). 2020 Zhonghua liu xing bing xue za zhi Abstract HBV G1764A;A1762T 62;55 68;61 32568442 The genetic polymorphism down-regulating HLA-DRB1 enhancer activity facilitates HBV persistence, evolution and hepatocarcinogenesis in the Chinese Han population. rs3135395-T, rs477515-T and rs2395178-G were inversely associated with the generation of A1762T/G1764A, T1753V and C1653T, the HCC-risk HBV mutations. 2020 Journal of viral hepatitis Abstract HBV G1764A;A1762T;T1753V;C1653T 96;89;104;115 102;95;110;121 Hepatocellular carcinoma 127 130 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Artificial elimination of rtA181S from the rtA181S + T184I + M204I mutant restored viral susceptibility to ADV but decreased viral replication capacity. 2020 Antiviral research Abstract HBV A181S;A181S;T184I;M204I 28;45;53;61 33;50;58;66 RT;RT 26;43 28;45 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Compared with wild-type, the rtA181S + T184I + M204I mutant had 53.7% lower replication capacity and >1000-, 3.9-, and 383.3-fold greater LAM, ADV, and ETV resistance, respectively, but remained sensitive to tenofovir. 2020 Antiviral research Abstract HBV T184I;M204I;A181S 39;47;31 44;52;36 RT 29 31 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Longitudinal analysis of the clinical course of resistant mutant evolution for four representative cases showed that rtA181S + T184I + M204I developed in all patients who had received LAM/telbivudine +- ADV and was receiving ETV or ADV + ETV. 2020 Antiviral research Abstract HBV A181S;T184I;M204I 119;127;135 124;132;140 RT 117 119 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Of 180 rtA181S-positive patients, 42 had no coexistent resistance mutations, 34 had coexisting LAM-resistance mutation (LAMr), 17 had coexisting ADV-resistance mutation (ADVr), and 86 had coexisting ETV-resistance mutation (ETVr), and one had ADVr + ETVr. 2020 Antiviral research Abstract HBV A181S 9 14 RT 7 9 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. Our study presented the first evidence that HBV rtA181S + T184I + M204I mutation had features of multidrug-resistance that contributed to resistance to both nucleoside and nucleotide analogs. 2020 Antiviral research Abstract HBV A181S;T184I;M204I 50;58;66 55;63;71 RT 48 50 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. rtA181S + T184I + M204I occurred in 79.1% (68/86) of patients with rtA181S + ETVr and 37.8% (68/180) of all rtA181S-positive patients. 2020 Antiviral research Abstract HBV A181S;A181S;A181S;T184I;M204I 2;69;110;10;18 7;74;115;15;23 RT;RT;RT 0;67;108 2;69;110 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. rtA181S-positive patients had significantly higher lamivudine (LAM), adefovir (ADV), and entecavir (ETV) exposure than rtA181S-negative patients. 2020 Antiviral research Abstract HBV A181S;A181S 2;121 7;126 RT;RT 0;119 2;121 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. The rtA181S mutation was detected in 0.82% (180/22,009) of samples. 2020 Antiviral research Abstract HBV A181S 6 11 RT 4 6 32569703 Hepatitis B virus mutation pattern rtA181S+T184I+M204I may contribute to multidrug resistance in clinical practice: Analysis of a large cohort of Chinese patients. The study aimed to characterize the prevalence and virological features of the rtA181S + T184I + M204I mutant in a large cohort of patients with chronic HBV infection. 2020 Antiviral research Abstract HBV A181S;T184I;M204I 81;89;97 86;94;102 RT 79 81 Chronic HBV infection 145 166 32579776 Virology analysis of chronic hepatitis B virus-infected patients treated for 28 days with JNJ-56136379 monotherapy. A 25 mg JNJ-6379-treated patient had on-treatment enrichment of Y118F variant (HBV DNA decline 2.13 log10 IU/mL). 2020 Journal of viral hepatitis Abstract HBV Y118F 64 69 32579776 Virology analysis of chronic hepatitis B virus-infected patients treated for 28 days with JNJ-56136379 monotherapy. One 75 mg JNJ-6379-treated patient had an emerging T109S substitution (FC = 1.8; HBV DNA decline 3.18 log10 IU/mL). 2020 Journal of viral hepatitis Abstract HBV T109S 51 56 32579776 Virology analysis of chronic hepatitis B virus-infected patients treated for 28 days with JNJ-56136379 monotherapy. Two JNJ-6379-treated patients carried a Y118F baseline core polymorphism known to reduce JNJ-6379 activity in vitro (FC = 6.6) and had HBV DNA declines of 2.77 (75 mg) and 2.19 log10 IU/mL (150 mg) at the end of treatment. 2020 Journal of viral hepatitis Abstract HBV Y118F 40 45 C 55 59 32592870 Identification of mutations in the S gene of hepatitis B virus in HIV positive Mexican patients with occult hepatitis B virus infection. The most common mutations were: C19Y, Q129H, E164D, and I195M, with a frequency of 44%, 36%, 39% and 48% respectively. 2020 Annals of hepatology Abstract HBV C19Y;Q129H;E164D;I195M 32;38;45;56 36;43;50;61 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The differences in dynamics when comparing HBV and human Cp149-Y132A as well as the differences in dynamics when comparing the HBV and WHV Cps allowed us to map an allosteric network within the HBV dimer. 2020 ACS chemical biology Abstract HBV Y132A 63 68 C;C 57;139 59;141 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. To understand what blocks assembly, we took advantage of an assembly incompetent mutant dimer, Cp149-Y132A, located in the interdimer interface. 2020 ACS chemical biology Abstract HBV Y132A 101 106 C 95 97 32679130 Immunoreactivity pattern of monoclonal antibodies against Hepatitis B vaccine with global Hepatitis B virus genotypes. Comparing amino acids sequences inside the antigenic loop (AGL) showed that D2/ayw3 contains a T118A/P127T double substitution, E/ayw4 contains P127L/T140S, F2/adw4 contains P127L/T140S/ F158L, and H/adw4 contains P127L substitution. 2020 Clinica chimica acta; international journal of clinical chemistry Abstract HBV P127T;T140S;T140S;T118A;P127L;P127L;F158L;P127L 101;150;180;95;144;174;187;214 106;155;185;100;149;179;192;219 32679130 Immunoreactivity pattern of monoclonal antibodies against Hepatitis B vaccine with global Hepatitis B virus genotypes. Interestingly, the amino acid alignment of the samples in this WHO panel showed that P127T substitution can also be found in C2/adr. 2020 Clinica chimica acta; international journal of clinical chemistry Abstract HBV P127T 85 90 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. Conclusion: In the present study, mutations were identified at positions T113S and N131T within the MHR region of S protein; these mutations can potentially decrease the effect of hepatitis B vaccination in vaccine recipients. 2020 Heliyon Abstract HBV T113S;N131T 73;83 78;88 S 114 115 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. Results: We found major hydrophilic region (MHR) mutations at "a" determining region that included K122R, N131T, F134Y, P142L, and T126N mutations. 2020 Heliyon Abstract HBV K122R;N131T;F134Y;P142L;T126N 99;106;113;120;131 104;111;118;125;136 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Multiple-point mt were found only in 8 cases (5.6%): 6 children carried double mt (rtV207M + rtL229V; rtV207M + rtI233V; rtV207I + rtV207M x 2 cases; rtV207M + rtS213T; rtN238A + rtS256G) relating to LMV or/and ADF resistance and 3 children carried triple mt (rtL180M + rtM204I + rtN238T; rtV207M + rtS213T + rtS256G) or quadruple mt (rtL180M + rtM204V + rtV207I/M) for LMV-ADF resistance and Entecavir-reduced susceptibility. 2020 Diagnostics (Basel, Switzerland) Abstract HBV V207M;L229V;V207M;I233V;V207I;V207M;V207M;S213T;N238A;S256G;L180M;M204I;N238T;V207M;S213T;S256G;L180M;M204V;V207I;V207M 85;95;104;114;123;133;152;162;171;181;262;272;282;291;301;311;337;347;357;357 90;100;109;119;128;138;157;167;176;186;267;277;287;296;306;316;342;352;364;364 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 83;93;102;112;121;131;150;160;169;179;260;270;280;289;299;309;335;345;355 85;95;104;114;123;133;152;162;171;181;262;272;282;291;301;311;337;347;357 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Single-point mt associated to LMV and ADF resistance were detected in 59.9% of the tested children with rtV207M (38.0%) and rtN238T (9.9%) being the most frequent. 2020 Diagnostics (Basel, Switzerland) Abstract HBV V207M;N238T 106;126 111;131 RT;RT 104;124 106;126 32748602 [Preparation and characterization of HBc virus like particles with site-directed coupling function]. After expression and purification, high purity HBc(A80C) monomer protein was assembled into HBc-VLPs nanoparticles in Phosphate Buffer. 2020 Sheng wu gong cheng xue bao Abstract HBV A80C 51 55 C;C 47;92 50;95 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. HBV variants, particularly the G1896A pre-core (PC) and A1762T/G1764A basal core promoter (BCP) mutations, are established risk factors for cirrhosis and HCC, but the molecular biological basis is unclear. 2020 Frontiers in microbiology Abstract HBV G1764A;A1762T;G1896A 63;56;31 69;62;37 BCP;BCP;Precore;Precore 70;91;48;38 89;94;50;46 Liver cirrhosis;Hepatocellular carcinoma 140;154 149;157 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. RESULTS: HBeAg expression was reduced in PC and BCP variants, and higher supernatant HBV DNA and HBV RNA levels were found with A1762T/G1764A vs. G1896A mutant (p聽< 0.05). 2020 Frontiers in microbiology Abstract HBV G1764A;G1896A;A1762T 135;146;128 141;152;134 32763811 The sK122R mutation of hepatitis B virus (HBV) is associated with occult HBV infection: Analysis of a large cohort of Chinese patients. CONCLUSIONS: The study clarified the clinical prevalence of OBI, verified the influence of immune escape-associated mutations, and identified the role of the sK122R mutation in multiple OBI patients. 2020 Journal of clinical virology Abstract HBV K122R 158 164 S 158 159 Occult Hepatitis B;Occult Hepatitis B 60;186 63;189 32763811 The sK122R mutation of hepatitis B virus (HBV) is associated with occult HBV infection: Analysis of a large cohort of Chinese patients. Specifically, the prevalence rates of sT118 K, sK122R, and sV168A were increased in OBI patients. 2020 Journal of clinical virology Abstract HBV T118K;K122R;V168A 38;47;59 45;53;65 S;S;S 38;47;59 39;48;60 Occult Hepatitis B 84 87 32763811 The sK122R mutation of hepatitis B virus (HBV) is associated with occult HBV infection: Analysis of a large cohort of Chinese patients. Strains with sK122R mutants (sK122R, sK122R + D144E, sK122R + C121R + D144E, and sK122R + F134L + D144E) from a follow-up OBI patient all showed significantly lower levels of HBsAg production than a wild-type strain. 2020 Journal of clinical virology Abstract HBV D144E;C121R;D144E;F134L;D144E;K122R;K122R;K122R;K122R;K122R 46;62;70;90;98;13;29;37;53;81 51;67;75;95;103;19;35;43;59;87 S;S;S;S;S;S 175;13;29;37;53;81 180;14;30;38;54;82 Occult Hepatitis B 122 125 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Primary and secondary DR variants were found in 7.3% (15/206) of patients, including rtL80I/V, rtI169T, rtV173L rtL180M, rtA181T/V, rtM204I/V, and rtN236T. 2020 Infection and drug resistance Abstract HBV L80I;L80V;I169T;V173L;L180M;A181T;A181V;M204I;M204V;N236T 87;87;97;106;114;123;123;134;134;149 93;93;102;111;119;130;130;141;141;154 RT;RT;RT;RT;RT;RT;RT 85;95;104;112;121;132;147 87;97;106;114;123;134;149 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. Further, antibody binding was not affected by the mutations in the antigenic 'a' determinant found in many clinical variants, including the immune escape mutant G145R. 2020 PloS one Abstract HBV G145R 161 166 S 78 92 32791794 [Effect of hepatitis B virus preC/C and S gene antigen epitope mutations on HBeAg serological status in patients with chronic hepatitis B]. After adjusting for confounding factors such as age, gender, HBV genotype, serum alanine aminotransferase level and precw28 * mutations in the longitudinal studies, the results showed that TC cell epitope (prec47-56, prec117-125, s208-216) and Th cell epitope (prec176-185) were the main independent risk factors affecting the host HBeAg serological status. 2020 Zhonghua gan zang bing za zhi Abstract HBV W28X 120 125 C;Precore;Precore;Precore;Precore;S 332;116;206;217;261;230 337;120;210;221;265;231 32840739 An antiviral drug-resistant mutant of hepatitis B virus with high replication capacity in association with a large in-frame deletion in the preS1 region of viral surface gene. In addition, all the clones harbored another nonsense mutation in the S gene (C69*) and a 207nt in-frame deletion in the preS1 region. 2020 Virus genes Abstract HBV C69X 78 82 PreS1;S 121;70 126;71 32840739 An antiviral drug-resistant mutant of hepatitis B virus with high replication capacity in association with a large in-frame deletion in the preS1 region of viral surface gene. Mutation(s) in the polymerase gene responsible for ADV resistance included rtA181T (all clones) and rtN236T (four clones). 2020 Virus genes Abstract HBV A181T;N236T 77;102 82;107 RT;RT;P 75;100;19 77;102;29 32840739 An antiviral drug-resistant mutant of hepatitis B virus with high replication capacity in association with a large in-frame deletion in the preS1 region of viral surface gene. The rtA181T mutation caused the W172* nonsense mutation in the overlapping S gene. 2020 Virus genes Abstract HBV A181T;W172X 6;32 11;37 S;RT 75;4 76;6 32860463 Precore and Basal Core Promoter Hepatitis B Virus (HBV) Variants Are Present From a Young Age and Differ Across HBV Genotypes. CONCLUSIONS: PC variants can be present in HBV genotype A and are usually associated with C1858T, which preserves the pregenome encapsidation sequence. 2021 Hepatology (Baltimore, Md.) Abstract HBV C1858T 90 96 Precore 13 15 32860463 Precore and Basal Core Promoter Hepatitis B Virus (HBV) Variants Are Present From a Young Age and Differ Across HBV Genotypes. Seventeen of 20 participants with genotype A and PC had a compensatory C1858T mutation. 2021 Hepatology (Baltimore, Md.) Abstract HBV C1858T 71 77 Precore 49 51 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. CONCLUSIONS: The percentage of A1762T/G1764A mutations after HBeAg seroconversion was associated with liver fibrosis. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 38;31 44;37 C 61 66 Liver fibrosis 102 116 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. Hepatitis B e antigen seroconversion age is positively correlated with the percentages of A1762T/G1764A mutation at inflammatory phase before HBeAg seroconversion. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 97;90 103;96 C;C 12;142 21;147 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. RESULTS: We demonstrated that the percentages of A1762T/G1764A mutation are significantly higher in subjects with an LSM >7 kPa than in those with an LSM <=7 kPa after HBeAg seroconversion. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 56;49 62;55 C 168 173 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. Subjects who underwent interferon, entecavir, or tenofovir disoproxil fumarate therapy before HBeAg seroconversion possessed a lower percentage of A1762T/G1764A mutation after HBeAg seroconversion. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 154;147 160;153 C;C 94;176 99;181 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. The A1762T/G1764A mutation may evoke hepatic inflammation by suppressing PD-L1 in hepatocytes. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 11;4 17;10 Liver inflammation 37 57 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. The percentage of A1762T/G1764A >=20% after HBeAg seroconversion was predictive of an LSM >7 kPa (hazard ratio = 6.37, P = .001). 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 25;18 31;24 C 44 49 32860707 Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion. The presence of A1762T/G1764A led to downregulated messenger ribonucleic acid and protein levels of programmed-death ligand-1 (PD-L1) in hepatocytes. 2021 The Journal of infectious diseases Abstract HBV G1764A;A1762T 23;16 29;22 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Some of these mutants introduce premature stop codons in the overlapping surface (s) gene, including rtA181T/sW172*, which has been shown to enhance oncogenicity. 2020 International journal of molecular sciences Abstract HBV W172X;A181T 109;103 115;108 RT;S;S;S 101;82;109;73 103;83;110;80 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The oncogenicity of another drug-resistant mutant, rtM204I/sW196*, has not been studied. 2020 International journal of molecular sciences Abstract HBV W196X;M204I 59;53 65;58 RT;S 51;59 53;60 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The rtM204I/sW196* preS/S truncation may endorse the cell transformation and tumorigenesis ability via altered host gene expressions, including MGST2, HIF1A, and TGFbi. 2020 International journal of molecular sciences Abstract HBV W196X;M204I 12;6 18;11 PreS;S;RT;S 19;24;4;12 23;25;6;13 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The rtM204I/sW196* transformants, compared with the control or wild type, showed enhanced transactivation activities for c-fos, increased cell proliferation, decreased apoptosis, more anchorage-independent growth, and enhanced tumor growth in mouse xenografts. 2020 International journal of molecular sciences Abstract HBV W196X;M204I 12;6 18;11 RT;S 4;12 6;13 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. We constructed plasmids harboring rtM204I/sW196* and assessed the in vitro cell transformation, endoplasmic reticulum (ER) stress response, and xenograft tumorigenesis of the transformants. 2020 International journal of molecular sciences Abstract HBV W196X;M204I 42;36 48;41 RT;S 34;42 36;43 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. All the patients harbouring rtA194T or CYE/CYEI at baseline achieved viral suppression by week 96 after TDF or TAF treatment. 2021 Journal of viral hepatitis Abstract HBV A194T 30 35 RT 28 30 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. Both the A194T and a quadruple mutation CYEI (S106C, H126Y, D134E and L269I) in hepatitis B virus (HBV) polymerase reverse transcriptase domain (pol/RT) are suggested to be associated with treatment failure with tenofovir disoproxil fumarate (TDF). 2021 Journal of viral hepatitis Abstract HBV S106C;H126Y;D134E;L269I;A194T 46;53;60;70;9 51;58;65;75;14 P;P;RT;RT 145;104;115;149 148;114;136;151 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. In total, six out of 3886 (0.2%) patients carried the rtA194T mutation, while only 1 patient carried a triple CYE and 2 patients carried a quadruple CYEI mutation at baseline. 2021 Journal of viral hepatitis Abstract HBV A194T 56 61 RT 54 56 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. No evidence of rtA194T and CYEI conferring resistance to TDF or TAF was observed based on the treatment responses to TDF or TAF in patients with mutations at baseline, the lack of selection of mutations after starting TDF or TAF treatment and no change in susceptibility to TFV or TAF in vitro. 2021 Journal of viral hepatitis Abstract HBV A194T 17 22 RT 15 17 32894807 Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance. No patients developed an rtA194T mutation or > 1 substitution of CYEI, and the number of patients losing any substitutions of CYEI (n = 17) was similar to the number who developed a single substitution of CYEI (n = 32) during treatment. 2021 Journal of viral hepatitis Abstract HBV A194T 27 32 RT 25 27 32911905 [Clinical significance and mutation characteristics in the core promoter/pre-C region of different HBV genotypes in children]. Further analysis showed that the age of G1721A/A1775G/T1858C containing combined mutation group was significantly lower than that of the non-mutation group [(4.58 +- 2.53) years vs. 2020 Zhonghua gan zang bing za zhi Abstract HBV A1775G;T1858C;G1721A 47;54;40 53;60;46 32911905 [Clinical significance and mutation characteristics in the core promoter/pre-C region of different HBV genotypes in children]. The mutation rates of G1721a, C1856t and T1858c of genotype C samples were 30.9%, 16.2% and 30.9%, respectively, while the mutation rates of genotype B samples were 0.4%, 0, 0, P < 0.001, respectively. 2020 Zhonghua gan zang bing za zhi Abstract HBV C1856T 30 36 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Resistance mutations included rtL80I, rtV173L, rtL180M, rtM204I/V and the overlapping sE164D, sW182*, sI195M and sW196LS variants. 2020 PloS one Abstract HBV L80I;V173L;L180M;M204I;M204V;E164D;W182X;I195M;W196L;W196S 32;40;49;58;58;86;94;102;113;113 36;45;54;65;65;92;100;108;120;120 RT;RT;RT;RT;S;S;S;S 30;38;47;56;86;94;102;113 32;40;49;58;87;95;103;114 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. By sequencing analysis, we revealed mutations at the "a" determinant of HBsAg, including Q129R, T131N, M133S, F134L and D144E. 2020 International journal of medical sciences Abstract HBV Q129R;T131N;M133S;F134L;D144E 89;96;103;110;120 94;101;108;115;125 S 72 77 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. Conclusions: Our study clarifies the prevalence of OBI in MHD patients in Sichuan Province(4.2% in the test group, 2.1% in the overall dialysis cohort), and demonstrate the mutations of Q129R and M133S in the "a" determinant of HBsAg for the first time. 2020 International journal of medical sciences Abstract HBV Q129R;M133S 186;196 191;201 S 228 233 Occult Hepatitis B 51 54 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. The Q129R and M133S mutations were first reported. 2020 International journal of medical sciences Abstract HBV Q129R;M133S 4;14 9;19 32978866 Case of hepatitis B virus reactivation after ibrutinib therapy in which the patient remained negative for hepatitis B surface antigens throughout the clinical course. Interestingly, the patient remained negative for HBsAg throughout the clinical course owing to triple HBsAg escape mutations: Q101K, M133L, and G145A. 2021 Hepatology research Abstract HBV Q101K;M133L;G145A 126;133;144 131;138;149 S;S 49;102 54;107 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Among these, sA159V was detected in 1.95% (136/6982) of patients with resistance mutations and 1.08% (134/12,458) of patients lacking resistance mutations (P < 0.05). 2020 World journal of gastroenterology Abstract HBV A159V 13 19 S 13 14 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. HBsAg production was significantly lower and the replication capacity was significantly higher, without a significant difference in LAM/ETV susceptibility, in sA159V-containing LAM/ETV-resistant mutants than in their sA159V-lacking counterparts. 2020 World journal of gastroenterology Abstract HBV A159V;A159V 159;217 164;222 S;S;S 0;159;217 5;160;218 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In particular, these mutations were sQ101H/K/R, sS114A/L/T, sT118A/K/M/R/S/V, sP120A/L/Q/S/T, sT/I126A/N/P/S, sM133I/L/T, sC137W/Y, sG145A/R, and sA159G/V. 2020 World journal of gastroenterology Abstract HBV T126A;T126N;T126P;T126S;I126A;I126N;I126P;I126S;Q101H;Q101K;Q101R;S114A;S114L;S114T;T118A;T118K;T118M;T118R;T118S;T118V;P120A;P120L;P120Q;P120S;P120T;M133I;M133L;M133T;C137W;C137Y;G145A;G145R;A159G;A159V 94;94;94;94;94;94;94;94;36;36;36;48;48;48;60;60;60;60;60;60;78;78;78;78;78;110;110;110;122;122;132;132;146;146 108;108;108;108;108;108;108;108;46;46;46;58;58;58;76;76;76;76;76;76;92;92;92;92;92;120;120;120;130;130;140;140;154;154 S;S;S;S;S;S;S;S;S 36;48;60;78;94;110;122;132;146 37;49;61;79;95;111;123;133;147 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Phenotypic analyses were performed to evaluate HBsAg production, replication capacity, and drug-induced viral inhibition of patient-derived drug-resistant mutants with or without the coexistence of sA159V. 2020 World journal of gastroenterology Abstract HBV A159V 198 204 S;S 47;198 52;199 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. sA159V might increase the fitness of LAM/ETV-resistant mutants under environmental pressure in some cases. 2020 World journal of gastroenterology Abstract HBV A159V 0 6 S 0 1 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The coexistence of sA159V with lamivudine (LAM) and entecavir (ETV)-resistance mutations in the same viral genome was identified during follow-up in some patients with drug resistance. 2020 World journal of gastroenterology Abstract HBV A159V 19 25 S 19 20 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. One escape mutation (T123A) associated with OBI and various amino acid substitutions for genotype A1 and E were observed. 2020 Memorias do Instituto Oswaldo Cruz Abstract HBV T123A 21 26 Occult Hepatitis B 44 47 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Calculation of the pgRNA secondary structure suggests a destabilization of the pgRNA structure by A1762T/G1764A that was compensated by GCAC1809-1812TTCT. 2020 JCI insight Abstract HBV G1764A;A1762T 105;98 111;104 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. GCAC1809-1812TTCT was strongly associated with coexistence of basal core promoter (BCP) double mutation A1762T/G1764A and lower HBV DNA levels. 2020 JCI insight Abstract HBV G1764A;A1762T 111;104 117;110 BCP;BCP 62;83 81;86 33090103 Molecular epidemiology of Hepatitis B virus, Hepatitis C virus, and Hepatitis D virus in general population of Afghanistan. C316N mutation was prevalent in 72.7% of HCV 1b participants. 2020 The Turkish journal of gastroenterology Abstract HBV C316N 0 5 33090103 Molecular epidemiology of Hepatitis B virus, Hepatitis C virus, and Hepatitis D virus in general population of Afghanistan. Likewise, S213T 10%, Q215P 5% and N248H 100% mutations were detected in the HBV polymerase region. 2020 The Turkish journal of gastroenterology Abstract HBV S213T;Q215P;N248H 10;21;34 15;26;39 P 80 90 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. A typical putative resistance mutation rtL229V was further studied using in-vitro susceptibility assays and molecular modeling. 2020 Emerging microbes & infections Abstract HBV L229V 41 46 RT 39 41 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. It contributed to the most potent suppression of viral replication and reduced the in-vitro drug susceptibility to entecavir (ETV) when coexisting with rtM204V, consistent with the hypothesis based on the molecular modeling and clinical data analysis. 2020 Emerging microbes & infections Abstract HBV M204V 154 159 RT 152 154 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. rtL229V was the major substitution at the site of rt229. 2020 Emerging microbes & infections Abstract HBV L229V 2 7 RT;RT 0;50 2;52 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. rtV191I and rtA181T/V were the only resistance mutations identified as genotype-specific mutation. 2020 Emerging microbes & infections Abstract HBV V191I;A181T;A181V 2;14;14 7;21;21 RT;RT 0;12 2;14 33245644 Optimization of the algorithm diagnosis chronic hepatitis B markers in patients with newly diagnosed HIV infection. Three HBV isolates (8.3%) were identified with drug resistance mutations to lamivudine, entericavir, telbivudine and tenofovir, which are amino acid substitutions in the HBV polymerase gene at positions L180M, T184A, M204V. 2020 Klinicheskaia laboratornaia diagnostika Abstract HBV L180M;T184A;M204V 203;210;217 208;215;222 P 174 184 33245644 Optimization of the algorithm diagnosis chronic hepatitis B markers in patients with newly diagnosed HIV infection. When analyzing the basal nucleus promoter, Precore and Core regions, 22.2% of patients with the double mutation A1762T / G1764A, 25% with the mutation G1896A were identified. 2020 Klinicheskaia laboratornaia diagnostika Abstract HBV A1762T;G1764A;G1896A 112;121;151 118;127;157 C;Precore 55;43 59;50 33247709 Compartmentalized evolution of hepatitis B virus contributes differently to the prognosis of hepatocellular carcinoma. APOBECs-related HBV mutations, including G1764A, were more frequent in the sera than in the adjacent tissues. 2021 Carcinogenesis Abstract HBV G1764A 41 47 33247709 Compartmentalized evolution of hepatitis B virus contributes differently to the prognosis of hepatocellular carcinoma. HBV QC and A1762T/G1764A in the sera and tumors have contrary prognostic effects in HCC. 2021 Carcinogenesis Abstract HBV G1764A;A1762T 18;11 24;17 Hepatocellular carcinoma 84 87 33247709 Compartmentalized evolution of hepatitis B virus contributes differently to the prognosis of hepatocellular carcinoma. High-frequent A1762T/G1764A in the sera predicted an unfavorable RFS (P < 0.001), whereas, in the tumors, it predicted a favorable RFS (P = 0.035). 2021 Carcinogenesis Abstract HBV G1764A;A1762T 21;14 27;20 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. In contrast to widely used commercial assays, the NTR-HBeAg completely eliminated the cross-reactivity with secreted HBcAg from precore mutant (G1896A) virus in either cell culture or patient sera. 2021 Emerging microbes & infections Abstract HBV G1896A 144 150 C;C;Precore 117;54;128 122;59;135 33333207 Identification of a novel long-acting 4'-modified nucleoside reverse transcriptase inhibitor against HBV. E-CFCP also reduced HBVETV-RL180M/S202G/M204V-viremia by 2 logs over 2 weeks, while ETV completely failed to reduce HBVETV-RL180M/S202G/M204V-viremia. 2021 Journal of hepatology Abstract HBV S202G;M204V;S202G;M204V;L180M;L180M 34;40;130;136;123;27 39;45;135;141;129;33 33333207 Identification of a novel long-acting 4'-modified nucleoside reverse transcriptase inhibitor against HBV. E-CFCP's 4'-cyano and fluorine interact with both HBVWT-RT and HBVETV-RL180M/S202G-M204 -RT via Van der Waals and polar forces, being important for E-CFCP-triphosphate's interactions and anti-HBV potency. 2021 Journal of hepatology Abstract HBV S202G;R180M;L180M 77;70;70 82;76;76 RT;RT 56;89 58;91 33333207 Identification of a novel long-acting 4'-modified nucleoside reverse transcriptase inhibitor against HBV. RESULTS: E-CFCP potently blocked HBVWTD1 production (IC50qPCR_cell=1.8 nM) in HepG2.2.15 cells and HBVWTC2 (IC50SB_cell=0.7 nM), entecavir (ETV)-resistant HBVETV-RL180M/S202G/M204V (IC50SB_cell=77.5 nM), and adefovir-resistant HBVADV-RA181T/N236T production (IC50SB_cell=14.1 nM) in Huh7 cells. 2021 Journal of hepatology Abstract HBV N236T;S202G;M204V;L180M;R181T;A181T 241;169;175;162;234;234 246;174;180;168;240;240 33357228 Viral hepatitis B and C in HIV-exposed South African infants. The rtM204I mutation associated with lamivudine resistance was identified in one infant, a second infant harboured the double A1762T/G1764A BCP mutation. 2020 BMC pediatrics Abstract HBV G1764A;M204I;A1762T 133;6;126 139;11;132 BCP;RT 140;4 143;6 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. HCC-associated mutations were detected in 33.7% of the sequences, with significantly higher frequency of C1653T, T1753V and A1762T/G1764A in genotype G than C (P < 0.001). 2020 Frontiers in microbiology Abstract HBV G1764A;C1653T;T1753V;A1762T 131;105;113;124 137;111;119;130 Hepatocellular carcinoma 0 3 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Immune escape mutations were detected in 10.7% of the sequences, the most common being I/T126S (1.8%), G145R (1.2%), M133T (1.2%), and Q129R (1.0%). 2020 Frontiers in microbiology Abstract HBV I126S;T126S;G145R;M133T;Q129R 87;87;103;117;135 94;94;108;122;140 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. HBV DRMs V173L, L180M, S202I and M204V/I, which are associated with lamivudine resistance, were detected in 32.2% (n = 10/31) of the HBV DNA-positive samples. 2021 Virology journal Abstract HBV V173L;L180M;S202I;M204V;M204I 9;16;23;33;33 14;21;28;40;40 33453326 Role of core protein mutations in the development of occult HBV infection. An analysis of the effect of Cp mutants on intracellular or extracellular viral protein production indicated that the W62R mutation in Cp had a critical impact on the reduction of HBcAg and HBeAg production during HBV replication, whereas P50H and/or S74G mutations played a limited role in influencing viral protein production invivo. 2021 Journal of hepatology Abstract HBV W62R;P50H;S74G 118;239;251 122;243;255 C;C;C;C 29;135;180;190 31;137;185;195 33453326 Role of core protein mutations in the development of occult HBV infection. CONCLUSIONS: W62R and its combination mutations in HBV Cp might massively affect HBcAg and HBeAg production during viral replication, which, in turn, might contribute to the occurrence of OBI. 2021 Journal of hepatology Abstract HBV W62R 13 17 C;C;C 55;81;91 57;86;96 Occult Hepatitis B 188 191 33453326 Role of core protein mutations in the development of occult HBV infection. The W62R mutation in Cp majorly reduces HBcAg and HBeAg production during HBV replication, potentially contributing to the occurrence of OBI. 2021 Journal of hepatology Abstract HBV W62R 4 8 C;C;C 21;40;50 23;45;55 Occult Hepatitis B 137 140 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. Through application of deep whole-genome sequencing we typed the isolate as genotype-D1, and identified several minority variants including G1764A and G1986A substitutions in the pre-core promoter and pre-core regions, which support CHB-AR rather than AHB. 2020 Wellcome open research Abstract HBV G1764A;G1986A 140;151 146;157 Precore;Precore promoter 201;179 209;196 Acute Hepatitis B;Chronic Hepatitis B 252;233 255;236 33462964 Virologic analysis of tenofovir resistance in a patient with chronic hepatitis B experiencing viral breakthrough during combination treatment with tenofovir disoproxil fumarate and entecavir. A recent Korean report showed that two patients with viral breakthrough during treatment with TDF-containing regimens were found to carry five reverse transcriptase (rt) mutations ([rt]S106C[C], rtH126Y[Y], rtD134E[E], rtM204I/V, and rtL269I [I]), with the C, Y, E, and I mutations being associated with tenofovir resistance. 2021 Hepatology research Abstract HBV H126Y;D134E;M204I;M204V;L269I;S106C 197;209;221;221;236;184 202;214;228;228;241;190 RT;RT;RT;RT;RT;RT;RT 143;166;182;195;207;219;234 164;168;184;197;209;221;236 33462964 Virologic analysis of tenofovir resistance in a patient with chronic hepatitis B experiencing viral breakthrough during combination treatment with tenofovir disoproxil fumarate and entecavir. Four mutations (rtS106C, rtD134N/S[N/S], rtM204V, and rtL269I) plus ETV resistance (rtL180M and rtS202G) existed when she developed viral breakthrough during ETV and TDF combination therapy in April 2013. 2021 Hepatology research Abstract HBV S106C;D134N;D134S;M204V;L269I;L180M;S202G 18;27;27;43;56;86;98 23;34;34;48;61;91;103 RT;RT;RT;RT;RT;RT 16;25;41;54;84;96 18;27;43;56;86;98 33462964 Virologic analysis of tenofovir resistance in a patient with chronic hepatitis B experiencing viral breakthrough during combination treatment with tenofovir disoproxil fumarate and entecavir. In conclusion, three mutations (CN/SI) plus ETV resistance (rtL180M, rtM204V, and rtS202G) can cause tenofovir resistance. 2021 Hepatology research Abstract HBV L180M;M204V;S202G 62;71;84 67;76;89 RT;RT;RT 60;69;82 62;71;84 33462964 Virologic analysis of tenofovir resistance in a patient with chronic hepatitis B experiencing viral breakthrough during combination treatment with tenofovir disoproxil fumarate and entecavir. Moreover, three mutations (rtS106C, rtD134N, and rtL269I) existed at baseline. 2021 Hepatology research Abstract HBV S106C;D134N;L269I 29;38;51 34;43;56 RT;RT;RT 27;36;49 29;38;51 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A high-frequency mutation, T1719G (93.3%), was detected in the BCP/PC region, which reduced the viral replication. 2021 BMC infectious diseases Abstract HBV T1719G 27 33 BCP;Precore 63;67 66;69 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Mutations were found in the S gene, including Y100C, Y103I, G145R, and L175S, which can affect the detection of HBsAg. 2021 BMC infectious diseases Abstract HBV Y100C;Y103I;G145R;L175S 46;53;60;71 51;58;65;76 S;S 112;28 117;29 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. A cell-based phenotypic assay revealed that the rtT301A mutation dramatically impaired the replication ability with meaningful reduction in sensitivity to tenofovir in hepatoma cell lines. 2021 International journal of molecular sciences Abstract HBV T301A 50 55 RT 48 50 Hepatocellular carcinoma 168 176 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. However, attenuated viral replication by the rtT301A mutation was significantly restored in primary human hepatocytes (PHHs). 2021 International journal of molecular sciences Abstract HBV T301A 47 52 RT 45 47 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Interestingly, a threonine to alanine mutation at the 301 amino acid position of the reverse-transcriptase (RT) domain, (rtT301A), was commonly accompanied with CYELMVI at a high rate (72.7%). 2021 International journal of molecular sciences Abstract HBV T301A 123 128 RT;RT;RT 85;108;121 106;110;123 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Since the rtT301A mutation has not been reported yet, we investigated the role of this naturally occurring mutation on the viral replication and susceptibility to tenofovir in various liver cells (hepatoma cells as well as primary human hepatocytes). 2021 International journal of molecular sciences Abstract HBV T301A 12 17 RT 10 12 Hepatocellular carcinoma 197 205 33571155 Multiple drug-resistant HBV mutation may contribute to poor response of adefovir + entecavir in entecavir-resistant patients. RESULTS: ETV-resistant mutants were continuously detected in 10 of the 12 patients, and multidrug-resistant (MDR) mutants, including a novel strain (rtL180M+A181V+T184A+S202G+M204V), were detected in two patients. 2021 Journal of infection in developing countries Abstract HBV L180M;A181V;T184A;S202G;M204V 151;157;163;169;175 156;162;168;174;180 RT 149 151 33595430 Transcriptome analysis of hepatoma cells transfected with Basal Core Promoter (BCP) and Pre-Core (PC) mutant hepatitis B virus full genome construct. Infections with Basal Core Promoter (BCP) (A1762T/G1764A) and Pre-Core (PC) (G1896A) hepatitis B virus HBeAg mutants are associated with severe liver injury. 2021 The Journal of general virology Abstract HBV G1764A;A1762T;G1896A 50;43;77 56;49;83 BCP;BCP;C;Precore;Precore 16;37;103;72;62 35;40;108;74;70 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. A genotype D-specific pattern of mutations (A12S/P33S/P46S/T36D-G) was identified in CI (median frequency, 81.7%), which determined a reduction in HBV DNA release of up to 1.5 log in vitro. 2021 Scientific reports Abstract HBV P33S;P46S;T36D;T36G;A12S 49;54;59;59;44 53;58;65;65;48 33687074 Occult and active hepatitis B virus detection in donated blood in Sao Paulo, Brazil. Among them, T123N, G145A, and D144G high-impact immune escape mutations were identified. 2021 Transfusion Abstract HBV T123N;G145A;D144G 12;19;30 17;24;35 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. Other HBV precore region mutations that were detected include: G1899A, T1846A, G1862C, G1888A, T1821C, C1826T, A1827C, A1850T, C1858T, precore start codon Kozak sequence mutations and some novel core region mutations such as G/A1951T and G1957A. 2021 International journal of health sciences Abstract HBV A1951T;G1951T;G1899A;T1846A;G1862C;G1888A;T1821C;C1826T;A1827C;A1850T;C1858T;G1957A 225;225;63;71;79;87;95;103;111;119;127;238 233;233;69;77;85;93;101;109;117;125;133;244 C;Precore;Precore 195;10;135 199;17;142 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. It is controversial whether the rtA194T mutation truly confers resistance against TDF. 2021 Infection and drug resistance Abstract HBV A194T 34 39 RT 32 34 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. These observations suggest that rtA194T mutation emerges under LAM monotherapy and remains sensitive to TDF. 2021 Infection and drug resistance Abstract HBV A194T 34 39 RT 32 34 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. We present here a 62-year-old CHB patient who occurred rtL180M, rtM204V and rtA194T mutants after lamivudine (LAM) monotherapy for 9 years. 2021 Infection and drug resistance Abstract HBV L180M;M204V;A194T 57;66;78 62;71;83 RT;RT;RT 55;64;76 57;66;78 Chronic Hepatitis B 30 33 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. We also found that there are a total of 19 signature single nucleotide polymorphisms (SNPs), of which 2 and 17 nonsynonymous mutation types were specific to rt269L and rt269I, respectively: Of these, most are HBeAg negative infections (preC-W28*, X-V5M and V131I), lowered HBV DNA or virion production (C-I97F/L, rtM204I/V) or preexisting nucleot(s)ide analog resistance (NAr) (rtN139K/H, rtM204I/V and rtI224V) or disease severity (preC-W28*, C-I97F/L, C-Q182K/*, preS2-F141L, S-L213I/S, V/L5M, T36P/S/A, V131I, rtN139K/H, rtM204I/V and rtI224V). 2021 Microorganisms Abstract HBV M204I;M204V;N139K;N139H;M204I;M204V;I224V;N139K;N139H;M204I;M204V;I224V;V131I;I97F;I97L;I97F;I97L;Q182K;F141L;L213I;L213S;T36P;T36S;T36A;V131I;W28X;V5M;W28X;Q182X;L5M;V5M 315;315;380;380;391;391;405;515;515;526;526;540;257;305;305;446;446;456;471;478;478;496;496;496;506;241;247;438;456;489;489 322;322;387;387;398;398;410;522;522;533;533;545;262;311;311;452;452;461;476;487;487;504;504;504;511;245;252;442;463;494;494 C;C;C;C;Precore;Precore;PreS2;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;X 303;444;454;209;236;433;465;157;168;313;378;389;403;513;524;538;478;247 304;445;455;214;240;437;470;159;170;315;380;391;405;515;526;540;479;248 33836203 Natural variability in surface antigen and reverse transcriptase domain of hepatitis B virus in treatment-naive chronic HBV-infected Egyptian patients. Additionally, 11 occult samples (19 %) were detected, in which the predominant mutations of HBsAg were S143L (7 samples) followed by D144A and T125M (4 samples each). 2021 Virus research Abstract HBV S143L;D144A;T125M 103;133;143 108;138;148 S 92 97 33836203 Natural variability in surface antigen and reverse transcriptase domain of hepatitis B virus in treatment-naive chronic HBV-infected Egyptian patients. Additionally, we detected viral quasispecies and revealed Y124H as a characteristic substitution in the RT domain for HBV isolates in Egypt. 2021 Virus research Abstract HBV Y124H 58 63 RT 104 106 33836203 Natural variability in surface antigen and reverse transcriptase domain of hepatitis B virus in treatment-naive chronic HBV-infected Egyptian patients. Eleven substitutions were found in the major hydrophilic region, including two novel ones (M103T and G130E) that were not correlated before with genotype D. 2021 Virus research Abstract HBV M103T;G130E 91;101 96;106 33836203 Natural variability in surface antigen and reverse transcriptase domain of hepatitis B virus in treatment-naive chronic HBV-infected Egyptian patients. The most predominant mutation was Y124H (47 samples, 82 %). 2021 Virus research Abstract HBV Y124H 34 39 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. Almost 29% (24/82) of the cases remarkably had the presence of G1896A mutation confirmed by LCR and direct sequencing. 2021 Journal of infection and public health Abstract HBV G1896A 63 69 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. G1896A switch is one of the hotspots in subjects affected with hepatitis B. 2021 Journal of infection and public health Abstract HBV G1896A 0 6 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. Polymerase chain reaction (PCR) and Nucleotide Sequencing was done to identify the G1896A mutation in the precore region of the genome. 2021 Journal of infection and public health Abstract HBV G1896A 83 89 Precore 106 113 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. The major purpose of the study was to screen G1986A mutations at a large scale and also to establish ligase chain reaction as a mutation testing tool. 2021 Journal of infection and public health Abstract HBV G1986A 45 51 33857724 LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B. The precore G1896A mutation is responsible for one third of the patients suffering from precore stop codon mutation. 2021 Journal of infection and public health Abstract HBV G1896A 12 18 Precore;Precore 4;88 11;95 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. RAM M204I/V had the highest prevalence, occurring in 3.8% (109/2838) of all HBV sequences in our data set, and a significantly higher rate in genotype C at 5.4% (60/1102, p = 0.0007). 2021 Journal of viral hepatitis Abstract HBV M204I;M204V 4;4 11;11 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. Only the substitution M204I was detected in the HBV polymerase region. 2021 Molecular and clinical oncology Abstract HBV M204I 22 27 P 52 62 33933516 Identification of hepatitis B virus core protein residues critical for capsid assembly, pgRNA encapsidation and resistance to capsid assembly modulators. In addition, we also found that WT Cp, but not the assembly incompetent Cp, such as Y132A Cp, interacted with HBV DNA polymerase (Pol). 2021 Antiviral research Abstract HBV Y132A 84 89 C;C;C;P;P 35;72;90;130;118 37;74;92;133;128 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The peptide "GSLLGRMKGA" binds weakly to hepatitis B core protein capsids and mutant capsids with a premature (F97L) or low-secretion phenotype (L60V and P5T). 2021 Microorganisms Abstract HBV F97L;L60V;P5T 111;145;154 115;149;157 Capsid;Capsid;C 66;85;53 73;92;57 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. With electron cryo microscopy, we provide novel structures for L60V and P5T and demonstrate that binding occurs at the tips of the spikes at the dimer interface, splaying the helices apart independent of the secretion phenotype. 2021 Microorganisms Abstract HBV L60V;P5T 63;72 67;75 33959934 Spontaneous reactivation of hepatitis B virus with a frameshift mutation in the precore region in an elderly hepatitis B virus carrier with lifestyle-related diseases. Her HBV genome was typed as subgenotype B1 and possessed a frameshift mutation due to an insertion of T after nucleotide (nt) 1817 and G to A mutations at nt 1896 and nt 1899 (G1896A/G1899A) in the precore region as well as serine to glutamine substitution of amino acid 21 in the core protein. 2021 Clinical journal of gastroenterology Abstract HBV G1899A;G1896A;G1896A 183;135;176 189;162;182 C;Precore 281;198 285;205 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Among them, 75.0% of patients with rtM204I positive had HBV DNA load >=103 IU/mL at delivery, which was comparable with the subjects without rtM204I (75.0% vs. 2021 The Canadian journal of infectious diseases & medical microbiology Abstract HBV M204I;M204I 37;143 42;148 RT;RT 35;141 37;143 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. No changes were found in the frequencies and the complexity of HBV quasispecies of rtM204I mutation after the TVB treatment. 2021 The Canadian journal of infectious diseases & medical microbiology Abstract HBV M204I 85 90 RT 83 85 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. RESULTS: Before TBV treatment, the complexity of HBV quasispecies of all subjects was 0.40 +- 0.09; 41.1% (30/73) and 53.4% (39/73) subjects had rtM204I/V and rtN236 T/A detected, respectively; and 9.6% (7/73) patients had more than 20% frequency mutation of rtM204I/V, which was also similar with high frequency of rtN236 T/A mutation (41.1% vs. 2021 The Canadian journal of infectious diseases & medical microbiology Abstract HBV M204I;M204V;N236T;N236A;M204I;M204V;N236T;N236A 147;147;161;161;261;261;318;318 154;154;169;169;268;268;326;326 RT;RT;RT;RT 145;159;259;316 147;161;261;318 34002910 Hepatitis B virus genome diversity in adolescents: Tenofovir disoproxil fumarate treatment effect and HBeAg serocon version. The basal core promoter (BCP) variants, A1762T and G1764A, and the pC variant, G1896A, were most often enriched at or after seroconversion. 2021 Journal of viral hepatitis Abstract HBV A1762T;G1764A;G1896A 40;51;79 46;57;85 BCP;BCP;Precore 4;25;67 23;28;69 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. A plasmid containing the M204V mutation was synthesized and standard curves plotted. 2021 Journal of clinical and translational hepatology Abstract HBV M204V 25 30 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. CONCLUSIONS: These results show that our method can be used to detect HBV M204V mutations with the advantages of sensitivity, specificity and efficiency, providing a new choice for monitoring drug resistance. 2021 Journal of clinical and translational hepatology Abstract HBV M204V 74 79 34029727 Increased hepatitis B virus quasispecies diversity is correlated with liver fibrosis progression. Specific mutations, such as A1762T, G1764A and G1896A, in the BCP/PC region were more common in patients with advanced liver disease and formed the majority of the viral quasispecies pool in patients with LC and HCC. 2021 Infection, genetics and evolution Abstract HBV A1762T;G1764A;G1896A 28;36;47 34;42;53 BCP;Precore 62;66 65;68 Liver disease;Hepatocellular carcinoma;Liver cirrhosis 119;212;205 132;215;207 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. Collectively, our results provide novel insights into the mechanism of ETV resistance of HBV RT caused by L180M and M204V mutations. 2021 Journal of virology Abstract HBV M204V;L180M 116;106 121;111 RT 93 95 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. Crystallography of HIV RTY115F/F116Y/Q151M/F160M/M184V, mimicking HBV RT L180M/M204V, showed that the F115 bulge (F88 in HBV RT) caused by the F160M mutation induced deviated binding of dCTP from its normal tight binding position. 2021 Journal of virology Abstract HBV M204V;M184V;L180M 79;49;73 84;54;78 RT;RT;RT 23;70;125 25;72;127 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. ETV-triphosphate (ETV-TP) exhibited competitive inhibition with dGTP in both wild-type (wt) RT and M204V RT, as observed using Lineweaver-Burk plots. 2021 Journal of virology Abstract HBV M204V 99 104 RT;RT 92;105 94;107 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. In contrast, RT L180M or L180M/M204V did not fit either competitive, uncompetitive, noncompetitive, or typical mixed inhibition, although ETV-TP was a competitive inhibitor of dGTP. 2021 Journal of virology Abstract HBV M204V;L180M;L180M 31;16;25 36;21;30 RT 13 15 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. Therefore, in HBV RT L180M/M204V, ETV-TP may be stuck at M171, a residue that is conserved in almost all HBV isolates, leading to the strange inhibition pattern observed in the kinetic analysis. 2021 Journal of virology Abstract HBV M204V;L180M 27;21 32;26 RT 18 20 34076480 Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations. To understand the mechanism underlying the development of ETV resistance by HBV RT, we analyzed the L180M, M204V, and L180M/M204V mutants using a combination of biochemical and structural techniques. 2021 Journal of virology Abstract HBV M204V;M204V;L180M;L180M 124;107;100;118 129;112;105;123 RT 80 82 34111075 Molecular characterization of hepatitis B virus basal core promoter and precore region of isolates from chronic hepatitis B patients. A rare G1764T mutation was also detected in 6(12%) isolates. 2021 JPMA. The Journal of the Pakistan Medical Association Abstract HBV G1764T 7 13 34111075 Molecular characterization of hepatitis B virus basal core promoter and precore region of isolates from chronic hepatitis B patients. Classic A1762T/G1764A double mutation was noted in 15(30%) isolates. 2021 JPMA. The Journal of the Pakistan Medical Association Abstract HBV G1764A;A1762T 15;8 21;14 34111075 Molecular characterization of hepatitis B virus basal core promoter and precore region of isolates from chronic hepatitis B patients. Precore stop codon mutation G1896A was detected in 19 (38%) isolates; 17(34%) among negative patients and 2(4%) in positive patients. 2021 JPMA. The Journal of the Pakistan Medical Association Abstract HBV G1896A 28 34 Precore 0 7 34111075 Molecular characterization of hepatitis B virus basal core promoter and precore region of isolates from chronic hepatitis B patients. The CG1802-1803 mutation was detected in 47(94%) isolates, while all the 50(100%) isolates had T1858A. 2021 JPMA. The Journal of the Pakistan Medical Association Abstract HBV T1858A 95 101 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. IEM Q129H was detected in eight out of the 44 (18.2%) HBV isolates sequenced in this study; however, no DRMs were observed. 2021 Viruses Abstract HBV Q129H 4 9 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. This study confirms the circulation of HBV IEMs and reports the presence of Q129H IEM for the first time in Nigeria. 2021 Viruses Abstract HBV Q129H 76 81 34214504 Evolution and phenotypic characterization of whole HBV genome in compliant patients experiencing unexplained entecavir treatment failure. Core promoter mutations T1753G, A1762T and G1764A were present as major mutations before and after treatment in patient #1. 2021 Antiviral research Abstract HBV T1753G;A1762T;G1764A 24;32;43 30;38;49 Core promoter 0 13 34214504 Evolution and phenotypic characterization of whole HBV genome in compliant patients experiencing unexplained entecavir treatment failure. HBs Ag immune escape mutations were present as major mutations before and after treatment in patients #2 (sK122R, sT126I, sP127S and sG145R) and #3 (sM133I). 2021 Antiviral research Abstract HBV K122R;T126I;P127S;G145R;M133I 106;114;122;133;149 112;120;128;139;155 S;S;S;S;S;S 0;106;114;122;133;149 6;107;115;123;134;150 34214504 Evolution and phenotypic characterization of whole HBV genome in compliant patients experiencing unexplained entecavir treatment failure. Mutations Q206K (pre-core/core), Q120K (pre-S1/pre-S2, T-cell epitope) and A300E (spacer domain) were selected during entecavir treatment in patient #1 but were not associated with an increased level of resistance to entecavir or an increase in HBV replication capacity. 2021 Antiviral research Abstract HBV Q206K;Q120K;A300E 10;33;75 15;38;80 C;Precore;PreS1;PreS2 26;17;40;47 30;25;46;53 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. The observed mutations were T115S (3/20, 15%), P120T/S (3/20, 15%), T126S (1/20, 5%), Q129R (2/20, 10%), M133T (2/20, 10%), S143L (5/20, 25%), D144E/A (3/20, 15%), and G145R/A (4/20, 20%). 2021 Infection and drug resistance Abstract HBV T115S;P120T;P120S;T126S;Q129R;M133T;S143L;D144E;D144A;G145R;G145A 28;47;47;68;86;105;124;143;143;168;168 33;54;54;73;91;110;129;150;150;175;175 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. Six patients (13.3%) had rtV173L, rtL180M, and rtM204V mutations; five subjects (11.1%) with rtL180M and rtM204V while 1 patient (2.2%) had rtM204V mutations. 2021 International journal of health sciences Abstract HBV V173L;L180M;M204V;L180M;M204V;M204V 27;36;49;95;107;142 32;41;54;100;112;147 RT;RT;RT;RT;RT;RT 25;34;47;93;105;140 27;36;49;95;107;142 34319801 Fast and Sensitive Real-Time PCR Detection of Major Antiviral-Drug Resistance Mutations in Chronic Hepatitis B Patients by Use of a Predesigned Panel of Locked-Nucleic-Acid TaqMan Probes. Multiple-point mt, including rtL180M-rtM204V- rtN238A and rtL180M-rtM204I, were identified in only two children, resulting in LMV-ADF resistance and reduced ETV susceptibility. 2021 Journal of clinical microbiology Abstract HBV L180M;M204V;N238A;M204I;L180M 31;39;48;68;60 36;44;53;73;65 RT;RT;RT;RT;RT 29;37;46;58;66 31;39;48;60;68 34319801 Fast and Sensitive Real-Time PCR Detection of Major Antiviral-Drug Resistance Mutations in Chronic Hepatitis B Patients by Use of a Predesigned Panel of Locked-Nucleic-Acid TaqMan Probes. Single-point mt for LMV and ADF resistance were detected in 57.7% and 54.1% of the child and adult samples, respectively, with rtV207M (children, 42.3%; adults, 36.7%) and rtN238T/A (children, 15.4%; adults, 16.3%) being the most frequent mt in these populations. 2021 Journal of clinical microbiology Abstract HBV N238T;N238A;V207M 174;174;129 181;181;134 RT;RT 127;172 129;174 34319801 Fast and Sensitive Real-Time PCR Detection of Major Antiviral-Drug Resistance Mutations in Chronic Hepatitis B Patients by Use of a Predesigned Panel of Locked-Nucleic-Acid TaqMan Probes. We developed a novel real-time PCR assay that simultaneously evaluates 11 major nucleos(t)ide antiviral (NA) drug resistance mutations (mt) in chronic hepatitis B patients (CHB), including L180M, M204I/V, and V207M (lamivudine [LMV] resistance), N/H238A/T (adefovir [ADF] resistance), which are circulating in Vietnam; and T184G/L, S202I, and M250V (entecavir [ETV] resistance) and A194T (tenofovir resistance), which have been recently reported in several studies across the globe. 2021 Journal of clinical microbiology Abstract HBV N238A;N238T;H238A;H238T;L180M;V207M;M204I;M204V;T184G;T184L;S202I;M250V;A194T 246;246;246;246;189;209;196;196;323;323;332;343;382 255;255;255;255;194;214;203;203;330;330;337;348;387 Chronic Hepatitis B;Chronic Hepatitis B 143;173 162;176 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. CONCLUSIONS: The I97L substitution reduces the level of cccDNA through the generation of immature virions with single-stranded genomes. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 17 21 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBV-I97L exhibited lower infectivity than HBV-I97wt in both infection systems with reporter HBV and cell culture-generated HBV. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 4 8 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBV-I97L virions exhibiting low infectivity primarily contained a single-stranded HBV genome. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 4 8 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In this study, we attempted to identify the point at which I97L affects the hepatitis B virus (HBV) life cycle and to elucidate the underlying mechanisms governing the stabilization of hepatitis. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 59 63 Hepatitis 185 194 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. METHODS: To confirm the clinical features of I97L, we used a cohort of hepatitis B e antigen-negative patients with chronic hepatitis B infected with HBV-I97 wild-type (wt) or HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L;I97L 45;180 49;184 C 83 92 Chronic Hepatitis B 116 135 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Previously, we identified the substitution of isoleucine to leucine at amino acid 97 (I97L) in the hepatitis B core region as a key predictor among patients with stable hepatitis. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L;I97L 86;46 90;84 C 111 115 Hepatitis 169 178 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. RESULTS: The ratios of reduction in hepatitis B surface antigen and HBV DNA were higher in patients with HBV-I97L than in those with HBV-I97wt. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 109 113 S 48 55 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The effects of I97L on viral characteristics were evaluated by in vitro HBV production and infection systems with the HBV reporter virus and cell culture-generated HBV. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 15 19 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The lower efficiency of cccDNA synthesis was demonstrated after infection of HBV-I97L or transfection of the molecular clone of HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L;I97L 81;132 85;136 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. This I97L-associated low efficiency of cccDNA synthesis may be involved in the stabilization of hepatitis. 2021 Cellular and molecular gastroenterology and hepatology Abstract HBV I97L 5 9 Hepatitis 96 105 34406663 Multiple epitopes of hepatitis B virus surface antigen targeted by human plasma-derived immunoglobulins coincide with clinically observed escape mutations. We then tested in binding assays HBsAg peptides containing clinically relevant mutations previously reported within these sites, such as Y134S, P142S, and G145R, and observed a significant reduction in anti-HBs binding activity to the mutated sites, suggesting a mechanism the virus may use to avoid HBIG-mediated neutralization. 2022 Journal of medical virology Abstract HBV Y134S;P142S;G145R 137;144;155 142;149;160 S;S 207;33 210;38 34432346 A DNA Nanoflower-Assisted Separation-Free Nucleic Acid Detection Platform with a Commercial Pregnancy Test Strip. It is able to correctly identify the unmutated and rtL180M genome types of HBV in clinical samples. 2021 Angewandte Chemie (International ed. in English) Abstract HBV L180M 53 58 RT 51 53 34432346 A DNA Nanoflower-Assisted Separation-Free Nucleic Acid Detection Platform with a Commercial Pregnancy Test Strip. This simple, separation-free platform is highly specific, as demonstrated with the detection of rtL180M, a single-nucleotide polymorphism observed in hepatitis B virus (HBV) associated with antiviral drug resistance. 2021 Angewandte Chemie (International ed. in English) Abstract HBV L180M 98 103 RT 96 98 34697871 Regulatory function of interferon-inducible 44-like for hepatitis B virus covalently closed circular DNA in primary human hepatocytes. METHODS: Primary human hepatocytes were infected with HBV using genomic plasmids carrying the basic core promoter mutation A1762T/G1764A and/or the precore mutation G1896A and treated with IFN-gamma and IFN-alpha. 2022 Hepatology research Abstract HBV G1764A;A1762T;G1896A 130;123;165 136;129;171 BCP;Precore 94;148 113;155 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. Resistance mutations (rtM204V/I/S) associated or not with compensatory mutations (rtL180M, rtV173L) were identified in 13.9% (5/36) of patients undergoing viral treatment and 1.1% (1/90) of naive patients. 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Abstract HBV M204V;M204I;M204S;L180M;V173L 24;24;24;84;93 33;33;33;89;98 RT;RT;RT 22;82;91 24;84;93 34826506 Preclinical characterization of AB-506, an inhibitor of HBV replication targeting the viral core protein. Evaluation of AB-506 against a panel of core variants showed that T33N/Q substitutions results in >200-fold increase in EC50 values, while L30F, L37Q, and I105T substitutions showed an 8 to 20-fold increase in EC50 values in comparison to the wild-type. 2022 Antiviral research Abstract HBV T33N;T33Q;L30F;L37Q;I105T 66;66;139;145;155 72;72;143;149;160 C 40 44 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Similar changes occur in mutants with low secretion phenotypes (P5T and L60V) and in a mutant with a pre-mature secretion phenotype (F97L). 2021 Viruses Abstract HBV P5T;L60V;F97L 64;72;133 67;76;137 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In this study, we constructed an HBV-producing vector that expresses W3S HBs (pHB-W3S) along with a wild-type HBV-producing plasmid (pHB-WT) in order to analyze the physicochemical properties, replication, and antiviral drug response of the mutant. 2021 Viruses Abstract HBV W3S;W3S 69;82 72;85 S 73 76 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Transfection of either pHB-WT or W3S into HepG2 cells yielded similar CsCl density profiles and eAg expression, as did transfection of a glycosylation defective mutant, pHB-W3S (N146G), in which a glycosylation site at the 146aa asparagine (N) site of HBs was mutated to glycine (G). 2021 Viruses Abstract HBV W3S;W3S;N146G 33;173;178 36;176;183 S 252 255 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Virion secretion, however, seemed to be severely impaired in cases of pHB-W3S and pHB-W3S (N146G), compared with pHB-WT, as determined by qPCR and Southern blot analysis. 2021 Viruses Abstract HBV W3S;W3S;N146G 74;86;91 77;89;96 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. We previously identified a diagnostic escape mutant (W3S) HBV that produces massively glycosylated HBsAg. 2021 Viruses Abstract HBV W3S 53 56 S 99 104 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. By complementation assay, we demonstrated that the wild type small envelope protein alone is sufficient to rescue the virion secretion defect of a small loop mutant M198P. 2021 Journal of biomedical science Abstract HBV M198P 165 170 S 61 75 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. E2 mutations (E2G/A/V/D) existed in 21.8% (26/119) of OBIs, while no E2 mutations were found in the control group. 2021 Frontiers in microbiology Abstract HBV E2G;E2A;E2V;E2D 14;14;14;14 23;23;23;23 Occult Hepatitis B 54 58 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. E2G/A/V/D mutations could strongly affect extracellular and intracellular level of HBsAg (p < 0.05). 2021 Frontiers in microbiology Abstract HBV E2G;E2A;E2V;E2D 0;0;0;0 9;9;9;9 S 83 88 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Furthermore, N-terminal signal peptides, with a typical cleavage site for peptidase at positions 27 and 28, were exclusively detected in S proteins with secretion-defective mutants (E2G/A). 2021 Frontiers in microbiology Abstract HBV E2G;E2A 182;182 187;187 S 137 138 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Meanwhile, for E2G/A mutations, the relative intracellular HBsAg (110.7-338.3% vs. extracellular) and its fluorescence intensity (1.5-2.4-fold vs. with genotype-matched pHBV1.3B/C) were significantly higher (p聽< 0.05). 2021 Frontiers in microbiology Abstract HBV E2G;E2A 15;15 20;20 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Notably, unlike E2G in genotype B that could cause HBsAg intracellular accumulation and secretion decrease (p < 0.05), E2G in genotype C could lead to a very significant HBsAg decrease both extracellularly (0.46% vs. 2021 Frontiers in microbiology Abstract HBV E2G;E2G 16;119 19;122 S;S 51;170 56;175 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Our findings suggest that: (1) E2G/A/V/D mutations were confirmed to significantly influence the detection of HBsAg, (2) the underlying mechanism of OBI caused by E2G mutation is quite different between genotype B and genotype C, and (3) E2G/A could produce a N-terminal truncated S protein, which might attribute to the HBsAg secretion impairment in the OBIs. 2021 Frontiers in microbiology Abstract HBV E2G;E2A;E2V;E2D;E2G;E2G;E2A 31;31;31;31;163;238;238 40;40;40;40;166;243;243 S;S;S 110;321;281 115;326;282 Occult Hepatitis B;Occult Hepatitis B 149;355 152;359 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Our previous research found that novel OBI-related mutation within S protein, E2G, could cause the hepatitis B surface antigen (HBsAg) secretion impairment, which resulted in intracellular accumulation in OBI of genotype B. 2021 Frontiers in microbiology Abstract HBV E2G 78 81 S;S;S 128;67;111 133;68;118 Occult Hepatitis B;Occult Hepatitis B 39;205 42;208 34899733 The Impact of HBV Quasispecies Features on Immune Status in HBsAg+/HBsAb+ Patients With HBV Genotype C Using Next-Generation Sequencing. Especially, mutations in antigenic epitopes, such as I126S in CHB and I126T in HCC, could impact the conformational structure and alter the antigenicity/immunogenicity of HBsAg. 2021 Frontiers in immunology Abstract HBV I126S;I126T 53;70 58;75 S 171 176 Hepatocellular carcinoma;Chronic Hepatitis B 79;62 82;65 34902556 Analysis of entire hepatitis B virus genomes reveals reversion of mutations to wild type in natural infection, a 15 year follow-up study. Some sequences from subject CC246 had predicted escape substitutions (T123N, G145R) in the surface protein in 2004, 2013 and 2019 but none of the sequences from 2007 had these changes. 2022 Infection, genetics and evolution Abstract HBV T123N;G145R 70;77 75;82 S 91 98 34920100 Novel X gene point mutations in chronic hepatitis B and HBV related cirrhotic patients. A higher rate of A1635T, C1678T, A1727T, A1762T, G1764A, and C1773T was observed in cirrhotic patients. 2022 Infection, genetics and evolution Abstract HBV A1635T;C1678T;A1727T;A1762T;G1764A;C1773T 17;25;33;41;49;61 23;31;39;47;55;67 Liver cirrhosis 84 93 34920100 Novel X gene point mutations in chronic hepatitis B and HBV related cirrhotic patients. RESULT: Novel mutations were detected, including C1491G, C1500T, G1613T, and G1658T in the N-terminal of the X gene. 2022 Infection, genetics and evolution Abstract HBV C1491G;C1500T;G1613T;G1658T 49;57;65;77 55;63;71;83 X 109 110 34920100 Novel X gene point mutations in chronic hepatitis B and HBV related cirrhotic patients. The frequency of C1481T/G1479A, T1498C, C1500T, G1512A, A1635T, C1678T, A1727T, and A1762T/ G1764A/ C1773T was significantly higher in cirrhotic patients compared to chronically HBV infected ones. 2022 Infection, genetics and evolution Abstract HBV G1479A;C1481T;T1498C;C1500T;G1512A;A1635T;C1678T;A1727T;A1762T;G1764A;C1773T 24;17;32;40;48;56;64;72;84;92;100 30;23;38;46;54;62;70;78;90;98;106 Chronic HBV infection;Liver cirrhosis 166;135 190;144 34920663 Signal-On Electrochemical Detection for Drug-Resistant Hepatitis B Virus Mutants through Three-Way Junction Transduction and Exonuclease III-Assisted Catalyzed Hairpin Assembly. The rtN236T mutation, an error encoded by codon 236 of the reverse transcriptase region of HBV DNA, was employed as the model gene target. 2022 Analytical chemistry Abstract HBV N236T 6 11 RT;RT 59;4 80;6 34951036 Combining the HBcrAg decline and HBV mutations predicts spontaneous HBeAg seroconversion in chronic hepatitis B patients during the immune clearance phase. Baseline A1574T, G1862A, G1896A, and C1913G mutations and HBcrAg levels with a sharp decrease at Week 28 were associated with spontaneous HBeAg seroconversion. 2022 Journal of medical virology Abstract HBV A1574T;G1862A;G1896A;C1913G 9;17;25;37 15;23;31;43 C 138 143 34951036 Combining the HBcrAg decline and HBV mutations predicts spontaneous HBeAg seroconversion in chronic hepatitis B patients during the immune clearance phase. The mutation frequencies of A1574T (51.11% vs. 18.18%, p = 0.001), G1862A (30.00% vs. 13.03%, p = 0.001), G1896A (27.22% vs. 5.45%, p = 0.001), and C1913G (32.78% vs. 12.73%, p = 0.001) in Group A were significantly higher than Group B. 2022 Journal of medical virology Abstract HBV G1862A;G1896A;C1913G;A1574T 67;106;148;28 73;112;154;34 34954390 Hepatitis B virus genetic multiplicity and the associated HBV lamivudine resistance mutations in HBV/HIV co-infection in Western Kenya: A review article. HBV polymerase rtV173L, rtL180M, and rtM204V major substitutional mutations were identified. 2022 Infection, genetics and evolution Abstract HBV V173L;L180M;M204V 17;26;39 22;31;44 P;RT;RT;RT 4;15;24;37 14;17;26;39 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Importantly, the high frequency of some notable mutations such as E109A/Y, A110S/K, Y111D/E, and F112L was first time reported in the entire study population. 2022 PloS one Abstract HBV E109A;E109Y;A110S;A110K;Y111D;Y111E;F112L 66;66;75;75;84;84;97 73;73;82;82;91;91;102 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. The highest frequency of mutations S101F (62.2%), A102V/R/G/I (56.25%), M103L/A (68.75%)were found in HCC, followed in LC and CH patients as 57.1%, 42.8%, 28.52% 16%, 15.2% and 18.4% respectively. 2022 PloS one Abstract HBV S101F;A102V;A102R;A102G;A102I;M103L;M103A 35;50;50;50;50;72;72 40;61;61;61;61;79;79 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 102;126;119 105;128;121 35084739 Establishment of monoclonal antibodies broadly neutralize infection of hepatitis B virus. In addition, the antibodies neutralized the infection of hepatitis D virus possessing a Gly145 mutation to Arg in S protein, which is a well-known escape mutation against HBIG treatment. 2022 Microbiology and immunology Abstract HBV G145R 88 110 S 114 115 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. An HIV-coinfected patient presented the rtM204V/I-rtL180M double resistance mutation in serum and DBS. 2022 Scientific reports Abstract HBV M204V;M204I;L180M 42;42;52 49;49;57 RT;RT 40;50 42;52 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. As a result, our study revealed that rtL180M (M) and rtM204V (V) mutations, already known as lamivudine-resistant mutations, confer resistance to BSV in the CHB patient. 2022 Biomedicines Abstract HBV L180M;M204V 39;55 44;60 RT;RT 37;53 39;55 Chronic Hepatitis B 157 160 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. The ten mutations include rtV23I (I), rtH55R (R), rtY124H (H), rtD134E (E), rtN139K (K), rtL180M (M), rtM204V (V), rtQ267L (L), rtL269I (I) and rtL336M (M). 2022 Biomedicines Abstract HBV V23I;H55R;Y124H;D134E;N139K;L180M;M204V;Q267L;L269I;L336M 28;40;52;65;78;91;104;117;130;146 32;44;57;70;83;96;109;122;135;151 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 26;38;50;63;76;89;102;115;128;144 28;40;52;65;78;91;104;117;130;146 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Here, we compared the effects of recombinant HBsAg antigens, wild-type and mutated at G145R, both included in the new vaccine, on activation of a human high-density culture of peripheral blood mononuclear cells (PBMC) in vitro. 2022 Vaccines Abstract HBV G145R 86 91 S 45 50 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, the G145R mutant alone did not affect CD86 expression, it induced less CD69, and stimulated IL-2 along with lowering levels of TNF-alpha, IL-10, and IFN-gamma. 2022 Vaccines Abstract HBV G145R 17 22 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Recently, the multivalent vaccine Bubo -Unigep has been developed to protect against both wild-type HBV and the most significant G145R mutant. 2022 Vaccines Abstract HBV G145R 129 134 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The dramatic differences in the immune responses elicited by wild-type HBsAg and the G145R mutant HBsAg suggest distinct adaptive capabilities of the G145R mutant HBV. 2022 Vaccines Abstract HBV G145R;G145R 85;150 90;155 S;S 71;98 76;103 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The G145R mutant also suppressed PHA-induced activation of CD69. 2022 Vaccines Abstract HBV G145R 4 9 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. Wild-type HBx (WT-HBx) and four HBx mutants (M1, A1762T/G1764A; M2, T1674G+T1753C+A1762T/G1764A; M3, C1653T+T1674G+A1762T/G1764A; and Ct-HBx, carboxylic acid-terminal truncated HBx) were delivered into Sleeping Beauty (SB) mouse models. 2022 Frontiers in oncology Abstract HBV G1764A;G1764A;G1764A;A1762T;A1762T;T1753C;T1674G;C1653T;T1674G;A1762T 56;89;122;82;49;75;68;101;108;115 62;95;128;88;55;81;74;107;114;121 X;X;X;X;X 10;18;32;137;177 13;21;35;140;180 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Of note, the conversion of Ala Val at amino acid 168 (A168V) and Thr Pro at amino acid 127 (T127P) were detected in HBsAg of the occult HBV strain. 2022 PloS one Abstract HBV A168V;T127P 54;92 59;97 S 116 121 35293188 [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. CONCLUSION: ELISA-based detection of escape mutations S143L, D144E and G145R can be used for routine diagnostics, especially in the risk groups. 2022 Voprosy virusologii Abstract HBV S143L;D144E;G145R 54;61;71 59;66;76 35293188 [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. The G145R mutation was recognized using ELISA kit in almost all cases. 2022 Voprosy virusologii Abstract HBV G145R 4 9 35293188 [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. The kit specifically recognized the S143L substitution in contrast to the S143T variant. 2022 Voprosy virusologii Abstract HBV S143L;S143T 36;74 41;79 35293188 [Identification by enzyme immunoassay of escape mutants S143L and G145R of hepatitis B virus (Hepadnaviridae: Orthohepadnavirus: Hepatitis B virus)]. The presence of neighbor mutation D144E can be assumed due to it special serological fingerprint. 2022 Voprosy virusologii Abstract HBV D144E 34 39 35314401 In vitro investigation of HBV clinical isolates from Chinese patients reveals that genotype C isolates possess higher infectivity than genotype B isolates. Moreover, we identified a naturally occurring mutation sL21S in small hepatitis B surface protein, which markedly decreased the infectivity of HBV genotype C isolates, but not that of genotype B isolates. 2022 Virologica Sinica Abstract HBV L21S 55 60 S;S 55;82 56;89 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. Genetic sequencing of HBV showed the mutants of S143T, D144G, and G145R in the S gene region, and the mutant of site 1896 in the pre-Core region coexisted with the wild type (G1896A/G). 2022 Frontiers in microbiology Abstract HBV S143T;D144G;G145R;G1896A;G1896G 48;55;66;175;175 53;60;71;183;183 Precore;S 129;79 137;80 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. In addition to the LAM mutations (rtS256G and rtM267L), missense mutations in B-cell, T-cell, HLA class I and II-restricted epitopes emerged, which were to evade and escape host surveillance, leading to delayed viral clearance, persistence and disease progression. 2022 BMC pediatrics Abstract HBV S256G;M267L 36;48 41;53 RT;RT 34;46 36;48 35380862 Comparative analysis of HBV basic core promoter/pre-core gene mutations and viral quasispecies diversity in HIV/HBV co-infected and HBV mono-infected patients. Among the patients infected with HBV genotype C and HBeAg-negative status, the frequency of A1762T/G1764A double mutations was significantly lower in HIV/HBV co-infected patients than in HBV mono-infected patients (53.3% vs. 2022 Acta virologica Abstract HBV G1764A;A1762T 99;92 105;98 C 52 57 HBV-HIV coinfections 150 169 35380862 Comparative analysis of HBV basic core promoter/pre-core gene mutations and viral quasispecies diversity in HIV/HBV co-infected and HBV mono-infected patients. However, A1762T/G1764A double mutations did not differ in the other groups (P >0.05). 2022 Acta virologica Abstract HBV G1764A;A1762T 16;9 22;15 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Most of S point-mutations were presented with low rates such as T47A/E/V/K (9.3%), P120S/T (8.5%), G145R (2%). 2022 PloS one Abstract HBV T47A;T47E;T47V;T47K;P120S;P120T;G145R 64;64;64;64;83;83;99 74;74;74;74;90;90;104 S 8 9 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. On multivariable analysis, males (OR = 4.51, 95%CI 1.78-11.4, p = 0.001), age>=40 (OR = 5.5, 95%CI 2.06-14.68, p = 0.001), W4P/R/Y on PreS1 (OR = 11.56, 95%CI 1.99-67.05, p = 0.006) and 4 S point-mutations as: T47A/E/V/K (OR = 3.67, 95%CI 1.19-11.29, p = 0.023), P120S/T (OR = 3.38, 95%CI 1.09-10.49, p = 0.035), S174N (OR = 29.73, 95%CI 2.12-417.07, p = 0.012), P203R (OR = 8.45, 95%CI 1.43-50.06, p = 0.019) were associated with HCC. 2022 PloS one Abstract HBV W4P;W4R;W4Y;T47A;T47E;T47V;T47K;P120S;P120T;S174N;P203R 123;123;123;210;210;210;210;263;263;313;363 130;130;130;220;220;220;220;270;270;318;368 PreS1;S 134;188 139;189 Hepatocellular carcinoma 431 434 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The most common point-mutations included N/H51Y/T/S/Q/P (30.4%), V68T/S/I (44.9%), T/N87S/T/P (46.2%) on PreS1 gene; T125S/N/P (30.8%), I150T (42.5%) on PreS2 gene; S53L (37.7%), A184V/G (39.3%), S210K/N/R/S (39.3%) on S gene. 2022 PloS one Abstract HBV T87S;T87T;T87P;N87S;N87T;N87P;N51Y;N51T;N51S;N51Q;N51P;H51Y;H51T;H51S;H51Q;H51P;V68T;V68S;V68I;T125S;T125N;T125P;I150T;S53L;A184V;A184G;S210K;S210N;S210R;S210S 83;83;83;83;83;83;41;41;41;41;41;41;41;41;41;41;65;65;65;117;117;117;136;165;179;179;196;196;196;196 93;93;93;93;93;93;55;55;55;55;55;55;55;55;55;55;73;73;73;126;126;126;141;169;186;186;207;207;207;207 PreS1;PreS2;S 105;153;219 110;158;220 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Conclusions: Our results indicated a high frequency of W28* mutation in HBV studied patients. 2022 Clinical and experimental hepatology Abstract HBV W28X 55 59 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Results: The stop codon of W28*(G1896A) was determined as the most prevalent mutation (55%) of the precore region. 2022 Clinical and experimental hepatology Abstract HBV W28X;G1896A 27;32 31;38 Precore 99 106 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. The most frequently encountered RAMs are M204V/I: 48.8%, L180M: 33.3%, L80V: 28.8%, and V173L: 42.2%. 2022 Medicina (Kaunas, Lithuania) Abstract HBV M204V;M204I;L180M;L80V;V173L 41;41;57;71;88 48;48;62;75;93 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. There are no significant differences in the distribution of RAMs in patients infected with different HBV genotypes, except for the L80V and N236T mutations, which were more frequently found in HBV genotype A infections (p = 0.032 and p = 0.004, respectively). 2022 Medicina (Kaunas, Lithuania) Abstract HBV L80V;N236T 131;140 135;145 35487093 Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. CONCLUSIONS: Our findings indicate that changes at the conserved residue 35 (H35N/Q) in the HBV RT may be associated with tenofovir resistance. 2022 Journal of clinical virology Abstract HBV H35Q;H35N 77;77 83;83 RT 96 98 35487093 Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. H35N was maintained during final tenofovir treatment. 2022 Journal of clinical virology Abstract HBV H35N 0 4 35487093 Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. Two of the SNPs were in the reverse transcriptase (RT; H35Q and D263E). 2022 Journal of clinical virology Abstract HBV H35Q;D263E 55;64 59;69 RT;RT 28;51 49;53 35487093 Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. Two RT mutations (H35N and P237T) emerged during subsequent 5-year entecavir treatment. 2022 Journal of clinical virology Abstract HBV H35N;P237T 18;27 22;32 RT 4 6 7474444 [Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. I. Identification of mutations in the precore region by PCR-direct sequencing and ASO probe method]. Five unknown mutations (I10N, C12W, C14S, V17F and A19D), three known mutations (I9V, W28X and G29D) and for novel nucleotide insertions were identified in anti-HBe positive sera. 1995 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV C12W;C14S;I10N;V17F;A19D;I9V;W28X;G29D 30;36;24;42;51;81;86;95 34;40;28;46;55;84;90;99 C 161 164 7474444 [Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. I. Identification of mutations in the precore region by PCR-direct sequencing and ASO probe method]. The W28X mutation was found in anti-HBe positive but not in any of HBeAg positive sera. 1995 Rinsho byori. The Japanese journal of clinical pathology Abstract HBV W28X 4 8 C;C 36;67 39;72 7489968 Hepatitis B virus infection: precore mutants and its relation to viral genotypes and core mutations. In genotype A, the M1 mutation coexisted with a second mutation (C-->T at position 1858 in codon 15), and both mutations were paired in the secondary structure of the RNA encapsidation signal, which justified the rare presence of precore mutants in this genotype. 1995 Hepatology (Baltimore, Md.) Abstract HBV C1858T 65 99 Precore 230 237 7539089 Fulminant reactivation of hepatitis B due to envelope protein mutant that escaped detection by monoclonal HBsAg ELISA. PCR sequencing revealed a substitution of arginine for glycine at position 145 of HBsAg in the major neutralising epitope cluster, the a determinant, as well as a 2-aminoacid insertion of asparagine and threonine between positions 122 and 123, immediately upstream of this determinant. 1995 Lancet (London, England) Abstract HBV G145R 42 78 S;S 135;82 148;87 7553156 [Expression of 12 antibody escape mutants of hepatitis B virus surface antigen gene in mammalian cell by using an Epstein-Barr based vector]. The results of detection of HBsAg excreted by resistant cell clones with monoclonal antibody to HBsAg showed that all antibody escape mutants of HBsAg except mutant 145R, a substitution of arginine for glycine at amino acid 145 position in HBsAg, were positive. 1995 Zhonghua yi xue za zhi Abstract HBV G145R 189 227 S;S;S;S 28;96;145;240 33;101;150;245 7557146 Hepatitis B virus core promoter sequence analysis in fulminant and chronic hepatitis B. BACKGROUND & AIMS: It was recently reported that two point mutations within the hepatitis B virus (HBV) core promoter region (A to T at position 1762 and G to A at position 1764) are associated with fulminant hepatitis and lead to hepatitis B e antigen (HBeAg)-negative phenotype. 1995 Gastroenterology Abstract HBV A1762T;G1764A 126;154 149;177 Core promoter;C;C 104;243;254 117;252;259 Fulminant Hepatitis B 199 218 7636505 Mutations of some critical amino acid residues in the hepatitis B virus surface antigen. Mutation of cysteine 149 to serine or of glycine 145 to arginine (imitating naturally occurring mutants), lysine, or glutamatic acid all led to loss of cross-reactivity with polyclonal antisera. 1995 Journal of medical virology Abstract HBV C149S;G145R 12;41 34;64 7645207 The mechanism of natural occurrence of two closely linked HBV precore predominant mutations. At nt 1899, a G to A mutation changes glycine at codon 29 to aspartic acid. 1995 Virology Abstract HBV G29D 38 74 7645207 The mechanism of natural occurrence of two closely linked HBV precore predominant mutations. The preferential occurrence of the G to A mutation at nt 1896 and 1899, instead of at other nonpredominant positions, is likely to be a combined consequence of both selection and higher intrinsic mutation frequency at these positions. 1995 Virology Abstract HBV G1896A 35 61 7699256 Detection of hepatitis B precore mutants by the fluorescent linear polymerase chain reaction sequencing method. Precore variants were detected in one HBeAg positive and in all 20 anti-HBe positive patients: in 19 cases, G to A at position 1896, with or without the substitution G to A at position 1899, in two cases C to T substitution at position 1817 which also produces a stop codon (CAA to TAA), one accompanied by the mutation G to A at position 1896. 1994 Journal of hepatology Abstract HBV G1896A;G1899A;C1817T;G1896A 108;166;204;320 131;189;240;343 C;C;Precore 72;38;0 75;43;7 7699256 Detection of hepatitis B precore mutants by the fluorescent linear polymerase chain reaction sequencing method. The only mutation observed in the patient who was initially HBeAg positive patient was a G to A substitution at position 1899. 1994 Journal of hepatology Abstract HBV G1899A 89 125 C 60 65 7699256 Detection of hepatitis B precore mutants by the fluorescent linear polymerase chain reaction sequencing method. These results indicate that the main cause of non-expression of HBeAg in chronic hepatitis B in our country is the substitution of G to A at nucleotide 1896, alone or accompanied by other variants. 1994 Journal of hepatology Abstract HBV G1896A 131 156 C 64 69 Chronic Hepatitis B 73 92 7706802 Precore mutant of hepatitis B virus in childhood fulminant hepatitis B: an infrequent association. A precore mutation from G to A at nucleotide 1896 was found in 5 of 14 FHB patients and in 3 of 10 AHB patients. 1995 The Journal of infectious diseases Abstract HBV G1896A 24 49 Precore 2 9 Fulminant Hepatitis B;Acute Hepatitis B 71;99 74;102 7730438 Demonstration of the presence of protease-cutting site in the spacer of hepatitis B viral Pol protein. By using a novel method called the LacZ localization assay (LLA), it was demonstrated that a tripartite fusion protein containing the nucleus localization sequence (NLS) of SV40 large T Ag, the putative thrombin cutting sequence (Ile-Arg-Ile-Pro-Arg320-Thr) of HBV Pol protein and the full length beta-galactosidase of E. 1995 Journal of virological methods Abstract HBV R320T 246 256 P 265 268 7798663 Detection of hepatitis B virus precore TAG mutant by an amplification-created restriction site method. A new method for detecting the hepatitis B virus (HBV) precore 1896 G-->A mutation is described. 1995 The Journal of infectious diseases Abstract HBV G1896A 63 73 Precore 55 62 7798663 Detection of hepatitis B virus precore TAG mutant by an amplification-created restriction site method. This method of detecting HBV precore 1896 G-->A should be useful for evaluation and follow-up of patients and for prevalence studies. 1995 The Journal of infectious diseases Abstract HBV G1896A 37 47 Precore 29 36 7821093 Nucleotide sequence analysis of precore and proximal core regions in patients with chronic hepatitis B treated with interferon. Mutations that prevent HBeAg synthesis were found in three patients, all of whom had G-to-A substitution at nt 1896 and two of them were anti-HBe positive. 1995 Digestive diseases and sciences Abstract HBV G1896A 85 115 C;C 142;23 145;28 7825758 Hepatitis B virus strains with mutations in the core promoter in patients with fulminant hepatitis. RESULTS: A point mutation from G to A at nucleotide 1896 in the precore region was detected in 519 (98%) of 529 HBV DNA clones from 38 patients. 1995 Annals of internal medicine Abstract HBV G1896A 31 56 Precore 64 71 7825758 Hepatitis B virus strains with mutations in the core promoter in patients with fulminant hepatitis. Two point mutations in the core promoter, from A to T at nucleotide 1762 and from G to A at nucleotide 1764, were detected in all 130 clones from the remaining 5 patients, who did not have mutations in the precore region, and in 20 (63%) of 32 clones from a patient with chronic hepatitis B who had transmitted HBV to 1 of these other 5 patients. 1995 Annals of internal medicine Abstract HBV A1762T;G1764A 47;82 72;107 Core promoter;Precore 27;206 40;213 Chronic Hepatitis B 271 290 7851832 Mutations in the transcriptional regulatory region of the precore and core/pregenome of a hepatitis B virus with defective HBeAg production. The deduced amino acid substitutions were 28 Arg--Gln, 94 His--Tyr, 131 Val--Ile and 132 Phe--Tyr of HBx and 715 Met--Val and 789 Asp--Asn of pol. 1994 Fukuoka igaku zasshi Abstract HBV R28Q;H94Y;V131I;F132Y;M715V;D789N 42;55;68;85;109;126 53;66;80;97;121;138 X;P 101;142 104;145 7890897 Different prevalence of precore mutants in five members of a hepatitis-B-virus-infected family: evidence for a precore variant type in an asymptomatic anti-HBs patient. A method for rapid screening of a large number of cloned polymerase chain reaction products was developed for the presence of the most frequent pre-C mutations (G to A substitution at nucleotide position 1896 and 1899). 1994 Journal of hepatology Abstract HBV G1896A 161 208 Precore 144 149 7895545 Glycine-to-arginine substitution at codon 145 of HBsAg in two infants born to hepatitis B e antigen-positive carrier. Amino acid residues 122-160 of HBsAg were identical between the daughters and their mother except for a glycine-to-arginine substitution at codon 145. 1995 Digestive diseases and sciences Abstract HBV G145R 104 149 S 31 36 7930478 The role of pre-core hepatitis B virus mutants on the long-term outcome of chronic hepatitis B virus hepatitis. A longitudinal study. Anti-HBe seroconversion was accompanied by a dramatic reduction of hepatitis B virus replication and normalization of alanine aminotransferase in all, except one, and by the emergence of mutated strains with a pre-core stop codon (point mutation G to A at nt 1896) that replaced the wild type in seven of the 12. 1994 Journal of hepatology Abstract HBV G1896A 246 263 C;Precore 5;210 8;218 7966600 Hepatitis B virus with mutations in the core promoter for an e antigen-negative phenotype in carriers with antibody to e antigen. Two point mutations in the core promoter, from A to T at nt 1762 and from G to A at nt 1764, were most prevalent. 1994 Journal of virology Abstract HBV A1762T;G1764A 47;74 64;91 Core promoter 27 40 8082510 Nucleotide sequence analysis of the precore region in patients with spontaneous reactivation of chronic hepatitis B. Prior to reactivation, none of the group I patients harbored an HBV strain having a mutation that prevented HBeAg synthesis; however, 2/5 developed such a mutation during reactivation (G to A transition at nt 1896). 1994 Digestive diseases and sciences Abstract HBV G1896A 185 213 C 108 113 8083656 Mutation specific PCR and direct solid phase sequencing assay for the detection of hepatitis B virus pre-C/C mutants in anti-HBe-positive, chronic hepatitis B. Sequence analysis of the HBV DNA from patients with anti-HBe+, chronic hepatitis B revealed that the lack of HBeAg is mostly due to a single G-->A transition at nucleotide position 1896, resulting in a translational stop codon. 1994 Journal of medical virology Abstract HBV G1896A 141 185 C;C 57;109 60;114 Chronic Hepatitis B 63 82 8113769 A novel hepatitis B virus variant in the sera of immunized children. A unique nucleotide change from adenosine to guanosine at nucleotide 421 was found, resulting in an amino acid substitution at residue 141 from lysine to glutamic acid. 1994 The Journal of general virology Abstract HBV K141E 135 167 8171038 Mutations in the pre-core region of hepatitis B virus serve to enhance the stability of the secondary structure of the pre-genome encapsidation signal. Four major missense/nonsense mutations (M) were found: (M1) C-->T at nucleotide position 1856, Pro-->Ser at codon 15; (M2) G-->A at position 1896, Trp-->stop at codon 28; (M3) G-->A at position 1898, Gly-->Ser at codon 29; and (M4) G-->A at position 1899, Gly-->Asp at codon 29. 1994 Proc Natl Acad Sci U S A Abstract HBV C1856T;P15S;W28X;G29S;G1896A;G1898A;G1899A;G29A 60;95;147;199;123;176;232;256 93;116;169;220;145;198;254;277 8171038 Mutations in the pre-core region of hepatitis B virus serve to enhance the stability of the secondary structure of the pre-genome encapsidation signal. The commonest conserved mutation was M0: T-->C at position 1858, Pro-->Pro at codon 15. 1994 Proc Natl Acad Sci U S A Abstract HBV P15P;T1858C 65;41 86;63 8188166 Detection of precore hepatitis B virus mutants in asymptomatic HBsAg-positive family members. M0, a conserved mutation (T-to-C at nucleotide 1858, codon 15), was detected in 81% and 12% family members of index patients with and without M0, respectively (p < 0.0001). 1994 Hepatology (Baltimore, Md.) Abstract HBV T1858C 26 51 8188166 Detection of precore hepatitis B virus mutants in asymptomatic HBsAg-positive family members. We previously reported two novel mutations: M1 (C-to-T change at nucleotide 1856 [proser at codon 15]) and M3 (G-to-A change at nucleotide 1898 [gly-ser at codon 29]) in addition to two well-described mutations: M2 (G-to-A change at nucleotide 1896 [trp-stop at codon 28]); and M4 (G-to-A change at nucleotide 1899 [gly-asp at codon 29]) in Chinese patients. 1994 Hepatology (Baltimore, Md.) Abstract HBV C1856T;G1898A;G1896A;G1899A 48;111;216;282 80;143;248;314 8291231 Complete genomes, phylogenetic relatedness, and structural proteins of six strains of the hepatitis B virus, four of which represent two new genotypes. Most notable is the Ser81 to Ala81 substitution in an immunodominant region of HBcAg, and the four extra cysteine residues in HBsAg at residues 19, 183, 206, and 220, which might be engaged in additional disulphide bridges. 1994 Virology Abstract HBV S81A 20 34 C;S 79;126 84;131 8308523 Variant of hepatitis B virus isolated in Zimbabwe. Within the second loop of the "a" determinant, two mutations resulting in substitution of serine or threonine with the hydrophobic amino acids, methionine at position 143 and with alanine in place of glycine at position 145, are predicted from the consensus nucleotide sequence of the PCR-derived clones. 1994 Journal of medical virology Abstract HBV G145A 180 223 8359657 Fibrosing cholestatic hepatitis in a transplant recipient with hepatitis B virus precore mutant. Sequencing of the HBV precore region of the pretransplant serum sample confirmed the presence of the precore stop-codon mutant (G-->A mutation in codon 1896) only. 1993 Gastroenterology Abstract HBV G1896A 128 156 Precore;Precore 22;101 29;108 8405863 Nucleotide sequence analysis of the precore region in patients with fulminant hepatitis B in the United States. RESULTS: Four patients (10.8%) harbored nonsense mutants likely to produce an HBeAg negative HBV infection; two such mutants had a G to A substitution at position 1896, one lost the precore initiation codon, and one harbored a stop codon immediately downstream of the precore initiation codon. 1993 Gastroenterology Abstract HBV G1896A 131 167 C;Precore;Precore 78;182;268 83;189;275 HBV infections 93 106 8551270 Probable implication of mutations of the X open reading frame in the onset of fulminant hepatitis B. A C-to-T substitution was found at nucleotide (nt) 1655, an A-to-T substitution at nt 1764 and a G-to-A substitution at nt 1766 in 4, 5 and 5 patients, respectively, out of the seven with fulminant hepatitis. 1995 Journal of medical virology Abstract HBV C1655T;A1764T;G1766A 1;60;97 55;90;127 Fulminant Hepatitis B 188 207 8574843 A family cluster of an immune escape variant of hepatitis B virus infecting a mother and her two fully immunized children. A hepatitis B virus (HBV) immune escape variant which results from a substitution of glycine by arginine at position 145 (arginine-145) in the immunodominant neutralization epitope of the S protein was found to infect one child in a seroepidemiologic survey of 1,812 vaccinated children. 1995 Clinical and diagnostic laboratory immunology Abstract HBV G145R 85 120 S 188 189 8636711 Emergence of hepatitis B virus S gene mutant in a liver transplant recipient. A double mutation generating an amino acid change (glycine to lysine) at residue 145, able to impair recognition by monoclonal antibodies, was observed in the post-transplant serum from one patient. 1995 Journal of medical virology Abstract HBV G145K 50 84 8636719 Hepatitis B virus strains in Thailand: genomic variants in chronic carriers. Glycine 145 was changed to alanine in one strain, and this position showed an apparent mixture of glycine and arginine in another. 1995 Journal of medical virology Abstract HBV G145A 0 34 8724860 Mutations in the core promoter/enhancer II regions of naturally occurring hepatitis B virus variants and analysis of the effects on transcription activities. Predominant mutations were found to occur naturally in nucleotide positions 1762 (A to T) and 1764 (G to A) in chronic hepatitis patients and in asymptomatic carriers after seroconversion, but were not observed in HBeAg-positive healthy carriers. 1995 Intervirology Abstract HBV A1762T;G1764A 55;94 89;107 C 214 219 Chronic Hepatitis B 111 128 8731842 [Genetic variation in the cleavage site of the precore region of hepatitis B virus in Chinese patients with fulminant hepatitis]. Double amino acid substitutions were seen in the precore region in the isolates: one from glycine to aspartic acid at codon 29 previously reported; the other substitution of phenylalanine for valine at codon 17 in the cleavage site of hepatitis B virus. 1995 Zhonghua nei ke za zhi Abstract HBV G29D;V17F 90;174 126;210 Precore 49 56 8758427 [Identification of vertical transmission of hepatitis B virus from mother to children by direct sequencing a segment of surface gene of hepatitis B virus]. In one child of family three, with coexisted HBsAg and anti-HBs, sequencing result revealed a point mutation which predicted a change from glycine to arginine at residue 145 in the second loop of the determinant. 1996 Zhonghua yi xue za zhi Abstract HBV G145R 139 173 S;S 60;45 63;50 8781313 Hepatitis B virus carriers without precore mutations in hepatitis B e antigen-negative stage show more severe liver damage. The G-->A mutation at nucleotide 1896 may mediate viral escape by creating a TAG stop codon in the precore region, thus preventing HBeAg production. 1996 Hepatology (Baltimore, Md.) Abstract HBV G1896A 4 37 C;Precore 131;99 136;106 8834756 A new immune escape mutant of hepatitis B virus with an Asp to Ala substitution in aa144 of the envelope major protein. A new hepatitis B virus (HBV) mutant with an Asp to Ala substitution in aa144 of the envelope major protein was identified from the blood samples of two persistently infected patients. 1995 Research in virology Abstract HBV D144A 45 77 S 85 93 8835351 Complete nucleotide sequences of hepatitis B virus genomes associated with epidemic fulminant hepatitis. One was located in the pre-surface 1 gene; two were in the surface gene; three were in the pre-core gene, including codons 28 (tryptophan to stop codon) and 29 (glycine to aspartic acid); eight were in the core gene; and 11 were in the polymerase gene. 1996 Journal of medical virology Abstract HBV G29D 157 186 C;P;Precore;S;S 206;236;91;27;59 210;246;99;34;66 8847524 The precore/core promoter mutant (T1762A1764) of hepatitis B virus: clinical significance and an easy method for detection. Recently, a new hepatitis B virus (HBV) mutant with HBe antigen-negative phenotype has been characterized, in which one TATA box-like motif of the precore/core promoter had degenerated: most frequently by both A-->T and G-->A mutations at positions 1762 and 1764, respectively. 1995 The Journal of general virology Abstract HBV G1762A 220 253 Core promoter;C;Precore 155;52;147 168;55;154 8871875 Rare pre-core stop-codon mutant nt. 1897 predominates over wide-spread mutant nt. 1896 in an unusual course of chronic hepatitis B. Direct sequencing of polymerase chain reaction (PCR) products derived from consecutive sera showed a rare pre-core stop-codon mutation at nucleotide (nt.) 1897 G --> A with an accompanying mutation nt. 1857 C --> T as well as a stop-codon mutation nt. 1896 G --> A. 1996 Journal of viral hepatitis Abstract HBV C1857T;G1896A;G1897A 202;252;155 214;264;167 Precore 106 114 8915879 Pre-core mutants of hepatitis B virus in patients receiving immunosuppressive treatment after orthotopic liver transplantation. In one of eight patients in addition to wildtype HBV a mutant strain (nt. 1899 G-->A) was detected. 1996 Journal of medical virology Abstract HBV G1899A 74 84 8915879 Pre-core mutants of hepatitis B virus in patients receiving immunosuppressive treatment after orthotopic liver transplantation. In one of the latter two, a pre-core start-codon mutant (nt. 1816 G-->T), not detectable before OLT, emerged, in the other a nt. 1897 G-->A stop-codon mutant persisted. 1996 Journal of medical virology Abstract HBV G1816T;G1897A 61;129 71;139 Precore 28 36 8915879 Pre-core mutants of hepatitis B virus in patients receiving immunosuppressive treatment after orthotopic liver transplantation. Six of nine patients of group B were reinfected with the same mutant population; in one, an additional pre-core mutation emerged; two patients lost pre-core mutant HBV (nt. 1896 and 1899 G-->A). 1996 Journal of medical virology Abstract HBV G1899A 182 192 Precore;Precore 103;148 111;156 8938164 Mutations in the hepatitis B virus precore/core gene and core promoter in patients with severe recurrent disease following liver transplantation. Previously, we reported that infection with HBV strains containing a mutation in the precore region (G-to-A at nucleotide 1896) was associated with severe recurrent disease posttransplantation. 1996 Hepatology (Baltimore, Md.) Abstract HBV G1896A 101 126 Precore 85 92 8941643 Two core promotor mutations identified in a hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication. Analysis of viral replication showed that two adjacent mutations in the HBV core promotor (C to T at nucleotide 1768 and T to A at nucleotide 1770) led to high level replication. 1996 The Journal of clinical investigation Abstract HBV C1768T;T1770A 91;121 116;146 C 76 80 8952268 [Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. II. Identification of mutations in the core gene by PCR-direct sequencing and ASO probe method]. The analysis of nucleotide sequences (codon 27-100) of HBV DNA in anti-HBe positive sera showed that there were two hypervariable segments of codon 31-49 and codon 87-97, where amino acid substitutions of L31I, S49T, S87G/N, K96N and I87F/1 frequently occurred regardless of the presence or absence of the mutation in the pre-core region. 1996 Kansenshogaku zasshi Abstract HBV L31I;S49T;S87G;S87N;K96N;I87F 205;211;217;217;225;234 209;215;223;223;229;238 C;Precore 71;322 74;330 8955047 Reduced precore transcription and enhanced core-pregenome transcription of hepatitis B virus DNA after replacement of the precore-core promoter with sequences associated with e antigen-seronegative persistent infections. The mutant with coexisting A1762T and G1764A substitutions produced less than one-fifth of the wild-type level of HBeAg. 1996 Virology Abstract HBV A1762T;G1764A 27;38 33;44 C 114 119 8973525 Semiquantitative assessment of pre-core stop-codon mutant and wildtype hepatitis B virus during the course of chronic hepatitis B using a new PCR-based assay. 1896 G-->A mutant from wildtype HBV. 1996 Archives of virology Abstract HBV G1896A 0 10 8973525 Semiquantitative assessment of pre-core stop-codon mutant and wildtype hepatitis B virus during the course of chronic hepatitis B using a new PCR-based assay. 1896 G-->A mutant HBV and to determine the ratio of mutant and wildtype HBV in patients' sera. 1996 Archives of virology Abstract HBV G1896A 0 10 8973525 Semiquantitative assessment of pre-core stop-codon mutant and wildtype hepatitis B virus during the course of chronic hepatitis B using a new PCR-based assay. 1896 G-->A mutant HBV could be determined semiquantitatively. 1996 Archives of virology Abstract HBV G1896A 0 10 8985297 Nucleic acid sequence analysis of the precore region of hepatitis B virus from sera of southern African black adult carriers of the virus. The presence of C instead of T in position 1858 precludes the G-to-A mutation at 1896 because the coexistence of these two mutations would destabilize the stem-loop structure of the RNA encapsidation signal, a finding confirmed by our observation that the CCC polymorphism and the 1896 mutation were mutually exclusive. 1997 Hepatology (Baltimore, Md.) Abstract HBV G1896A 62 85 8991934 Mutations in the core promoter region of hepatitis B virus in patients with chronic hepatitis B. Especially, A to T mutations at nucleotide 1762 and G to A mutations at nucleotide 1764 were found in five anti-HBe-positive asymptomatic carriers, and 22 patients with chronic liver disease. 1996 Journal of medical virology Abstract HBV A1762T;G1764A 12;52 47;87 C 112 115 9011456 Pathogenesis of chronic liver disease in patients with chronic hepatitis B virus infection without serum HBeAg. Chronic hepatitis B in patients lacking hepatitis B e antigen has been attributed to a hepatitis B virus variant (G-to-A mutation at nucleotide 1896 in the precore region of the genome). 1996 Digestive diseases and sciences Abstract HBV G1896A 114 148 C;Precore 52;156 61;163 Chronic Hepatitis B 0 19 9041321 Infectivity and pathogenicity in chimpanzees of a surface gene mutant of hepatitis B virus that emerged in a vaccinated infant. Dilutions of serum that contained the first such described HBV mutant, with an Arg-for-Gly substitution at codon 145 of the S gene, were inoculated into 6 seronegative chimpanzees. 1997 The Journal of infectious diseases Abstract HBV G145R 79 116 S 124 125 9093945 Genotype F prevails in HBV infected patients of hispanic origin in Central America and may carry the precore stop mutant. Since the three published precore sequences of genotype F strains have a C1858, which is known to prevent the precore stop mutation from G to A at position 1896, the precore and part of the core genes were sequenced from 19 anti-HBe positive sera with HBV DNA, 17 with genotype F and 2 with genotype A. 1997 Journal of medical virology Abstract HBV G1896A 137 160 C;C;Precore;Precore;Precore 190;229;26;110;166 194;232;33;117;173 9122641 Increasing heterogeneity of the 'a' determinant of HBsAg found in the presumed late phase of chronic hepatitis B virus infection. Most prevalent was a point mutation from adenine to guanine at nucleotide 530 resulting in a change from threonine to alanine at amino acid position 126. 1996 Scandinavian journal of infectious diseases Abstract HBV T126A 105 152 9237708 Detection of hepatitis B surface gene mutation in carrier children with or without immunoprophylaxis at birth. A precore mutant (G to A) at nucleotide 1896 was detected in sera from 11 carriers without vaccination. 1997 The Journal of infectious diseases Abstract HBV G1896A 17 44 Precore 2 9 9267007 Effects of a frequent double-nucleotide basal core promoter mutation and its putative single-nucleotide precursor mutations on hepatitis B virus gene expression and replication. A double mutation in the BCP which converts nucleotide (nt) 1762 from A to T and nt 1764 from G to A is frequently observed in patients with chronic hepatitis B. 1997 The Journal of general virology Abstract HBV G1764A 84 100 BCP 25 28 Chronic Hepatitis B 141 160 9303514 Surface gene mutants of hepatitis B virus in infants who develop acute or chronic infections despite immunoprophylaxis. An S mutant (residue 126, Thr to Ala) initially found in an infant with fulminant hepatitis was replaced by another S mutant (residue 145, Gly to Arg) 4 days later. 1997 Hepatology (Baltimore, Md.) Abstract HBV T126A;G415R 13;126 36;149 S;S 3;116 4;117 Fulminant Hepatitis B 72 91 9335928 [Genomic heterogeneity of hepatitis B virus, genotype A circulating in the metropolitan area of Buenos Aires, Argentina]. pHB4 shows a mutation at the T 3182-Leu in the preS1 region that change Pro for Leu, this mutation is absent in 125 sequences selected (having a 65% or more of homology) from NCBI by Blast algortm. 1996 Acta gastroenterologica Latinoamericana Abstract HBV T3182L 29 39 PreS1 47 52 9425945 Hepatitis B virus with antigenically altered hepatitis B surface antigen is selected by high-dose hepatitis B immune globulin after liver transplantation. In addition to already-known variants sG145R/K/E, we could demonstrate that newly described variants sX144G and sG145A were antigenically altered and showed impaired recognition by polyclonal HBIG in vitro. 1998 Hepatology (Baltimore, Md.) Abstract HBV G145R;G145K;G145E;X144G;G145A 38;38;38;101;112 48;48;48;107;118 S;S;S 38;101;112 39;102;113 9439156 Precore codon 28 stop mutation in hepatitis B virus from patients with hepatocellular carcinoma. OBJECTIVES: Hepatitis B virus (HBV) with a stop mutation at precore codon 28 (TGG-->TAG, tryptophan-->stop) was investigated to clarify if such a mutant virus might play a role in hepatocarcinogenesis. 1997 The Korean journal of internal medicine Abstract HBV C28A 68 87 Precore 60 67 9462667 Hepatitis B virus mutants associated with 3TC and famciclovir administration are replication defective. Double mutants with the L515M substitution showed intermediate defect between the YI/VDD or F501L and the L515M single-mutant strains. 1998 Hepatology (Baltimore, Md.) Abstract HBV L515M;F501L;L515M 24;92;106 29;97;111 9462667 Hepatitis B virus mutants associated with 3TC and famciclovir administration are replication defective. In addition, other mutations in the reverse-transcriptase "B domain" involving either a phenylalanine (F)-to-leucine (L) at amino acid 501 (F501L) or an L-to-M substitution at amino acid 515 (L515M) have been observed during 3TC and Famciclovir therapy as well. 1998 Hepatology (Baltimore, Md.) Abstract HBV F501L;F501L;L515M;L515M 88;140;192;153 138;145;197;190 RT 36 57 9462667 Hepatitis B virus mutants associated with 3TC and famciclovir administration are replication defective. In both HCC and HEK 293 cells, the mutant viruses carrying the F501L substitution showed a decreased pregenomic RNA encapsidation level, suggesting that the defect in HBV DNA synthesis occurs at the RNA packaging level. 1998 Hepatology (Baltimore, Md.) Abstract HBV F501L 63 68 Hepatocellular carcinoma 8 11 9462667 Hepatitis B virus mutants associated with 3TC and famciclovir administration are replication defective. In contrast, when transfected into HEK 293 cells, the viruses bearing the YI/VDD or L515M mutation replicated as wild-type. 1998 Hepatology (Baltimore, Md.) Abstract HBV L515M 84 89 9462667 Hepatitis B virus mutants associated with 3TC and famciclovir administration are replication defective. In transiently transfected HCC cells, the viruses bearing the YI/VDD or F501L mutations had greatly impaired replication as compared to wild-type virus, whereas the virus carrying the L515M substitution showed the least defect. 1998 Hepatology (Baltimore, Md.) Abstract HBV F501L;L515M 72;184 77;189 Hepatocellular carcinoma 27 30 9472623 Wild-type levels of pregenomic RNA and replication but reduced pre-C RNA and e-antigen synthesis of hepatitis B virus with C(1653) --> T, A(1762) --> T and G(1764) --> A mutations in the core promoter. Hepatitis B virus (HBV) isolates with A-1762 to T and G-1764 to A mutations in the core promoter have been associated with active hepatitis, severe liver disease following liver transplantation, hepatocellular carcinoma and acute fulminant courses--in the latter case combined with a C-1653 to T mutation. 1998 The Journal of general virology Abstract HBV A1762T;G1764A;C1653T 38;54;284 49;65;295 Core promoter 83 96 Liver disease;Hepatocellular carcinoma;Hepatitis 148;195;130 161;219;139 9519838 Proline-138 is essential for the assembly of hepatitis B virus core protein. We report a mutation study of the region that we have suggested forms an arm-like structure, which reveals that a single mutation, Pro-138 --> Gly, prevents the full-length HBV core protein self-assembling into particles. 1998 The Journal of general virology Abstract HBV P138G 131 146 C 177 181 9551691 Transient emergence of hepatitis B variants in a patient with chronic hepatitis B resistant to lamivudine. RESULTS: Sequencing studies of HBV DNA at week 52 showed the emergence of a lamivudine-resistant variant associated with two point mutations in the hepatitis B virus polymerase gene: one mutation led to amino acid substitution of methionine to valine at residue 552, in the highly conserved tyrosine-methionineaspartate-aspartate motif, part of the active site of the polymerase; the second mutation consisted of a substitution of leucine to methionine at residue 528. 1998 Journal of hepatology Abstract HBV M552V;L528M 230;431 265;467 P;P 166;368 176;378 9593029 Identification of more than one mutation in the hepatitis B virus polymerase gene arising during prolonged lamivudine treatment. Analysis of the HBV DNA polymerase gene from 8 chronic hepatitis B patients with suspected resistance to lamivudine showed that in addition to a mutation in the YM552DD motif, a second mutation located in the B domain of this gene, a Leu528-to-Met528 change, was consistently and exclusively found in 4 patients showing the YV552DD motif. 1998 The Journal of infectious diseases Abstract HBV L528M 234 250 P 24 34 Chronic Hepatitis B 47 66 9620341 Identification and characterization of mutations in hepatitis B virus resistant to lamivudine. Lamivudine Clinical Investigation Group. HBV DNA from the sera of patients in Group I exhibits a substitution of valine for methionine at residue 552, accompanied by a substitution of methionine for leucine at residue 528. 1998 Hepatology (Baltimore, Md.) Abstract HBV M552V;L528M 72;143 108;180 9620341 Identification and characterization of mutations in hepatitis B virus resistant to lamivudine. Lamivudine Clinical Investigation Group. Patients in Group II had only an isoleucine-for-methionine substitution at position 552. 1998 Hepatology (Baltimore, Md.) Abstract HBV M552I 33 87 9624604 Mutation of nucleotide 1,762 in the core promoter region during hepatitis B e seroconversion and its relation to liver damage in hepatitis B e antigen carriers. The results show that the nucleotide (nt) 1,762 A-->T mutation often develops during HBe seroconversion, particularly in strains without precore mutations that prevent HBeAg production. 1998 Journal of medical virology Abstract HBV A1762T 42 53 C;C;Precore 85;168;137 88;173;144 9638436 Point mutations in the S and pre-S2 genes observed in two hepatitis B virus carriers positive for antibody to hepatitis B surface antigen. Seven out of nine S gene clones from case 1 and six out of nine S gene clones from case 2 had an amino acid replacement from Thr or Ile to Ser at codon 126 in the alpha-determinant of the S gene. 1998 Hepato-gastroenterology Abstract HBV I126S 132 155 S;S;S 18;64;188 19;65;189 9658127 Naturally occurring mutations define a novel function of the hepatitis B virus core promoter in core protein expression. In this study, we define the molecular mechanism whereby the two core promoter mutations (C to T at nucleotide [nt] 1768 and T to A at nt 1770) result in enhanced viral encapsidation and replication. 1998 Journal of virology Abstract HBV C1768T;T1770A 90;125 120;142 Core promoter 65 78 9687422 The M539V polymerase variant of human hepatitis B virus demonstrates resistance to 2'-deoxy-3'-thiacytidine and a reduced ability to synthesize viral DNA. To determine the biological relevance of the Met-to-Val substitution, we mutated a plasmid that contained a cDNA copy of the HBV pregenomic RNA such that when virus replication occurred during transient transfection of HepG2 cells, an M539V polymerase variant was produced. 1998 Antimicrobial agents and chemotherapy Abstract HBV M539V 234 240 P 241 251 9696024 Incidence and clinical consequences of surface and polymerase gene mutations in liver transplant recipients on hepatitis B immunoglobulin. The most frequently identified amino acid substitution was glycine to arginine at position 145 (present in 4 of 6 patients who failed HBIg after at least 6 months of treatment). 1998 Hepatology (Baltimore, Md.) Abstract HBV G145R 59 94 9722876 Effect of 3-beta-hydroxysteroid dehydrogenase gene deletion on virulence and immunogenicity of different vaccinia viruses and their recombinants. 3-beta-Hydroxysteroid dehydrogenase (3-beta-HSD) activity coded for by the A44L gene of vaccinia virus (VV) was demonstrated in CV-1 cultures infected by all five VV strains tested, viz. 1998 Archives of virology Abstract HBV A44L 75 79 9722876 Effect of 3-beta-hydroxysteroid dehydrogenase gene deletion on virulence and immunogenicity of different vaccinia viruses and their recombinants. Deletion of the A44L gene in two Praha virus-derived clones (the moderately virulent P13 and the highly attenuated P20), the WR and DD viruses resulted in absence of 3-beta-HSD activity from infected cultures. 1998 Archives of virology Abstract HBV A44L 16 20 9722876 Effect of 3-beta-hydroxysteroid dehydrogenase gene deletion on virulence and immunogenicity of different vaccinia viruses and their recombinants. Recombinant VVs expressing either varicella-zoster virus glycoprotein E (VZV-gE) or hepatitis B virus preS2-S protein (HBV-preS2-S) and their respective A44L deleted mutants were used in immunogenicity tests in mice. 1998 Archives of virology Abstract HBV A44L 153 157 PreS2;PreS2;S;S 102;123;108;129 107;128;109;130 9722876 Effect of 3-beta-hydroxysteroid dehydrogenase gene deletion on virulence and immunogenicity of different vaccinia viruses and their recombinants. The virulence for mice of P13 was not affected, and that of WR was only slightly decreased, by the A44L gene deletion. 1998 Archives of virology Abstract HBV A44L 99 103 9728561 Emergence of an S gene mutant during thymosin alpha1 therapy in a patient with chronic hepatitis B. Sequence analysis revealed an S gene mutant in HBsAg-seronegative serum with two consecutive amino acid substitutions: threonine115-to-isoleucine and threonine116-to-asparagine, whereas no amino acid substitution or deletion was found in the pre-S region. 1998 The Journal of infectious diseases Abstract HBV T115I;T116N 119;150 145;176 S;PreS;S 47;242;30 52;247;31 9751010 Incidence and clinical significance of hepatitis B virus precore gene translation initiation mutations in e antigen-negative patients. All HBeAg-negative patients (100%) harboured the m1896 mutation and 20 (64.5%) also had a G to A mutation at nucleotide 1899 (m1899). 1998 Journal of viral hepatitis Abstract HBV G1899A 90 124 C 4 9 9763505 Molecular analysis of the a determinant of HBsAg in children of HBeAg-positive mothers upon failure of postexposure prophylaxis. Only two exhibited a point mutation within the a determinant, one of which consisted of a substitution of glycine with alanine at position 145, and the other of a substitution of glutamine with arginine at position 129. 1998 International journal of infectious diseases Abstract HBV G145A;Q129R 106;179 142;218 S 47 60 9813205 Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus. In a mixed infection of ducklings with G133E and a small amount of wild-type virus, the wild-type virus was detected as the predominant genotype after recovery of normal liver histology. 1998 Virology Abstract HBV G133E 39 44 9813205 Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus. In vivo liver damage caused by this variant (G133E) occurred only during the first 2 weeks p.i., after which time cccDNA levels and liver histology returned to near normal despite continued virus replication. 1998 Virology Abstract HBV G133E 45 50 Liver disease 8 20 9813205 Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus. The results support the conclusion that the recovery from liver damage in G133E-infected ducklings was due to the emergence of spontaneous noncytopathic revertants rather than to host suppression of virus cytotoxicity. 1998 Virology Abstract HBV G133E 74 79 Liver disease 58 70 9813205 Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus. Two candidate revertant viral genomes were cloned directly from the serum virus of G133E-infected birds after recovery and tested for (i) control of cccDNA levels in primary hepatocyte cultures and (ii) their ability to compete with wild-type virus in a mixed infection. 1998 Virology Abstract HBV G133E 83 88 9824137 Prevalence of mutations in core promoter/precore region in Japanese patients with chronic hepatitis B virus infection. Furthermore, a mutation at nucleotide 1753 from T to C or G was frequently found in anti-HBe positive patients and was often accompanied by the double mutation. 1998 Digestive diseases and sciences Abstract HBV T1753C;T1753G 38;38 59;59 C 89 92 9824278 The sequential occurrence of viral mutations in a liver transplant recipient re-infected with hepatitis B: hepatitis B immune globulin escape, famciclovir non-response, followed by lamivudine resistance resulting in graft loss. One mutation I533L was detected during HBIg treatment. 1998 Journal of hepatology Abstract HBV I533L 13 18 9824278 The sequential occurrence of viral mutations in a liver transplant recipient re-infected with hepatitis B: hepatitis B immune globulin escape, famciclovir non-response, followed by lamivudine resistance resulting in graft loss. Three amino acid changes were selected while the patient was on lamivudine treatment, which include L533I, S559T and M550I. 1998 Journal of hepatology Abstract HBV L533I;S559T;M550I 100;107;117 105;112;122 9828233 Mutations in hepatitis B DNA polymerase associated with resistance to lamivudine do not confer resistance to adefovir in vitro. HBV DNA polymerase mutants M552I, M552V, and L528M/M552V showed resistance to lamivudine triphosphate with inhibition constants (Ki) increased by 8.0-fold, 19.6-fold, and 25.2-fold compared with that of wild-type HBV DNA polymerase. 1998 Hepatology (Baltimore, Md.) Abstract HBV M552V;L528M;M552I;M552V 51;45;27;34 56;50;32;39 P;P 8;221 18;231 9828233 Mutations in hepatitis B DNA polymerase associated with resistance to lamivudine do not confer resistance to adefovir in vitro. The L528M single mutation, identified in patients with increasing HBV DNA levels during therapy with famciclovir, also remained sensitive to adefovir diphosphate with the inhibition constant increased by only 2.3-fold. 1998 Hepatology (Baltimore, Md.) Abstract HBV L528M 4 9 9841851 Identification of hepatitis B surface antigen variants with alterations outside the "a" determinant in immunized Singapore infants. Decreased binding to "a" determinant-specific monoclonal antibody was observed for variants Pro120 to Ser120, Ala159 to Val159, and Phe183 to Cys183. 1999 The Journal of infectious diseases Abstract HBV P120S;A159V;F183C 92;110;132 108;126;148 9841851 Identification of hepatitis B surface antigen variants with alterations outside the "a" determinant in immunized Singapore infants. These include Asn116 to Thr116, Val118 to Ala118, Pro120 to Ser120, Ala159 to Val159, Phe183 to Cys183, and Val184 to Ala184. 1999 The Journal of infectious diseases Abstract HBV N116T;V118A;P120S;A159V;F183C;V184A 14;32;50;68;86;108 30;48;66;84;102;124 9841851 Identification of hepatitis B surface antigen variants with alterations outside the "a" determinant in immunized Singapore infants. Unlike other HBsAg variants, the Asn116-to-Thr116 HBsAg variant had the wild type threonine in the infant, whereas the mutated asparagine was found in the mother. 1999 The Journal of infectious diseases Abstract HBV N116T 33 49 S;S 13;50 18;55 9841851 Identification of hepatitis B surface antigen variants with alterations outside the "a" determinant in immunized Singapore infants. Vertical transmission is indicated for Phe183-to-Cys183 and Val184-to-Ala184 HBsAg variants, as they were found in both the infants and mothers. 1999 The Journal of infectious diseases Abstract HBV F183C;V184A 39;60 55;76 S 77 82 9857356 Current aspects of hepatitis B surface antigen mutants in Singapore. These vaccine-escape HBsAg mutants display a predominance of the Gly145-to-Arg145 mutation in the antigenic 'a' determinant. 1998 Journal of viral hepatitis Abstract HBV G145R 65 81 S;S 109;21 123;26 9862871 Transient selection of a hepatitis B virus polymerase gene mutant associated with a decreased replication capacity and famciclovir resistance. The impaired replication capacity of this V542I mutant may have contributed to the absence of outgrowth of this viral strain in vivo. 1999 Hepatology (Baltimore, Md.) Abstract HBV V542I 42 47 9862871 Transient selection of a hepatitis B virus polymerase gene mutant associated with a decreased replication capacity and famciclovir resistance. The results showed that the V542I mutant has a decreased replication capacity compared with wild type virus and does not produce HBsAg. 1999 Hepatology (Baltimore, Md.) Abstract HBV V542I 28 33 S 129 134 9862871 Transient selection of a hepatitis B virus polymerase gene mutant associated with a decreased replication capacity and famciclovir resistance. The results showed the transient selection of a V542I mutant in the C domain of the viral polymerase. 1999 Hepatology (Baltimore, Md.) Abstract HBV V542I 48 53 P 90 100 9862871 Transient selection of a hepatitis B virus polymerase gene mutant associated with a decreased replication capacity and famciclovir resistance. The sensitivity of the V542I mutant to penciclovir, the active metabolite of famciclovir, was further studied in tissue culture. 1999 Hepatology (Baltimore, Md.) Abstract HBV V542I 23 28 9870800 Association of mutations in the core promoter and precore region of hepatitis virus with fulminant and severe acute hepatitis in Japan. The presence of HBV mutants was examined by using a point mutation assay to detect a G to A transition at position 1896 in the precore region and an A to T transition at position 1762 and a G to A transition at position 1764 in the core promoter region. 1998 Journal of gastroenterology and hepatology Abstract HBV G1896A;A1762T;G1764A 85;149;190 119;183;224 Core promoter;Precore 232;127 245;134 9875378 The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. A variant of hepatitis B virus (HBV) containing a Met-to-Val substitution (M539V) in the YMDD motif of the polymerase nucleoside-binding domain exhibited resistance to the cytosine analogue lamivudine (3TC). 1998 Antiviral chemistry & chemotherapy Abstract HBV M539V 75 80 P;P 107;89 117;93 9875378 The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. The M539V polymerase variant produced in this cell line was approximately 26-fold less sensitive to the antiviral effects of 3TC than wild-type virus. 1998 Antiviral chemistry & chemotherapy Abstract HBV M539V 4 9 P 10 20 9875378 The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. This mutation results in a Met-to-Val substitution at amino acid 539 of the polymerase. 1998 Antiviral chemistry & chemotherapy Abstract HBV M539V 27 68 P 76 86 9875378 The hepatitis B virus M539V polymerase variation responsible for 3TC resistance also confers cross-resistance to other nucleoside analogues. To determine if the mutation responsible for the M539V polymerase variant affected the sensitivity of the virus to other nucleoside analogues, we constructed a tetracycline-responsive cell line, HepAD79. 1998 Antiviral chemistry & chemotherapy Abstract HBV M539V 49 54 P 55 65 9882327 Mechanism of suppression of hepatitis B virus precore RNA transcription by a frequent double mutation. A double mutation which converts nucleotide 1765 from A to T and nucleotide 1767 from G to A is frequently found in the hepatitis B virus (HBV) genome isolated from HBV patients with chronic hepatitis symptoms. 1999 Journal of virology Abstract HBV G1767A 76 92 Chronic Hepatitis B 183 209 9882327 Mechanism of suppression of hepatitis B virus precore RNA transcription by a frequent double mutation. In addition, this double mutation also resides in the X protein coding sequence, converting codon 130 from Lys to Met and codon 131 from Val to Ile. 1999 Journal of virology Abstract HBV K130M;V131I 98;128 117;147 X 54 55 9918936 Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus. A single amino acid change of glycine to glutamic acid at position 133 (G133E) in the preS protein of duck hepatitis B virus (DHBV) caused an increase in the intranuclear pool of viral covalently closed circular DNA (cccDNA), resulting in a transient elevation of viral replication and eventual hepatocyte destruction. 1999 Hepatology (Baltimore, Md.) Abstract HBV G133E;G133E 72;30 77;70 PreS 86 90 9918936 Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus. Birds infected with the G133E virus had increased periportal cellular proliferation and numerous lysed apoptotic hepatocytes following 100% infection of hepatocytes. 1999 Hepatology (Baltimore, Md.) Abstract HBV G133E 24 29 9918936 Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus. In vivo viral infection with the G133E virus was compared with infection with wild-type virus over a 72-day period. 1999 Hepatology (Baltimore, Md.) Abstract HBV G133E 33 38 9918936 Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus. The liver damage within G133E virus-infected birds subsided over time, resulting in mild chronic hepatitis that was similar to that observed within wild-type virus-infected birds. 1999 Hepatology (Baltimore, Md.) Abstract HBV G133E 24 29 Liver disease;Chronic Hepatitis B 4;89 16;106 9918936 Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus. The subsidence of liver damage in G133E virus-infected birds coincided with a reduction of viral cccDNA to wild-type virus levels in the liver. 1999 Hepatology (Baltimore, Md.) Abstract HBV G133E 34 39 Liver disease 18 30 9930189 Hepatitis B virus genomic sequence in the circulation of hepatocellular carcinoma patients: comparative analysis of 40 full-length isolates. G-to-A at nt 1613 and C-to-T at nt 1653 within enhancer II and T-to-C/A at nt 1753 within core promoter were also evident: 38%, 53%, and 40%, respectively. 1998 Archives of virology Abstract HBV G1613A;C1653T 0;22 17;39 Core promoter;Enh II 90;47 103;58 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The most common of these mutations is a G to A substitution at nucleotide (nt) 1896, that prevents the production of HBeAg by introducing a premature stop codon into the open reading frame (ORF) of the precore region. 2001 BMC microbiology Introduction HBV G1896A 39 84 C;Precore 117;202 122;209 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The presence of a C at position 1858 precludes the G to A mutation at nt 1896 as this would destabilize the stem-loop structure of the RNA encapsidation signal. 2001 BMC microbiology Introduction HBV G1896A 51 77 15308845 Detection of YMDD motif mutants by oligonucleotide chips in lamivudine-untreated patients with chronic hepatitis B virus infection. The most common mutants have a change at codon 552 from M to V (M552V) or from M to I (M552I). 2004 Journal of Korean medical science Introduction HBV M552V;M552I 64;87 69;92 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Most of these mutations usually affect the YMDD motif of the HBV DNA polymerase, by replacement of a methionine residue at position 550 with either valine (M550V) or isoleucine (M550I). 2004 BMC infectious diseases Introduction HBV M550V;M550I 156;178 161;183 P;P 69;43 79;47 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. A double point mutation with a transversion nucleotide from adenine to thymine at nucleotide 1762, K130M with a transition from adenine to guanine at position 1764 V131I (T-A mutations), has been found more frequently in patients with hepatic tumors than in asymptomatic chronic patients from China and Africa. 2005 Virology journal Introduction HBV K130M;V131I 99;164 104;169 Hepatocellular carcinoma 235 249 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. However, new adefovir-resistant mutations have been reported, such as the rtA181V mutation which is closely located to the rtL180M mutation conferring resistance to lamivudine. 2006 Comparative hepatology Introduction HBV A181V;L180M 76;125 81;130 RT;RT 74;123 76;125 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. In the few cases published thus far, adefovir-resistant HBV displayed the rtN236T mutation and maintained susceptibility to lamivudine in vivo . 2006 Comparative hepatology Introduction HBV N236T 76 81 RT 74 76 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. The patient had both an rtN236T and a rare rtA181T mutation. 2006 Comparative hepatology Introduction HBV N236T;A181T 26;45 31;50 RT;RT 24;43 26;45 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. In addition, a second lamivudine resistance mutation (rtL180M), located in the B domain of rt, has been identified. 2008 BMC microbiology Introduction HBV L180M 56 61 RT;RT 54;91 56;93 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. More than 90% of the HIV-HBV co-infected patients under lamivudine treatment display the double resistant mutation rtL180M/rtM204V. 2008 BMC microbiology Introduction HBV M204V;L180M 125;117 130;122 RT;RT 115;123 117;125 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. These mutations usually affect the YMDD motif located in the C domain of the HBV reverse transcriptase (rt), by replacement of a methionine residue at position 204 to either valine (rtM204V, occidental population) or isoleucine (rtM204I, oriental population). 2008 BMC microbiology Introduction HBV M204V;M204I 184;231 189;236 RT;RT;RT;RT;P 81;104;182;229;35 102;106;184;231;39 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. HBV genotype C and the BCP A1762T/G1764A mutant were independent risk factors for HCC, and the precore G1896A mutant was associated with a decreased risk of HCC. 2008 Journal of the National Cancer Institute Introduction HBV G1764A;A1762T;G1896A 34;27;103 40;33;109 BCP;Precore 23;95 26;102 Hepatocellular carcinoma;Hepatocellular carcinoma 82;157 85;160 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The most common of these mutations is a G to A substitution at nucleotide 1896 (G1896A), which prevents the production of HBeAg by introducing a premature stop codon into the open reading frame of the precore region. 2008 Journal of the National Cancer Institute Introduction HBV G1896A;G1896A 80;40 86;78 C;Precore 122;201 127;208 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The most frequent BCP mutation is a double mutation involving an A to T substitution at nucleotide 1762 and a G to A substitution at nucleotide 1764 (hereafter referred to as BCP A1762T/G1764A), which results in a substantial decrease in HBeAg expression but enhanced viral genome replication in vitro. 2008 Journal of the National Cancer Institute Introduction HBV G1764A;A1762T;A1762T;G1764A 186;179;65;110 192;185;103;148 BCP;BCP;C 18;175;238 21;178;243 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. This mutation (hereafter referred to as precore G1869A) is frequently detected in patients with HBeAg-negative chronic hepatitis B and in some patients with fulminant hepatitis B. 2008 Journal of the National Cancer Institute Introduction HBV G1869A 48 54 C;Precore 96;40 101;47 Chronic Hepatitis B;Fulminant Hepatitis B 111;157 130;176 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. The aim of present molecular modeling study is to elucidate the structural features of HBV-polymerase in terms of qualitative and quantitative changes conferred by B and C domain mutations (3TC; Lamivudine associated resistance: rtL180M and rtM204V/I) on the binding of different class of anti-HBV nucleosides (1-5). 2008 Antiviral research Introduction HBV M204V;M204I;L180M 243;243;231 250;250;236 P;RT;RT 91;229;241 101;231;243 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The common precore mutation (G1896A), mutations in enhancer II (C1653T) and the basal core promoter (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC. 2008 The American journal of gastroenterology Introduction HBV G1896A;C1653T;T1753V;A1762T;G1764A 29;64;101;134;142 35;70;107;140;148 BCP;Enh II;Precore;PreS 80;51;11;172 99;62;18;177 Hepatocellular carcinoma 245 248 19070921 The association of HBV core promoter double mutations (A1762T and G1764A) with viral load differs between HBeAg positive and anti-HBe positive individuals: a longitudinal analysis. One of the most critical changes is the appearance of double mutations at nt 1762 (A-T) and 1764 (G-A) in the BCP. 2009 Journal of hepatology Introduction HBV A1762T;G1764A 77;92 87;102 BCP 110 113 19077239 Occult hepatitis B infection: an evolutionary scenario. In this clade, a T-to-G mutation at position 173 truncates a splice-promoting polypyrimidine tract and also affects the local secondary structure of the viral RNA. 2008 Virology journal Introduction HBV T173G 17 48 19077239 Occult hepatitis B infection: an evolutionary scenario. Posttranscriptional reduction of surface protein and mRNA expression to a background level was due to a single G458A substitution and could also be caused by deletion of 30 nucleotides immediately downstream of this site. 2008 Virology journal Introduction HBV G458A 111 116 S 33 40 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. The most common BCP mutations are A to T at nt 1762 and G to A at nt 1764 (T1762/A1764). 2009 Journal of medical virology Introduction HBV G1764A;A1762T 56;34 73;51 BCP 16 19 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. The most common PC mutation is a G to A transition at nucleotide (nt) 1896 (A1896) that creates a premature stop codon and abolishes HBeAg translation. 2009 Journal of medical virology Introduction HBV G1896A 32 75 C;Precore 133;16 138;18 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Clone 4B with quadruple core promoter mutation (T1753C, A1762T, G1764A, and C1766T) had 10-20 times higher replication capacity than clone 2A, which has a wild-type core promoter sequence. 2009 Virology Introduction HBV T1753C;A1762T;G1764A;C1766T 48;56;64;76 54;62;70;82 Core promoter;Core promoter 24;165 37;178 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. On the other hand, a naturally occurring I97L mutation in the core protein caused an "immature secretion phenotype" of predominantly single stranded DNA. 2009 Virology Introduction HBV I97L 41 45 C 62 66 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The hot-spot double mutation in the core promoter, A1762T/G1764A, was found by site-directed mutagenesis to moderately increase genome replication and decrease HBeAg expression in transiently transfected human hepatoma cell lines. 2009 Virology Introduction HBV G1764A;A1762T 58;51 64;57 Core promoter;C 36;160 49;165 Hepatocellular carcinoma 210 218 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A and precore G1896A (a G-to-A substitution at nucleotide 1896) have been associated with active exacerbation of chronic hepatitis B, liver cirrhosis, and acute fulminant hepatitis. 2009 Journal of the National Cancer Institute Introduction HBV G1764A;A1762T;G1896A;G1896A 7;0;26;36 13;6;32;74 Precore 18 25 Chronic Hepatitis B;Liver cirrhosis 125;146 144;161 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Frequent examination of patients with chronic HBV infections for the presence of PreS mutations, C1653T, T1753V, and A1762T/G1764A may be useful for identifying which patients require preventive antiviral treatment and for the prediction of HCC. 2009 Journal of the National Cancer Institute Introduction HBV G1764A;C1653T;T1753V;A1762T 124;97;105;117 130;103;111;123 PreS 81 85 HBV infections;Hepatocellular carcinoma 38;241 60;244 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. HBV genotype- or HBV subgenotype-specific mutations, including C1653T (a C-to-T substitution at nucleotide 1653) in the EnhII region, T1753V (a T-to-V [C or A or G] substitution at nucleotide 1753), and the double mutant A1762T/G1764A (an A-to-T substitution at nucleotide 1762 and a G-to-A substitution at nucleotide 1764) in the BCP region, have been found to be independent risk factors for HCC. 2009 Journal of the National Cancer Institute Introduction HBV G1764A;C1653T;T1753V;A1762T;C1653T;A1762T;G1764A 228;63;134;221;73;239;284 234;69;140;227;111;277;322 BCP;Enh II 331;120 334;125 Hepatocellular carcinoma 394 397 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. PreS mutations, C1653T, T1753V, and A1762T/G1764A were each associated with an increased risk of HCC and were increasingly more prevalent as chronic HBV infection progressed from the asymptomatic hepatitis B surface antigen carrier state to liver cirrhosis or HCC. 2009 Journal of the National Cancer Institute Introduction HBV G1764A;C1653T;T1753V;A1762T 43;16;24;36 49;22;30;42 PreS;S 0;208 4;215 Hepatocellular carcinoma;Chronic HBV infection;Liver cirrhosis;Hepatocellular carcinoma 97;141;241;260 100;162;256;263 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. The most frequently encountered point mutation involving the lower stem of the epsilon structure is the A instead of G mutation at position 1896 that induces a stop codon in the preC gene, affects HBeAg expression and has been associated with a severe course of acute hepatitis. 2009 Journal of medical case reports Introduction HBV G1896A 104 144 C;Precore 197;178 202;182 Acute Hepatitis B 262 277 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. A higher prevalence of the BCP double mutation A1762T/G1764A and the G1896A PC mutation have been reported in ALF than in acute hepatitis B patients. 2010 Journal of viral hepatitis Introduction HBV G1764A;A1762T;G1896A 54;47;69 60;53;75 BCP;Precore 27;76 30;78 Liver disease 110 113 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. In addition, single mutations including the T1753V (C/A/G), C1766T, T1768A, G1862T and G1899A in the BCP/PC region have been reported to be associated with increased HBV replication capacity and/or reduced HBeAg expression in vitro, and in some cases associated with ALF in the clinic. 2010 Journal of viral hepatitis Introduction HBV T1753V;C1766T;T1768A;G1862T;G1899A 44;60;68;76;87 50;66;74;82;93 BCP;C;Precore 101;206;105 104;211;107 Liver disease 267 270 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Among adefovir (ADV) treated patients, rtA181T or rtA181V mutations have been associated with a 2-6 fold decrease in sensitivity to LMV. 2010 Journal of Korean medical science Introduction HBV A181T;A181V 41;52 46;57 RT;RT 39;50 41;52 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In LMV treated patients, the P120A mutation in the S region results in hepatitis B surface antigen (HBsAg) detection failure. 2010 Journal of Korean medical science Introduction HBV P120A 29 34 S;S;S 100;51;83 105;52;90 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In this patient, they detected deletions of nucleotides 23 to 55 (amino acids 12 to 22) in the Pre-S2 region, and amino acid substitutions at I126S, T131N, M133T, and S136Y in the 'a' determinant region of HBsAg. 2010 Journal of Korean medical science Introduction HBV I126S;T131N;M133T;S136Y 142;149;156;167 147;154;161;172 S;S;PreS2 181;206;95 195;211;101 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Overlap of surface gene mutations, such as sW172stop in patients carrying rtA181T, and sL173F in patients carrying rtA181V, have been reported in chronic hepatitis B patients receiving ADV treatment. 2010 Journal of Korean medical science Introduction HBV A181T;A181V;L173F;W172X 76;117;87;43 81;122;93;52 RT;RT;S;S;S 74;115;43;87;11 76;117;44;88;18 Chronic Hepatitis B 146 165 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Patients with lamivudine (LMV)-resistant rtM204I/V (+-rtL180M) mutations in the catalytic tyrosine-methionine-aspartate-aspartate (YMDD) motif are less responsive to entecavir (ETV). 2010 Journal of Korean medical science Introduction HBV M204I;M204V;L180M 43;43;56 50;50;61 RT;RT;P;P 41;54;90;131 43;56;129;135 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The goal of this study was to evaluate the surface gene sequence in ADV-resistant patients carrying A181T/V mutations and to determine the associated clinical significance. 2010 Journal of Korean medical science Introduction HBV A181V;A181T 100;100 107;107 S 43 50 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Both patients were infected with HBV with M204V+L180M LVDr substitutions at study entry and developed additional substitutions T184G & S202I, or M250V on therapy. 2010 PloS one Introduction HBV M204V;L180M;T184G;S202I;M250V 42;48;127;135;145 47;53;132;140;150 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. In addition, ETVr substitutions in isolates with only the M204I substituted LVDr HBV and not the M204V+L180M LVDr virus, phenotypic resistance to ETV is diminished. 2010 PloS one Introduction HBV M204I;M204V;L180M 58;97;103 63;102;108 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. In this study we reported a novel 12-nucleotide(nt) insertion between nt494 and nt495 in S gene, which led 4-aa insertion between aa113 and aa114 compared with wildtype HBsAg. 2010 Virology journal Introduction HBV Ins nt494-495;Ins nt113-114 52;112 85;145 S;S 169;89 174;90 20573234 Infection with hepatitis B virus carrying novel pre-S/S gene mutations in female siblings vaccinated at birth: two case reports. In 1990, a child developing protective antibody level after hepatitis B immunization was found to carry mutant HBV with a surface gene mutation at position 587 (guanine to adenosine), resulting in a change of glycine to arginine at amino acid 145 of the major surface antigen. 2010 Journal of medical case reports Introduction HBV G145R 209 246 S;S 122;260 129;267 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. A Precore stop codon substitution at amino acid (aa) 28 (W28 stop, nucleotide (nt) G1896A) is associated with failure to synthesize hepatitis B e antigen (HBeAg). 2010 Virology Introduction HBV W28X;G1896A 57;83 65;89 C;C;Precore 144;155;2 153;160;9 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. Both the BCP A1762T/G1764A mutations and the Precore stop codon mutation have been associated with advanced liver disease including hepatocellular carcinoma (HCC) and cirrhosis in mono-infected patients. 2010 Virology Introduction HBV G1764A;A1762T 20;13 26;19 BCP;Precore 9;45 12;52 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 108;132;158;167 121;156;161;176 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. In the basal core promoter (BCP) region, two associated nt changes, A1762T and G1764A have been associated with reduced Precore mRNA transcription and reduced HBeAg production. 2010 Virology Introduction HBV A1762T;G1764A 68;79 74;85 BCP;BCP;C;Precore 7;28;159;120 26;31;164;127 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Although the 1762T/1764A double mutation, commonly occurring in HBeAg-negative patients, was observed in vivo to suppress the production of preC mRNA independent of G1896A, recent in vitro research suggested other single site substitutions rather than these two may be responsible for the reduction of HBeAg expression. 2010 BMC infectious diseases Introduction HBV G1896A 165 171 C;C;Precore 64;302;140 69;307;144 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Studies have been shown that G1896A is involved in HBeAg negativity by introducing a stop codon in the preC region. 2010 BMC infectious diseases Introduction HBV G1896A 29 35 C;Precore 51;103 56;107 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Triple core promoter mutations C1753T/A1762T/G1764A occurred more commonly in genotype C compared with genotype B. 2010 BMC infectious diseases Introduction HBV A1762T;G1764A;C1753T 38;45;31 44;51;37 Core promoter 7 20 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Several investigations have shown that the substitutions L60V, S87G and I97L in the HBV core antigen (HBcAg, referred to as the HBc protein) were the most frequent in patients with CHB, and HBV with these "hot-spot" mutations show different characteristics in replication cycle in vitro compared to the wild-type strain. 2010 Virology journal Introduction HBV L60V;S87G;I97L 57;63;72 61;67;76 C;C;C 88;128;102 92;131;107 Chronic Hepatitis B 181 184 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. In this study, the role of Y100C substitution in reducing amount of HBsAg or changing HBsAg affinity by commercial antibodies was investigated by comparison of HBsAg levels obtained from recombinant plasmids with or without Y100C substitution. 2011 Hepatitis research and treatment Introduction HBV Y100C;Y100C 27;224 32;229 S;S;S 68;86;160 73;91;165 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Tyrosine (Y) to cysteine (C) substitution in HBsAg residue 100 (Y100C) has been associated with HBsAg-negative phenotype in blood donors from Venezuela and Spain, and is frequently found in cases of occult HBV infection in Brazil. 2011 Hepatitis research and treatment Introduction HBV Y100C 64 69 S;S 45;96 50;101 HBV infections 206 219 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Cross-resistance (usually rtM204I) also exists between LdT and LAM [20]. 2011 Journal of viral hepatitis Introduction HBV M204I 28 33 RT 26 28 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. In addition, rtA181T seems to be an atypical substitution associated with LAM and ADV selection and may reduce the typical extent of virologic breakthrough [21]. 2011 Journal of viral hepatitis Introduction HBV A181T 15 20 RT 13 15 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtM204I and rtM204V are classic LAM-resistant mutations and often coexist with compensatory mutations (rtV173L and rtL180M) [9, 10, 11]. 2011 Journal of viral hepatitis Introduction HBV M204V;M204I;V173L;L180M 18;6;109;121 23;11;114;126 RT;RT;RT;RT 4;16;107;119 6;18;109;121 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtN236T and rtA181V are two well-recognized ADV-resistant mutations [12, 13], and some purported mutations such as rtV84M, rtV214A, rtQ215S, rtL217R and rtI233V may reduce susceptibility to ADV, although these are still controversial [13, 14, 15, 16]. 2011 Journal of viral hepatitis Introduction HBV A181V;V84M;I233V;N236T;V214A;Q215S;L217R 18;121;159;6;129;138;147 23;125;164;11;134;143;152 RT;RT;RT;RT;RT;RT;RT 4;16;119;127;136;145;157 6;18;121;129;138;147;159 21438026 Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival. One hotspot mutation involves an adenine to thymine transversion at nucleotide 1762, and a guanine to adenine transition at nucleotide 1764 of the viral genome, and both mutations fall within the X gene (A1762T/G1764A). 2011 Molecular carcinogenesis Introduction HBV G1764A;A1762T 211;204 217;210 X 196 197 21438026 Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival. This observation is of particular interest to our investigation since the A1762T/G1764A double mutation impacts amino acids 130 and 131 of HBx, causing a lysine to methionine change at amino acid 130 and a valine to isoleucine change at amino acid 131. 2011 Molecular carcinogenesis Introduction HBV G1764A;A1762T;K130M;V131I 81;74;154;206 87;80;199;251 X 139 142 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. Precore mutations, such as G1896A (guanine-to-adenine mutation at nucleotide 1,896), and core promoter (CP) mutations, including A1762T (adenine-to-thymine mutation at nucleotide 1,762) and G1764A (guanine-to-adenine mutation at nucleotide 1,764), are known to be associated with HBeAg status in adults. 2011 Journal of Korean medical science Introduction HBV G1896A;A1762T;G1764A 27;129;190 33;135;196 Core promoter;Core promoter;C;Precore 89;104;280;0 102;106;285;7 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. The precore stop-codon mutation (G1896A) abolishes HBeAg and the dual mutation in the CP region (A1762T, G1764A) down-regulates HBeAg production. 2011 Journal of Korean medical science Introduction HBV G1896A;A1762T;G1764A 33;97;105 39;103;111 Core promoter;C;C;Precore 86;51;128;4 88;56;133;11 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations in HBV core gene, destroying the cleavage sites of Tsp509I, were demonstrated to correlate with the decreases in serum HBV DNA levels and HBV replication in chronic hepatitis B patients, and moreover, A336C/A336T variations caused the substitution of Glu-83 with Asp in HBcAg. 2011 Virology journal Introduction HBV A336T;A336T;T337C;A336C;A336C;E83D 236;6;12;0;230;280 241;11;17;5;235;295 C;C 36;299 40;304 Chronic Hepatitis B 186 205 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. G1896A variation was mainly present in patients who were HBeAg-negative natives of Asian or Mediterranean basin, whereas A1762T/G1764A dual variations were detected in a similar proportion of HBeAg-negative and HBeAg-positive patients. 2011 Virology journal Introduction HBV G1764A;G1896A;A1762T 128;0;121 134;6;127 C;C;C 57;192;211 62;197;216 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. HBeAg is transcribed from the precore/core gene like HBcAg, therefore, A336C/A336T variations also cause the change of amino acid composition of HBeAg. 2011 Virology journal Introduction HBV A336T;A336C 77;71 82;76 C;C;C;C;Precore 38;53;0;145;30 42;58;5;150;37 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. In addition to genotype B, G1896A variation, not A1762T/G1764A dual variations, is proposed to be another major mechanism to explain spontaneous HBeAg loss in the natural history of chronic HBV infection. 2011 Virology journal Introduction HBV G1764A;G1896A;A1762T 56;27;49 62;33;55 C 145 150 Chronic HBV infection 182 203 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. In order to investigate whether there was correlation between A336C/A336T/T337C variations and spontaneous HBeAg loss, the cumulative rates of spontaneous HBeAg loss between patients with C336/T336/C337 variants and the wild type A336/T337 were compared by analyzing a cohort of 166 Chinese chronic hepatitis B patients without any antiviral therapy. 2011 Virology journal Introduction HBV A336T;T337C;A336C 68;74;62 73;79;67 C;C 107;155 112;160 Chronic Hepatitis B 291 310 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Therefore, it was reasonable to suspect that A336C/A336T/T337C variations caused the decrease in serum HBV DNA levels by down-regulating HBeAg expression or promoting HBeAg loss. 2011 Virology journal Introduction HBV A336T;T337C;A336C 51;57;45 56;62;50 C;C 137;167 142;172 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. However, about 9% HBeAg-positive patients had G1896A mutant as dominant species. 2011 Journal of clinical virology Introduction HBV G1896A 46 52 C 18 23 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. It was shown that the appearance of G1896A or G1899A mutation in the precore region correlated with increased risk of HCC, although inconsistent results were also reported. 2011 Journal of clinical virology Introduction HBV G1896A;G1899A 36;46 42;52 Precore 69 76 Hepatocellular carcinoma 118 121 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. The G1896A mutation in particular creates a premature stop codon in the hepatitis B e antigen (HBeAg) open reading frame, thereby abolishing HBeAg production. 2011 Journal of clinical virology Introduction HBV G1896A 4 10 C;C;C 84;95;141 93;100;146 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. Besides the TA mutation, other core promoter mutations, notably T1753V and T1768A, have also been reported to be associated with an increased risk of HCC. 2011 Gastroenterology Introduction HBV T1753V;T1768A 64;75 70;81 Core promoter 31 44 Hepatocellular carcinoma 150 153 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. Clinical studies have shown that the common double mutation A1762T/G1764A (TA) in the HBV basal core promoter (CP) region is independently associated with HCC. 2011 Gastroenterology Introduction HBV G1764A;A1762T 67;60 73;66 BCP;Core promoter 90;111 109;113 Hepatocellular carcinoma 155 158 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In BCP region, a double mutation, A1762T/G1764A, is commonly found to associate with HBV genotype C, which affects the viral replications. 2011 PloS one Introduction HBV G1764A;A1762T 41;34 47;40 BCP 3 6 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In our previous study, the G1613A mutation was identified as a hotspot in HCC patients. 2011 PloS one Introduction HBV G1613A 27 33 Hepatocellular carcinoma 74 77 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In this study, we set out to elucidate the functional consequences of the G1613A mutation on the synthesis of HBV serological markers, HBeAg and HBV surface antigen (HBsAg), as well as the production of viral DNA and RNA. 2011 PloS one Introduction HBV G1613A 74 80 C;S;S 135;166;149 140;171;156 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Overall, our data demonstrated the functional consequences of the G1613A mutation, and suggested a possible molecular link between the mutation and the resulted phenotype of the virus. 2011 PloS one Introduction HBV G1613A 66 72 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. We showed that the G1613A mutation is associated to high viral load in HBV carriers with statistically significance. 2011 PloS one Introduction HBV G1613A 19 25 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Because of the overlap between the S and polymerase genes, a great proportion of patients carrying the rtA181T mutation also possessed the sW172* nonsense mutation, resulting in truncation of the pre-S/S reading frames. 2011 BMC cancer Introduction HBV A181T;W172X 105;139 110;145 P;PreS;S;RT;S;S 41;196;202;103;35;139 51;201;203;105;36;140 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. However, in the presence of rtM204I/V mutations, ETV resistance can occur if the rtI169T, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutation coexists. 2011 BMC cancer Introduction HBV M204I;M204V;T184A;T184F;T184G;T184I;T184L;T184S;S202G;S202I;I169T;M250V 30;30;92;92;92;92;92;92;111;111;83;125 37;37;107;107;107;107;107;107;118;118;88;130 RT;RT;RT;RT;RT 28;81;90;109;123 30;83;92;111;125 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Previous studies have indicated that several virological factors including HBV-DNA level, HBV e antigen (HBeAg) status, genotype, pre-S internal deletion mutant and basal core promoter (BCP) A1762T/G1764A mutation are closely associated with development of HCC in treatment naive, chronic hepatitis B patients. 2011 BMC cancer Introduction HBV G1764A;A1762T 198;191 204;197 BCP;BCP;C;C;PreS 165;186;94;105;130 184;189;103;110;135 Hepatocellular carcinoma;Chronic Hepatitis B 257;281 260;300 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The major ADV resistant mutants were rtN236T and rtA181T/V. 2011 BMC cancer Introduction HBV A181T;A181V;N236T 51;51;39 58;58;44 RT;RT 37;49 39;51 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The major resistant mutant was rtM204I. 2011 BMC cancer Introduction HBV M204I 33 38 RT 31 33 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The most frequently encountered LAM-resistant mutant is rtM204V/I, which possesses a mutation located at the catalytic YMDD motif. 2011 BMC cancer Introduction HBV M204V;M204I 58;58 65;65 RT;P 56;119 58;123 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The rtA181T mutation has also been reported in a substantial proportion of LAM-resistant patients, which has been shown to confer LAM-resistance in cell-based assays. 2011 BMC cancer Introduction HBV A181T 6 11 RT 4 6 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The rtL180M mutation usually occurs concurrently with the rtM204V mutation and serves as a compensatory mutation. 2011 BMC cancer Introduction HBV L180M;M204V 6;60 11;65 RT;RT 4;58 6;60 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. As for deletions and point mutations, which are more subtle genetic variations than genotype, previous studies have found some clues, such as codon 38 in x gene, A1762T/G1764A basal core promoter (BCP) mutation, and deletion of pre-S and x protein, but definitive conclusions have not yet been made. 2011 BMC cancer Introduction HBV G1764A;A1762T 169;162 175;168 BCP;BCP;PreS;X;X 176;197;228;154;238 195;200;233;155;239 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. Since the precore G1896A and BCP A1762T/G1764A mutants make no or reduced level of HBeAg, they could escape the anti-HBe immunity and be selected passively due to a survival advantage. 2012 Journal of hepatology Introduction HBV G1764A;G1896A;A1762T 40;18;33 46;24;39 BCP;C;C;Precore 29;117;83;10 32;120;88;17 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. The BCP A1762T/G1764A double mutation can reduce the production of HBeAg by around 50% and thus may also contribute to HBeAg seroconversion. 2012 Journal of hepatology Introduction HBV G1764A;A1762T 15;8 21;14 BCP;C;C 4;67;119 7;72;124 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. The precore G1896A mutation and/or the A1762T/G1764A double mutation in the basal core promoter (BCP) region have been studied extensively using the qualitative DNA sequencing technology. 2012 Journal of hepatology Introduction HBV G1764A;G1896A;A1762T 46;12;39 52;18;45 BCP;BCP;Precore 76;97;4 95;100;11 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. The precore G1896A mutation creates a premature stop codon that abolishes the synthesis of HBeAg, thus the dominance of this mutant could easily account for HBeAg seronegativity. 2012 Journal of hepatology Introduction HBV G1896A 12 18 C;C;Precore 91;157;4 96;162;11 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. We have recently overcome this technical difficulty and established reliable quantitative assays for the detection of the BCP A1762T/G1764A double mutation and the precore mutations (G1896A and G1896A/G1899A). 2012 Journal of hepatology Introduction HBV G1764A;G1899A;A1762T;G1896A;G1896A 133;201;126;183;194 139;207;132;189;200 BCP;Precore 122;164 125;171 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. with the most important occurring in the highly conserved tyrosine-methionine-asparate-aspartate (YMDD) motif, involving a change from methionine at position 204 in the reverse transcriptase domain (rt204) to either a valine or isoleucine residue (rtM204V/I) or, more rarely, a serine residue. 2011 BMC research notes Introduction HBV M204V;M204I 250;250 257;257 RT;RT;RT;P 169;199;248;98 190;201;250;102 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. For example, studies demonstrated that the rtA194T mutation in the HBV genome led to a decrease in HBV replication capacity with TDF treatment; however, additional and more long-term data investigating the effects of TDF treatment on HBV resistance are needed . 2011 Hepatitis monthly Introduction HBV A194T 45 50 RT 43 45 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. LdT selects for mutations in the YMDD motif, and to date, only rtM204I (but not rtM204V) has been observed . 2011 Hepatitis monthly Introduction HBV M204I;M204V 65;82 70;87 RT;RT;P 63;80;33 65;82;37 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Moreover, studies conducted in Turkish patients having treated or untreated CHB infections indicated that HBV drug resistance is frequently mediated by rtM204V (YVDD variant) and rtM204I (YIDD variant) mutations, and rtM204S (YSDD variant) mutations with or without compensatory mutations such as rtV173L and rtL180M are also found, but occur much less frequently . 2011 Hepatitis monthly Introduction HBV M204S;L180M;M204V;M204I;V173L 219;311;154;181;299 224;316;159;186;304 RT;RT;RT;RT;RT;P;P;P 152;179;217;297;309;188;226;161 154;181;219;299;311;192;230;165 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Nine major mutation patterns associated with LAM resistance have been reported: (i) rtM204I/V + rtL180M; (ii) rtM204I; (iii) rtV173L + rtL180M + rtM204V; (iv) rtL80I + rtM204I; (v) rtQ215S + rtM204I/V +- rtL180M; (vi) rt169T + rtV173L + rtL180M + rtM204V; (vii) rtA181T; (viii) rtT184S + rtM204I/V +- rtL180M, and (ix) rtM204S + rtL180M. 2011 Hepatitis monthly Introduction HBV M204I;M204V;L180M;M204I;V173L;L80I;M204I;M204I;M204V;A181T;M204V;L180M;M204V;Q215S;L180M;V173L;L180M;M204V;T184S;M204I;L180M;M204S;L180M 86;86;98;112;127;161;170;193;193;264;290;137;147;183;206;229;239;249;280;290;303;321;331 93;93;103;117;132;165;175;200;200;269;297;142;152;188;211;234;244;254;285;297;308;326;336 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 84;96;110;125;135;145;159;168;181;191;204;218;227;237;247;262;278;288;301;319;329 86;98;112;127;137;147;161;170;183;193;206;220;229;239;249;264;280;290;303;321;331 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Similarly, the mechanism mediating ADV resistance has been characterized, with major resistance mutations located at rtN236T and/or rtA181T/V , and a number of other mutations found in 3 clusters within the rt region of the HBV polymerase. 2011 Hepatitis monthly Introduction HBV N236T;A181T;A181V 119;134;134 124;141;141 P;RT;RT;RT 228;117;132;207 238;119;134;209 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Some of these mutations can act as compensatory mutations, such as rtL80I/V and rtV173L. 2011 Hepatitis monthly Introduction HBV L80I;L80V;V173L 69;69;82 75;75;87 RT;RT 67;80 69;82 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The main mutation associated with LAM and L-nucleoside resistances is rtM204I/V, a mutation that occurs within the YMDD motif of the reverse transcriptase (rt) region of the polymerase. 2011 Hepatitis monthly Introduction HBV M204I;M204V 72;72 79;79 P;RT;RT;RT;P 174;133;70;156;115 184;154;72;158;119 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Two patterns of ETV resistance have been characterized, and they include the LAM-resistance mutation rtM204I/V plus an additional mutation of either rtT184G + rtS202I/C or rtM250V + rtI169T . 2011 Hepatitis monthly Introduction HBV M204V;S202I;S202C;I169T;M204I;T184G;M250V 103;161;161;184;103;151;174 110;168;168;189;110;156;179 RT;RT;RT;RT;RT 101;149;159;172;182 103;151;161;174;184 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Moreover, a few studies of Turkish patients with treated or untreated CHB infections have frequently indicated HBV drug resistance as rtM204V (YVDD variant), rtM204I (YIDD variant) and, rarely, as rtM204S (YSDD variant) mutations with or without compensatory mutations, such as rtV173L and rtL180M . 2010 Hepatitis monthly Introduction HBV M204S;L180M;M204V;M204I;V173L 199;292;136;160;280 204;297;141;165;285 RT;RT;RT;RT;RT;P;P;P 134;158;197;278;290;167;206;143 136;160;199;280;292;171;210;147 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. G145R was the major variation in the HBV isolates responsible for the occult HBV infections in Xiamen, China. 2012 Virology journal Introduction HBV G145R 0 5 HBV infections 77 91 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Lamivudine resistance is primarily associated with rtM204I or rtM204V substitution (rtM204I/V) in the YMDD motif of the RT domain. 2012 Nature communications Introduction HBV M204I;M204V;M204V;M204I 53;86;64;86 58;93;69;93 RT;RT;RT;RT;P 51;62;84;120;102 53;64;86;122;106 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Other mutations that have been reported to be associated with lamivudine resistance include rtA181V/T and several secondary RT mutations, for example, rtV173L and rtL180M. 2012 Nature communications Introduction HBV A181V;A181T;L180M;V173L 94;94;165;153 101;101;170;158 RT;RT;RT;RT 92;124;151;163 94;126;153;165 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Based on the abundant genetic information obtained by ultra-deep sequencing, we clarified the precise prevalence of HBV clones with G1896A pre-C mutations in association with HBe serostatus in chronically infected patients with or without NA treatment. 2012 PloS one Introduction HBV G1896A 132 138 C;Precore 175;139 178;144 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. For example, in chronic infection, G to A point mutation at nucleotide (nt) 1896 in the pre-core (pre-C) region as well as A1762T and G1764A mutations in the core-promoter region are highly associated with HBeAg seroconversion that in general results in the low levels of viremia and consequent clinical cure. 2012 PloS one Introduction HBV G1896A;A1762T;G1764A 34;123;134 81;129;140 Core promoter;C;Precore;Precore 158;206;98;88 171;211;103;96 Chronic HBV infection 16 33 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. In contrast, acute infection with the G1896A pre-C mutant represents a high risk for fulminant hepatic failure. 2012 PloS one Introduction HBV G1896A 38 44 Precore 45 50 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The region analyzed extends from codon rt148 to rt208 in the P ORF, which includes most RT codons corresponding to reported relevant NA-resistant aa substitutions (rtI169T, rtV173L, rtL180M, rtA181T/V, rtT184S/A/I/L/G/C/M, rtA194T, rtA202C/G/I, rtM204V/I, rtW153Q, rtV191I and rtV207I), and spans a part of the S ORF, from codon s140 to s200, containing the C-terminal region of the immunodominant epitope "a determinant" (codon s124 to s147) (Figure 1). 2012 PloS one Introduction HBV A181T;A181V;T184S;T184A;T184I;T184L;T184G;T184C;T184M;A202C;A202G;A202I;M204V;M204I;I169T;V173L;L180M;A194T;W153Q;V191I;V207I 193;193;204;204;204;204;204;204;204;234;234;234;247;247;166;175;184;225;258;267;279 200;200;221;221;221;221;221;221;221;243;243;243;254;254;171;180;189;230;263;272;284 S;P;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S;S 407;61;39;48;88;164;173;182;191;202;223;232;245;256;265;277;311;329;337;429;437 420;62;41;50;90;166;175;184;193;204;225;234;247;258;267;279;312;330;338;430;438 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. Compensatory mutations in the rt domain (rtL180M, rtV173L, rtL80I/V) that partially restore replication efficiency are often co-selected in HBV rt204 mutants. 2012 BMC microbiology Introduction HBV L80I;L80V;L180M;V173L 61;61;43;52 67;67;48;57 RT;RT;RT;RT;RT 30;41;50;59;144 32;43;52;61;146 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. The main site within the HBV rt protein that is associated with LAM resistance is residue 204 in the highly conserved tyrosine-methionine-aspartate-aspartate (YMDD) motif of the nucleotide-binding site; in general, the methionine in this sequence is replaced by either valine or isoleucine (rtM204V/I). 2012 BMC microbiology Introduction HBV M204V;M204I 293;293 300;300 RT;RT;P;P 29;291;118;159 31;293;157;163 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. This primary LAM-resistant mutant, rtM204V/I, affects viral replication fitness. 2012 BMC microbiology Introduction HBV M204V;M204I 37;37 44;44 RT 35 37 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Besides, a new mutation pattern G1899A in precore region appears to significantly correlate with the incremental risk of HCC as well. 2012 PloS one Introduction HBV G1899A 32 38 Precore 42 49 Hepatocellular carcinoma 121 124 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Several prospective studies demonstrated that patients who had A1762T/G1764A double mutation were more predisposed to HCC than those with the wild type. 2012 PloS one Introduction HBV G1764A;A1762T 70;63 76;69 Hepatocellular carcinoma 118 121 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Therefore we reappraised the relationship between the ubiquitous mutations and the risk of suffering from HCC in this study, with great attention paying to Precore G1896A and the HCC risk. 2012 PloS one Introduction HBV G1896A 164 170 Precore 156 163 Hepatocellular carcinoma;Hepatocellular carcinoma 106;179 109;182 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Those mutations include G1613A, C1653T in the EnhII region; T1753V, the double mutation A1762T/G1764A at the BCP region, G1896A and G1899A in the precore region. 2012 PloS one Introduction HBV G1764A;G1613A;C1653T;T1753V;A1762T;G1896A;G1899A 95;24;32;60;88;121;132 101;30;38;66;94;127;138 BCP;Enh II;Precore 109;46;146 112;51;153 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Till now, much more studies (around 40 more case-control studies) focusing on the correlation of HBV mutations with HCC have emerged and increasing studies demonstrated a significant correlation between Precore G1896A and the risk of HCC. 2012 PloS one Introduction HBV G1896A 211 217 Precore 203 210 Hepatocellular carcinoma;Hepatocellular carcinoma 116;234 119;237 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. To illuminate the controversy, a related meta-analysis was performed and demonstrated a positive relationship between the mutations like BCP double mutation, Pre-S mutation, C1653T and T1753V and the occurrence of HCC, while no significance was observed in Precore mutation G1896A. 2012 PloS one Introduction HBV C1653T;T1753V;G1896A 174;185;274 180;191;280 BCP;Precore;PreS 137;257;158 140;264;163 Hepatocellular carcinoma 214 217 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Although the T1762/A1764 double mutation, commonly occurring in HBeAg-negative patients, was observed in vivo to suppress the production of preC mRNA independent of G1896A, recent in vitro research suggested other single site substitutions rather than these two which may be responsible for the reduction of HBeAg expression.Unknown mutation in this core promoter may impede the seroconversion of HBeAg during antiviral treatment. 2012 PloS one Introduction HBV G1896A 165 171 Core promoter;C;C;C;Precore 350;64;308;397;140 363;69;313;402;144 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Studies have shown that G1896A is involved in HBeAg negativity by introducing a stop codon in the preC region. 2012 PloS one Introduction HBV G1896A 24 30 C;Precore 46;98 51;102 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. In addition, studies have observed that amino acid (AA) substitutions in other positions of RT, such as rtV191I and rtT128I/N, were selected during prolonged NA therapy and affected the replication capacity of HBV. 2012 Liver international Introduction HBV T128I;T128N;V191I 118;118;106 125;125;111 RT;RT;RT 92;104;116 94;106;118 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Published data showed that approximately 65% of patients on lamivudine monotherapy developed YMDD motif mutations (rtM204I/V) after 5 years of treatment. 2012 Liver international Introduction HBV M204I;M204V 117;117 124;124 RT;P 115;93 117;97 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. A1762T/G1764A double mutation has been frequently reported to be associated with the progression of liver disease and increased risk for HCC, but it has also been found in patients without AdLD. 2012 PloS one Introduction HBV G1764A;A1762T 7;0 13;6 Liver disease;Hepatocellular carcinoma;Aggressive Hepatitis and advanced liver disease 100;137;189 113;140;193 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1896A mutation was seen at a higher frequency in genotype D strains, while A1762T/G1764A double mutation was observed predominantly in genotype A strains. 2012 PloS one Introduction HBV G1764A;G1896A;A1762T 83;0;76 89;6;82 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Moreover, other studies reported no association between G1896A and clinical outcome. 2012 PloS one Introduction HBV G1896A 56 62 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Our previous study focused only on pre-C G1896A and G1899A mutations by using selective oligonucleotide hybridization, and showed a predominance of these variants. 2012 PloS one Introduction HBV G1896A;G1899A 41;52 47;58 Precore 35 40 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Recently, additional mutations in the pre-C and CP regions, including G1899A, C1653T, T1753V, C1766T and T1768A have become increasingly recognized to be associated with severe clinical outcome and HCC development. 2012 PloS one Introduction HBV G1899A;C1653T;T1753V;C1766T;T1768A 70;78;86;94;105 76;84;92;100;111 Core promoter;Precore 48;38 50;43 Hepatocellular carcinoma 198 201 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The clinical significance of G1896A mutation is unclear, with reports of its association with severe forms of liver disease and others of its occurrence in a large number of patients who had inactive liver disease. 2012 PloS one Introduction HBV G1896A 29 35 Liver disease;Liver disease 110;200 123;213 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The most common mutation involves a G A transition at position 1896 (G1896A), which creates a premature stop codon at codon 28, causing the termination of HBeAg translation without affecting the replicative ability of the virus. 2012 PloS one Introduction HBV G1896A 69 75 C 155 160 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The most frequent mutation is an A T substitution at nt 1762 combined with G A substitution at nt 1764 (A1762T/G1764A), which results in a decreased transcription of pre-C RNA by 50 to 70%, but enhanced viral replication in vitro . 2012 PloS one Introduction HBV G1764A;A1762T 111;104 117;110 Precore 166 171 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Finally, G145A was reported in one O-HBV infection of unknown genotype. 2012 Journal of viral hepatitis Introduction HBV G145A 9 14 HBV-HIV coinfections 35 50 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. K122R - which indicates a sub-serotype change from d to y - has also been identified in one genotype A O-HBV infection. 2012 Journal of viral hepatitis Introduction HBV K122R 0 5 HBV-HIV coinfections 101 118 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. M103I had been previously identified in 2 O-HBV infections, although these patients harbored genotype C or D. 2012 Journal of viral hepatitis Introduction HBV M103I 0 5 HBV infections 44 58 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Three O-HBV mutations - M103I, K122R, and G145A - from a genotype A infection were significant by signature pattern analysis. 2012 Journal of viral hepatitis Introduction HBV M103I;K122R;G145A 24;31;42 29;36;47 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. The two types of mutations related to clinical severity, the F141L preS2 mutation and W182* leading to premature termination in the HBV surface antigen (HBsAg), were recently noted in Korean chronic patients. 2012 PloS one Introduction HBV W182X;F141L 86;61 91;66 S;PreS2;S 153;67;136 158;72;143 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The basal core promoter (BCP) gene is a gene frequently changed in HBV as a double mutation (A1762T/G1764T) and has been found to be a codeterminant of HCC development and rapid disease progression in several populations. 2013 Annals of surgical oncology Introduction HBV G1764T;A1762T 100;93 106;99 BCP;BCP 4;25 23;28 Hepatocellular carcinoma 152 155 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The precore G1896A mutation results in a premature stop codon during transcription, thus preventing hepatitis B e antigen (HBeAg) synthesis. 2013 Annals of surgical oncology Introduction HBV G1896A 12 18 C;C;Precore 112;123;4 121;128;11 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The X gene mutations (two of the most common being C1653T and T1753V) and pre-S2 gene deletions have been associated with increased incidence of HCC. 2013 Annals of surgical oncology Introduction HBV C1653T;T1753V 51;62 57;68 PreS2;X 74;4 80;5 Hepatocellular carcinoma 145 148 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. A1762T/G1764A in liver tissue can independently predict postoperative survival. 2012 Hepatitis monthly Introduction HBV G1764A;A1762T 7;0 13;6 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. Another mutant, rtA181T, may arise during prolonged LAM therapy, conferring cross resistance to ADV. 2012 Hepatitis monthly Introduction HBV A181T 18 23 RT 16 18 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. As for other NAs, the rtN236T mutation is associated with ADV resistance. 2012 Hepatitis monthly Introduction HBV N236T 24 29 RT 22 24 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. C1653T, T1753V, A1762T/G1764A, T1674C/G, C1766T/T1768A, T53C, preS2 start codon mutation, preS1 deletion, C2964A, A2962G, C3116T, C7A, and their combinations are HBV mutations that are significantly associated with an increased risk of HCC occurrence. 2012 Hepatitis monthly Introduction HBV G1764A;T1768A;T1674G;C7A;C1653T;T1753V;A1762T;T1674C;C1766T;T53C;C2964A;A2962G;C3116T 23;48;31;130;0;8;16;31;41;56;106;114;122 29;54;39;133;6;14;22;39;47;60;112;120;128 PreS1;PreS2 90;62 95;67 Hepatocellular carcinoma 236 239 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. However, in the presence of rtM204I/V mutations, ETV resistance arose with the coexistence of rtI169T, rtL180M, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutations. 2012 Hepatitis monthly Introduction HBV M204I;M204V;T184A;T184F;T184G;T184I;T184L;T184S;S202G;S202I;I169T;L180M;M250V 30;30;114;114;114;114;114;114;133;133;96;105;147 37;37;129;129;129;129;129;129;140;140;101;110;152 RT;RT;RT;RT;RT;RT 28;94;103;112;131;145 30;96;105;114;133;147 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. Importantly, since the HBV S and polymerase genes overlap with each other, a great proportion of patients with the rtA181T mutation also carry the SW172 nonsense mutation, resulting in truncation of the preS/S reading frames, which significantly increases the risk of HCC during subsequent courses of NA therapy. 2012 Hepatitis monthly Introduction HBV A181T 117 122 P;PreS;S;RT;S 33;203;208;115;27 43;207;209;117;28 Hepatocellular carcinoma 268 271 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. The major TBV resistant mutant is rtM204I. 2012 Hepatitis monthly Introduction HBV M204I 36 41 RT 34 36 23166535 Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation. The most frequently encountered LAM-resistant mutation at the catalytic YMDD motif is rtM204V/I. 2012 Hepatitis monthly Introduction HBV M204V;M204I 88;88 95;95 RT;P 86;72 88;76 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. However, the effect of the rtA181T/sW172* mutation on HBV virology in vivo remains unclear. 2012 Virology journal Introduction HBV W172X;A181T 35;29 41;34 RT;S 27;35 29;36 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. In this study, a mouse model for the replication of the HBV rtA181T/sW172* mutant was established using a hydrodynamic-based procedure . 2012 Virology journal Introduction HBV W172X;A181T 68;62 74;67 RT;S 60;68 62;69 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Previous studies in vitro also demonstrated that the rtA181T/sW172* mutation may impair HBsAg secretion, and may be an oncogenic potential factor leading to advanced hepatocellular carcinoma (HCC) . 2012 Virology journal Introduction HBV W172X;A181T 61;55 67;60 S;RT;S 88;53;61 93;55;62 Hepatocellular carcinoma;Hepatocellular carcinoma 157;192 190;195 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. So it is thus necessary to study the biological characteristics of the HBV rtA181T/sW172* mutation in vivo environment. 2012 Virology journal Introduction HBV W172X;A181T 83;77 89;82 RT;S 75;83 77;84 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. The effect of the rtA181T/sW172* mutation on HBV transcription, replication and HBsAg secretion were investigated. 2012 Virology journal Introduction HBV W172X;A181T 26;20 32;25 S;RT;S 80;18;26 85;20;27 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. The HBV rtA181T/sW172* mutant strain researched in this study is that the rtA181T mutation in the viral polymerase encodes a stop codon in the overlapping surface gene at amino acid 172 (sW172) resulting in truncation of the last 55 amino acids of the C-terminal hydrophobic region of the surface proteins. 2012 Virology journal Introduction HBV W172X;A181T;A181T 16;10;76 22;15;81 P;RT;RT;S;S;S;S 104;8;74;16;187;155;289 114;10;76;17;188;162;296 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. The rtA181T mutation causes drug resistance to adefovir (ADV) clinically . 2012 Virology journal Introduction HBV A181T 6 11 RT 4 6 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. The rtA181T/sW172* mutation also reduces the typical extent of virological breakthrough . 2012 Virology journal Introduction HBV W172X;A181T 12;6 18;11 RT;S 4;12 6;13 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Among these, A1762T was almost accompanied with G1764A nucleotide acid substitution. 2012 Iranian journal of public health Introduction HBV A1762T;G1764A 13;48 19;54 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV mutations were often observed in the pre-C and basal core promoter (BCP) regions, such as T1753C, A1762T, G1764A, G1862T, G1896A and G1899A nucleotide acid substitution. 2012 Iranian journal of public health Introduction HBV T1753C;A1762T;G1764A;G1862T;G1896A;G1899A 94;102;110;118;126;137 100;108;116;124;132;143 BCP;BCP;Precore 51;72;41 70;75;46 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Hou and Ledesma described that A1762T/G1764A mutations were associated with chronic hepatitis B (CHB) with negative HBV e antigen (HBeAg). 2012 Iranian journal of public health Introduction HBV G1764A;A1762T 38;31 44;37 C;C 120;131 129;136 Chronic Hepatitis B;Chronic Hepatitis B 76;97 95;100 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. In this study, we randomly collected the sera of 160 CHB patients, 150 LC patients, and 156 HCC patients to investigate the risk factors that affect the progression of chronic HBV infection, including HBV genotypes/subgenotypes, A1762T/G1764A mutations, and some serologic markers. 2012 Iranian journal of public health Introduction HBV G1764A;A1762T 236;229 242;235 Chronic Hepatitis B;Hepatocellular carcinoma;Chronic HBV infection;Liver cirrhosis 53;92;168;71 56;95;189;73 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Meanwhile, the data is limited on the relationship among HBV genotypes/subgenotypes, A1762T/G1764A mutations and Clinicopathological characteristics in HCC patients. 2012 Iranian journal of public health Introduction HBV G1764A;A1762T 92;85 98;91 Hepatocellular carcinoma 152 155 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Studies suggested that genotype C infection could induce A1762T/G1764A mutations easier and it was related to LC and HCC, but no relationship with advanced liver disease (LC and HCC) was also reported. 2012 Iranian journal of public health Introduction HBV G1764A;A1762T 64;57 70;63 HBV infections;Hepatocellular carcinoma;Liver disease;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 23;117;156;178;171;110 43;120;169;181;173;112 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. Mutations at the BCP region such as A1762T/G1764A and T1753V were found in high prevalence (59.5% and 40.5%, respectively) and were associated with severe liver disease. 2013 Virology journal Introduction HBV G1764A;A1762T;T1753V 43;36;54 49;42;60 BCP 17 20 Liver disease 155 168 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. Several epidemiological studies have shown that HBV genotype D was predominant in the Tunisian population, and frequencies of double mutation A1762T /G1764A in BCP region and common mutation G1896A in PC region of viral B genome were higher among asymptomatic chronic carriers. 2012 Hepatitis monthly Introduction HBV G1764A;A1762T;G1896A 150;142;191 156;148;197 BCP;Precore 160;201 163;203 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Another common mutation is the G to A transition at nucleotide 1896 (G1896A) in the precore (PC) region. 2013 Journal of viral hepatitis Introduction HBV G1896A;G1896A 69;31 75;67 Precore;Precore 93;84 95;91 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. One of the most well known mutations in the HBV genome is the basal core promoter (BCP) double mutation that consists of the nucleotide substitution of A to T at position 1762 and of G to A at 1764 (A1762T/G1764A) in the core promoter region. 2013 Journal of viral hepatitis Introduction HBV G1764A;A1762T;A1762T;G1764A 206;199;152;183 212;205;175;197 BCP;BCP;Core promoter 62;83;221 81;86;234 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Several studies showed that two common mutations in the region encoding HBx, a nonstructural regulatory protein of HBV, include a nucleotide substitution from C to T at position 1653 (C1653T) of the enhancer II region and a substitution from T to V (C/A/G) at position 1753 (T1753V) of the core promoter region are associated with HCC development. 2013 Journal of viral hepatitis Introduction HBV C1653T;T1753V;C1653T 184;275;159 190;281;182 Core promoter;Enh II;X 290;199;72 303;210;75 Hepatocellular carcinoma 331 334 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. 2003 showed that PC WT virus (G1896) was significantly more prevalent in patients who cleared the virus (negative HBeAg) compared to the G1896A precore mutant which persisted in patients who developed HCC. 2013 The open virology journal Introduction HBV G1896A 137 143 C;Precore;Precore 114;17;144 119;19;151 Hepatocellular carcinoma 201 204 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. 2009 found that G1862T has no effect on HBeAg expression. 2013 The open virology journal Introduction HBV G1862T 16 22 C 40 45 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Among 52 FH patients, G1862T was detected in 7 patients (Table 3). 2013 The open virology journal Introduction HBV G1862T 22 28 Fulminant Hepatitis B 9 11 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1862T and G1896A Mutations. 2013 The open virology journal Introduction HBV G1862T;G1896A 0;11 6;17 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1862T was also implicated in reducing DNA replication severely. 2013 The open virology journal Introduction HBV G1862T 0 6 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1899A mutations increased DNA replication but the double mutation G1899A/G1862T was associated with considerably more replication compared to G1862T alone. 2013 The open virology journal Introduction HBV G1862T;G1899A;G1899A;G1862T 74;0;67;143 80;6;73;149 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. In a study of in vitro translation, G1862T mutation abolished precore/core proteins synthesis but not entirely impaired. 2013 The open virology journal Introduction HBV G1862T 36 42 C;Precore 70;62 74;69 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Interestingly, U:G pair is converted into U:A in the lower stem (epsilon) in the two positions 1855/1899 if HBV strain possesses G1899A mutation. 2013 The open virology journal Introduction HBV G1899A 129 135 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. PC mutation (G1896A) prevents HBeAg precursor translation whereas T1762/A1764 core mutation interfered with core mRNAs transcription leading to suppressed HBeAg synthesis and was associated with high replication phenotype. 2013 The open virology journal Introduction HBV G1896A 13 19 C;C;C;C;Precore 78;108;30;155;0 82;112;35;160;2 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. the bulge of epsilon signal is affected by G1862T mutation. 2013 The open virology journal Introduction HBV G1862T 43 49 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. The G1896A precore stop codon mutation at the codon 28 decreased HBV replication if paired with T1858 mutation. 2013 The open virology journal Introduction HBV G1896A 4 10 Precore 11 18 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Using western blot analysis, core protein expression was reduced by G1862T mutation. 2013 The open virology journal Introduction HBV G1862T 68 74 C 29 33 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Pretreatment mutations (such as T38A, Y124H, D134E, N139K/H, I224V, and R242A) were defined as amino acid substitutions that have been reported among NA-naive patients but their relationships with antiviral resistance development have not been clarified yet. 2013 Virology journal Introduction HBV T38A;Y124H;D134E;N139K;N139H;I224V;R242A 32;38;45;52;52;61;72 36;43;50;59;59;66;77 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Recently, HBVrt domain mutations which have been reported in the literature as supposed drug resistant mutations but are not verified experimentally were classified as putative NA resistant (NAr) mutations (such as S53N, T54N, L82M, V84M, S85A, I91L, Y126C, T128I, T128N, N139D, W153Q, F166L). 2013 Virology journal Introduction HBV S53N;T54N;L82M;V84M;S85A;I91L;Y126C;T128I;T128N;N139D;W153Q;F166L 215;221;227;233;239;245;251;258;265;272;279;286 219;225;231;237;243;249;256;263;270;277;284;291 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. It has been documented that rtI233V mutation occurs in approximately 2% of treatment-naive chronic hepatitis B virus carriers . 2013 Bioinformation Introduction HBV I233V 30 35 RT 28 30 Chronic Hepatitis B 91 110 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Some studies have shown rtI233V mutation to be associated with adefovir resistance . 2013 Bioinformation Introduction HBV I233V 26 31 RT 24 26 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The primary adefovir-resistant mutations significantly associated with treatment failure are rtN236T and rtA181T/V . 2013 Bioinformation Introduction HBV A181T;A181V;N236T 107;107;95 114;114;100 RT;RT 93;105 95;107 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The role of rtI233V mutation and adefovir response remains contradictory. 2013 Bioinformation Introduction HBV I233V 14 19 RT 12 14 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. We attempted to study the impact of this putative rtI233V substitution and adefovir binding by molecular modeling and docking studies. 2013 Bioinformation Introduction HBV I233V 52 57 RT 50 52 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. We have previously reported the putative rtI233V mutation in 4 treatment-naive subjects. 2013 Bioinformation Introduction HBV I233V 43 48 RT 41 43 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Exchange of Gly2 to Ala (G2A) disrupts the myristoylation motif Met-Gly recognized by N-myristoyl transferase and this mutation was introduced in an expression vector for generation of L protein deletion variants without a myristoylation signal. 2013 Virology journal Introduction HBV G2A;G2A 25;12 28;23 S 185 194 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. For example, the triple mutation in HBV polymerase rtV173L+rtL180M+rtM204V, associated with lamivudine drug resistance, confers changes to the envelope gene because of overlapping reading frames that result in an HBV vaccine escape phenotype while compensating for the loss in viral fitness. 2013 Journal of virological methods Introduction HBV V173L;L180M;M204V 53;61;69 58;66;74 S;P;RT;RT;RT 143;40;51;59;67 151;50;53;61;69 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Furthermore, this combination of mutations also alters the overlapping envelope reading frame causing surface antigen (HBsAg) mutations E164D and I195M, which confer a vaccine escape phenotype. 2013 Journal of virological methods Introduction HBV E164D;I195M 136;146 141;151 S;S;S 71;119;102 79;124;109 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Given the current limitations of existing minority variant assessment techniques and the importance of identifying of multiple mutations on the same genome, it was important to create a highly sensitive and specific, rapid, and inexpensive assay to detect minority variant viral quasispecies of the drug resistant/vaccine escape triple mutant rtV173L+rtM204V+rtL180M directly from clinical samples. 2013 Journal of virological methods Introduction HBV V173L;M204V;L180M 345;353;361 350;358;366 RT;RT;RT 343;351;359 345;353;361 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Recent data suggests a threshold of 2000 copies/mL of the K103N mutation predicts failure of efavirenz containing regimens. 2013 Journal of virological methods Introduction HBV K103N 58 63 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. The primary lamivudine resistance mutation, rtM204V in the HBV polymerase, reduces replicative capacity, but additional mutations rtV173L and rtL180M are associated with compensated fitness. 2013 Journal of virological methods Introduction HBV L180M;M204V;V173L 144;46;132 149;51;137 P;RT;RT;RT 63;44;130;142 73;46;132;144 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. Long term usage of lamivudine leads to development of drug resistance which is mainly associated with mutations in the YMDD motifs, substitution of methionine by either valine (rtM204I) or isoleucine (rtM204I) in the tyrosine-methionine-aspartate-aspartate (YMDD) motif of the HBV polymerase C domain. 2013 Iranian journal of microbiology Introduction HBV M204I;M204I 179;203 184;208 P;RT;RT;P;P;P 281;177;201;217;119;258 291;179;203;256;123;262 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. The rtL180M mutation may occur concurrently with YMDD mutations and serves as a compensation for better replication fitness. 2013 Iranian journal of microbiology Introduction HBV L180M 6 11 RT;P 4;49 6;53 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. Two mutations of A1762T and G1764A reported as the most prevalent mutations in the basal core region and described in different stages of HBV infection. 2013 Hepatitis monthly Introduction HBV A1762T;G1764A 17;28 23;34 C 89 93 HBV infections 138 151 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Interestingly, resistance to ETV includes LAM resistance mutations, rtM250V+-rtI169T+rtM204V+rtL180M and rtT184G+rtS202I+rtM204V+rtL180M. 2013 Gut and liver Introduction HBV M250V;I169T;M204V;L180M;M204V;L180M;T184G;S202I 70;79;87;95;123;131;107;115 75;84;92;100;128;136;112;120 RT;RT;RT;RT;RT;RT;RT;RT 68;77;85;93;105;113;121;129 70;79;87;95;107;115;123;131 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The main mutation associated with LAM resistance is rtM204I/V. 2013 Gut and liver Introduction HBV M204I;M204V 54;54 61;61 RT 52 54 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The rtL180M mutation is the most common compensatory mutation, contributing to increasing either replication efficiency and/or antiviral resistance. 2013 Gut and liver Introduction HBV L180M 6 11 RT 4 6 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. In addition, study of C1653T, T1753V, G1899A, and other mutations in the enhII/BCP/precore regions has just begun. 2013 Brazilian journal of medical and biological research Introduction HBV C1653T;T1753V;G1899A 22;30;38 28;36;44 BCP;Enh II;Precore 79;73;83 82;78;90 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Multiple mutations have been identified in the enhII/BCP/precore regions, of which the BCP mutations (A1762T/G1764A) and the precore stop codon mutation (G1896A) have been extensively studied. 2013 Brazilian journal of medical and biological research Introduction HBV G1764A;A1762T;G1896A 109;102;154 115;108;160 BCP;BCP;Enh II;Precore;Precore 53;87;47;57;125 56;90;52;64;132 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The A1762T/G1764A mutations are associated with severe liver disease, including liver failure, LC, and HCC, and are considered potential biomarkers for HCC ~9. 2013 Brazilian journal of medical and biological research Introduction HBV G1764A;A1762T 11;4 17;10 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 55;103;152;95 68;106;155;97 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The G1896A mutation correlates with increased risk of HCC in a newly updated meta-analysis. 2013 Brazilian journal of medical and biological research Introduction HBV G1896A 4 10 Hepatocellular carcinoma 54 57 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. ALT levels in the serum of HBsAg positive, HBeAg negative, and HBV DNA detectable patients infected with the wild-type HBV was 43.7 +- 36.0 IU/L (mean +- SD) compared with 91.6 +- 67.3 IU/L in the serum of the patients with precore G1896A mutant HBV infection. 2009 Brazilian journal of microbiology Introduction HBV G1896A 232 238 C;S;Precore 43;27;224 48;32;231 HBV infections 246 259 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Among the 200 inactive HBV carriers, 176 (88%) were pre-S1 antigen negative (108 with undetectable HBV DNA, 56 with wild-type precore sequence, and 12 with precore G1896A mutation (Table 3). 2009 Brazilian journal of microbiology Introduction HBV G1896A 164 170 Precore;Precore;PreS1 126;156;52 133;163;58 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Among the 48 pre-S1 antigen negative patients with HBeAg-negative CHB, 16 (33.3%) had precore G1896A mutation. 2009 Brazilian journal of microbiology Introduction HBV G1896A 94 100 C;Precore;PreS1 51;86;13 56;93;19 Chronic Hepatitis B 66 69 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. However, of the 224 patients with serum negative pre-S1 antigen, only 28 (12.5%) had precore G1896A mutation. 2009 Brazilian journal of microbiology Introduction HBV G1896A 93 99 Precore;PreS1 85;49 92;55 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. In conclusion, the prevalence of precore G1896A mutation in HBeAg-negative CHB patients is much higher than that in inactive HBV carriers. 2009 Brazilian journal of microbiology Introduction HBV G1896A 41 47 C;Precore 60;33 65;40 Chronic Hepatitis B 75 78 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. In the present study, we examined the prevalence of naturally occurring HBV precore G1896A mutation in Chinese patients with HBeAg-negative HBV infection. 2009 Brazilian journal of microbiology Introduction HBV G1896A 84 90 C;Precore 125;76 130;83 HBV infections 140 153 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Jardi et al reported that among HBeAg negative CHB, patients with precore G1896A mutation and elevated ALT showed highest HBV DNA, and simultaneous presence of the main BCP and precore mutations was associated with the degree of histological injury. 2009 Brazilian journal of microbiology Introduction HBV G1896A 74 80 BCP;C;Precore;Precore 169;32;66;177 172;37;73;184 Chronic Hepatitis B 47 50 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Moreover, serum pre-S1 antigen is more often detected in patients with precore G1896A mutation. 2009 Brazilian journal of microbiology Introduction HBV G1896A 79 85 Precore;PreS1 71;16 78;22 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Most patients with precore G1896A had detectable serum pre-S1 antigen. 2009 Brazilian journal of microbiology Introduction HBV G1896A 27 33 Precore;PreS1 19;55 26;61 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Of the 272 patients with serum positive pre-S1 antigen, 248 (91.2%) had precore G1896A mutation. 2009 Brazilian journal of microbiology Introduction HBV G1896A 80 86 Precore;PreS1 72;40 79;46 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Of the 296 patients with HBeAg negative CHB, serum pre-S1 antigen and precore G1896A mutation were simultaneously detected in 232 (78.4%) patients. 2009 Brazilian journal of microbiology Introduction HBV G1896A 78 84 C;Precore;PreS1 25;70;51 30;77;57 Chronic Hepatitis B 40 43 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Of the 380 patients with detectable HBV DNA, 276 patients (72.6%) had precore G1896A mutation. 2009 Brazilian journal of microbiology Introduction HBV G1896A 78 84 Precore 70 77 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Our results showed that precore G1896A mutation does exist in inactive HBV carriers with detectable serum HBV DNA. 2009 Brazilian journal of microbiology Introduction HBV G1896A 32 38 Precore 24 31 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Our results showed that the overall prevalence of precore G1896A mutation in Chinese HBeAg-negative, serum HBV DNA detectable population was 72.6%. 2009 Brazilian journal of microbiology Introduction HBV G1896A 58 64 C;Precore 85;50 90;57 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Patients with precore G1896A mutation have significantly higher serum HBV DNA and ALT levels than those with wild-type virus infection. 2009 Brazilian journal of microbiology Introduction HBV G1896A 22 28 Precore 14 21 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Precore G1896A mutants were found in 248 (83.8%) of 296 patients with CHB, while only 28 (33.3%) of 84 inactive HBV carriers with detectable HBV DNA had precore G1896A mutation (Table 2). 2009 Brazilian journal of microbiology Introduction HBV G1896A;G1896A 8;161 14;167 Precore;Precore 0;153 7;160 Chronic Hepatitis B 70 73 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. Precore G1896A mutation was more frequent in patients with fulminant than acute self-limited hepatitis and was independently associated with the fulminant outcome. 2009 Brazilian journal of microbiology Introduction HBV G1896A 8 14 Precore 0 7 Acute Hepatitis B 74 102 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The G1896A mutation is found predominantly in HBV genotypes B, C, and D, due to a genotype-specific nucleotide difference upstream from rt1896 that can critically alter the secondary conformation of the HBV encapsidation signal. 2009 Brazilian journal of microbiology Introduction HBV G1896A 4 10 RT 136 138 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The G1896A precore mutation was detected by a molecular-beacon assay described by Wartz et al. 2009 Brazilian journal of microbiology Introduction HBV G1896A 4 10 Precore 11 18 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The influence of precore G1896A and basal core promoter mutations on the virulence of HBV infection remains controversial. 2009 Brazilian journal of microbiology Introduction HBV G1896A 25 31 BCP;Precore 36;17 55;24 HBV infections 86 99 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The median prevalence of the G1896A mutation in HBeAg-negative patients is 50% in Asia, 92% in the Mediterranean, and 24% in America. 2009 Brazilian journal of microbiology Introduction HBV G1896A 29 35 C 48 53 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The percentage of the precore G1896A mutant in total virus is negatively associated with HBV DNA and ALT. 2009 Brazilian journal of microbiology Introduction HBV G1896A 30 36 Precore 22 29 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The prevalence of G1896A mutation is significantly higher in HBeAg-negative patients with CHB than in HBeAg-negative inactive carriers. 2009 Brazilian journal of microbiology Introduction HBV G1896A 18 24 C;C 61;102 66;107 Chronic Hepatitis B 90 93 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. The prevalence of precore G1896A mutation varies geographically and depends on the genotypes of HBV. 2009 Brazilian journal of microbiology Introduction HBV G1896A 26 32 Precore 18 25 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. These results support the suggestion that precore G1896A mutation may lead to evade immune clearance of the virus. 2009 Brazilian journal of microbiology Introduction HBV G1896A 50 56 Precore 42 49 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. A glycine to lysine point mutation at position 145 (sG145K) or a threonine to methionine substitution at position 118 (sT118M) has also been detected, and both mutations have been reported to significantly change the antigenic profile of HBsAg compared with that of wild type . 2013 Virology journal Introduction HBV G145K;T118M;G145K;T118M 52;119;2;65 58;125;50;117 S;S;S 238;52;119 243;53;120 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Although substitutions outside of the 'a' determinant appear to be readily detected by current commercially available HBsAg immunoassays, there is limited information as to the combined effects of immune-escaped (T118M, G145K, G145R) and drug-resistant (rtM204I = sI195M, rtM204V = sW196S) point mutations on the antigenicity profiles of HBsAg. 2013 Virology journal Introduction HBV M204I;M204V;I195M;W196S;T118M;G145K;G145R 256;274;264;282;213;220;227 261;279;270;288;218;225;232 S;S;S;RT;RT;S;S 39;118;338;254;272;264;282 53;123;343;256;274;265;283 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. An amino acid change from glycine to arginine at position 145 (sG145R) for the immunodominant determinant of HBsAg, which alone can be responsible for vaccine escape, is most commonly reported and has been well documented . 2013 Virology journal Introduction HBV G145R;G145R 63;26 69;61 S;S 109;63 114;64 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Interestingly, because of the overlap of the open reading frame (ORF) S for the HBsAg and ORF P for viral polymerase, rtM204I and rtM204V mutations produce sI195M and sW196S in the HBsAg . 2013 Virology journal Introduction HBV M204I;M204V;I195M;W196S 120;132;156;167 125;137;162;173 S;S;P;P;RT;RT;S;S;S 80;181;94;106;118;130;70;156;167 85;186;95;116;120;132;71;157;168 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The substitution of methionine by isoleucine (I) or valine (V) in the tyrosine-methionine-aspartate-aspartate (YMDD) motif (C domain) at position 204 (rtM204I or rtM204V) has been shown to confer lamivudine resistance on HBV . 2013 Virology journal Introduction HBV M204I;M204V 153;164 158;169 RT;RT;P;P 151;162;70;111 153;164;109;115 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. According to previously studies, the patterns of genotypic resistance in the HBV polymerase can be categorized into five specific evolutionary pathways, including L-nucleoside pathway (rtM204I [or V or I/V]), the acyclic phosphonate pathway (rtN236T), the shared pathway (rtA181T [or V or T/V]) of both L-nucleoside and acyclic phosphonate, ETV resistance pathway (rtL180M+rtM204V with one of either rtT184, S202 or M250 residue changes) and multidrug resistance pathways (rtA181T+rtI233V+rtN236T+rtM250L). 2013 Virology journal Introduction HBV A181T;M204I;N236T;L180M;M204V;N236T;A181T;I233V;M250L 274;187;244;367;375;491;475;483;499 279;192;249;372;380;496;480;488;504 P;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 81;185;242;272;365;373;400;473;481;489;497 91;187;244;274;367;375;402;475;483;491;499 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. In this study, the association of serum TLR2 with clinical findings in chronic hepatitis B patients especially in patients with G1896A stop codon mutation has been investigated. 2013 Advances in virology Introduction HBV G1896A 128 134 Chronic Hepatitis B 71 90 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Also, genotypes B, T1753V, and G1899A were more frequently found in ACLF patients than CHB patients. 2013 Hepatitis monthly Introduction HBV T1753V;G1899A 19;31 25;37 Acute on chronic liver failure;Chronic Hepatitis B 68;87 72;90 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In addition, the mutation in the basic core promoter (BCP), such as double mutation A1762T/G1764A, has been found to enhance HBV replication in vitro. 2013 Hepatitis monthly Introduction HBV G1764A;A1762T 91;84 97;90 BCP;BCP 33;54 52;57 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In comparison with CHB patients, liver cirrhosis (LC) patients have more frequent mutations in BCP/PC region such as A1762T/G1764A, T1753V, and/or G1896A. 2013 Hepatitis monthly Introduction HBV G1764A;A1762T;T1753V;G1896A 124;117;132;147 130;123;138;153 BCP;Precore 95;99 98;101 Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 19;33;50 22;48;52 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. The mutations in the precore region (PC), such as G1896A, generated a stop codon and halt translation of HBeAg. 2013 Hepatitis monthly Introduction HBV G1896A 50 56 C;Precore;Precore 105;37;21 110;39;28 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. A combination of mutations in the B, C, or D domain, such as rtI169T, rtM250I/V, and a background of rtM204V/I confer resistance to ETV. 2013 Hepatitis monthly Introduction HBV M250I;M250V;M204V;M204I;I169T 72;72;103;103;63 79;79;110;110;68 RT;RT;RT 61;70;101 63;72;103 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Although rtQ267H only led to slight resistance to LMV and LdT, enhanced HBV replication, aggravated existing LMV-resistance, and was proved to be another adaptive mutation of LMV, except rtL180M and rtV173L. 2013 Hepatitis monthly Introduction HBV Q267H;L180M;V173L 11;189;201 16;194;206 RT;RT;RT 9;187;199 11;189;201 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Among them, rtQ267H was found to be closely related to LMV therapy. 2013 Hepatitis monthly Introduction HBV Q267H 14 19 RT 12 14 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. In vitro analysis demonstrated that rtQ267H, rtM204V/Q267H, rtL180M/M204V, and rtL180M/M204V/Q267H resulted in 1.41-, 24.96-, 27.43, and 30.76-fold increases in resistance toward LMV, and 1.86-, 7.28-, 7.17- and 8.93-fold increases in resistance toward LdT, respectively. 2013 Hepatitis monthly Introduction HBV Q267H;M204V;Q267H;M204V;L180M;Q267H;M204V;L180M 53;68;93;87;62;38;47;81 58;73;98;92;67;43;52;86 RT;RT;RT;RT 36;45;60;79 38;47;62;81 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Mutations rtP177G and rtF249A predicted by computer were reported lately to confer resistance to TDF both in vivo and in vitro. 2013 Hepatitis monthly Introduction HBV P177G;F249A 12;24 17;29 RT;RT 10;22 12;24 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtA181V/T and/or rtN236T can reduce the anti-HBV effect of ADV, rtN238R, rtT240Y and rtN248H of HBV were newly reported to decrease susceptibility to ADV (8). 2013 Hepatitis monthly Introduction HBV A181V;A181T;N236T;N248H;N238R;T240Y 15;15;32;100;79;88 22;22;37;105;84;93 RT;RT;RT;RT;RT 13;30;77;86;98 15;32;79;88;100 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtA194T was reported to be a TDF resistance mutation which needs further confirmation. 2013 Hepatitis monthly Introduction HBV A194T 15 20 RT 13 15 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The most common resistance mutations to LMV and LdT are rtM204I/V, located at the YMDD motif within the C domain of RT, usually accompanied with compensatory mutations of rtL180M and/or rtV173L to restore HBV replication capacity. 2013 Hepatitis monthly Introduction HBV M204I;M204V;L180M;V173L 58;58;173;188 65;65;178;193 RT;RT;RT;RT;P 56;116;171;186;82 58;118;173;188;86 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. The most common mutation involved substitution of methionine for valine or isoleucine rtM204V/I. 2014 Hepatitis monthly Introduction HBV M204V;M204I 88;88 95;95 RT 86 88 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Compensatory mutations rtL180M, rtV173L, and rtL80I to LAM are often co-selected to restore viral replication efficacy. 2014 PloS one Introduction HBV L80I;L180M;V173L 47;25;34 51;30;39 RT;RT;RT 23;32;45 25;34;47 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Signature LAM resistance mutations have been mapped to the tyrosine-methionine-aspartate-aspartate (YMDD) locus in the catalytic or C domain of HBV reverse transcriptase (RT) region, and the primary resistance mutations are isoleucine (I), valine (V), or occasionally serine (S) that were designated rtM204I/V/S. 2014 PloS one Introduction HBV M204I;M204V;M204S 302;302;302 311;311;311 RT;RT;RT;S;P;P 148;171;300;276;59;100 169;173;302;277;98;104 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204I also confers cross-resistance to LdT. 2014 PloS one Introduction HBV M204I 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. This study aimed to clarify whether a newly-found rtM204Q mutant from patients was associated with drug resistance. 2014 PloS one Introduction HBV M204Q 52 57 RT 50 52 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Additional functional studies of these mutations revealed transforming activities in all 3 mutations, especially the nonsense mutation at the codon for tryptophane182 (sW182*). 2014 PloS one Introduction HBV W182X 168 174 S 168 169 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. Methionine substituted by valine or isoleucine in codon 204 (i.e., rtM204V/I) were confirmed to confer resistance to LMV. 2014 PloS one Introduction HBV M204V;M204I 69;69 76;76 RT 67 69 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. The rtM204I can not only cause the selection of Lamivudine and Telbivudine resistance, but can also lead to Entecavir-resistance. 2014 PloS one Introduction HBV M204I 6 11 RT 4 6 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. For example, the classical A1762T/G1764A double mutation within the basal core promoter (nt 1742-1849 from EcoRI site) and the G1896A mutation in the precore (PC) (nt 1814-1900 from EcoRI site) region are often reported to be associated with advanced liver diseases including liver cirrhosis and HCC in HBV mono-infection. 2014 PloS one Introduction HBV G1764A;A1762T;G1896A 34;27;127 40;33;133 BCP;Precore;Precore 68;159;150 87;161;157 Liver disease;Liver cirrhosis;Hepatocellular carcinoma;HBV infections 251;276;296;303 265;291;299;321 24693312 The Effect of HBV Genotype C on the Development of HCC Differs Between Wild-Type Viruses and Those With BCP Double Mutations (T(1762)A(1764)). Some mutations in HBV genome such as G1896A, C1653T, T1753V, the BCP double mutations (T1762A1764), and pre-S region deletions have been reported to be associated with HCC development. 2014 Hepatitis monthly Introduction HBV G1896A;C1653T;T1753V 37;45;53 43;51;59 BCP;PreS 65;104 68;109 Hepatocellular carcinoma 168 171 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A recent meta-analysis including a total of 11,582 HBV-infected participants revealed that deletions in the pre-S gene and mutations of C1653T, T1753V and A1762T/G1764A in the basal core promoter (BCP)/enhancer II (EnhII) region had statistically significant summary odds ratios (OR) for HCC. 2014 PloS one Introduction HBV G1764A;C1653T;T1753V;A1762T 162;136;144;155 168;142;150;161 BCP;BCP;Enh II;Enh II;PreS 176;197;202;215;108 195;200;213;220;113 Hepatocellular carcinoma;HBV infections 288;51 291;63 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. For example, resistance to lamivudine and telbivudine is conferred by mutation rtM204V or rtM204I in the YMDD motif, and this is often associated with compensatory mutations rtL180M and/or rtV173L restoring a higher replication capacity. 2014 PloS one Introduction HBV M204V;M204I;L180M;V173L 81;92;176;191 86;97;181;196 RT;RT;RT;RT;P 79;90;174;189;105 81;92;176;191;109 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. In addition, A2159G and A2189C in the core gene and G1896A and G1899A in the pre-C gene have also been reported to increase the risk of HCC. 2014 PloS one Introduction HBV A2159G;A2189C;G1896A;G1899A 13;24;52;63 19;30;58;69 C;Precore 38;77 42;82 Hepatocellular carcinoma 136 139 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Over the past few years, we defined that a high prevalence of the HBV C1 genotype, pre-S deletion and pre-S2 start codon mutation, C1653T, T1753A/G, C1766T, and T1768A mutations in the BCP/EnhII region, and A2159G, A2189C, and G2203W in the core gene are associated with HCC in Qidong. 2014 PloS one Introduction HBV T1753G;C1653T;T1753A;C1766T;T1768A;A2159G;A2189C;G2203W 139;131;139;149;161;207;215;227 147;137;147;155;167;213;221;233 BCP;C;Enh II;PreS;PreS2 185;241;189;83;102 188;245;194;88;108 Hepatocellular carcinoma 271 274 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. Mutation profiles emerged during LAM therapy was associated with clinical outcome of rescue therapy and rtM204I were associated with favorable outcome during ADV rescue therapy in several reports. 2015 Gut and liver Introduction HBV M204I 106 111 RT 104 106 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. A dual mutation in the basal core promoter (BCP) region of the HBV genome involving an A-T substitution at nucleotide 1762 and a G-A substitution at nucleotide 1764 has been associated with HCC development. 2014 Hepatitis monthly Introduction HBV A1762T;G1764A 87;129 122;164 BCP;BCP 23;44 42;47 Hepatocellular carcinoma 190 193 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. Another common mutation is a double mutation in BCP region (A1762T/G1764A), which aborts the transcription of precore mRNA, but does not seriously affect the viral pregenome RNA, resulting in a decrease of HBeAg expression up to 70% and enhanced viral genome replication. 2014 Hepatitis monthly Introduction HBV G1764A;A1762T 67;60 73;66 BCP;C;Precore 48;206;110 51;211;117 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. Moreover, a mutation in the precore (PC) region of the HBV genome involving a G-A substitution at nucleotide 1896 has been described in HBeAg-negative patients. 2014 Hepatitis monthly Introduction HBV G1896A 78 113 C;Precore;Precore 136;37;28 141;39;35 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Recently, through a molecular epidemiological study, we discovered novel preS1 substitutions (W4P) related to HCC, in which tryptophan changed to proline at the fourth codon from the preS1 start. 2015 Molecular cancer Introduction HBV W4P 94 97 PreS1;PreS1 73;183 78;188 Hepatocellular carcinoma 110 113 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Therefore, we hypothesize that the LHB variant with a W4P mutation may contribute to the male predominance in HCC. 2015 Molecular cancer Introduction HBV W4P 54 57 S 35 38 Hepatocellular carcinoma 110 113 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. To address the hypothesis, we investigated whether an LHB variant with a W4P mutation from an HCC patient would exhibit gender disparity in tumorigenicity. 2015 Molecular cancer Introduction HBV W4P 73 76 S 54 57 Hepatocellular carcinoma 94 97 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. In addition, clinical and mechanistic importance of pre-core mutations are unclear; especially G1896A, which results in a premature stop codon and termination of HBeAg translation, but does not seem to affect viral replication. 2015 Hepatitis monthly Introduction HBV G1896A 95 101 C;Precore 162;52 167;60 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. G1896A and the A1762T and G1764A double mutation are the most frequent isolated mutations in the precore and basal core promoter (BCP) regions of the HBV genome isolated from HBeAg-negative patients. 2015 PloS one Introduction HBV G1896A;A1762T;G1764A 0;15;26 6;21;32 BCP;BCP;C;Precore 109;130;175;97 128;133;180;104 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The mutation G1896A creates a premature stop codon (28th codon) that prevents the production of HBeAg, and the A1762T and G1764A double mutation in the BCP region can reduce the synthesis of HBeAg and enhance viral replication. 2015 PloS one Introduction HBV G1896A;A1762T;G1764A 13;111;122 19;117;128 BCP;C;C 152;96;191 155;101;196 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. Based on the stability of the encapsidation signal (nt 1847-1907) it has been established that genotypes carrying 1858T (B, C2, C3, D, E, F1 and F4) favor the emergence and selection of G1896A, whereas the double mutation A1762T/G1764A in the BCP is more prone to occur in those genotypes carrying 1858C (A, C1, F2, F3 and H). 2015 PloS one Introduction HBV G1764A;G1896A;A1762T 229;186;222 235;192;228 BCP 243 246 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. In this study, the G1896A precore mutation and its effect on HBeAg detection were investigated in chronic HBV patients, using polymerase chain reaction (PCR) and subsequent sequencing method, rather than the restriction fragment length polymorphism (RFLP), because of improving the sensitivity of the detection. 2015 Jundishapur journal of microbiology Introduction HBV G1896A 19 25 C;Precore 61;26 66;33 Chronic Hepatitis B 98 109 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. The most common of these mutations is a guanine (G) to adenine (A) substitution at nucleotide1896, which prevents the production of HBeAg by introducing a premature stop codon into the open reading frame (ORF) of the PC. 2015 Jundishapur journal of microbiology Introduction HBV G1896A 39 98 C;Precore 132;217 137;219 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. The predominant mutation involves a GtoA change at nucleotide1896 (A1896), which creates a premature stop codon at codon 28. 2015 Jundishapur journal of microbiology Introduction HBV G1896A 36 65 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. We and others have reported that HBV mutations C1653T, T1753V, A1762T/G1764A, T1674C/G, and C1766T/T1768A in the enhancer II/basal core promoter (EnhII/BCP) region; G1899A, C2002T, A2159G, A2189C, and G2203A/T in the precore/core region; as well as T53C, preS2 start codon mutation, preS1 deletion, C2964A, A2962G, C3116T, and C7A in the preS region of HBV genome are significantly associated with an increased risk of HCC. 2015 Chinese medical journal Introduction HBV G1764A;T1768A;T1674G;G2203T;C7A;C1653T;T1753V;A1762T;T1674C;C1766T;G1899A;C2002T;A2159G;A2189C;G2203A;T53C;C2964A;A2962G;C3116T 70;99;78;201;327;47;55;63;78;92;165;173;181;189;201;249;299;307;315 76;105;86;209;330;53;61;69;86;98;171;179;187;195;209;253;305;313;321 BCP;BCP;C;Enh II;Enh II;Precore;PreS;PreS1;PreS2 125;152;225;113;146;217;338;283;255 144;155;229;124;151;224;342;288;260 Hepatocellular carcinoma 419 422 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The HBc particle introducing the R154G mutation showed a drastic decrease in all capacities of cellular uptake for HeLa, NuE and A431 cells. 2015 Journal of nanobiotechnology Introduction HBV R154G 33 38 C 4 7 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. They include rtA181V/T and rtN236T. 2015 International journal of medical sciences Introduction HBV A181V;A181T;N236T 15;15;29 22;22;34 RT;RT 13;27 15;29 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. This may be attributed to an ADV-resistant variant, rtA181V/T, which is responsible for cross-resistance to LAM and ADV. 2015 International journal of medical sciences Introduction HBV A181V;A181T 54;54 61;61 RT 52 54 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. However, certain HBV variants that acquired 3TC-associated amino acid substitutions such as M204V and L180M (HBVM204V and HBVL180M/M204V) are less susceptible to ETV by factors of 20 to 30 and tend to develop high levels of ETV resistance. 2015 Hepatology (Baltimore, Md.) Introduction HBV M204V;M204V;L180M 131;92;102 136;97;107 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. Those harboring HBVM204V, and/or HBVL180M/M204V are, therefore, recommended to receive TDF or ADV; however, a long-term treatment with TDF or ADV has been associated with certain adverse effects such as renal toxicity. 2015 Hepatology (Baltimore, Md.) Introduction HBV M204V;L180M 42;35 47;41 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. M204V/I mutations associated with LMV and LdT resistance also confer cross-resistance to other L-nucleosides and reduce sensitivity to ETV (but not to ADV or TDF). 2015 BMC complementary and alternative medicine Introduction HBV M204V;M204I 0;0 7;7 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. The L80V/I mutation was first detected in patients with severe hepatitis after apparent LMV failure. 2015 BMC complementary and alternative medicine Introduction HBV L80V;L80I 4;4 10;10 Hepatitis 63 72 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. The most common mutation associated with LMV resistance is the substitution of methionine 204 with isoleucine, valine, or serine (M204I/V/S) at the YMDD active site motif within the P protein RT domain. 2015 BMC complementary and alternative medicine Introduction HBV M204I;M204V;M204S 130;130;130 139;139;139 P;RT;P 182;192;148 183;194;152 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. An in vitro drug susceptibility assay demonstrated the association of similar mutations, namely rtA194T, rtL181T/V, and/or rtN236T, with TDF resistance. 2015 PloS one Introduction HBV L181T;L181V;A194T;N236T 107;107;98;125 114;114;103;130 RT;RT;RT 96;105;123 98;107;125 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Finally, the clinical relevance of the rtL269I substitution was investigated. 2015 PloS one Introduction HBV L269I 41 46 RT 39 41 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Genotypic analyses have revealed that rtN236T and/or rtA181T/V mutations confer ADV resistance. 2015 PloS one Introduction HBV N236T;A181T;A181V 40;55;55 45;62;62 RT;RT 38;53 40;55 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In addition, a molecular modeling study suggested that the rtL269I substitution affects replication. 2015 PloS one Introduction HBV L269I 61 66 RT 59 61 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. On the other hand, rtL229V behaved as a compensatory mutation to rescue replication of the rtM204I mutant. 2015 PloS one Introduction HBV L229V;M204I 21;93 26;98 RT;RT 19;91 21;93 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The most common mutation during viral breakthrough in CLV-failure patients is rtM204I. 2015 PloS one Introduction HBV M204I 80 85 RT 78 80 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The primary mutation conferring LMV resistance is rtM204I/V in the YMDD motif. 2015 PloS one Introduction HBV M204I;M204V 52;52 59;59 RT;P 50;67 52;71 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The well-characterized compensatory mutations include rtL180M, rtL80I/V, and rtV173L; they enhance replication of the rtM204I/V mutants. 2015 PloS one Introduction HBV L80I;L80V;M204I;M204V;L180M;V173L 65;65;120;120;56;79 71;71;127;127;61;84 RT;RT;RT;RT 54;63;77;118 56;65;79;120 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. They include rtI169T, rtL180M, rtS184S/A/I/L/G/C/M, M204I/V, rtS202G/I, and rtM250I/V. 2015 PloS one Introduction HBV S184S;S184A;S184I;S184L;S184G;S184C;S184M;S202G;S202I;M250I;M250V;I169T;L180M;M204I;M204V 33;33;33;33;33;33;33;63;63;78;78;15;24;52;52 50;50;50;50;50;50;50;70;70;85;85;20;29;59;59 RT;RT;RT;RT;RT 13;22;31;61;76 15;24;33;63;78 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. We have previously identified a multi-drug resistant HBV mutant (clone 50-2), which harbored the quintuple mutations (rtM129L+V173L+M204I+L269I+H337N) that conferred robust replicative ability and strong cross-resistance to LMV, CLV, and ETV. 2015 PloS one Introduction HBV M129L;V173L;M204I;L269I;H337N 120;126;132;138;144 125;131;137;143;149 RT 118 120 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Considering these aspects, we performed a crystallographic study of the HIV-1 RT Q151M mutant to investigate the mutational effect on HIV-1 RT and the structural details of the HBV Pol dNTP-binding site. 2015 Acta crystallographica. Section F, Structural biology communications Introduction HBV Q151M 81 86 P;RT;RT 181;78;140 184;80;142 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. It has been reported that a Q151M mutation in HIV-1 RT induces the development of NRTI resistance in mutant viruses (Shirasaka et al., 1993, 1995). 2015 Acta crystallographica. Section F, Structural biology communications Introduction HBV Q151M 28 33 RT 52 54 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. It is also known that the Q151M mutant confers resistance to almost all NRTIs, while maintaining sensitivity to lamivudine and tenofovir (Iversen et al., 1996; Mbisa et al., 2011; Harada et al., 2007). 2015 Acta crystallographica. Section F, Structural biology communications Introduction HBV Q151M 26 31 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Moreover, the Q151M mutant appears to confer hypersensitivity to entecavir, a powerful NRTI used for the treatment of HBV infection (Zennou et al., 2007). 2015 Acta crystallographica. Section F, Structural biology communications Introduction HBV Q151M 14 19 HBV infections 118 131 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. A predominant mutation in the pre-core region involves a G to A change at nucleotide1896 (G1896A), which generates a premature stop codon at codon 28. 2015 Hepatitis monthly Introduction HBV G1896A;G1896A 90;57 96;88 Precore 30 38 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The aim of this study was to identify the presence of G1896A mutant in HBV virus isolated from Malaysian HBV carriers and determine the association of this mutation with several parameters such as clinical status, genotype and HBeAg status. 2015 Hepatitis monthly Introduction HBV G1896A 54 60 C 227 232 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. As a multi-drug resistant mutation, rtA181T/V has cross-resistance to LMV, LdT and TDF as well. 2015 Scientific reports Introduction HBV A181T;A181V 38;38 45;45 RT 36 38 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Combination of rtM204V/I, rtL180M plus one of the following mutations: rtT184S/C/I/A, rtS202G/C/I or rtM250V links to ETV resistance. 2015 Scientific reports Introduction HBV M204V;M204I;T184S;T184C;T184I;T184A;S202G;S202C;S202I;M250V;L180M 17;17;73;73;73;73;88;88;88;103;28 24;24;84;84;84;84;97;97;97;108;33 RT;RT;RT;RT;RT 15;26;71;86;101 17;28;73;88;103 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Two large-scale clinical studies from China found that rtM204I with or without rtL180V was more frequent in genotype C than genotype B. 2015 Scientific reports Introduction HBV L180V;M204I 81;57 86;62 RT;RT 55;79 57;81 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. BCP A1762T/G1764A double mutants increase the risk of liver cirrhosis and hepatocellular carcinoma (HCC), PC G1896A mutant decreases the risk of HCC, although the impact of PC G1896A mutant on HCC development remain controversial. 2015 Scientific reports Introduction HBV G1764A;A1762T;G1896A;G1896A 11;4;109;176 17;10;115;182 BCP;Precore;Precore 0;106;173 3;108;175 Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 54;74;100;145;193 69;98;103;148;196 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Regarding HBV mutations, the use of 3TC alone has been shown to be strongly associated with consistently high HBV viremia due to the rapid emergence of HBV mutants carrying the M204I/V mutation conferring resistance to 3TC/FTC. 2016 PloS one Introduction HBV M204I;M204V 177;177 184;184 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. HBV rtA181V/T mutants have been reported in chronic hepatitis B patients who received antiviral treatment with LMV, ADV, LdT, or CLV, and have been known to present cross-resistance against other NA, except ETV. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 6;6 13;13 RT 4 6 Chronic Hepatitis B 44 63 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. However, some studies reported that HBV rtA181V/T mutants could even induce cross-resistance to ETV. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 42;42 49;49 RT 40 42 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. However, there is no specific therapeutic recommendation or clinical study on HBV rtA181V/T single mutation. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 84;84 91;91 RT 82 84 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. In general, the majority of HBV rtA181V/T mutants are known to be induced after ADV therapy, along with the rtN236T mutant. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T;N236T 34;34;110 41;41;115 RT;RT 32;108 34;110 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. In other words, the aim of this study is to investigate the antiviral efficacy of ETV alone and in combination with ADV for HBV rtA181V/T single mutation. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 130;130 137;137 RT 128 130 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. In practice, a clinical investigation reported that HBV rtA181V/T mutants might present persistence of HBV DNA and showed an association with incomplete response, despite rescue therapy by ETV. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 58;58 65;65 RT 56 58 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Many guidelines published in Korea, the United States, and Europe recommend ETV plus TDF (or ADV if TDF is unavailable) as rescue therapy for HBV rtA181V/T mutants. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 148;148 155;155 RT 146 148 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Of NA-related HBV mutants, HBV rtA181V/T mutants develop as a result of mutation of the HBV reverse transcriptase gene at position 181, where an alanine (A) is substituted with a valine (V) or threonine (T). 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 33;33 40;40 RT;RT 92;31 113;33 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Thus, antiviral therapy should be determined to support the decision on which rescue therapy, add-on therapy with ETV or switch to ETV monotherapy, is to be applied in patients who received prior ADV therapy for HBV rtA181V/T mutants alone. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 218;218 225;225 RT 216 218 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Thus, ETV with high susceptibility in vitro has been used primarily as rescue therapy for HBV rtA181V/T mutants. 2016 Saudi journal of gastroenterology Introduction HBV A181V;A181T 96;96 103;103 RT 94 96 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. However, the roles that HBx mutations play in hepatocarcinogenesis remain controversial, particularly for the basal core promoter (BCP) A1762T/G1764A dual mutation. 2016 Oncotarget Introduction HBV G1764A;A1762T 143;136 149;142 BCP;BCP;X 110;131;24 129;134;27 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In this meta-analysis, we summarized the prevalence of A1762T/G1764A mutations from ASC, CHB, LC and HCC patients. 2016 Oncotarget Introduction HBV G1764A;A1762T 62;55 68;61 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 89;101;94 92;104;96 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Several prospective studies have demonstrated that patients with an A1762T/G1764A dual mutation were more predisposed to HCC than those with the wild type and that HBV mutations, including A1762T/G1764A, are associated with an increased risk of HCC. 2016 Oncotarget Introduction HBV G1764A;G1764A;A1762T;A1762T 75;196;68;189 81;202;74;195 Hepatocellular carcinoma;Hepatocellular carcinoma 121;245 124;248 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. The stable overexpression of HBx-Delta14 or HBx-Delta35 in HCC cell line Huh7 and immortalized normal liver cell line MIHA resulted in a significant increase of the cells ability to self-renew, resist 5-fluorouracil and sorafenib, migrate and induce capillary tube formation in endothelial cells. 2016 Oncotarget Introduction HBV del 35 48 55 X;X 29;44 32;47 Hepatocellular carcinoma 59 62 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. However, it has been shown that HBV resistance to 3TC occurs rapidly through the rtM204V/I substitutions. 2017 Antiviral therapy Introduction HBV M204V;M204I 83;83 90;90 RT 81 83 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. In this study, four mutations (sC124R, sC124Y, sK141E, and sD144A) strongly decreased the sensitivity of HBV detection in seven commercial HBsAg immunoassays. 2016 PloS one Introduction HBV C124R;C124Y;K141E;D144A 31;39;47;59 37;45;53;65 S;S;S;S;S 139;31;39;47;59 144;32;40;48;60 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. Recently, a novel vaccine escape S gene mutant (sP120Q+sD144A) was described. 2016 PloS one Introduction HBV P120Q;D144A 48;55 54;61 S;S;S 33;48;55 34;49;56 27303803 Hepatitis B Virus Core Promoter Double Mutations (A1762T, G1764A) Are Associated with Lower Levels of Serum Dihydrolipoyl Dehydrogenase. One of the most critical changes is the appearance of double mutations at nt 1,762 (A-T) and 1,764 (G-A) in the BCP. 2016 Intervirology Introduction HBV A762T;G764A 79;95 88;104 BCP 112 115 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. These resistant variants include rtM204V, rtM204I and the infrequently identified rtM204S. 2016 Experimental and therapeutic medicine Introduction HBV M204V;M204I;M204S 35;44;84 40;49;89 RT;RT;RT 33;42;82 35;44;84 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. 127 (isoleucine to asparagine/serine/threonine), 130 (lysine to methionine), 131 (valine to isoleucine), and 132 (phenylalanine to tyrosine), which might affect the biological activity of HBx.18, 19 However, the potential role of HBx Combo mutations in hepatocarcinogenesis is largely unknown. 2016 Cancer science Introduction HBV I127N;K130M;V131I;F132Y 0;49;77;109 47;75;103;140 X;X 188;230 191;233 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. A1762T/G1764A (TA) mutations in the core promoter, which overlap with the HBx gene, are found commonly in HCC and are independent risk factors for the progression of HCC during chronic HBV infection.12 In vivo studies suggest that the TA mutant increases the replication capacity of HBV and suppresses HBeAg serum levels.13 A1762T/G1764A mutations are also predictors of postoperative survival in patients with HBV-related HCC.14 A1762T/T1764A mutations in the HBx gene lead to Lys-Met 130 and Val-Ile 131 substitutions, which in turn affect the biological activities of HBx by abrogating its transcription activity and inhibitory effects on cell proliferation and transformation.15 T1753A/A1762T/G1764A/T1768A (Combo) mutations in the basal core promoter (BCP) of HBV and combinations of multiple point mutations (G1613A, C1653T, T1753V, A1762T, and G1764A) are closely related to HCC in patients infected with HBV.16, 17 The Combo mutations in BCP result in four a.a. 2016 Cancer science Introduction HBV G1764A;G1764A;T1764A;G1764A;T1768A;A1762T;A1762T;A1762T;A1762T;T1753A;G1613A;C1653T;T1753V;A1762T;G1764A;K130M;V131I 7;331;437;697;704;690;0;324;430;683;815;823;831;839;851;478;494 13;337;443;703;710;696;6;330;436;689;821;829;837;845;857;489;505 BCP;BCP;BCP;Core promoter;C;X;X;X 736;757;946;36;302;74;461;571 755;760;949;49;307;77;464;574 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Chronic HBV infection;Hepatocellular carcinoma 106;166;882;177;423 109;169;885;198;426 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Recently, more and more research works illustrate that YMDD variation is not a single mutation of rtM204I/V in the RT, but companied by compensatory mutation, such as rtL180M, etc. 2016 SpringerPlus Introduction HBV M204I;M204V;L180M 100;100;169 107;107;174 RT;RT;RT;P 98;115;167;55 100;117;169;59 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. The typical YMDD motif variation (rtM204I/V) could be found in the reverse transcriptase (RNA-dependent DNA polymerase, RT) from all the genotypes, after the patients with HBV infection took a long-term treatment of the lamivudine (Malmstrom et al.; Zhang et al.; Moskovitz et al.). 2016 SpringerPlus Introduction HBV M204I;M204V 36;36 43;43 P;RT;RT;RT;P 108;67;34;120;12 118;88;36;122;16 HBV infections 172 185 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. HBV mutants resistant to adefovir (ADV) monotherapy are complex and diverse, including rtA181T, rtV214A, and rtN236T. 2016 Oncotarget Introduction HBV A181T;V214A;N236T 89;98;111 94;103;116 RT;RT;RT 87;96;109 89;98;111 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. It has been reported that rtA181T+ rtN236T, rtA194T, rtP177G and rtF249A may increase viral replication and reduce the susceptibility to tenofovir. 2016 Oncotarget Introduction HBV A181T;N236T;P177G;F249A;A194T 28;37;55;67;46 33;42;60;72;51 RT;RT;RT;RT;RT 26;35;44;53;65 28;37;46;55;67 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R mutant has been reported in many cases of occult hepatitis B infection (OBI) because it decreases the HBsAg levels, often going undetected by routine assays and in patients who suffer from lamivudine-resistant mutants. 2016 Hepatitis monthly Introduction HBV G145R 0 5 S 108 113 Occult Hepatitis B 78 81 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R mutants have mainly been found in genotypes B, C, and D. 2016 Hepatitis monthly Introduction HBV G145R 0 5 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Naturally occurring G145R mutants are often detectable with monoclonal antibody-based assays, albeit at a reduced sensitivity. 2016 Hepatitis monthly Introduction HBV G145R 20 25 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The commonest type of these mutations, G145R, is created by the substitution of arginine for glycine has been shown to exhibit various degrees of altered binding of HBsAg to antibodies in different commercial assays. 2016 Hepatitis monthly Introduction HBV G145R 39 44 S 165 170 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The objectives of this de novo study were to assess the impact of the G145R mutation on the HBsAg structure at both the two-dimensional (2D) and three-dimensional (3D) levels. 2016 Hepatitis monthly Introduction HBV G145R 70 75 S 92 97 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. We also performed molecular docking studies of the HBsAg-antibody to investigate the antigen-antibody interactions in the G145R mutant compared with the wild-type HBsAg. 2016 Hepatitis monthly Introduction HBV G145R 122 127 S;S 51;163 56;168 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. However, some newly discovered SHBs mutations were under quantitated by the Architect assay, whereas sP142L, sP142S and sG145K mutations yielded lower results in the Elecsys system when compared with those obtained with the Architect system. 2017 Journal of hepatology Introduction HBV P142L;P142S;G145K 101;109;120 107;115;126 S;S;S;S 101;109;120;31 102;110;121;35 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. It is known that new qHBsAg assays have incorporated the impact of some classical SHBs AA substitutions on qHBsAg, such as sK122I, sI126S and sG145R. 2017 Journal of hepatology Introduction HBV K122I;I126S;G145R 123;131;142 129;137;148 S;S;S;S 123;131;142;82 124;132;143;86 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. reported that the rtA181T/sW172stop (sW172*) variant had a secretory defect and exerted a dominant negative effect on wild-type (WT) HBV virion secretion. 2017 Journal of hepatology Introduction HBV W172X;A181T;W172X 26;20;37 35;25;43 RT;S;S 18;26;37 20;27;38 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Additionally, pre-S deletion, T1753V mutation in BCP, and C1653T mutation in box-alpha of Enhancer II have been reported to be related with increased risk of HCC in several reports. 2016 International journal of molecular sciences Introduction HBV T1753V;C1653T 30;58 36;64 BCP;Enh II;PreS 49;90;14 52;101;19 Hepatocellular carcinoma 158 161 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. The most convincing association between viral mutation and the development of HCC is A1762T/G1764A double mutations in the basal core promoter (BCP). 2016 International journal of molecular sciences Introduction HBV G1764A;A1762T 92;85 98;91 BCP;BCP 123;144 142;147 Hepatocellular carcinoma 78 81 27779207 HBV core promoter mutations and AKT upregulate S-phase kinase-associated protein 2 to promote postoperative hepatocellular carcinoma progression. In addition to TA, other CP mutations, notably C1653T, T1674C/G, C1766T, T1753V and T1768A, have also been reported to be associated with an increased risk of HCC. 2016 Scientific reports Introduction HBV T1674G;C1653T;T1674C;C1766T;T1753V;T1768A 55;47;55;65;73;84 63;53;63;71;79;90 Core promoter 25 27 Hepatocellular carcinoma 159 162 27779207 HBV core promoter mutations and AKT upregulate S-phase kinase-associated protein 2 to promote postoperative hepatocellular carcinoma progression. The double mutation A1762T/G1764A (TA) in the HBV basal core promoter (CP) region has been widely recognized to be independently associated with HCC. 2016 Scientific reports Introduction HBV G1764A;A1762T 27;20 33;26 BCP;Core promoter 50;71 69;73 Hepatocellular carcinoma 145 148 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Among the VEMs, the mutant G145R, with a single mutation of amino acid 145 of the surface protein of HBV, which is located in the "a" determinant region (aa124-147), is well known as the most virulent mutant in breakthrough infections. 2016 PloS one Introduction HBV G145R 27 32 S 82 89 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Finally, a prospective study was conducted to clarify whether immunoprophylaxis failure could occur in infants who were born to HBV carrier mothers with the G145R mutant existing as a minor population. 2016 PloS one Introduction HBV G145R 157 162 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, it is difficult to detect the minor strain of G145R in HBV carriers by Sanger sequencing and conventional real-time PCR. 2016 PloS one Introduction HBV G145R 55 60 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In this study, the G145R mutant as a minor strain as well as a major strain was detected in chronically infected children with HBV due to breakthrough infection using LNA-based probe real-time PCR. 2016 PloS one Introduction HBV G145R 19 24 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Analysing the predicted base pairing patterns of pregenomic RNAs (pgRNAs), specific for HBV subgenotype A1 and A2, we demonstrate that the potent immune escape mutation G145R evolves specifically in the context of HBV subgenotype A2. 2016 World journal of virology Introduction HBV G145R 169 174 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Based on the RNA secondary structure predictions, we demonstrate that the selection and emergence of G145R within HBV subgenotype A2 sequences in the PBL compartment occurs due to the differential base pairing characteristics in the subgenotype A2 specific pgRNA. 2016 World journal of virology Introduction HBV G145R 101 106 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. G145R is the mutation signifying Glycine to Arginine substitution at amino acid residue 145 in the major hydrophilic loop (MHL), a B-cell epitope of the hepatitis B surface antigen (HBsAg), which provides a strong immune escape property. 2016 World journal of virology Introduction HBV G145R;G145R 0;33 5;91 S;S 182;165 187;172 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. In our previous studies, we have recognized the subgenotype A1 (Afro-Asian subgenotype) as the predominant subgenotype of HBV genotype A circulating in the sera/plasma of our study population and that the occurrence of G145R mutation therein was sporadic. 2016 World journal of virology Introduction HBV G145R 219 224 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. In sharp contrast, we documented the confined and exclusive existence of HBV subgenotype A2 with the potent "immune escape" mutation G145R within the peripheral blood leukocytes (PBL), across the study population, irrespective of the HBV genotype/subgenotype circulating in the serum/plasma of the respective individual. 2016 World journal of virology Introduction HBV G145R 133 138 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Taken together, the above observations led us to hypothesize that the subgenotype specific nucleotide substitutions might modulate the base pairing of the A2 specific pgRNA in a way, which favours the emergence of G145R. 2016 World journal of virology Introduction HBV G145R 214 219 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. The PBL compartment is exposed to strong anti-HBs immunity, and thus G145R is highly advantageous for the virus to persist. 2016 World journal of virology Introduction HBV G145R 69 74 S 46 49 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. These observations strongly signify that viral mutants with G145R does have an explicit replicative advantage within the PBLs, that are exposed to strong anti-HBs immunity and that this mutation emerges specifically in the perspective of subgenotype A2, but not in subgenotype A1. 2016 World journal of virology Introduction HBV G145R 60 65 S 159 162 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Clinical analysis showed that the rtA181T/sW172* mutation was associated with an increased risk of HCC in cirrhotic patients. 2016 Oncogenesis Introduction HBV W172X;A181T 42;36 48;41 RT;S 34;42 36;43 Hepatocellular carcinoma;Liver cirrhosis 99;106 102;115 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. For example, high serum or intrahepatic HBV-DNA levels and the presence of basal core promoter A1762T/G1764A mutation can independently predict outcomes of long-term chronic HBV infection as well as postoperative survival in HCC. 2016 Oncogenesis Introduction HBV G1764A;A1762T 102;95 108;101 BCP 75 94 Chronic HBV infection;Hepatocellular carcinoma 166;225 187;228 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. However, hepatic expression levels of the S truncation proteins derived from HBV integration was usually low and the sW172* mutation was not located on the characterized 'transactivation-on' region. 2016 Oncogenesis Introduction HBV W172X 117 123 S;S 42;117 43;118 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. In the present study, we aimed to provide transgenic mouse evidence for the increased oncogenicity of pre-S/S proteins carrying the rtA181T/sW172* mutation. 2016 Oncogenesis Introduction HBV W172X;A181T 140;134 146;139 PreS;S;RT;S 102;108;132;140 107;109;134;141 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Of them, the S gene truncation mutants, such as the rtA181T/sW172* mutant, were associated with hepatocarcinogenesis. 2016 Oncogenesis Introduction HBV W172X;A181T 60;54 66;59 RT;S;S 52;13;60 54;14;61 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. On the other hand, HBV carrying the rtA181T/sW172* mutation could accumulate to a high serum level, insuring the generation of significant amount of truncated pre-S/S proteins. 2016 Oncogenesis Introduction HBV W172X;A181T 44;38 50;43 PreS;S;RT;S 159;165;36;44 164;166;38;45 27920641 Severe de novo Hepatitis B Recovered from Late-Onset Liver Insufficiency with Prolonged Ascites and Hypoalbuminemia due to Hepatitis B Virus Genotype Bj with Precore Mutation. However, the prognosis of patients who develop hepatitis after chemotherapy including rituximab has shown to have high mortality, even when NA was administered; recently, the fulminant outcome of HBV reactivation associated with genotype Bj with precore mutation (PCm) (G1896A) has been reported. 2016 Case reports in gastroenterology Introduction HBV G1896A 270 276 Precore 246 253 Hepatitis 47 56 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. And our preliminary study also has revealed that the HBV rtA181T/sW172* mutant has a dominant secretion defect of HBsAg and viral DNA replication enhancement in liver tissue of mouse model with HBV replication. 2016 Scientific reports Introduction HBV W172X;A181T 65;59 71;64 S;RT;S 114;57;65 119;59;66 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As we known, HBV rtA181T mutant is an A T mutation at position 181 of the P gene in the RT domain. 2016 Scientific reports Introduction HBV A181T 19 24 P;RT;RT 74;17;88 75;19;90 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. For example, the result reported by Dr.Hiromi Yatsuji showed that there was no noticeable difference in replication ability between the rtA181T/sW172* and rtA181T/sW172L; while other two in vitro studies reported a reduced replication of rtA181T/sW172* mutant. 2016 Scientific reports Introduction HBV W172X;W172L;W172X;A181T;A181T;A181T 144;163;246;138;157;240 150;169;252;143;162;245 RT;RT;RT;S;S;S 136;155;238;144;163;246 138;157;240;145;164;247 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, due to the low genetic barrier, the HBV rtA181T/V mutations are selected during the long-term treatment of LAM or ADV, especially among patients with high viral load. 2016 Scientific reports Introduction HBV A181T;A181V 51;51 58;58 RT 49 51 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In theory, its overlapping S gene should have two types of mutation at amino acid 172, which include rtA181T/sW172L (TGG CTC TTA CTC) mutant coding substituted HBsAg protein and rtA181T/sW172*(TGG CTC TGA CTC) mutant coding truncated HBsAg protein. 2016 Scientific reports Introduction HBV W172L;W172X;A181T;A181T 109;186;103;180 115;192;108;185 S;S;RT;RT;S;S;S 160;234;101;178;27;109;186 165;239;103;180;28;110;187 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Recently, the HBV rtA181T/sW172* mutant has been strongly concerned, and the emergence of this mutant has reported an increased risk of hepatocellular carcinoma in LAM- or ADV-treated patients. 2016 Scientific reports Introduction HBV W172X;A181T 26;20 32;25 RT;S 18;26 20;27 Hepatocellular carcinoma 136 160 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. So, for getting a full understanding of HBV rtA181T mutants, the biological characteristics of both sW172L and sW172* mutants should be investigated. 2016 Scientific reports Introduction HBV A181T;W172L;W172X 46;100;111 51;106;117 RT;S;S 44;100;111 46;101;112 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Thus, to better and fully understand the characteristics of the HBV rtA181T mutant, we designed this study to investigate the impact of different overlapping S gene mutation (sW172L and sW172*) on rtA181T mutant DNA replication and viral protein expression, not only in vitro in cultured HepG2 cells but also in vivo in mouse model. 2016 Scientific reports Introduction HBV A181T;A181T;W172L;W172X 70;199;175;186 75;204;181;192 RT;RT;S;S;S 68;197;158;175;186 70;199;159;176;187 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. In this study, we cloned the ORFs of three wild-type HBsAgs, designated W1S, W3S and adr4 (all of which were isolated from HBV-infected patients) and constructed a total of 19 synthetic mutants into a mammalian expression vector. 2017 PloS one Introduction HBV W1S;W3S 72;77 75;80 S 53 59 HBV infections 123 135 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Single amino acid mutation of either P120K or T123D, or other positions such as 145 (G145R) or 146 (N146G), only marginally reduced the binding efficiency of HBsAg. 2017 PloS one Introduction HBV P120K;T123D;G145R;N146G 37;46;85;100 42;51;90;105 S 158 163 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The first vaccine-induced natural mutation (G145R) was found in a newborn of an HBsAg carrier mother, and mutations in this surface protein have also been shown to lead to a failure of immune prophylaxis in infants receiving HBV vaccines ("immune escape") and in a liver transplant patient receiving hepatitis B immune globulin (HBIG). 2017 PloS one Introduction HBV G145R 44 49 S;S 80;124 85;131 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Thus, double mutation of P120K and T123D will be crucial for the future design of hepatitis B vaccines and diagnostic assays. 2017 PloS one Introduction HBV P120K;T123D 25;35 30;40 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. W1S but not W3S was detected with commercial ELISA kits. 2017 PloS one Introduction HBV W1S;W3S 0;12 3;15 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Recently published high-resolution complex structures, using a non-assembled core protein mutant Y132A as a surrogate, greatly facilitate structure-based drug design of next-generation HAPs. 2017 Scientific reports Introduction HBV Y132A 97 102 C 77 81 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. To evaluate potential differences of these two classes of core protein modulators, we characterize the mechanisms of HAP and SBA and present the crystal structures of two reference compounds HAP_R01 and SBA_R01 in complex with the core protein mutant hexamer (Y132A). 2017 Scientific reports Introduction HBV Y132A 260 265 C;C 58;231 62;235 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. In the absence of G1896A mutation, alternative mutations to abolish HBeAg expression include C1817T converting codon 2 from CAA to TAA, various frameshift mutations, and mutated precore ATG codon. 2017 Virology Introduction HBV G1896A;C1817T 18;93 24;99 C;Precore 68;178 73;185 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Intriguingly, genotype G harbors both C1817T and G1896A nonsense mutations, and possesses a 36-nt insertion at the 5' end of the core gene. 2017 Virology Introduction HBV C1817T;G1896A 38;49 44;55 C 129 133 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. The G1896A nonsense mutation rarely develops in genotypes A, H, C1, F2, or F3, for which a preexisting C:G pair with C1858 would be disrupted by the mutation. 2017 Virology Introduction HBV G1896A 4 10 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. The hot-spot HBeAg-abrogating mutation for most HBV genotypes is G1896A converting precore codon 28 from TGG to TAG, at least partly because it would improve a base pair at the lower stem of the epsilon signal from U:G to U:A. 2017 Virology Introduction HBV G1896A 65 71 C;Precore 13;83 18;90 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Primary LMV resistance mutation has been mapped in the reverse transcriptase (RT) domain of HBV Pol and typically involved rtM204I/V, while compensatory mutations rtL180M, rtV173L, and rtL80I are often co-selected during therapy to restore HBV replication efficacy. 2017 Scientific reports Introduction HBV M204I;M204V;L80I;L180M;V173L 125;125;187;165;174 132;132;191;170;179 P;RT;RT;RT;RT;RT;RT 96;55;78;123;163;172;185 99;76;80;125;165;174;187 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. However, there is limited knowledge about the clinical features and quasispecies characteristics associated with infection by G145R mutant HBV. 2017 Emerging microbes & infections Introduction HBV G145R 126 131 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Mutations in the 'alpha' determinant of the major hydrophilic region (MHR), such as amino-acid (aa) substitution from glycine to arginine at aa 145 (G145R), have been reported in patients with coexistence of HBsAg and anti-HBs. 2017 Emerging microbes & infections Introduction HBV G145R;G145R 149;118 154;147 S;S;S 18;223;208 36;226;213 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. We herein describe the dynamic changes in the serological and virological markers in a case of hepatitis B with coexisting HBsAg and anti-HBs caused by a G145R immune escape mutant. 2017 Emerging microbes & infections Introduction HBV G145R 154 159 S;S 138;123 141;128 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Alternatively, HBeAg expression can be down regulated by mutations in the core promoter such as A1762T/G1764A, which reduce transcription of the pcRNA. 2017 Virus research Introduction HBV G1764A;A1762T 103;96 109;102 Core promoter;C 74;15 87;20 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Finally, the rising anti-HBs antibodies can select for amino acid substitutions in the antigenic epitopes in the S protein such as G145R. 2017 Virus research Introduction HBV G145R 131 136 S;S 25;113 28;114 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The G1896A nonsense mutation in the precore region, which blocks HBeAg expression at the translational level, is frequently selected at the HBeAg- negative phase of chronic HBV infection. 2017 Virus research Introduction HBV G1896A 4 10 C;C;Precore 65;140;36 70;145;43 Chronic HBV infection 165 186 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Additionally, in vitro studies have found the rtA181T/V mutation could affect virus replication, protein secretion and tumorigenesis. 2017 Virology journal Introduction HBV A181T;A181V 48;48 55;55 RT 46 48 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. But few studies reported the effect of ETV in rescuing rtA181T/V mutation patients. 2017 Virology journal Introduction HBV A181T;A181V 57;57 64;64 RT 55 57 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In general, the majority of HBV rtA181V/T mutants are known to be induced after ADV therapy, along with the rtN236T mutant. 2017 Virology journal Introduction HBV A181V;A181T;N236T 34;34;110 41;41;115 RT;RT 32;108 34;110 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Switching to ETV for rtA181T/V mutation patients was recommended by the Asian Pacific Association for the Study of the Liver (APASL). 2017 Virology journal Introduction HBV A181T;A181V 23;23 30;30 RT 21 23 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Therefore, we aimed to evaluate the antiviral efficacy of 12 months ETV rescue therapy in rtA181T/V single mutation or with rtN236T mutant. 2017 Virology journal Introduction HBV A181T;A181V;N236T 92;92;126 99;99;131 RT;RT 90;124 92;126 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Molecular analyses revealed the presence of the rtS78T mutation that created a stop codon (sC69*) for HBsAg. 2017 Journal of hepatology Introduction HBV S78T;C69X 50;91 54;96 S;RT;S 102;48;91 107;50;92 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The molecular explanation is that ETV resistance usually requires the LAM-resistant "YMDD mutation(s)" (rtM204V/I +-L180M) plus an additional ETV 'signature' substitution in the B domain (rtI169T or rtS184G), C domain (rtS202G/I), or E domain (rtM250V). 2017 Journal of hepatology Introduction HBV M204V;M204I;I169T;S202G;S202I;S184G;M250V;L180M 106;106;190;221;221;201;246;116 113;113;195;228;228;206;251;121 RT;RT;RT;RT;RT;P 104;188;199;219;244;85 106;190;201;221;246;89 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Accumulated evidence indicates that the most common mutations are a G to A substitution at nucleotide 1896 (G1896A) in the precore region, an A to T mutation at nucleotide 1762 (A1762T), a G to A mutation at nucleotide 1764 (G1764A), and the A1762T/G1764A double mutation in the BCP region. 2017 Medicine Introduction HBV G1764A;G1896A;A1762T;G1764A;A1762T;G1896A;A1762T;G1764A 249;108;178;225;242;68;142;189 255;114;184;231;248;106;176;223 BCP;Precore 279;123 282;130 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. In this meta-analysis, we analyzed the relationship between the risk of developing HCC and mutations G1896A, A1762T, and G1764A, in addition to the A1762T/G1764A double mutation. 2017 Medicine Introduction HBV G1764A;G1896A;A1762T;G1764A;A1762T 155;101;109;121;148 161;107;115;127;154 Hepatocellular carcinoma 83 86 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. There have been some meta-analyses investigating the relationship between mutations G1896A, A1762T, and G1764A and HCC, but the results were conflicting, and each of these studies was published before 2015. 2017 Medicine Introduction HBV G1896A;A1762T;G1764A 84;92;104 90;98;110 Hepatocellular carcinoma 115 118 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. G1896A mutation is most commonly associated with genotypes D, E, and B of HBV and is rare in other genotypes of HBV. 2017 Electronic physician Introduction HBV G1896A 0 6 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. The G1896A precore mutation leads to a conversion of codon 28 from TGG (tryptophan) to a premature stop codon TAG. 2017 Electronic physician Introduction HBV G1896A 4 10 Precore 11 18 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. The most naturally occurring mutation in the HBV precore gene is substitution of a guanine (G) to adenine (A) at position 1896. 2017 Electronic physician Introduction HBV G1896A 82 127 Precore 49 56 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. There is an association between mutations in the precore region of the HBV and HBV genotype, so the prevalence of infection with G1896A precore mutant is related to HBV genotypes in different geographic areas. 2017 Electronic physician Introduction HBV G1896A 129 135 Precore;Precore 49;136 56;143 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. According to several clinical practice guidelines and authoritative reviews, NUCr substitutions can be classified into two categories: primary NUCr substitutions at 8 codons (rtI169T, rtA181T/V, rtT184A/C/F/G/I/L/M/S, rtA194T, rtS202C/G/I, rtM204I/V, rtN236T and rtM250I/L/V) and secondary substitutions at 3 codons in RT (rtL80I/V, rtV173L and rtL180M), which are often found in treated patients and termed as classic amino acid (AA) substitutions. 2017 Viruses Introduction HBV A181T;A181V;T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M204I;M204V;N236T;M250I;M250L;M250V;L80I;L80V;V173L;L180M;I169T;A194T 186;186;197;197;197;197;197;197;197;197;229;229;229;242;242;253;265;265;265;325;325;335;347;177;220 193;193;216;216;216;216;216;216;216;216;238;238;238;249;249;258;274;274;274;331;331;340;352;182;225 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 175;184;195;218;227;240;251;263;319;323;333;345 177;186;197;220;229;242;253;265;321;325;335;347 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. characterized two novel substitutions, rtI163V and rtA186T, in an ETV-refractory patient. 2017 Viruses Introduction HBV I163V;A186T 41;53 46;58 RT;RT 39;51 41;53 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. For example, initial NUCr studies often investigated rtM204I/V substitution, while more AA substitution codons associated with NUCr in the RT domain have been included in more recent studies. 2017 Viruses Introduction HBV M204I;M204V 55;55 62;62 RT;RT 53;139 55;141 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. found a relatively high incidence of rtM204I/V substitution (23.3%) in 1042 untreated CHB patients. 2017 Viruses Introduction HBV M204I;M204V 39;39 46;46 RT 37 39 Chronic Hepatitis B 86 89 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. identified rtS78T as being partially responsible for multidrug resistance to ETV and TDF in two patients receiving ETV-TDF combination therapy. 2017 Viruses Introduction HBV S78T 13 17 RT 11 13 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Resistance to ADV is linked to rtA181T/V or rtN236T. 2017 Viruses Introduction HBV A181T;A181V;N236T 33;33;46 40;40;51 RT;RT 31;44 33;46 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Resistance to ETV needs a combination of substitutions of rtM204I/V and rtL180M plus one of the following substitutions: rtI169T, rtT184A/C/F/G/I/L/M/S, rtS202C/G/I or rtM250I/L/V. 2017 Viruses Introduction HBV M204I;M204V;T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M250I;M250L;M250V;L180M;I169T 60;60;132;132;132;132;132;132;132;132;155;155;155;170;170;170;74;123 67;67;151;151;151;151;151;151;151;151;164;164;164;179;179;179;79;128 RT;RT;RT;RT;RT;RT 58;72;121;130;153;168 60;74;123;132;155;170 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Resistance to LAM or LdT is conferred by rtM204I/V, which is often accompanied by rtL80I/V, rtL180M and/or rtV173L. 2017 Viruses Introduction HBV M204I;M204V;L80I;L80V;L180M;V173L 43;43;84;84;94;109 50;50;90;90;99;114 RT;RT;RT;RT 41;82;92;107 43;84;94;109 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Substitution of rtA181T/V can also cause decreased susceptibility to LAM or LdT. 2017 Viruses Introduction HBV A181T;A181V 18;18 25;25 RT 16 18 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. The rtA186T substitution was responsible for ETV resistance and significantly reduced viral replication efficacy, while rtI163V substitution could sustain viral fitness and rescue the variant. 2017 Viruses Introduction HBV A186T;I163V 6;122 11;127 RT;RT 4;120 6;122 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. G145R mutation was the first identified VEMs to be described in 1990, and later several other notable VEMs (I/T126S, Q129H, G130N, D144A, G145A) at different positions associated with HBV breakthrough infections have also been repeatedly documented worldwide. 2017 Scientific reports Introduction HBV T126S;I126S;G145R;Q129H;G130N;D144A;G145A 108;108;0;117;124;131;138 115;115;5;122;129;136;143 HBV infections 184 211 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. This is also the case for HBx C1653T and C1485T mutations associated with the occurrence of HCC in patients with HBV genotype C in Japan. 2017 Scientific reports Introduction HBV C1653T;C1485T 30;41 36;47 X 26 29 Hepatocellular carcinoma 92 95 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We herein demonstrated that HBx C1653T and C1485T mutations are associated with the development of HBV-related hepatocarcinogenesis and also that the latter mutation induces malignant transformation in hepatocytes upon over-expression. 2017 Scientific reports Introduction HBV C1653T;C1485T 32;43 38;49 X 28 31 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. In addition, mutations such as T1753 V (genotype A, C or G), T1754S (genotype C or G), G1862 T, T1961 V, C1962D (A, G or T), and A2339G were more frequently found in fulminant hepatitis. 2017 Virology journal Introduction HBV T1753V;T1754S;G1862T;T1961V;C1962D;A2339G 31;61;87;96;105;129 38;67;94;103;111;135 Fulminant Hepatitis B 166 185 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The A1762T/G1764A dual mutations in core promoter region were also implicated in fulminant hepatitis due to improved transcription of pregenomic (pg)-RNA and increased viral replication. 2017 Virology journal Introduction HBV G1764A;A1762T 11;4 17;10 Core promoter 36 49 Fulminant Hepatitis B 81 100 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The G1896A mutation in the precore region, which post-transcriptionally abrogates HBeAg expression, was associated with fulminant hepatitis B development. 2017 Virology journal Introduction HBV G1896A 4 10 C;Precore 82;27 87;34 Fulminant Hepatitis B 120 139 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Coexistence of circulating HBsAg and anti-HBs was reported to be associated with A1762T/G1764A double mutations in the basal core promoter (BCP) region in HBV genome, which might enhance the ability of HBV replication. 2017 Medical science monitor Introduction HBV G1764A;A1762T 88;81 94;87 BCP;BCP;S;S 119;140;42;27 138;143;45;32 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Moreover, a recent study showed that the prevalence of BCP double mutations (A1762T/G1764A) in patients with coexistent circulating HBsAg and anti-HBs was significantly higher than that in patients with positive HBsAg but negative anti-HBs. 2017 Medical science monitor Introduction HBV G1764A;A1762T 84;77 90;83 BCP;S;S;S;S 55;147;236;132;212 58;150;239;137;217 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. On the other hand, previous studies have revealed that the BCP double mutations A1762T/G1764A were associated with an increased risk of HCC. 2017 Medical science monitor Introduction HBV G1764A;A1762T 87;80 93;86 BCP 59 62 Hepatocellular carcinoma 136 139 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Recently, a meta-analysis showed a statistically significant summary odds ratios (OR) of HCC obtained for A1762T/G1764A (3.79, 95% CI=2.71 to 5.29) and T1753V (2.35, 95% CI=1.63 to 3.40) in the BCP region. 2017 Medical science monitor Introduction HBV G1764A;A1762T;T1753V 113;106;152 119;112;158 BCP 194 197 Hepatocellular carcinoma 89 92 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Several lines of in vitro evidence have indicated that the simultaneous presence of A1762T and G1764A mutations in the BCP region of HBV can enhance the viral replication, which possibly occurs through up-regulated synthesis of the core protein and increased transcription of the pregenomic RNA. 2017 Medical science monitor Introduction HBV A1762T;G1764A 84;95 90;101 BCP;C 119;232 122;236 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Site-directed mutagenesis (A1762T, G1764A, and T1753V) of the wild-type clone exhibited appreciably stronger replication capacity of the virus than double mutations (A1762T/G1764A). 2017 Medical science monitor Introduction HBV G1764A;A1762T;G1764A;T1753V;A1762T 173;27;35;47;166 179;33;41;53;172 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Taken together, it could be speculated that coexistence of circulating HBsAg and anti-HBs in CHB patients, possibly due to mutations (T1753V, A1762T, and G1764A) in the BCP region, may be associated with an augmented HBV replicative capacity and HBV reactivation, which could even contribute to a poor prognosis, including HCC. 2017 Medical science monitor Introduction HBV T1753V;A1762T;G1764A 134;142;154 140;148;160 BCP;S;S 169;86;71 172;89;76 Chronic Hepatitis B;Hepatocellular carcinoma 93;323 96;326 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Thus, patients with double mutations (A1762T/G1764A) or triple mutations (A1762T/G1764A/T1753V) in the BCP region could be more likely to develop HBV reactivation due to a higher HBV replicative ability. 2017 Medical science monitor Introduction HBV G1764A;G1764A;T1753V;A1762T;A1762T 45;81;88;38;74 51;87;94;44;80 BCP 103 106 29248936 Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis. Triple mutations (A1762T, G1764A, and T1753V) and enhanced ability of HBV replication. 2017 Medical science monitor Introduction HBV A1762T;G1764A;T1753V 18;26;38 24;32;44 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. In addition, K130M+V131I HBx double mutation has been reported to increase in frequency with the liver disease progression in HBV-infected Taiwanese patients. 2017 Oncotarget Introduction HBV K130M;V131I 13;19 18;24 X 25 28 Liver disease;HBV infections 97;126 110;138 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. It was suggested that K130M+V131I HBx double mutation might contribute to HCC development by initiating the increased nuclear factor kappa B (NF-kappaB) activity. 2017 Oncotarget Introduction HBV K130M;V131I 22;28 27;33 X 34 37 Hepatocellular carcinoma 74 77 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. A previous study indicated that the A799G, A987G, and T1055A mutations in the RT domain are predictive markers of HCC occurrence. 2017 PloS one Introduction HBV A799G;A987G;T1055A 36;43;54 41;48;60 RT 78 80 Hepatocellular carcinoma 114 117 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. A high rate (47.4%) of the mutation conferring resistance to Lamivudine (major mutation M204V/I) was registered. 2018 PloS one Introduction HBV M204V;M204I 88;88 95;95 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. By using capillary gel electrophoresis, we found that it was the short fragment, rather than larger fragment, contributing to the association of Pre-S deletion with HCC., In addition to the above novel findings, we also verified the association of some known HBV mutations, such as HBV pre-S2 start codon mutation, C1653T and T1753C, with HCC in Qidong. 2018 Hepatoma research Introduction HBV C1653T;T1753C 315;326 321;332 PreS;PreS2 145;286 150;292 Hepatocellular carcinoma;Hepatocellular carcinoma 165;339 168;342 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. By using the plasma samples from the members of the QBC, we found the A1762T/G1764A double mutation of the HBV basal core promoter (BCP) was frequently detected in HBV infected participants. 2018 Hepatoma research Introduction HBV G1764A;A1762T 77;70 83;76 BCP;BCP 111;132 130;135 HBV infections 164 176 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. However, the A1762T/G1764A double mutation alone was not sufficient to produce a statistically significant association with PLC. 2018 Hepatoma research Introduction HBV G1764A;A1762T 20;13 26;19 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. P53 G249T mutation is an indicator of aflatoxin exposure. 2018 Hepatoma research Introduction HBV G249T 4 9 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. These mutations include A2159G, A2189C and G2203W at C gene, A799G, A987G and T1055A at P gene, and A1479T at X gene. 2018 Hepatoma research Introduction HBV A2159G;A2189C;G2203W;A799G;A987G;T1055A;A1479T 24;32;43;61;68;78;100 30;38;49;66;73;84;106 C;P;X 53;88;110 54;89;111 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. While A1762T/G1764A, C1653T, A799G, A987G, T1055A, pre-S deletion could be detected in the plasma long before PLC diagnosis, T1753C, C1766T and T1768A mutations appeared only one or two years before PLC diagnosis.,,These observations provide valuable information for HCC prediction and screening when using HBV mutations as the marker. 2018 Hepatoma research Introduction HBV G1764A;A1762T;C1653T;A799G;A987G;T1055A;T1753C;C1766T;T1768A 13;6;21;29;36;43;125;133;144 19;12;27;34;41;49;131;139;150 PreS 51 56 Hepatocellular carcinoma 267 270 29479565 Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer. While the odd ratio (OR) of HCC patients with the A1762T/G1764A double mutation alone was 0.393 (95% CI=0.234-0.660), it increased to 1.861 (95% CI=1.161-2.984) with the triple mutation and to 4.434 (95% CI=1.630-12.063) with the quadruple mutation in BCP region. 2018 Hepatoma research Introduction HBV G1764A;A1762T 57;50 63;56 BCP 252 255 Hepatocellular carcinoma 28 31 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Furthermore, our results prove the utility of the developed W4P transgene mouse model for research into the mechanisms of HBV-caused liver diseases. 2018 World journal of gastroenterology Introduction HBV W4P 60 63 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Here, to gain further insight into the role of this mutation in the sex disparity of HBV-induced liver inflammation, we created transgenic (TG) mice carrying the full HBV genome with the W4P mutation and evaluated HBV virion replication and IL-6-mediated inflammation in male and female TG and WT individuals. 2018 World journal of gastroenterology Introduction HBV W4P 187 190 Liver inflammation 97 115 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. In a molecular epidemiological study, we have previously found that the W4P mutation in the preS1 start region is associated with HCC development in male but not female patients. 2018 World journal of gastroenterology Introduction HBV W4P 72 75 PreS1 92 97 Hepatocellular carcinoma 130 133 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. In addition, our further cell-based and nude mouse xenograft model studies supported the notion that the W4P mutation likely induced HCC progression in an IL-6-dependent manner in male patients. 2018 World journal of gastroenterology Introduction HBV W4P 105 108 Hepatocellular carcinoma 133 136 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Of note, our data showed that W4P transgene males of 10 mo of age, but not W4P transgene females, spontaneously developed liver damage due to IL-6-mediated liver inflammation, further supporting the previous finding regarding the contribution of the W4P mutation to sex disparity in susceptibility to HCC. 2018 World journal of gastroenterology Introduction HBV W4P;W4P;W4P 30;75;250 33;78;253 Liver disease;Liver inflammation;Hepatocellular carcinoma 122;156;301 134;174;304 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Our study in the nude mouse xenograft model indicated that the W4P mutation likely contributed to IL-6-dependent HCC progression, particularly in male individuals. 2018 World journal of gastroenterology Introduction HBV W4P 63 66 Hepatocellular carcinoma 113 116 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Recently, we introduced the novel W4P substitution into the preS1 region, which associated with HCC and notably occurred exclusively in male patients. 2018 World journal of gastroenterology Introduction HBV W4P 34 37 PreS1 60 65 Hepatocellular carcinoma 96 99 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Abolishing N-linked glycosylation in the S domain by either N146Q or N146S mutation prevented the secretion of virions but not subviral particles (HBsAg). 2018 Virology Introduction HBV N146Q;N146S 60;69 65;74 S;S 147;41 152;42 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. G145R, the classic immune escape mutation, also severely impaired virion secretion. 2018 Virology Introduction HBV G145R 0 5 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In the present study, we examined whether other novel N-linked glycosylation sites could rescue virion secretion of the G145R and N146Q mutants. 2018 Virology Introduction HBV G145R;N146Q 120;130 125;135 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Our previous study revealed that the M133T mutation, which creates a novel glycosylation site at N131 (131NST133), could rescue virion secretion of the N146Q and N146S mutants. 2018 Virology Introduction HBV M133T;N146Q;N146S 37;152;162 42;157;167 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Studies were performed to clarify whether the G145R and N146Q mutations impair virion secretion through the L, M, or S envelope protein, and whether M133T mutation in L, M, or S protein rescues virion secretion of the G145R or N146Q mutant. 2018 Virology Introduction HBV G145R;N146Q;M133T;G145R;N146Q 46;56;149;218;227 51;61;154;223;232 S;S;S 119;117;176 127;118;177 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation could also rescue virion secretion of G145R and other immune escape mutants. 2018 Virology Introduction HBV M133T;G145R 4;57 9;62 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The most common vaccine escape mutation, G145R, has been shown to impair the binding of antibodies raised against the wild-type (WT) S protein. 2018 Virology Introduction HBV G145R 41 46 S 133 134 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Additionally, clinical study indicated that HBV carrying rtA181T/sW172* mutation may have an increased oncogenic potential. 2018 Virology journal Introduction HBV W172X;A181T 65;59 71;64 RT;S 57;65 59;66 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. As we known, HBV rtA181T mutant is an A T mutation at position 181 of the P gene in the RT domain. 2018 Virology journal Introduction HBV A181T 19 24 P;RT;RT 76;17;90 77;19;92 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. HBV rtA181T/sW172* mutant had a dominant secretion defect of HBsAg which may cause the accumulation of viral core particles in liver cells, and the latter may damage the liver microenvironment. 2018 Virology journal Introduction HBV W172X;A181T 12;6 18;11 C;S;RT;S 109;61;4;12 113;66;6;13 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. However, because of a low genetic barrier to the development of resistance, HBV rtA181T/V mutation is common in real-life medical practice. 2018 Virology journal Introduction HBV A181T;A181V 82;82 89;89 RT 80 82 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. However, it is still unknown about the molecular mechanism of tumorigenesis of HBV rtA181T/sW172* mutant expressing truncated HBsAg protein. 2018 Virology journal Introduction HBV W172X;A181T 91;85 97;90 S;RT;S 126;83;91 131;85;92 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In theory, its overlapping S gene should have two types of mutation at amino acid 172, which include rtA181T/sW172L (TGG CTC TTA CTC) mutant coding substituted HBsAg protein and rtA181T/sW172*(TGG CTC TGA CTC) mutant coding truncated HBsAg protein. 2018 Virology journal Introduction HBV W172L;W172X;A181T;A181T 109;188;103;182 115;194;108;187 S;S;RT;RT;S;S;S 162;238;101;180;27;109;188 167;243;103;182;28;110;189 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Our previously studies showed that the replication capacity of HBV rtA181T/sW172* mutant was higher than that of HBV rtA181T/sW172L mutant. 2018 Virology journal Introduction HBV W172X;W172L;A181T;A181T 75;125;69;119 81;131;74;124 RT;RT;S;S 67;117;75;125 69;119;76;126 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Thus, to better and fully understand the tumorigenicity of HBV rtA181T mutants, we designed this study to investigate the impact of different overlapping S gene mutation (sW172L and sW172*) on the tumorigenicity of HBV rtA181T mutant and reveal the possible mechanism. 2018 Virology journal Introduction HBV A181T;A181T;W172L;W172X 65;221;171;182 70;226;177;188 RT;RT;S;S;S 63;219;154;171;182 65;221;155;172;183 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Other BCP mutations, notably T1753V and T1768A, have also been reported to be associated with an increased risk of HCC. 2018 Cancer management and research Introduction HBV T1753V;T1768A 29;40 35;46 BCP 6 9 Hepatocellular carcinoma 115 118 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The A1762T/G1764A BCP double mutation was associated with a hazard ratio (HR) of 1.73 for developing HCC. 2018 Cancer management and research Introduction HBV G1764A;A1762T 11;4 17;10 BCP 18 21 Hepatocellular carcinoma 101 104 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The most frequent BCP mutation is a double mutation involving an A to T substitution at nucleotide 1762 and a G to A substitution at nucleotide 1764. 2018 Cancer management and research Introduction HBV A1762T;G1764A 65;110 103;148 BCP 18 21 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The X gene mutations (two of the most common being C1653T and T1753V) and Pre S2 gene deletions have been associated with increased incidence of HCC. 2018 Cancer management and research Introduction HBV C1653T;T1753V 51;62 57;68 PreS2;X 74;4 80;5 Hepatocellular carcinoma 145 148 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. Specific single mutations, such as G145R, disrupt the structure of this epitope domain so that neutralizing antibodies (anti-HBs) cannot recognize it, thereby eliminating protection. 2018 World journal of hepatology Introduction HBV G145R 35 40 S 125 128 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. HBV resistance to TDF is not well characterised, but there are emerging data from in vitro studies associating Pol mutations rtA194T and rtN236T with decreased susceptibility. 2018 PLoS neglected tropical diseases Introduction HBV N236T;A194T 139;127 144;132 P;RT;RT 111;125;137 114;127;139 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Virological breakthrough on TDF therapy has been reported in two patients harbouring rtS78T/sC69 mutations, and in another patient with multi-site polymerase mutations; rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I. 2018 PLoS neglected tropical diseases Introduction HBV S78T;L80M;M204V;M204I;A200V;T184A;T184L;V191I;L180M;F221Y;S223A;R153Q 87;171;188;188;199;226;226;250;179;208;217;237 91;175;195;195;204;233;233;255;184;213;222;242 P;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S 147;85;169;177;186;197;206;215;224;235;248;92 157;87;171;179;188;199;208;217;226;237;250;93 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Whilst the S protein mutation sG145R has been identified as the major VEM, recently other mutations in S protein have been associated with immune escape Fig 1. 2018 PLoS neglected tropical diseases Introduction HBV G145R 30 36 S;S;S 11;30;103 12;31;104 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. For example, hepatitis B virus (BHV) 1762T/1764A double mutation (HBVDM) detection in urine was done with 250-fold WT while KRAS (G12V) point mutation (PM) detection in urine was done with 1000-fold WT. 2018 Biosensors & bioelectronics Introduction HBV G12V 130 134 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. HBVDM and KRAS G12V PM were chosen as the model double-stranded mutations for ease of comparison with detection of their single-stranded counterparts as both mutations have been extensively studied in single-stranded mutation detections. 2018 Biosensors & bioelectronics Introduction HBV G12V 15 19 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Furthermore, five HBcAg mutations identified in a Korean population, P5H/L/T, E83D, I97F/L, L100I, and Q182K/Stop, were shown to be significantly enriched in HCC patients compared with patients at earlier disease stages, including those with cirrhosis and chronic hepatitis (Kim et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV P5H;P5L;P5T;Q182X;E83D;I97F;I97L;L100I;Q182K 69;69;69;103;78;84;84;92;103 76;76;76;113;82;90;90;97;113 C 18 23 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B 158;242;256 161;251;273 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Mutations within the X gene, including V5M, I127T, K130M, and V131I/L, are risk factors for HCC and may promote the progression of liver degradation (Kim et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV V5M;I127T;K130M;V131I;V131L 39;44;51;62;62 42;49;56;69;69 X 21 22 Hepatocellular carcinoma;Liver disease 92;131 95;148 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. One of the most common precore mutations reported thus far is a G1896A, which prevents HBeAg production through the replacement of a tryptophan residue at amino acid position 28 with a premature stop codon (Tong et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV G1896A 64 70 C;Precore 87;23 92;30 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Similarly, a study of an Indian population showed that HBcAg residue 5 mutations P5H/L/T or P5R were found more frequently in HCC patients than in HBV-infected patients at other clinical stages of liver disease (Malik et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV P5H;P5L;P5T;P5R 81;81;81;92 88;88;88;95 C 55 60 Hepatocellular carcinoma;Liver disease;HBV infections 126;197;147 129;210;159 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Similarly, the role of the precore mutation G1896A and the basal core promoter double mutation A1762T/G1764A in the progression of HBV-related liver diseases has been intensively studied (Kim et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV G1764A;G1896A;A1762T 102;44;95 108;50;101 BCP;Precore 59;27 78;34 Liver disease 131 157 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. The pre-S2 mutation F141L and the pre-S1 mutation W182*, leading to the premature termination of HBsAg, are reportedly associated with more severe HBV infection (Mun et al.,; Lee et al.,). 2018 Frontiers in cellular and infection microbiology Introduction HBV W182X;F141L 50;20 55;25 S;PreS1;PreS2 97;34;4 102;40;10 HBV infections 147 160 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. An adequately rapid, specific and sensitive method for detection of this precore G1896A mutant is needed. 2018 Saudi journal of biological sciences Introduction HBV G1896A 81 87 Precore 73 80 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Preliminary studies conducted in South India suggest that G to A switch at nucleotide 1896 is the most common mutation of HBV genome in patients with chronic liver disease from the Indian subcontinent. 2018 Saudi journal of biological sciences Introduction HBV G1896A 58 90 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. With the above background, the current study was designed to look at the prevalence of precore G1896A mutations in HBeAg negative serology patients with different kinds of liver diseases. 2018 Saudi journal of biological sciences Introduction HBV G1896A 95 101 C;Precore 115;87 120;94 Liver disease 172 186 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. We previously demonstrated that resolved HBV carriers with the G1896A variant (guanine to adenine mutant at nucleotide 1896) in the precore gene of the HBV genome might have an increased risk of HBV reactivation and fatal acute liver failure. 2018 Scientific reports Introduction HBV G1896A 63 69 Precore 132 139 Liver disease 222 241 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. For instance, it was found that A1762T/G1764A were novel mutations within CP and could lead to decreased HBeAg expression but enhanced viral replication, which correlated with liver disease severity. 2019 Viruses Introduction HBV G1764A;A1762T 39;32 45;38 Core promoter;C 74;105 76;110 Liver disease 176 189 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition to the classical ETV-resistance mutations, a novel mutation pattern, rtL180M+M204V+rtA186 T(+-I163V) from an ETV-refractory patient were reported to account for ETV resistance. 2019 Emerging microbes & infections Introduction HBV A186T;L180M;M204V;I163V 97;83;89;106 103;88;94;111 RT;RT 81;95 83;97 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Moreover, HBV rtL269I and rtS78 T/sC69stop mutations were respectively reported being associated with enhanced viral replication of LAMr mutants and insufficient response to ETV treatment. 2019 Emerging microbes & infections Introduction HBV C69X;S78T;L269I 34;28;16 42;33;21 RT;RT;S 14;26;34 16;28;35 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. rtL180M+A181C+M204V. 2019 Emerging microbes & infections Introduction HBV L180M;A181C;M204V 2;8;14 7;13;19 RT 0 2 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Signature or classical ETV-resistance mutations require an HBV RT mutation at position rtT184, S202, or M250 in the presence of LAM-resistance mutations rtM204V+L180M or rtM204I +- L180M (abbreviated as LAMr). 2019 Emerging microbes & infections Introduction HBV M204V;M204I;L180M;L180M 155;172;161;181 160;177;166;186 RT;RT;RT;RT 63;87;153;170 65;89;155;172 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Among other commonly detected vaccine-escape mutants are: P120Q, Q129H, F134Y/L, S143L and D144A/E. 2019 PeerJ Introduction HBV P120Q;Q129H;F134Y;F134L;S143L;D144A;D144E 58;65;72;72;81;91;91 63;70;79;79;86;98;98 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The prototypic and most stable vaccine-escape mutant is G145R. 2019 PeerJ Introduction HBV G145R 56 61 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Nonetheless, using the transient expression system, we found that the LHBs sW182* protein can antagonize multiple tumor suppressor pathways involving p53 and Smad4. 2019 PloS one Introduction HBV W182X 75 81 S;S 70;75 74;76 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Of the 12, 6 cases cause immature stop codon at Tryptophane-182 of the S gene (sW182*). 2019 PloS one Introduction HBV W182X 79 85 S;S 71;79 72;80 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Probably because of the unstable nature of the sW182* protein in the liver cells, attempts to generate cell clones that express the mutant protein were unsuccessful. 2019 PloS one Introduction HBV W182X 47 53 S 47 48 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Therefore, in the current study we used Huh-7, a cell line of liver origin, to express LHBs sW182*, the most frequently identified nonsense mutant with the highest oncogenic potential in our previous study. 2019 PloS one Introduction HBV W182X 92 98 S;S 87;92 91;93 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. However, compensatory mutations have been reported to partially restore the viral replication capacity, including rtL80V/I, rtL82M, rtV173L and rtV207I, mostly in the RT region of pol. 2019 Antiviral research Introduction HBV L80V;L80I;L82M;V173L;V207I 116;116;126;134;146 122;122;130;139;151 P;RT;RT;RT;RT;RT 180;114;124;132;144;167 183;116;126;134;146;169 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. However, the mechanism of P5T-associated liver disease progression remains unclear. 2019 Antiviral research Introduction HBV P5T 26 29 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Moreover, it has also been suggested that P5T/A mutation is an independent factor for acute-on-chronic liver failure (ACLF). 2019 Antiviral research Introduction HBV P5T;P5A 42;42 47;47 Acute on chronic liver failure;Acute on chronic liver failure 118;86 122;116 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Our study revealed that the mutant core, predominantly P5T, boosts the levels of HBV capsid formation and pgRNA encapsidation, and subsequently enhances the viral replication competency, which may contribute to disease progression during LAM treatment. 2019 Antiviral research Introduction HBV P5T 55 58 Capsid;C 85;35 91;39 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Previous studies have shown that the substitution of proline (P) with threonine (T) at codon 5 of HBcAg caused lower levels of virion secretion, which, would revert to the wild type secretion phenotype when it coexisted with F97L mutation. 2019 Antiviral research Introduction HBV F97L 225 229 C;P 98;62 103;63 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. ADV-resistance has been associated with the rtN236T mutation in the D domain and/or the rtA181V/T mutation in the B domain. 2019 Experimental and therapeutic medicine Introduction HBV A181V;A181T;N236T 90;90;46 97;97;51 RT;RT 44;88 46;90 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. It has been indicated that LAM resistance is mostly associated with the rtM204I/V mutation in the tyrosine-methionine-aspartate-aspartate (YMDD) motif of the C domain of the polymerase gene. 2019 Experimental and therapeutic medicine Introduction HBV M204I;M204V 74;74 81;81 P;RT;P;P 174;72;98;139 184;74;137;143 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. A recent meta-analysis of 54 studies examining the association between these mutations and HCC showed that X_K130M/V131I are detected in 66.5% of HCC cases, compared to 39.8% of non-HCC cases. 2019 Molecular cancer research Introduction HBV V131I;K130M 115;108 120;114 X 107 108 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 91;146;182 94;149;185 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. HBV patients with chronic hepatitis, fulminant hepatitis or HCC are often detected with mutations at K130M/V131I sites and diagnosed as HBeAg negative. 2019 Molecular cancer research Introduction HBV V131I;K130M 107;101 112;106 C 136 141 Chronic Hepatitis B;Fulminant Hepatitis B;Hepatocellular carcinoma 18;37;60 35;56;63 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. Several HBx gene mutation hotspots, including A12T, V44I, A66T, H86Y, E109D, and K130M/V131I can be found in HBV carriers. 2019 Molecular cancer research Introduction HBV V131I;A12T;V44I;A66T;H86Y;E109D;K130M 87;46;52;58;64;70;81 92;50;56;62;68;75;86 X 8 11 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. The aim of the study reported herein was to discover the impact of K130M/V131I mutant and wild-type variants of HBx-B on HCC progression and explore the genetic mechanism(s) involved with liver tumorigenesis using the Fah/SB11 transgenic mouse model. 2019 Molecular cancer research Introduction HBV V131I;K130M 73;67 78;72 X 112 115 Hepatocellular carcinoma;Hepatocellular carcinoma 121;188 124;207 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. The dual amino acid changes at K130M/V131I, which overlaps both the HBx gene and basal core promoter (BCP), have been consistently shown to have the highest potential to promote HCC progression. 2019 Molecular cancer research Introduction HBV V131I;K130M 37;31 42;36 BCP;BCP;X 81;102;68 100;105;71 Hepatocellular carcinoma 178 181 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. These X protein changes are encoded by nucleotide changes in the BCP region A1762T/G1764A (BCP_A1762T/G1764A), and have been shown to be associated with decreased PreC/C RNA synthesis and decreased expression of HBeAg. 2019 Molecular cancer research Introduction HBV G1764A;G1764A;A1762T;A1762T 83;102;76;94 89;108;82;101 BCP;BCP;C;Precore;C;X 65;91;212;163;168;6 68;94;217;167;169;7 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Double mutations, A1762T and G1764A, in the basic core promoter region result in decreased HBeAg expression and enhanced viral genome replication; these mutations are frequently found in HBeAg-negative chronic hepatitis patients. 2019 Virology journal Introduction HBV A1762T;G1764A 18;29 24;35 BCP;C;C 44;91;187 63;96;192 Chronic Hepatitis B 187 219 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. One of the most common mutations of HBV is G1896A at the precore region that converts TGG to TAG, a stop codon, which abolishes the expression of hepatitis B e antigen (HBeAg). 2019 Virology journal Introduction HBV G1896A 43 49 C;C;Precore 158;169;57 167;174;64 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. The fourth category could be found before NA therapy, such as T38A, Y124H and D134E. 2019 Scientific reports Introduction HBV T38A;Y124H;D134E 62;68;78 66;73;83 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. The third category which named putative antiviral resistance mutation may relate to prolonged NA treatment or replication compensation, such as S53N, T54N and L82M. 2019 Scientific reports Introduction HBV S53N;T54N;L82M 144;150;159 148;154;163 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. These two categories are known as classical mutations, which include: (i) M204I/V mutation, which associates with LAM or LDT resistance; (ii) N236T or A181T/V mutations, which associate with ADV resistance; (iii) M204V + L180M and either T184A/G/I/L/S or S202G or M250V to develop resistance to ETV. 2019 Scientific reports Introduction HBV T184A;T184G;T184I;T184L;T184S;M204I;M204V;N236T;A181T;A181V;M204V;L180M;S202G;M250V 238;238;238;238;238;74;74;142;151;151;213;221;255;264 251;251;251;251;251;81;81;147;158;158;218;226;260;269 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. For instance, I195M in the S protein (sI195M) and sW196S can produce rtM204I and rtL180M/rtM204I in RT, which could confer resistance to LMV. 2019 Journal of clinical microbiology Introduction HBV M204I;L180M;M204I;I195M;W196S;I195M 71;83;91;38;50;14 76;88;96;44;56;19 RT;RT;RT;RT;S;S;S 69;81;89;100;27;38;50 71;83;91;102;28;39;51 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. For instance, M204V/I in RT (rtM204V/I) is a classical lamivudine (LMV) resistance mutation, which also greatly reduces susceptibility to telbivudine (LdT); rtA181T/V is not only reported as an adefovir dipivoxil (ADV) resistance mutation, but rtA181T/V also confers a decreased susceptibility to LMV, LdT, tenofovir disoproxil fumarate (TDF), and tenofovir alafenamide (TAF); rtM204V/I and rtL180M together with rtI169T, rtV173L, rtM250V, rtT184G, or S202I/G can lead to resistance to entecavir (ETV). 2019 Journal of clinical microbiology Introduction HBV M204V;M204I;A181T;A181V;A181T;A181V;L180M;M204V;M204I;I169T;V173L;M250V;T184G;M204V;M204I;S202I;S202G 31;31;159;159;246;246;393;379;379;415;424;433;442;14;14;452;452 38;38;166;166;253;253;398;386;386;420;429;438;447;21;21;459;459 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 25;29;157;244;377;391;413;422;431;440 27;31;159;246;379;393;415;424;433;442 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Apart from these findings, another truncated mutant (sC69*) was identified from CHB patients as shown in previous studies. 2019 Frontiers in microbiology Introduction HBV C69X 53 58 S 53 54 Chronic Hepatitis B 80 83 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, little is known about the influence of the sC69* mutant on viral infectivity and spread. 2019 Frontiers in microbiology Introduction HBV C69X 52 57 S 52 53 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, we found that the sC69* negatively impaired viral replication, infectivity and spread, which could be rescued by the WT. 2019 Frontiers in microbiology Introduction HBV C69X 31 36 S 31 32 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. On the contrary, the sC69* mutant inhibited the host innate immune response more potently than that of the WT. 2019 Frontiers in microbiology Introduction HBV C69X 21 26 S 21 22 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Our hypothesis for sC69* is that it can inhibit host innate immune responses, which does not only protect itself but also the WT from host immune surveillance. 2019 Frontiers in microbiology Introduction HBV C69X 19 24 S 19 20 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Our previous study showed that the sC69* mutant could restrict viral replication and secretion, but these defects could somehow be rescued by the WT HBs. 2019 Frontiers in microbiology Introduction HBV C69X 35 40 S;S 149;35 152;36 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Recently, it was shown that HBsAg truncated mutants such as sW172*, sW182*, and sW199* occurred in patients both with and without antiviral treatment. 2019 Frontiers in microbiology Introduction HBV W172X;W182X;W199X 60;68;80 66;74;86 S;S;S;S 28;60;68;80 33;61;69;81 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Recently, the sC69* was found in genotype A CHB patients, which was reported to be associated with entecavir (ETV) and tenofovir (TDF) resistance. 2019 Frontiers in microbiology Introduction HBV C69X 14 19 S 14 15 Chronic Hepatitis B 44 47 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Similarly, it was also shown that HBV WT rescued the replication and secretion of variants such as sW172*, sW182*, and sC69*. 2019 Frontiers in microbiology Introduction HBV W172X;W182X;C69X 99;107;119 105;113;124 S;S;S 99;107;119 100;108;120 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. These results indicate that HBV sC69* coexisting with WT might facilitate the viral fitness and surviving from the host surveillance. 2019 Frontiers in microbiology Introduction HBV C69X 32 37 S 32 33 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Thus, it is possible to use HepG2-NTCP cells as an HBV infection model to study the influence of sC69* on viral infectivity and spread. 2019 Frontiers in microbiology Introduction HBV C69X 97 102 S 97 98 HBV infections 51 64 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To characterize how the sC69* mutant exists in the host, we sequenced the SHBs coding region in HBV genotype C from a cohort of 435 CHB patients without or with antiviral therapy. 2019 Frontiers in microbiology Introduction HBV C69X 24 29 S;S 24;74 25;78 Chronic Hepatitis B 132 135 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We found that 19 patients harbored the sC69* mutant. 2019 Frontiers in microbiology Introduction HBV C69X 39 44 S 39 40 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We found that 4.37% (19/435) of the studied patients with genotype C HBV chronic infection carried the small hepatitis B surface (SHBs) sC69* mutant resulting in the truncated SHBs [about 1/3 length of wild-type (WT) SHBs]. 2019 Frontiers in microbiology Introduction HBV C69X 136 141 S;S;S;S;S 136;130;176;217;121 137;134;180;221;128 Chronic HBV infection 73 90 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We then performed in vitro experiments to study the impact of the sC69* on viral replication, infectivity and spread and innate immune responses. 2019 Frontiers in microbiology Introduction HBV C69X 66 71 S 66 67 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We therefore wondered if the sC69* mutant could also inhibit innate immune responses and promote HBV persistence in the host. 2019 Frontiers in microbiology Introduction HBV C69X 29 34 S 29 30 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The most common mutations involve G1896A in the PC region and the simultaneous presence of G1764A/A1762T in the BCP region, which results to the premature termination of HBeAg expression and decreased level of HBeAg, respectively. 2019 Mediterranean journal of hematology and infectious diseases Introduction HBV A1762T;G1896A;G1764A 98;34;91 104;40;97 BCP;C;C;Precore 112;170;210;48 115;175;215;50 31341412 Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations. The precore mutation (G1896A), mutations in enhancer II (C1653T) and the BCP (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC. 2019 International journal of medical sciences Introduction HBV G1896A;C1653T;T1753V;A1762T;G1764A 22;57;78;111;119 28;63;84;117;125 BCP;Enh II;Precore;PreS 73;44;4;149 76;55;11;154 Hepatocellular carcinoma 222 225 31341412 Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations. When we established the Long An cohort in 2004, we found that about half of the HBV-infected individuals have BCP double mutations (A1762T, G1764A) in the viral genome and more than 93% of HCC cases occurred in those with BCP double mutations. 2019 International journal of medical sciences Introduction HBV A1762T;G1764A 132;140 138;146 BCP;BCP 110;222 113;225 Hepatocellular carcinoma;HBV infections 189;80 192;92 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. We recently introduced some mutations in the reverse transcriptase (RT) region of Pol related to HCC from genotype C infected patients [rtM80I, rtN139K/T/H, and rtM204I/V]. 2019 Frontiers in immunology Introduction HBV M80I;N139K;N139T;N139H;M204I;M204V 138;146;146;146;163;163 142;155;155;155;170;170 P;RT;RT;RT;RT;RT 82;45;68;136;144;161 85;66;70;138;146;163 Hepatocellular carcinoma 97 100 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. In addition, double mutation in the basal core promoter (A1762T/G1764A) of HBV genotype C was commonly found as an independent risk factor for the development of HCC. 2019 Scientific reports Introduction HBV G1764A;A1762T 64;57 70;63 BCP 36 55 Hepatocellular carcinoma 162 165 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Mutations at C1653T and/or T1753V and A1762T/G1764A in Enhancer II/basal core promoter were also reported to be associated with HCC in 1999 compared with other liver disease statuses. 2019 Scientific reports Introduction HBV G1764A;C1653T;T1753V;A1762T 45;13;27;38 51;19;33;44 BCP;Enh II 67;55 86;66 Hepatocellular carcinoma;Liver disease 128;160 131;173 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The combination mutation involving the double mutation at A1762T/G1764A and mutation at C1653T and/or T1753V has now been shown to be a risk factor for HCC occurrence. 2019 Scientific reports Introduction HBV G1764A;A1762T;C1653T;T1753V 65;58;88;102 71;64;94;108 Hepatocellular carcinoma 152 155 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The assembly kinetics and thermodynamics of WT and D2N/D4N were investigated under different conditions. 2018 ACS omega Introduction HBV D4N;D2N 55;51 58;54 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Toward this goal, two aspartic acids (D) were replaced with neutral asparagines (N) to create a mutant Cp149 dimer D2N/D4N to remove two negative charges from each wild-type (WT) protein monomer (Figure 1a,b). 2018 ACS omega Introduction HBV D4N;D2N 119;115 122;118 C 103 105 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. A proline (P) residue at amino acids 5 and 130 is highly evolutionarily conserved even in woodchuck hepatitis B virus core protein. 2019 Journal of virology Introduction HBV P5P 1 39 C 118 122 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Both P130T and P5T could compensate for or rescue the immature secretion phenotype of mutant I97L. 2019 Journal of virology Introduction HBV P5T;P130T;I97L 15;5;93 18;10;97 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In addition to the trans-defect in virion secretion, a cis-defect in intracellular viral DNA synthesis was also detected in mutant F97L by a genetic complementation assay. 2019 Journal of virology Introduction HBV F97L 131 135 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In addition to this HBc 97L mutation, HBc P130T and P5T mutations were found frequently in patients. 2019 Journal of virology Introduction HBV P5T;P130T 52;42 55;47 C;C 20;38 23;41 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In both immunocompetent BALB/c and immunodeficient IFNAR-/-, STAT1-/-, and NOD/SCID mouse models, intracellular HBV DNA of mutant I97L is less abundant and more transient than the wild-type HBV. 2019 Journal of virology Introduction HBV I97L 130 134 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In contrast, mutant P130T exhibited a hypermaturation phenotype with accumulated mature RC form DNA in the mouse liver. 2019 Journal of virology Introduction HBV P130T 20 25 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In the double mutant I97L/P130T, mutation P130T can only partially rescue the immature secretion of mutant I97L. 2019 Journal of virology Introduction HBV P130T;I97L;P130T;I97L 26;21;42;107 31;25;47;111 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Interestingly, while a single HBc mutation L60V or P5T displayed a low-level secretion phenotype, a single mutation P130T led to a "hypermaturation phenotype" characterized by an increased abundance of both intracellular and extracellular fully mature full-length RC DNA. 2019 Journal of virology Introduction HBV P5T;L60V;P130T 51;43;116 54;47;121 C 30 33 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Near amino acid 97, an engineered HBc mutation L95A or K96A, blocked envelopment and virion secretion. 2019 Journal of virology Introduction HBV L95A;K96A 47;55 51;59 C 34 37 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Point mutation A119F in the pre-S1 region of the envelope protein can compensate for the immature secretion of mutant I97L. 2019 Journal of virology Introduction HBV A119F;I97L 15;118 20;122 S;PreS1 49;28 57;34 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Recently, in another cryoEM study, this pocket in the mutant F97L virions was found enlarged. 2019 Journal of virology Introduction HBV F97L 61 65 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Strikingly, relative to wild-type HBV, single mutant P130T significantly prolonged the persistence of intracellular HBV DNA genome. 2019 Journal of virology Introduction HBV P130T 53 58 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The immature secretion of HBc variant I97L can be fully recapitulated in vivo. 2019 Journal of virology Introduction HBV I97L 38 42 C 26 29 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The most common HBc variant contains a substitution mutation at amino acid 97, changing an isoleucine to leucine (I97L). 2019 Journal of virology Introduction HBV I97L 114 118 C 16 19 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Using a cis-trans genetic test design, we demonstrated that it is the trans-acting mutant F97L HBc protein, rather than the mutant F97L pgRNA, that is responsible for the extracellular immature virion secretion. 2019 Journal of virology Introduction HBV F97L;F97L 90;131 94;135 C 95 98 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. While HBc mutant I97L is frequent in the genotype C (serotype adr), mutant F97L is common in the genotype D (serotype ayw) (; see also references cited in reference). 2019 Journal of virology Introduction HBV I97L;F97L 17;75 21;79 C 6 9 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. For instance, rtM204I is a classic mutation reducing susceptibility to mono-therapy by NAs with low genetic barriers, such as lamivudine (LAM), telbivudine (L-dT) and clevudine (CLV). 2019 World journal of gastroenterology Introduction HBV M204I 16 21 RT 14 16 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Multivariate analyses showed that the naturally-occurring rtM204I variants were more frequently pre-existed in patients with liver fibrosis, and the pre-existence of the naturally-occurring rtM204I variants were significantly associated with incomplete viral response to nucleos(t)ide analogues. 2019 World journal of gastroenterology Introduction HBV M204I;M204I 60;192 65;197 RT;RT 58;190 60;192 Liver fibrosis 125 139 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Tenofovir is a more suitable nucleos(t)ide analogues than entecavir for treatment-naive CHB patients carrying the naturally occurring rtM204I mutations. 2019 World journal of gastroenterology Introduction HBV M204I 136 141 RT 134 136 Chronic Hepatitis B 88 91 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The newly developed locked nucleotide probe based real-time PCR method could discriminate the naturally-occurring rtM204I mutations from wild type with high sensitivity in treatment-naive patients. 2019 World journal of gastroenterology Introduction HBV M204I 116 121 RT 114 116 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The purpose of this study was to determine the prevalence and clinical characteristics of naturally occurring rtM204I mutations in treatment-naive patients infected with HBV genotype C2 strains by using a newly developed locked nucleotide probe (LNA probe) based real time PCR (LNA-RT-PCR) method, which can detect subspecies at 5% of the circulating HBV population. 2019 World journal of gastroenterology Introduction HBV M204I 112 117 RT 110 112 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. A total of 8 HBV classical mutation sites are conventionally tested for HBV patients in most clinical labs, including M204I/V, L180M, T184A/F/I/L/S, L181T/V, M250I/L/V, M236T, S202G, and V207I. 2019 Scientific reports Introduction HBV T184A;T184F;T184I;T184L;T184S;M250I;M250L;M250V;M204I;M204V;L180M;L181T;L181V;M236T;S202G;V207I 134;134;134;134;134;158;158;158;118;118;127;149;149;169;176;187 147;147;147;147;147;167;167;167;125;125;132;156;156;174;181;192 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. Moreover, some of the mutations in HBsAg, such as D144A, Q129R, and G145R, could reduce binding to HBsAbs from the hepatitis B vaccination, bypassing the neutralizing activity of these antibodies (antibody escape) and result in infecting HBV-vaccinated individuals. 2019 Scientific reports Introduction HBV D144A;Q129R;G145R 50;57;68 55;62;73 S;S 99;35 105;40 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. 3TC is also approved as an anti-HIV-1 agent, and M184V in HIV-1 RT, which corresponds to M204V in HBV RT, has also been reported as an amino acid substitution responsible for 3TC resistance in HIV-1. 2020 Scientific reports Introduction HBV M204V 89 94 RT;RT 64;102 66;104 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. Accordingly, we assumed that crystallographic studies of HIV-1 RT containing HBV-associated amino acids at the N-site should also provide important clues for understanding the mechanism of 3TC/ETV resistance caused by common M204V/I in HBV RT (M184V/I in HIV-1 RT). 2020 Scientific reports Introduction HBV M204V;M204I 225;225 232;232 RT;RT;RT 63;240;261 65;242;263 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. It is therefore of crucial importance to understand why the key M204V/I amino acid substitution leads to both 3TC and ETV resistance. 2020 Scientific reports Introduction HBV M204V;M204I 64;64 71;71 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. Previous characterization of HBV RT mutants suggested that the M204V/I mutation is crucial for both 3TC/ETV resistance. 2020 Scientific reports Introduction HBV M204V;M204I 63;63 70;70 RT 33 35 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. The amino acid substitutions, M204V/I and M204V/I + L180M, in HBV RT are known to cause 3TC resistance, and these mutations significantly reduce ETV effectiveness against HBV, thereby increasing the likelihood of subsequently developing greater ETV resistance through getting additional amino acid substitutions such as S202G in HBV RT. 2020 Scientific reports Introduction HBV S202G;M204V;M204V;M204I;M204I;L180M 320;30;42;30;42;52 325;37;49;37;49;57 RT;RT 66;333 68;335 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. By comparing the differences in dynamics between hCp149-Y132A and WT hCp149, an understanding of whether these proteins sample different conformations at different rates can start to be determined. 2020 ACS chemical biology Introduction HBV Y132A 56 61 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In HBV, Y132 makes up 10% of the buried surface area when the dimer is assembled into capsids, however HBV Cp149-Y132A can co-assemble with WT hCp149 to form fragile capsids . 2020 ACS chemical biology Introduction HBV Y132A 113 118 Capsid;Capsid;C;S 86;166;107;40 93;173;109;47 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In this study, we used hydrogen deuterium exchange coupled to mass spectrometry (HDX-MS), native mass spectrometry (NMS), and differential scanning fluorimetry (DSF) to investigate the biophysical differences between hCp149, wCp149, hCp149-Y132A, and wCp149-Y132A. 2020 ACS chemical biology Introduction HBV Y132A;Y132A 240;258 245;263 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. It is suspected that there is an allosteric relationship between the spike tip, at the intra-dimer interface, and the contact region, at the inter-dimer interface, based on biophysical studies of hCp149, wCp149, hCp149-Y132A, and wCp149-Y132A . 2020 ACS chemical biology Introduction HBV Y132A;Y132A 219;237 224;242 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Mutation of tyrosine at position 132 to an alanine (Y132A) in either hCp149 or wCp149 renders the dimer assembly incompetent. 2020 ACS chemical biology Introduction HBV Y132A;Y132A 52;12 57;50 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The assembly incompetent conformation of hCp149-Y132A shows a decrease in stability at the intra-dimer interface. 2020 ACS chemical biology Introduction HBV Y132A 48 53 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The structures of hCp149-Y132A and hCp149 are similar; however, it is somewhat surprising that the largest differences occur in the spike tip and intra-dimer interface, (Figure 1, panel C) leading us to propose that changes in protein dynamics, both at the site of the mutation and areas distal to the mutation, may be the reason for the functional difference. 2020 ACS chemical biology Introduction HBV Y132A 25 30 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The Y132A mutation is located in the inter-dimer contact region (Figure 1, panel C) . 2020 ACS chemical biology Introduction HBV Y132A 4 9 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. This suggests that decreased intra-dimer stability destabilizes a key conformation in the energy landscape, making the free energy of assembly for hCp149-Y132A unfavorable. 2020 ACS chemical biology Introduction HBV Y132A 154 159 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. Also, mutations may occur in association with either vaccine-induced immune-escape (P120T, K122R, T126S, Q129H, G130N, M133L, and M133T) or in relation to the patients with occult HBV infection (Y100C, C124R, C124Y, K141E, and D144A). 2020 Heliyon Introduction HBV P120T;K122R;T126S;Q129H;G130N;M133L;M133T;Y100C;C124R;C124Y;K141E;D144A 84;91;98;105;112;119;130;195;202;209;216;227 89;96;103;110;117;124;135;200;207;214;221;232 HBV infections 180 193 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. G145R is a common immune escape mutation that is induced by the vaccine and can lead to HBsAg detection failure by some tests. 2020 Heliyon Introduction HBV G145R 0 5 S 88 93 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. In the present study, no G145R mutation was detected in the S protein of both HBV isolates from Ahvaz. 2020 Heliyon Introduction HBV G145R 25 30 S 60 61 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. The nucleotide substitutions in the pre-S1 promoter region, particularly the G2765A mutation, reduce the L protein expression and regulate the biological situation of HBV and result in a low viral load and then less serious disease in chronic HBV infection. 2020 Heliyon Introduction HBV G2765A 77 83 S;S1 promoter 105;36 114;51 Chronic HBV infection 235 256 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. This study attempted to identify mutations (K122R, N131T, F134Y, P142L, and T126N) in S gene, N-glycosylation sites (4, 112, 166, and 309), compare Ahvaz samples with isolates from other regions of the world using the phylogenetic tree, and investigate the tertiary structures of isolates. 2020 Heliyon Introduction HBV K122R;N131T;F134Y;P142L;T126N 44;51;58;65;76 49;56;63;70;81 S 86 87 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Both the G1896A and A1762T/G1764A mutations are associated with the "HBeAg-negative hepatitis" phase of CHB. 2020 Frontiers in microbiology Introduction HBV G1764A;A1762T;G1896A 27;20;9 33;26;15 C 69 74 Chronic Hepatitis B 104 107 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. HBV X/BCP/PC mutations (i.e., G1896A pre-core and A1762T/G1764A double mutants) are strong predictors of HCC risk and frequently reported in large epidemiological studies of HBV-related HCC. 2020 Frontiers in microbiology Introduction HBV G1764A;G1896A;A1762T 57;30;50 63;36;56 BCP;Precore;Precore;X 6;10;37;4 9;12;45;5 Hepatocellular carcinoma;Hepatocellular carcinoma 105;186 108;189 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. In the current study, we evaluated in vitro the functional properties of two clinically important genetic variants of HBV associated with HCC, the G1896A and A1762T/G1764A mutations. 2020 Frontiers in microbiology Introduction HBV G1764A;A1762T;G1896A 165;158;147 171;164;153 Hepatocellular carcinoma 138 141 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. The A1762T/G1764 double mutation is located within the BCP region of the HBV genome which influences the expression of both the pre-core/core and the pregenomic (pg) RNA transcripts. 2020 Frontiers in microbiology Introduction HBV A1762T;A1762G 4;4 10;10 BCP;C;Precore 55;137;128 58;141;136 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. The G1896A pre-core mutation introduces a premature stop codon in the precore/core HBV transcript resulting in abrogated HBeAg production. 2020 Frontiers in microbiology Introduction HBV G1896A 4 10 C;C;Precore;Precore 78;121;70;11 82;126;77;19 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. There is conflicting data from in vitro studies on the replicative capacity of G1896A or A1762T/G1764A HBV compared to wild-type HBV. 2020 Frontiers in microbiology Introduction HBV G1764A;G1896A;A1762T 96;79;89 102;85;95 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. This study was designed to compare in vitro viral replication in the wild-type, G1896A, and A1762T/G1764A HBV variants. 2020 Frontiers in microbiology Introduction HBV G1764A;G1896A;A1762T 99;80;92 105;86;98 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. In this study, we proved the oncogenic potential of rtM204I/sW196* mutants via in vitro assays in order to assess the cellular transformation ability and mouse xenograft tumorigenesis. 2020 International journal of molecular sciences Introduction HBV W196X;M204I 60;54 66;59 RT;S 52;60 54;61 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. rtM204I is a common 3TC-resistant mutation emerging in antiviral therapy, and may result in truncation or missense mutations on the overlapping surface gene (sW196*/S/L). 2020 International journal of molecular sciences Introduction HBV M204I;W196X;W196S;W196L 2;159;158;158 7;168;168;168 RT;S;S 0;158;144 2;159;151 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. We investigated four such mutants (sL15*, sL21*, sW156*, and sW172*) in our 3TC-experienced HCC cases for their nearby locations to the transactivity-on-region, and proved sL15*, sL21*, and sW172* mutants to be oncogenic. 2020 International journal of molecular sciences Introduction HBV L15X;L21X;W156X;W172X;L15X;L21X;W172X 35;42;49;61;172;179;190 40;47;55;67;177;184;196 S;S;S;S;S;S;S 35;42;49;61;172;179;190 36;43;50;62;173;180;191 Hepatocellular carcinoma 92 95 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. A few drug-resistance mutations, such as rtS78T and rtA181T, introduce a stop codon in the overlapping S region and affect the immune response, thereby influencing the clinical presentation of NA-treated patients. 2020 World journal of gastroenterology Introduction HBV S78T;A181T 43;54 47;59 RT;RT;S 41;52;103 43;54;104 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Classical primary resistance mutations include rtM204I/V (LAM-r) for LAM (rtM204I also confers resistance to LdT), rtA181V/rtN236T for ADV as well as LAM-r along with at least one substitution at rt184 (A/C/F/G/I/L/M/S), rt202 (C/G/I), and rtM250 (I/L/V) for ETV. 2020 World journal of gastroenterology Introduction HBV M204I;M204V;M204I;A181V;N236T 49;49;76;117;125 56;56;81;122;130 RT;RT;RT;RT;RT;RT;RT 47;74;115;123;196;221;240 49;76;117;125;198;223;242 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Contribution of sA159V to resistance was found in multiple followed up patients, in particular sA159V reduced hepatitis B surface antigen but raised the replication capacity of lamivudine/entecavir-resistant mutants. 2020 World journal of gastroenterology Introduction HBV A159V;A159V 16;95 22;101 S;S;S 16;95;122 17;96;129 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In addition, rtS106C+rtH126Y+rtD134E+rtL269I quadruple mutations have recently been reported to confer TDF resistance. 2020 World journal of gastroenterology Introduction HBV S106C;H126Y;D134E;L269I 15;23;31;39 20;28;36;44 RT;RT;RT;RT 13;21;29;37 15;23;31;39 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In this study, we evaluated a large number of patients to determine whether immune escape-associated mutations are associated with drug-resistance mutations, with a focus on the sA159V mutation. 2020 World journal of gastroenterology Introduction HBV A159V 178 184 S 178 179 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. For example, the double mutation A1762T/G1764A is the most common mutation in BCP and was found in some studies to be associated with progression to advanced liver disease and HCC development. 2020 JCI insight Introduction HBV G1764A;A1762T 40;33 46;39 BCP 78 81 Liver disease;Hepatocellular carcinoma 158;176 171;179 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. However, although a pronounced prevalence of A1762T/G1764A was observed in patients with advanced liver disease, the frequency of this mutation is also approximately 50% in our cohort of HBV inactive carriers. 2020 JCI insight Introduction HBV G1764A;A1762T 52;45 58;51 Liver disease 98 111 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. In addition, we performed bioinformatical modeling of pregenomic RNA secondary structures and in vitro analyses of A1762T/G1764A and the quadruple point mutation GCAC1809-1812TTCT in hepatoma cells. 2020 JCI insight Introduction HBV G1764A;A1762T 122;115 128;121 Hepatocellular carcinoma 183 191 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. The present study aimed to further specify the A1762T/G1764A-related clinical phenotype and to establish additional biomarkers for HBV-related prognosis. 2020 JCI insight Introduction HBV G1764A;A1762T 54;47 60;53 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. These data are contradictory and further limit the specificity of A1762T/G1764A as a robust prognostic marker in clinical practice. 2020 JCI insight Introduction HBV G1764A;A1762T 73;66 79;72 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. As compensatory changes, some other additional mutations such as rtL180M, rtV173L can also be included when the LMV resistance is occurring. 2020 Emerging microbes & infections Introduction HBV L180M;V173L 67;76 72;81 RT;RT 65;74 67;76 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Furthermore, we performed in-vitro susceptibility assays to verify the resistance efficacy of the mutation rtL229 V, a potential ETV-resistance site found in the study. 2020 Emerging microbes & infections Introduction HBV L229V 109 115 RT 107 109 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Phenotypic studies showed that the LMV resistance arising from rtM204V/I in the YMDD motif, could negate sensitivity to LMV by more than 100-fold decrease compared with wild-type. 2020 Emerging microbes & infections Introduction HBV M204V;M204I 65;65 72;72 RT;P 63;80 65;84 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The classic ETV resistance mutations rtT184G/rtS202I/rtM250V will reduce susceptibility to ETV, only in conjunction with additional LMV resistance mutations, such as rtM204V/I. 2020 Emerging microbes & infections Introduction HBV S202I;M250V;M204V;M204I;T184G 47;55;168;168;39 52;60;175;175;44 RT;RT;RT;RT 37;45;53;166 39;47;55;168 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. G145R was the first escape mutation described and the most frequently detected HBV variant with proven vaccine escape properties in humans. 2020 Frontiers in microbiology Introduction HBV G145R 0 5 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Although the HBV mutants harboring CYEI mutations were dominantly found in two TDF-resistant patients, a rtT301A (A) mutant together with CYEI mutations (CYEIA) was also identified from one patient as a minor portion. 2021 International journal of molecular sciences Introduction HBV T301A 107 112 RT 105 107 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Despite its high genetic barrier to resistance, we have previously reported that a novel quadruple mutation (CYEI; rtS106C (C), rtH126Y (Y), rtD134E (E), and rtL269I (I)) is associated with tenofovir resistance. 2021 International journal of molecular sciences Introduction HBV S106C;H126Y;D134E;L269I 117;130;143;160 122;135;148;165 RT;RT;RT;RT 115;128;141;158 117;130;143;160 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Moreover, we tested the effect of the rtT301A mutation on replication capability and drug sensitivity in hepatoma cell lines and primary human hepatocytes (PHHs). 2021 International journal of molecular sciences Introduction HBV T301A 40 45 RT 38 40 Hepatocellular carcinoma 105 113 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Therefore, in this study, we aimed to identify the role of a naturally occurring rtT301A mutation in HBV replication ability and susceptibility to tenofovir, using patient-derived HBV RT mutants and artificially constructed clones. 2021 International journal of molecular sciences Introduction HBV T301A 83 88 RT;RT 81;184 83;186 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The HBV precore G1896A mutation is known to be associated with HBV reactivation. 2021 International journal of health sciences Introduction HBV G1896A 16 22 Precore 8 15 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The precore stop codon mutation (G1896A) is resistant to IFN treatment. 2021 International journal of health sciences Introduction HBV G1896A 33 39 Precore 4 11 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Here, we report a case of a CHB patient who developed rtM204V, rtL180M and rtA194T mutations in association with viral breakthrough on LAM monotherapy and was rescued by TDF. 2021 Infection and drug resistance Introduction HBV M204V;L180M;A194T 56;65;77 61;70;82 RT;RT;RT 54;63;75 56;65;77 Chronic Hepatitis B 28 31 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. However, Delaney WE had not found a clear association between rtA194T and viral load by using transfected-HepG2 cell culture. 2021 Infection and drug resistance Introduction HBV A194T 64 69 RT 62 64 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. In addition, Samad Amini-Bavil-Olyaee demonstrated that clones harboring rtA194T showed partial resistance (a fivefold to sevenfold increase in the EC50) to TDF in vitro, irrespective of additional mutations. 2021 Infection and drug resistance Introduction HBV A194T 75 80 RT 73 75 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. It appears that the potential impact of rtA194T mutation on TDF susceptibility remains unclear and therefore deserves further study. 2021 Infection and drug resistance Introduction HBV A194T 42 47 RT 40 42 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Meanwhile, phenotypic analyses revealed that constructs harboring rtA194T together with rtL180M and rtM204V displayed a 10-fold reduction in TDF susceptibility. 2021 Infection and drug resistance Introduction HBV A194T;L180M;M204V 68;90;102 73;95;107 RT;RT;RT 66;88;100 68;90;102 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. The rtA194T Hepatitis B Virus (HBV) polymerase mutation was firstly identified, along with LAM resistance-associated mutations (rtL180M and rtM204V), in two HIV/HBV-coinfected patients treated with long-term TDF and LAM therapy. 2021 Infection and drug resistance Introduction HBV A194T;L180M;M204V 6;130;142 11;135;147 P;RT;RT;RT 36;4;128;140 46;6;130;142 HBV-HIV coinfections 157 175 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. In particular, we showed that rt269I-type infection versus rt269L-type infection leads to enhanced mitochondrial stress-mediated type I interferon (IFN-I) production, resulting in HBV e antigen (HBeAg)-negative infections by generating preC mutations at 1896 (G to A). 2021 Microorganisms Introduction HBV G1896A 254 267 C;C;Precore;RT;RT 184;195;236;30;59 193;200;240;32;61 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. G145A/R is the best described mutation associated with resistance to HBV vaccine/HBIg. 2021 Journal of viral hepatitis Introduction HBV G145A;G145R 0;0 7;7 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. In fact, resistance to ETV appears to occur through a two-hit mechanism with primary LVD resistance (LVDr) substitutions (M204V/I with/without rtL180M) followed by amino acid substitutions at the rtI169, rtT184, rtS202 or rtM250 sites. 2021 Molecular and clinical oncology Introduction HBV L180M;M204V;M204I 145;122;122 150;129;129 RT;RT;RT;RT;RT 143;196;204;212;222 145;198;206;214;224 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Some naturally occurring mutations at this site is also implicated with either low-level secretion (P5T-HBc and L60V-HBc) or premature (F/I/97 L-HBc) secretion phenotypes. 2021 Microorganisms Introduction HBV P5T;L60V 100;112 103;116 C;C;C 104;117;145 107;120;148 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. reported that one of the 50 high HBV DNA loads subjects developed rtM204I drug-resistance mutation after receiving TBV treatment, but the time duration that the patient received TBV treatment in the study was not clear. 2021 The Canadian journal of infectious diseases & medical microbiology Introduction HBV M204I 68 73 RT 66 68 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. In addition to a background of the mutations rtM204V/I, the other mutations, such as rtI169T, rtS184G, rtS202I and rtM250V, are associated with the emergence of ETV resistance. 2021 Journal of clinical and translational hepatology Introduction HBV M204V;M204I;I169T;S184G;S202I;M250V 47;47;87;96;105;117 54;54;92;101;110;122 RT;RT;RT;RT;RT 45;85;94;103;115 47;87;96;105;117 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Moreover, rtM204V combined with some other mutations may lead to a resistance to TDF. 2021 Journal of clinical and translational hepatology Introduction HBV M204V 12 17 RT 10 12 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. The mutations rtM204V/I represent one of the most common primary resistance mutations in hepatitis B patients, which directly decrease the susceptibility to NAs, especially to LAM and LdT. 2021 Journal of clinical and translational hepatology Introduction HBV M204V;M204I 16;16 23;23 RT 14 16 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Therefore, we chose mutations rtM204V/I to be detected. 2021 Journal of clinical and translational hepatology Introduction HBV M204I;M204V 32;32 39;39 RT 30 32 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Furthermore, the IEMs Q129N, M133T, and F134Y have been predicted to cause HBV diagnostic failure. 2021 Viruses Introduction HBV Q129N;M133T;F134Y 22;29;40 27;34;45 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. In the following years, other mutations observed on the a-determinant, which are considered as immune escape variants, including T116N, P120S/E, I/T126A/N/I/S, Q129H/R, M133L, K141E, P142S, and D144A/E, have also been reported. 2021 Viruses Introduction HBV T126A;I126A;I126N;I126I;I126S;T126N;T126I;T126S;T116N;P120S;P120E;Q129H;Q129R;M133L;K141E;P142S;D144A;D144E 145;145;145;145;145;145;145;145;129;136;136;160;160;169;176;183;194;194 158;158;158;158;158;158;158;158;134;143;143;167;167;174;181;188;201;201 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The first described vaccine escape mutation, arising from the substitution of glycine (G) with arginine (R) at position 145 (G145R) within the a-determinant region of the S gene, was reported in the sera of Italian vaccinated children who had HBsAg and anti-HBs antibodies. 2021 Viruses Introduction HBV G145R 125 130 S;S;S 258;243;171 261;248;172 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBV-I97L was mainly detected in hepatitis B e antigen (HBeAg)-negative patients, and the patients infected with HBV-I97L exhibited low levels of HBsAg and HBV DNA and achieved ALT within the normal range. 2021 Cellular and molecular gastroenterology and hepatology Introduction HBV I97L;I97L 4;116 8;120 C;C;S 44;55;145 53;60;150 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In this study, we aimed to confirm the involvement of the I97L substitution in the observed ALT within the normal range and reductions in HBV DNA and HBsAg among HBeAg-negative patients. 2021 Cellular and molecular gastroenterology and hepatology Introduction HBV I97L 58 62 C;S 162;150 167;155 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The amino acid substitution I97L in the HBc region is associated with stable hepatitis achieving a functional cure with the sustained loss of HBsAg. 2021 Cellular and molecular gastroenterology and hepatology Introduction HBV I97L 28 32 C;S 40;142 43;147 Hepatitis 77 86 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. We identified the characteristic substitution of isoleucine with leucine at amino acid 97 (I97L) in the hepatitis B core (HBc) region among those with stable disease. 2021 Cellular and molecular gastroenterology and hepatology Introduction HBV I97L;I97L 91;49 95;89 C;C 116;122 120;125 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Lecoq and coworkers showed that the point mutations L60W and P5W, which block the access to the pocket, support the maturation of the genome but not the progression into enveloped virus particles. 2021 Viruses Introduction HBV P5W;L60W 61;52 64;56 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Naturally occurring point mutations like HBc-F/I97L with an immature secretion phenotype or point mutations with a low secretion phenotype, such as HBc-L60V and HBc-P5T, are located in the area surrounding the pocket. 2021 Viruses Introduction HBV I97L;F97L;P5T;L60V 45;45;165;152 51;51;168;156 C;C;C 41;148;161 44;151;164 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. We asked what the underlying conformational changes were and whether these changes differed between CLPs of wt HBc, mutants with immature secretion phenotype (HBc-F97L) or mutants with low secretion phenotypes (HBc-P5Tand HBc-L60V). 2021 Viruses Introduction HBV F97L;L60V 163;226 167;230 C;C;C;C 111;159;211;222 114;162;214;225 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Additional glycosylation sites on HBsAg other than the acceptor site at position N146, such as T123N or K160N, impaired or reduced the antibody recognition, respectively, while also reducing the virion formation. 2021 Viruses Introduction HBV T123N;K160N 95;104 100;109 S 34 39 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Confocal microscopy revealed that the L77R mutant HBsAg are largely accumulated within the ER and Golgi. 2021 Journal of biomedical science Introduction HBV L77R 38 42 S 50 55 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. In addition, a single amino acid substitution R79K near the end of the large loop also blocked HBV virion secretion, while the secretion of HBsAg subviral particles was normal. 2021 Journal of biomedical science Introduction HBV R79K 46 50 S 140 145 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. In our earlier studies, a naturally occurring S gene mutation L77R at the large loop CYL-I resulted in more than tenfold reduced HBV virion secretion, and 2.8-fold reduced HBsAg in the medium of transfected HuH-7 cells. 2021 Journal of biomedical science Introduction HBV L77R 62 66 S;S 172;46 177;47 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. This phenomenon can be rescued by another naturally occurring mutation W74L in the same large loop. 2021 Journal of biomedical science Introduction HBV W74L 71 75 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Using a small loop mutant M198P defective in virion secretion, we conducted a complementation experiment, and demonstrated that it is the small S envelope protein, but not L and M, that can successfully restore virion secretion. 2021 Journal of biomedical science Introduction HBV M198P 26 31 S 138 154 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Recently, our research has found some novel OBI-related mutations within S gene, among which E2G was the most noteworthy mutation because it led to the intracellular accumulation and secretion decrease of HBsAg in OBI of genotype B. 2021 Frontiers in microbiology Introduction HBV E2G 93 96 S;S 205;73 210;74 Occult Hepatitis B;Occult Hepatitis B 44;214 47;217 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. A set of recognition defects characteristic of the natural G145R mutant detected in sera of chronic HBsAg carriers was determined, and the depth of these defects was assessed semiquantitatively using a four-step scoring system. 2022 Vaccines Introduction HBV G145R 59 64 S 100 105 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Across different genotypes, the most frequent substitutions were I/T126S (1.8%), G145R (1.2%), M133T (1.2%), Q129R (1.0%), I/T126A (0.8%), and P120T (0.8%). 2022 Vaccines Introduction HBV T126S;T126A;I126S;I126A;G145R;M133T;Q129R;P120T 65;123;65;123;81;95;109;143 72;130;72;130;86;100;114;148 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Although several patents for candidate vaccines protecting against the G145R mutant have been filed, none of those have been further developed and approved. 2022 Vaccines Introduction HBV G145R 71 76 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. As shown by Waters et al., monoclonal antibodies that recognize peptides containing 139-147 amino acid (aa) and 124-137 aa residues of HBsAg of subtypes ay and ad, either did not bind to the G145R mutant at all or were required at 10 times higher concentrations compared with wild-type HBsAg. 2022 Vaccines Introduction HBV G145R 191 196 S;S 135;286 140;291 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Computer simulations proposed that the G145R substitution results in an insertion of a new beta-fold in the HBsAg alpha-determinant and alters the orientation of the transmembrane segments of the protein, which in turn changes the membrane topology of HBsAg. 2022 Vaccines Introduction HBV G145R 39 44 S;S 108;252 113;257 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Electron microscopy revealed unusual oval-shaped 60-70 nm HBV structures in serum and 100-200 nm structures in a preparation of the purified G145R mutant, which were not seen in samples of wild-type HBV or an S143L escape mutant. 2022 Vaccines Introduction HBV G145R;S143L 141;209 146;214 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. For example, immunization of chimpanzees with licensed recombinant HBV vaccines stimulated production of broadly reactive anti-HBsAg antibodies that protected against infection with the G145R mutant. 2022 Vaccines Introduction HBV G145R 186 191 S 127 132 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. For example, the cell line transfected with the G145R mutant expressed significantly less L-HBsAg, whereas the expression of S-HBsAg did not change. 2022 Vaccines Introduction HBV G145R 48 53 S;S 90;125 97;132 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Further assessment of recombinant antigens with the G145R mutation using the same technique demonstrated that not all of them reproduced the natural serological profile of the given mutant. 2022 Vaccines Introduction HBV G145R 52 57 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Furthermore, endocytosis of full-length HBsAg-specific IgG inhibited the secretion of wild-type but not the G145R mutant HBsAg and HBV virions from cell lines. 2022 Vaccines Introduction HBV G145R 108 113 S;S 40;121 45;126 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Given the aforementioned features of the G145R mutant HBsAg folding, the recombinant analogue of the antigen included in the vaccine should have the same biological activity. 2022 Vaccines Introduction HBV G145R 41 46 S 54 59 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Hence, the G145R mutation can increase the rigidity, compactness, and aggregation potential of the alpha-determinants, affecting the immunogenicity and secretion of HBsAg as well as the morphogenesis of virions. 2022 Vaccines Introduction HBV G145R 11 16 S 165 170 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. However, it was later shown that the single-substitution mutant G145R is unstable in chimpanzees, as it reverts to the wild type during viremia. 2022 Vaccines Introduction HBV G145R 64 69 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In 2019, CJSK "RPC COMBIOTECH" designed a new trivalent vaccine Bubo -Unigep, containing antigens that confer protection against wild forms of HBV subtypes ay and ad, as well as a determinant of serotype ay with the G145R mutation at 10 mug/mL of suspension. 2022 Vaccines Introduction HBV G145R 216 221 S 178 191 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In addition, studies of sera from vaccinated people have shown that the widely used vaccines provide virtually no cross-reactive protection against the G145R mutant in the virus neutralization assay, in contrast to, for example, another immune-escape mutant S143L. 2022 Vaccines Introduction HBV G145R;S143L 152;258 157;263 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, monoclonal antibodies recognizing the mutant G145R HBsAg did not bind to HBsAg containing other substitutions. 2022 Vaccines Introduction HBV G145R 58 63 S;S 64;86 69;91 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, the HBV variant with three mutations in the polymerase gene (rtV173L + rtL180M + rtM204V), also generating the G145R mutation in S-HBsAg due to overlapping reading frames, was stable. 2022 Vaccines Introduction HBV V173L;L180M;M204V;G145R 76;86;96;124 81;91;101;129 P;RT;RT;RT;S 57;74;84;94;142 67;76;86;96;149 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In Japan in 2016, in a cohort of children born to HBV-carrier mothers who became HBV carriers despite immunoprophylaxis, the frequency of the G145R mutant ranged from 0.54% to 6.58%. 2022 Vaccines Introduction HBV G145R 142 147 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In the latter case, researchers used sera of chronic HBsAg carriers that were characterized by deep sequencing and shown to contain the G145R mutation in HBV adw3 and ayw2 genotype D subtypes (ENA ERZ377006 and ENA ERZ377011) with 99% homogeneity, and applied a method developed for assessing an antibody level specific to different native variants of HBsAg. 2022 Vaccines Introduction HBV G145R 136 141 S;S 53;352 58;357 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In this control cohort, the frequency of the G145R mutant ranged from 0.42% to 4.1%. 2022 Vaccines Introduction HBV G145R 45 50 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. It is noteworthy that in the work of Araujo et al., the G145R mutant was found only in genotypes G (5.0%), D (2.5%), C (2.1%), and B (0.2%), while Datta et al. 2022 Vaccines Introduction HBV G145R 56 61 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Nevertheless, the data suggested that the mechanism of the immune response against the G145R mutant is slightly different than for wild-type HBsAg. 2022 Vaccines Introduction HBV G145R 87 92 S 141 146 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Previously, we have selected a recombinant analogue of the G145R mutant that is almost identical to the natural protein. 2022 Vaccines Introduction HBV G145R 59 64 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. reported the G145R mutant of the HBV Ae/A2 subgenotype, and in most subjects this mutant was detected only in leukocytes. 2022 Vaccines Introduction HBV G145R 13 18 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Studies in Taiwan showed that escape mutations were detected at a frequency of 28.1% among vaccinated children, with the proportion of the G145R mutant being 15.4%. 2022 Vaccines Introduction HBV G145R 139 144 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Taken together, the data, along with results of mathematical models, indicate that the G145R mutant may be epidemiologically dangerous. 2022 Vaccines Introduction HBV G145R 87 92 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The aim of the current work was to conduct in-depth in vitro studies of the immunological mechanisms implemented by the G145R mutant, using the recombinant analogue of the natural HBsAg G145R mutant and its wild-type prototype, both included in the Bubo -Unigep vaccine. 2022 Vaccines Introduction HBV G145R;G145R 120;186 125;191 S 180 185 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The analysis of the spectrum of postvaccination antibodies was carried out both against the immunogen and the natural HBV G145R mutant. 2022 Vaccines Introduction HBV G145R 122 127 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The main reason for the ineffectiveness of postvaccination antibodies against the G145R mutant is the mutant's distinct antigenic properties. 2022 Vaccines Introduction HBV G145R 82 87 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The preliminary selection of rHBsAg containing the G145R mutation, similar to the native analogue in antigenic and immunogenic properties, allowed for developing a component of the hepatitis B vaccine with the G145R escape mutation in HBsAg. 2022 Vaccines Introduction HBV G145R;G145R 51;210 56;215 S;S 235;29 240;35 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The recombinant G145R mutant and wild-type HBV differ significantly in immunogenicity and determinant specificity. 2022 Vaccines Introduction HBV G145R 16 21 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The rHBsAg with the G145R mutation is capable of eliciting antibodies at the level comparable to the wild-type antigen, and the antibodies that are generated recognize not only the HBsAg G145R mutant but also wild-type HBsAg. 2022 Vaccines Introduction HBV G145R;G145R 20;187 25;192 S;S;S 181;219;4 186;224;10 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The urgency of the problem, however, dictates the need for developing a vaccine that would elicit a protective humoral immune response against both individual HBV subtypes (ay and ad) and epitopes of the G145R and other escape mutants. 2022 Vaccines Introduction HBV G145R 204 209 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. There is currently no registered vaccine globally that is active against the G145R escape mutant. 2022 Vaccines Introduction HBV G145R 77 82 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. These findings stress the ongoing spread of the G145R escape mutant despite large-scale vaccination, especially among children. 2022 Vaccines Introduction HBV G145R 48 53 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. These major mutations were more common in genotypes A (P120T, 3.2%), B (I/T126A, 2.8%; Q129R, 2.2%), C (I/T 126S, 3.9%; M133T, 1.9%), and G (G145R, 5.0%). 2022 Vaccines Introduction HBV T126A;T126S;I126A;P120T;Q129R;M133T;G145R 72;104;72;55;87;120;141 79;112;79;60;92;125;146 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Thus, HBsAg with the G145R mutation is less immunogenic, requiring large doses and time for the development of an immune response. 2022 Vaccines Introduction HBV G145R 21 26 S 6 11 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. When assessing the interaction of an anti-HBsAg monoclonal antibody with wild-type HBV and the G145R mutant by the Ouchterloni double immunodiffusion method, a "cross" where the precipitation lines intersect was observed, indicating that the antigenic determinants are not identical. 2022 Vaccines Introduction HBV G145R 95 100 S 42 47 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. HBV mutations, including A1762T/G1764A, C1653T, T1753V, and T1674G/C, in the core promoter (CP) region of the viral genome are typically the ones that increase the risk of HCC. 2022 Frontiers in oncology Introduction HBV G1764A;T1674C;A1762T;C1653T;T1753V;T1674G 32;60;25;40;48;60 38;68;31;46;54;68 Core promoter;Core promoter 77;92 90;94 Hepatocellular carcinoma 172 175 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. Here, we investigated tumorigenic effects of combo HBx mutations (A1762T/G1764A, C1653T, T1753C, and T1674G), Ct-HBx, and wild-type (WT) HBx on HCC using the Sleeping Beauty (SB) transposon system to deliver WT-HBx and HBx mutants into the livers of fumarylacetoacetate hydrolase (Fah)-deficient mice. 2022 Frontiers in oncology Introduction HBV G1764A;A1762T;C1653T;T1753C;T1674G 73;66;81;89;101 79;72;87;95;107 X;X;X;X;X 51;113;137;211;219 54;116;140;214;222 Hepatocellular carcinoma 144 147 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2017) described more concretely about point-mutations (N38E 71.9%, N38K 71.1%, A60V/E 100% on the PreS1 region, L126T/S 77% on the PreS2 and N3S 27.4% on the S region). 2022 PloS one Introduction HBV N3S;N38E;N38K;A60V;A60E;L126T;L126S 142;56;68;80;80;113;113 145;60;72;86;86;120;120 PreS1;PreS2;S 99;132;159 104;137;160 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (n = 187) had reported a rate of 31% cases with point-mutation in the immunodominant 'a' region, especially two major vaccine escape mutations with minor rates as G145A/R (2.2%) and P120L/Q/S/T (5.3%) had been detected. 2022 PloS one Introduction HBV P120L;P120Q;P120S;P120T;G145A;G145R 182;182;182;182;163;163 193;193;193;193;170;170 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Mutations at T53C, PreS deletions, PreS2 start codon, C7A, A2962G, C2964A and C3116T in the PreS region have been proved that significantly increase risk of HCC. 2022 PloS one Introduction HBV C7A;T53C;A2962G;C2964A;C3116T 54;13;59;67;78 57;17;65;73;84 PreS;PreS;PreS2 19;92;35 23;96;40 Hepatocellular carcinoma 157 160 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Additionally, they reported that A2051C increased the viral replication in vivo and in vitro. 2022 Clinical and experimental hepatology Introduction HBV A2051C 33 39 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. In a study conducted in the Korean population, the five HBcAg mutations P5H/L/T, E83D, I97F/L, L100I, and Q182K/Stop were significantly more frequent in subjects with chronic hepatitis and cirrhosis. 2022 Clinical and experimental hepatology Introduction HBV P5H;P5L;P5T;Q182X;E83D;I97F;I97L;L100I;Q182K 72;72;72;106;81;87;87;95;106 79;79;79;116;85;93;93;100;116 C 56 61 Chronic Hepatitis B;Liver cirrhosis 167;189 184;198 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. showed that the core mutations such as T1938C (V13A) and A2051C (N51H) were correlated with HBV-related HCC and played a role in progression of liver disease in an Alaskan native population with HBV genotype F1b. 2022 Clinical and experimental hepatology Introduction HBV T1938C;V13A;A2051C;N51H 39;47;57;65 45;51;63;69 C 16 20 Hepatocellular carcinoma;Liver disease 104;144 107;157 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The HBeAgphenotype arises due to some substitutions and more particularly a stop codon W28* in the precore sequence which is associated with abrogation of expression in the HBeAg level . 2022 Clinical and experimental hepatology Introduction HBV W28X 87 91 C;Precore 173;99 178;106 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Trends in the age-specific prevalence of HBV genotype C and precore G1896A and BCP A1762T/G1764A mutants were evaluated using the Cochran-Armitage trend test. 2008 Journal of the National Cancer Institute Method HBV G1764A;G1896A;A1762T 90;68;83 96;74;89 BCP;Precore 79;60 82;67 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Various mutants (L180M, M204V, M204I, L180M+M204V and L180M+M204I) of HBV polymerase were generated using builder module of Maestro (Schrodinger, LLC) and were subsequently subjected for all the modeling calculations as described above. 2008 Antiviral research Method HBV L180M;M204V;M204I;M204V;L180M;L180M;M204I 17;24;31;44;38;54;60 22;29;36;49;43;59;65 P 74 84 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Cp149-Y132A eluted at about 0.2 M NaCl. 2009 Biochemistry Method HBV Y132A 6 11 C 0 2 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Fractions were evaluated by SDS-PAGE and absorbance; Cp149-Y132A typically eluted at about 800 ml, consistent with a dimer rather than a capsid state. 2009 Biochemistry Method HBV Y132A 59 64 Capsid;C 137;53 143;55 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Preparation and purification of Cp149 and Cp149-Y132A. 2009 Biochemistry Method HBV Y132A 48 53 C;C 32;42 34;44 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. The Cp149-Y132A mutant was generated from pCp149 using a Quik-Change kit (Strategene). 2009 Biochemistry Method HBV Y132A 10 15 C;Precore 4;42 6;44 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Established NRTI-resistance mutations included the following RT mutations: rtL80V/I, rtI169T, rtV173L, rtL180M, rtA181TV, rtT184S/A/I/L/F/G, rtA194T, rtS202G/I, rtM204V/I/S, rtN236T, and rtM250V. 2009 The Journal of infectious diseases Method HBV L80V;L80I;T184S;T184A;T184I;T184L;T184F;T184G;S202G;S202I;M204V;M204I;M204S;M250V;I169T;V173L;L180M;A194T;N236T 77;77;124;124;124;124;124;124;152;152;163;163;163;189;87;96;105;143;176 83;83;139;139;139;139;139;139;159;159;172;172;172;194;92;101;110;148;181 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 61;75;85;94;103;112;122;141;150;161;174;187 63;77;87;96;105;114;124;143;152;163;176;189 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Mutations at 10 S envelope protein positions were considered possible vaccine-escape mutations, including sP120T, sI/T126N/A, sQ129H, sM133L, sK141E, sP142S, sD144A, sG145R, sF158Y, and sF161Y. 2009 The Journal of infectious diseases Method HBV T126N;T126A;P120T;I126N;I126A;Q129H;M133L;K141E;P142S;D144A;G145R;F158Y;F161Y 114;115;106;114;114;126;134;142;150;158;166;174;186 124;124;112;124;124;132;140;148;156;164;172;180;192 S;S;S;S;S;S;S;S;S;S;S;S 18;16;106;114;126;134;142;150;158;166;174;186 26;17;107;115;127;135;143;151;159;167;175;187 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. Although the T1762/A1764 double mutation does not create a novel restriction site, introduction of artificial A1767T mutation into the antisense primer B-Bc1 produces a BclI cleavage site (TGATCA) in conjunction with the double mutation. 2009 Journal of medical virology Method HBV A1767T 110 116 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. Similarly, due to the artificial G1888C/T1889C/G1890T mutations in the sense primer C-Xag, an XagI cleavage site (CCTN5AGG) was created in the presence of the A1896. 2009 Journal of medical virology Method HBV T1889C;G1890T;G1888C 40;47;33 46;53;39 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The core- mutants contain a C2044A change that converts codon 48 from TGC to TGA. 2009 Virology Method HBV C2044A 28 34 C 4 8 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The epsilon-/p- mutants harbor G1879T/T1880A double mutation that abolishes pg RNA encapsidation as well as a C2589T nonsense mutation of the 95th codon of P gene. 2009 Virology Method HBV T1880A;G1879T;C2589T 38;31;110 44;37;116 P 156 157 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. In our evaluation of the BCP A1762T/G1764A double mutant, subjects with either single mutation or a deletion at either site were not included in the analysis. 2009 Journal of the National Cancer Institute Method HBV G1764A;A1762T 36;29 42;35 BCP 25 28 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Summary estimates of HCC for PreS mutations, C1653T, T1753V, A1762T/G1764A, G1896A, and C1858T (a C-to-T substitution at nucleotide 1858) for patients with HCC were calculated with the use of Stata software (version 9.1; Stata Corp, College Station, TX). 2009 Journal of the National Cancer Institute Method HBV G1764A;C1653T;T1753V;A1762T;G1896A;C1858T;C1858T 68;45;53;61;76;88;98 74;51;59;67;82;94;136 PreS 29 33 Hepatocellular carcinoma;Hepatocellular carcinoma 21;156 24;159 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The remaining thirteen patients were ADV-resistant, having an rtA181T mutation, rtA181V mutation, or both mutations (ADV polymerase mutation group, Group P). 2010 Journal of Korean medical science Method HBV A181T;A181V 64;82 69;87 P;RT;RT 121;62;80 131;64;82 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The serum collected at the time of ADV-resistant rtA181T/V mutation detection was used for sequencing analysis. 2010 Journal of Korean medical science Method HBV A181V;A181T 51;51 58;58 RT 49 51 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. These patients developed ADV resistance while undergoing ADV monotherapy as rescue therapy for LMV-resistant HBV (rtM204I/V+-rtL180M). 2010 Journal of Korean medical science Method HBV M204I;M204V;L180M 116;116;127 123;123;132 RT;RT 114;125 116;127 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. We conducted the Fisher's exact tests for categorical variables and Mann-Whitney's U-tests for continuous variables to compare patients with the rtA181T/V mutation to those without the rtA181T/V mutation. 2010 Journal of Korean medical science Method HBV A181T;A181V;A181T;A181V 147;147;187;187 154;154;194;194 RT;RT 145;185 147;187 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Additional HBV-RT homology models were constructed with the LVD (M204V+L180M) and adefovir (A181T/V and N236T) resistance substitutions, and the ETVr signature substitutions T184G & S202I, or M250V were constructed on the LVDr (M204V+L180M) model. 2010 PloS one Method HBV M204V;L180M;A181T;A181V;N236T;T184G;S202I;M250V;M204V;L180M 65;71;92;92;104;174;182;192;228;234 70;76;99;99;109;179;187;197;233;239 RT 15 17 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. An additional model of the M250V was also constructed in WT HBV RT. 2010 PloS one Method HBV M250V 27 32 RT 64 66 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. We also analyzed the mutations that have been reported to possibly contribute to resistance at 10 additional positions: L82M, V84M, S85A, A194T, A200V, V214A, Q215S, I233V, P237H and NASH238TD. 2010 Antiviral research Method HBV L82M;V84M;S85A;A194T;A200V;V214A;Q215S;I233V;P237H 120;126;132;138;145;152;159;166;173 124;130;136;143;150;157;164;171;178 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. We analyzed the following mutations at 10 well-characterized DRM positions L80IV, I169T, V173L, L180M, A181TV, T184SAILFG, S202GI, M204VIS, N236T, and M250V. 2010 Antiviral research Method HBV I169T;V173L;L180M;N236T;M250V 82;89;96;140;151 87;94;101;145;156 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. After 24 h, Huh7 cells were transfected with 0.5 mug pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G), pCMV-HBc (I97L) and control DNA (pCMV-Tag1 and salmon DNA), respectively, using FuGene HD transfection reagent (Roche). 2010 Virology journal Method HBV L60V;S87G;I97L 78;95;112 82;99;116 C;C;C;C 58;73;90;107 61;76;93;110 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Huh7 cells were seeded in 12-well plates at 2 x 105 cells per well and, after 24 h, pMxA550-Luc (0.25 mug) was co-transfected in Huh7 cells with 0.5 mug pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G), pCMV-HBc (I97L) and control DNA (pCMV-Tag1 and salmon DNA), respectively, using FuGene HD (Roche). 2010 Virology journal Method HBV L60V;S87G;I97L 178;195;212 182;199;216 C;C;C;C 158;173;190;207 161;176;193;210 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G) and pCMV-HBc (I97L) were confirmed by sequencing and these vectors were able to express the HBc protein/Flag-tag fused protein. 2010 Virology journal Method HBV L60V;S87G;I97L 25;42;62 29;46;66 C;C;C;C;C 5;20;37;57;140 8;23;40;60;143 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G), pCMV-HBc (I97L) and pCMV-Tag1 were transfected into Huh7 cells as described above, using 0.5 mug of DNA. 2010 Virology journal Method HBV L60V;S87G;I97L 25;42;59 29;46;63 C;C;C;C 5;20;37;54 8;23;40;57 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Using pCMV-HBc (WT), the other three plasmids [pCMV-HBc (L60V), pCMV-HBc (S87G) and pCMV-HBc (I97L)] expressing HBc proteins with the substitutions L60V, I97L and S87G, respectively, were constructed using the Quick Change Site-Directed Mutagenesis Kit (Stratagene, USA) and the primers described previously. 2010 Virology journal Method HBV L60V;S87G;I97L;L60V;I97L;S87G 57;74;94;148;154;163 61;78;98;152;158;167 C;C;C;C;C 11;52;69;89;112 14;55;72;92;115 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V. 2010 Mediators of inflammation Method HBV T184G;T184S;T184A;T184C;I169T;V173L;L180M;A181V;A181T;A194T;S202G;S202I;M204V;M204I;N236T;M250V 146;146;146;146;116;123;130;137;137;159;166;166;175;175;184;195 157;157;157;157;121;128;135;144;144;164;173;173;182;182;189;200 P 104 114 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. The other has a unique Y100C variation in its amino acid sequence. 2011 Hepatitis research and treatment Method HBV Y100C 23 28 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. These two viral strains were used to construct two recombinant expression plasmids under CMV promoter, representing a wild-type and a Y100C variant of HBV S gene (named pcDNA3-SA1 and pcDNA3-Y100C, resp.). 2011 Hepatitis research and treatment Method HBV Y100C;Y100C 134;191 139;196 S 155 156 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Wild-type and Y100C variant sequences determined have been deposited in the GenBank database, accession numbers HQ840709 and EF690524, respectively. 2011 Hepatitis research and treatment Method HBV Y100C 14 19 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. In addition to signature mutations, rtV173L, rtL180M and rtA181T/S were included in drug-resistant mutational patterns when they were present with signature resistance mutations. 2011 Journal of viral hepatitis Method HBV A181T;A181S;V173L;L180M 59;59;38;47 66;66;43;52 RT;RT;RT 36;45;57 38;47;59 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtA181V and rtN236T were defined as the signature ADV-resistant mutations (ADV-R). 2011 Journal of viral hepatitis Method HBV A181V;N236T 6;18 11;23 RT;RT 4;16 6;18 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtM204I/V was defined as the signature LAM-resistant mutations (LAM-R) which also encompassed LdT-resistant mutations. 2011 Journal of viral hepatitis Method HBV M204I;M204V 6;6 13;13 RT 4 6 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtT184A/C/F/G/I/L/M/S, rtS202C/G/I and rtM250I/L/V were defined as the signature ETV-resistant mutations (ETV-R) if concomitant with rtM204I/V. 2011 Journal of viral hepatitis Method HBV T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M250I;M250L;M250V;M204I;M204V 6;6;6;6;6;6;6;6;29;29;29;45;45;45;139;139 25;25;25;25;25;25;25;25;38;38;38;54;54;54;146;146 RT;RT;RT;RT 4;27;43;137 6;29;45;139 21438026 Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival. Site-directed mutagenesis was then performed on pTracer-WtHBx using mutagenic primers and the QuickChange Site-Directed Mutagenesis Kit (Stratagene, La Jolla, CA), ultimately creating pTracer-MutHBx, which harbors the naturally occurring HBx double mutation A1762T/G1764A. 2011 Molecular carcinogenesis Method HBV G1764A;A1762T 265;258 271;264 X;X;X 238;195;58 241;198;61 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Detection of G1896A variation in HBV core gene. 2011 Virology journal Method HBV G1896A 13 19 C 37 41 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. G1896A variation in HBV core gene was detected with PCR-fluorescence detection kit based on Taqman MGB (minor groove binder) probes (Biocore, Hangzhou, China). 2011 Virology journal Method HBV G1896A 0 6 C 24 28 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. The presence of HBV core gene A336C/A336T/T337C variations in patient's sera were determined by a modified PCR-RFLP assay and cleaved PCR products were electrophoresed on 2.5% agarose gel, and five PCR amplicons per RFLP pattern were sequenced directly to confirm the accuracy of PCR-RFLP assay. 2011 Virology journal Method HBV A336T;T337C;A336C 36;42;30 41;47;35 C 20 24 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. A two-step assay was developed for the quantification of G1896A and/or G1899A mutants with high sensitivity. 2011 Journal of clinical virology Method HBV G1896A;G1899A 57;71 63;77 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. G1896A and G1899A occurred frequently either separately or together as a G1896A/G1899A double mutation. 2011 Journal of clinical virology Method HBV G1899A;G1896A;G1899A;G1896A 80;0;11;73 86;6;17;79 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Precore G1896A and G1899A quantification assay. 2011 Journal of clinical virology Method HBV G1896A;G1899A 8;19 14;25 Precore 0 7 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Serial diluted plasmids carrying G1896A were included in the first step PCR so that a standard concentration curve can be generated. 2011 Journal of clinical virology Method HBV G1896A 33 39 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. Another study reported of 5 HBV-infected patients also harboring the rtA194T mutation in association with LAM-resistance. 2009 Infection and drug resistance Method HBV A194T 71 76 RT 69 71 HBV infections 28 40 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. In contrast, in a study by Delaney et al the rtA194T mutation, whether or not in combination with LAM-resistant mutations, did not confer resistance to TDF in vitro. 2009 Infection and drug resistance Method HBV A194T 47 52 RT 45 47 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. In one patient a HBV subpopulation with mutations rtM204V, rtL180M, and rtA194T could be detected. 2009 Infection and drug resistance Method HBV M204V;L180M;A194T 52;61;74 57;66;79 RT;RT;RT 50;59;72 52;61;74 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. In vitro studies show that the rtA194T mutation alone resulted in a 7.6-fold decrease in susceptibility, but in conjunction with rtM204V and rtL180M led to a more than 10-fold decrease in susceptibility to TDF. 2009 Infection and drug resistance Method HBV A194T;M204V;L180M 33;131;143 38;136;148 RT;RT;RT 31;129;141 33;131;143 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. In vitro studies, however, show that both rtN236T and rtA181V/T HBV mutants remain sensitive to TDF, and are only associated with small decreases in susceptibility. 2009 Infection and drug resistance Method HBV A181V;A181T;N236T 56;56;44 63;63;49 RT;RT 42;54 44;56 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. The other patient presented with mutations in the HBV polymerase of rtM204V, rtL180M, rtV173L, and rtA194T, but there was a progressive decline in both HBV DNA and alanine aminotransferase (ALT) levels. 2009 Infection and drug resistance Method HBV M204V;L180M;V173L;A194T 70;79;88;101 75;84;93;106 P;RT;RT;RT;RT 54;68;77;86;99 64;70;79;88;101 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. The rtA194T mutation was detected 48 and 77 weeks after initiation of TDF. 2009 Infection and drug resistance Method HBV A194T 6 11 RT 4 6 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. Until now TDF resistance has only been described in 2 HIV-HBV co-infected patients demonstrating the A194T mutation in addition to LAM-resistance. 2009 Infection and drug resistance Method HBV A194T 101 106 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. In addition, a combination mutant of I127N/K130M/V131/I/F132Y (abbreviated as Combo mutant) was generated. 2011 Gastroenterology Method HBV I132Y;K130M;F132Y;I127N 54;43;56;37 61;48;61;42 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. To generate HBx mutants that correspond to mutations in the basal core promoter region, site-directed mutagenesis was performed at amino acid positions I127N (T1753A), K130M/V131I (A1762T/G1764A) (abbreviated as TA mutant) and F132Y (T1768A) using a Quikchange kit (Stratagene) according to the manufacturer's protocol. 2011 Gastroenterology Method HBV V131I;G1764A;I127N;T1753A;K130M;A1762T;F132Y;T1768A 174;188;152;159;168;181;227;234 179;194;157;165;173;187;232;240 BCP;X 60;12 79;15 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Construction of 1.3x HBV genomes of G1613A mutants with/without the BCP mutation. 2011 PloS one Method HBV G1613A 36 42 BCP 68 71 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Patients in the study of viral load and G1613A mutation. 2011 PloS one Method HBV G1613A 40 46 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The G1613A mutation and the BCP mutation were introduced into both 5' and 3' copy of the core promoter in the genome by site directed mutagenesis. 2011 PloS one Method HBV G1613A 4 10 BCP;Core promoter 28;89 31;102 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. As such, we developed an amplification created restriction enzyme site (ACRES) method to detect a small percentage of the rtA181T mutant. 2011 BMC cancer Method HBV A181T 124 129 RT 122 124 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Logistic regression analysis was performed to evaluate the association of the clinical and virological variables with occurrence of the rtA181T mutant. 2011 BMC cancer Method HBV A181T 138 143 RT 136 138 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Previous studies indicated that the rtA181T mutant usually coexisted with wild type or mutant type viruses as a mixture. 2011 BMC cancer Method HBV A181T 38 43 RT 36 38 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The methods to detect HBV basal core promoter (BCP) A1762T/G1764A mutations, precore stop codon G1896A mutation, rtM204I mutation, rtM204V mutation, rtL180M mutation were described previously. 2011 BMC cancer Method HBV G1764A;M204I;M204V;L180M;A1762T;G1896A 59;115;133;151;52;96 65;120;138;156;58;102 BCP;BCP;Precore;RT;RT;RT 26;47;77;113;131;149 45;50;84;115;133;151 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. A plasmid carrying both A1762T/G1764A and G1896A mutations was used as the concentration standard to ensure consistency in quantification in different assays. 2012 Journal of hepatology Method HBV G1764A;A1762T;G1896A 31;24;42 37;30;48 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. Of all the potential mutations in the BCP region, only the A1762T/G1764A double mutation is designated here as the "BCP mutation". 2012 Journal of hepatology Method HBV G1764A;A1762T 66;59 72;65 BCP;BCP 38;116 41;119 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. Only the G1896A and G1896A/G1899A mutations are designated as the "precore mutations". 2012 Journal of hepatology Method HBV G1899A;G1896A;G1896A 27;9;20 33;15;26 Precore 67 74 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. The G1899A mutation alone (in the absence of G1896A mutation) has not been reported to affect HBeAg production, thus it was not counted as the "precore mutation" in this study. 2012 Journal of hepatology Method HBV G1899A;G1896A 4;45 10;51 C;Precore 94;144 99;151 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. The precore mutation assay could detect G1896A, G1899A and G1896A/G1899A mutations. 2012 Journal of hepatology Method HBV G1899A;G1896A;G1899A;G1896A 66;40;48;59 72;46;54;65 Precore 4 11 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Real-time PCR for the G145R and G145A mutants. 2012 BMC research notes Method HBV G145R;G145A 22;32 27;37 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The point mutation at nt 587 (G145R, mutant 1: G to A, mutant 2: G to C) and nt 588 (G145A, mutant 3: G to C) were applied to the sequence of the probes. 2012 BMC research notes Method HBV G145R;G145A 30;85 35;90 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. To detect the G145R and G145A mutants as minor strains in patients, we designed 3 probes based on the sequences of the G145R and G145A mutants. 2012 BMC research notes Method HBV G145R;G145A;G145R;G145A 14;24;119;129 19;29;124;134 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Allele-specific quantitative real-time PCR and semiquantitative PCR to determine the relative proportion of G1896A pre-C mutant. 2012 PloS one Method HBV G1896A 108 114 Precore 115 120 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Oligonucleotide primers were designed individually to amplify the pre-C region of wild-type and the G1896A pre-C mutant HBV. 2012 PloS one Method HBV G1896A 100 106 Precore;Precore 66;107 71;112 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Performance of this assay was tested using mixtures of two previously described plasmids, pcDNA3-HBV-wt#1 and pcDNA3-HBV-G1896A pre-C mutant. 2012 PloS one Method HBV G1896A 121 127 Precore 128 133 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Quantification of wild-type and the G1896A pre-C mutant was individually performed by real-time PCR using a Light Cycler 480 and Fast Start Universal SYBR Master (Roche, Mannheim, Germany). 2012 PloS one Method HBV G1896A 36 42 Precore 43 48 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. The relative proportion of the G1896A pre-C mutant was determined to calculate the G1896A pre-C mutant/total HBV ratios. 2012 PloS one Method HBV G1896A;G1896A 31;83 37;89 Precore;Precore 38;90 43;95 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Three primers were used for this protocol, two allele-specific sense primers, 1896WT_F (for wild-type) and 1896MT_F (for the G1896A pre-C mutant), and one common antisense primer, 2037_R (Table S1). 2012 PloS one Method HBV G1896A 125 131 Precore 132 137 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. To determine the relative proportion of the G1896A pre-C mutant, allele-specific quantitative real-time PCR was performed based on the previously described method. 2012 PloS one Method HBV G1896A 44 50 Precore 51 56 22592516 HIV and Hepatitis B coinfection among perinatally HIV-infected Thai adolescents. HBV Mutation Analysis assessed the presence of rtM204V/I by pinpointing the change in the YMDD motif; HBV nucleotides were translated into amino acid sequences using the translation tool provided by the ExPASy Proteomics Server (available at: http://www.expasy.ch/tools/dna.html) at the Center of Excellence in Clinical Virology, Department of Pediatrics, Faculty of Medicine, Chulalongkorn University. 2012 The Pediatric infectious disease journal Method HBV M204V;M204I 49;49 56;56 RT;P 47;90 49;94 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In addition, to assess the changes in the most important epitopes of the overlapped S ORF, the fragment included the largest part possible of the C-terminal region of the immunodominant epitope "a determinant", which had the main immunotherapy escape mutation sG145R, associated with the rtW153Q NA compensatory variant. 2012 PloS one Method HBV W153Q;G145R 290;260 295;266 S;RT;S;S 195;288;84;260 208;290;85;261 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In patient 4, LMV failure was associated with emergence of the rtA181T variant (Figure 4). 2012 PloS one Method HBV A181T 65 70 RT 63 65 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. NA-resistance-related aa substitutions outside the B and C domains, such as rtI233V, rtN236T and rtM250I/V, were not considered relevant for the aims of the study, since they had not been detected during follow-up in any of the patients studied. 2012 PloS one Method HBV M250I;M250V;I233V;N236T 99;99;78;87 106;106;83;92 RT;RT;RT 76;85;97 78;87;99 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. For whole-genome amplification: fragment C amplification was performed as for fragment B but with primers POLF1 and P5W in the first round and POLF2 and P4WRS in the second round. 2012 PloS one Method HBV P5W 116 119 C;P;P 41;106;143 42;109;146 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. A mutation type was referred to the replacement of the consensus AA of the corresponding genotype with a novel one; for instance, rtM204I and rtM204V were described as two mutation types. 2012 Liver international Method HBV M204I;M204V 132;144 137;149 RT;RT 130;142 132;144 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. The primary drug resistant mutations were defined as nucleotide mutation(s) caused an amino acid substitution that resulted in reduced susceptibility to an antiviral drup, such as rtL180M, rt204I/V for lamivudine, rtL180M+rtM204I/V+rtS202C or rtM250I/V for entecavir; rtA181T/V, rtN236T for adefovir dipivoxil; rtM204I for telbivudine. 2012 Liver international Method HBV M250I;M250V;A181T;A181V;N236T;L180M;L180M;M204I;M204V;S202C;M204I 245;245;270;270;281;182;216;224;224;234;313 252;252;277;277;286;187;221;231;231;239;318 RT;RT;RT;RT;RT;RT;RT;RT;RT 180;189;214;222;232;243;268;279;311 182;191;216;224;234;245;270;281;313 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Cells were transfected with 2ug wild-type vector 1, G145A, M103I+K122R+G145A, or pCMV-HA. 2012 Journal of viral hepatitis Method HBV G145A;G145A;M103I;K122R 52;71;59;65 57;76;64;70 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Three mutations within the small HBsAg - M103I, K122R, and G145A - from an individual with a genotype A infection, were evaluated in the current study, since genotype A represents the most common HBV genotype in the US. 2012 Journal of viral hepatitis Method HBV M103I;K122R;G145A 41;48;59 46;53;64 S 33 38 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The sequencing conditions including BCP double mutation (A1762T/G1764A) in the core promoter region, G1896A in the PC region, C1653T or T1753V in the region encoding HBx, or pre-S2 deletion were specified in the protocol for the Taq DyeDeoxy Terminator Cycle Sequencing Kit (ABI; Applied Biosystems, Foster City, CA, USA). 2013 Annals of surgical oncology Method HBV G1764A;A1762T;G1896A;C1653T;T1753V 64;57;101;126;136 70;63;107;132;142 BCP;Core promoter;X;Precore;PreS2 36;79;166;115;174 39;92;169;117;180 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. A point mutation (rtA181T) in the RT region replacing Alanine (A) 181 with Threonine (T) was introduced via site-directed mutagenesis (QuikChange mutagenesis kit, Stratagene) according to the manufacturer's instructions using the forward primer: 5'-CAGCCCGTTTCTCCTGACTCAGTTTACTAGTGC-3' and the reverse primer: 5'-GCACTAGTAAACTGAGTCAGGAGAAACGGGCTG-3'. 2012 Virology journal Method HBV A181T 20 25 RT;RT 18;34 20;36 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Association analysis of HBV subgenotype C2, A1762T/G1764A mutations with progression of CHB. 2012 Iranian journal of public health Method HBV G1764A;A1762T 51;44 57;50 Chronic Hepatitis B 88 91 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV A1762T/G1764A mutations were determined by real-time fluorescence quantitative polymerase chain reaction (FQ-PCR), according to previous report with some modifies. 2012 Iranian journal of public health Method HBV G1764A;A1762T 11;4 17;10 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. To further understand the risks in progression of chronic HBV infection for HBV subgenotype C2 infection and A1762T/G1764A mutations, the association analysis was used in this study. 2012 Iranian journal of public health Method HBV G1764A;A1762T 116;109 122;115 Chronic HBV infection;HBV infections 50;92 71;104 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The amino acid sequence containing rtI233V mutation was substituted with valine for the construction of wild type model for comparison. 2013 Bioinformation Method HBV I233V 37 42 RT 35 37 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. 2.1 Preparation of wild type (WT) and mutant (rtV173L+rtL180M+rtM204V) plasmid standards. 2013 Journal of virological methods Method HBV V173L;L180M;M204V 48;56;64 53;61;69 RT;RT;RT 46;54;62 48;56;64 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Additional specificity reactions of each single mutant template, rtV173L, rtL180M, and rtM204V, and the clinically significant double mutant rtM204V+rtL180M were also testing for potential false amplification. 2013 Journal of virological methods Method HBV V173L;L180M;M204V;L180M;M204V 67;76;89;151;143 72;81;94;156;148 RT;RT;RT;RT;RT 65;74;87;141;149 67;76;89;143;151 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Allele-specific LNA forward and reverse primers were designed to detect the rtV173L and rtM204V mutations, respectively. 2013 Journal of virological methods Method HBV V173L;M204V 78;90 83;95 RT;RT 76;88 78;90 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. An allele-specific MGB probe was designed to detect the rtL180M mutation. 2013 Journal of virological methods Method HBV L180M 58 63 RT 56 58 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. In order to detect rtV173L, rtL180M and rtM204V simultaneously within a single template, a combination of oligonucleotide binding specificity-enhancing technologies was employed in a qPCR assay. 2013 Journal of virological methods Method HBV L180M;V173L;M204V 30;21;42 35;26;47 RT;RT;RT 19;28;40 21;30;42 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Site directed mutagenesis using the Stratagene Quickchange II XL kit (Agilent Technologies La Jolla, CA, USA) was used to create rtV173L (G>C), rtL180M (T>A), and rtM204V (A>G) mutations alone or in combination in polymerase (see figure 1) to serve as "Mutant" plasmids. 2013 Journal of virological methods Method HBV L180M;M204V;V173L;L180A;M180A;T180A;M204G;V204G;A204G 146;165;131;146;146;146;165;165;165 151;170;136;157;157;157;176;176;176 P;RT;RT;RT 214;129;144;163 224;131;146;165 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Subsequently, the rtL180M specific MGB probe was designed to have a compatible Tm for use with the LNA primers using Primer Express software (Applied Biosystems, Foster City, CA, USA). 2013 Journal of virological methods Method HBV L180M 20 25 RT 18 20 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. The primer and probe sequences are (see also Figure 1, nt positions are relative to gtA reference sequence X02763): MGB rtL180M probe (nt 658-674) 5' - 6FAM CCG TTT CTC ATG GCT CA MBGNFQ (Applied Biosystems, Foster City, CA, USA), LNA rtV173L forward primer (nt 629-647) 5' GCAAAATACCTATGGGA+CT and, LNA rtM204V reverse primer (nt 756-739) 5' CAATACCACATCATCC+AC, with LNA bases denoted as +C, +A, respectively. 2013 Journal of virological methods Method HBV L180M;V173L;M204V 122;237;306 127;242;311 RT;RT;RT 120;235;304 122;237;306 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. WT and rtV173L+rtL180M+rtM204V triple mutant plasmids were then 10-fold serially diluted from 109 to 10 copies/microL, plus an extra point at 50 copies/microL, in order to generate standard curves. 2013 Journal of virological methods Method HBV V173L;M204V;L180M 9;25;17 14;30;22 RT;RT;RT 7;15;23 9;17;25 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. The methods to detect HBV basal core promoter (BCP) A1762T/G1764A mutations, precore stop codon G1896A mutation and pre-S deletion were performed as previously described. 2013 PloS one Method HBV G1764A;A1762T;G1896A 59;52;96 65;58;102 BCP;BCP;Precore;PreS 26;47;77;116 45;50;84;121 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Mutations were verified by sequencing prior to cloning into similarly digested empty parent vector pJW4303 to yield recombinant plasmids; pJW4303-sT118M-rtM204I, pJW4303-sT118M-rtM204V, pJW4303-sG145K-rtM204I, pJW4303-sG145K-rtM204V, pJW4303-sG145R-rtM204I, and pJW4303-sG145R-rtM204V. 2013 Virology journal Method HBV M204V;M204I;M204I;M204V;M204I;M204V;T118M;T118M;G145K;G145K;G145R;G145R 179;155;203;227;251;279;146;170;194;218;242;270 184;160;208;232;256;284;152;176;200;224;248;276 RT;RT;RT;RT;RT;RT;S;S;S;S;S;S 153;177;201;225;249;277;146;170;194;218;242;270 155;179;203;227;251;279;147;171;195;219;243;271 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The ability of each of the ELISA to detect immune-escaped mutants (sT118M, sG145R, sG145K) had been confirmed in previous experiments (unpublished data). 2013 Virology journal Method HBV T118M;G145R;G145K 67;75;83 73;81;89 S;S;S 67;75;83 68;76;84 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Precore G1896A Mutation Detection and Direct Sequencing. 2013 Advances in virology Method HBV G1896A 8 14 Precore 0 7 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. The Mann-Whitney U test was utilized to test equality of TLR2 and ALT between patients with G1896A precore mutation and patients without mutation. 2013 Advances in virology Method HBV G1896A 92 98 Precore 99 106 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In the BCP region, the two-nucleotide substitutions, A-T at nucleotide 1762 and G-A at nucleotide 1764 (A1762T/G1764A), signal the double mutant BCP phenotype. 2013 PloS one Method HBV G1764A;A1762T;A1762T;G1764A 111;104;53;80 117;110;75;102 BCP;BCP 7;145 10;148 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In the PC region, two nucleotide changes were analyzed: the presence of a point mutation from G to A at nucleotide 1896 (G1896A), which signals the mutant PC phenotype; and the change C to T at position 1858, which defines the C1858T mutation. 2013 PloS one Method HBV G1896A;G1896A;G1896A;C1858T;G1896A;C1858T 93;120;121;227;94;184 200;207;127;233;119;207 Precore;Precore 7;155 9;157 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. For determining the role of LHBs or mutation of LHBs in endoplasmic reticulum stress, we cultured L02 cell for 24 hrs, then transfected with pCDNA3.1 (-), pCDNA3.1 (-)-LHBs, pCDNA3.1 (-)-N15S, pCDNA3.1 (-)-N123S, pCDNA3.1 (-)-N177S, and pCDNA3.1 (-)-N320K respectively. 2013 Hepatitis monthly Method HBV N15S;N123S;N177S;N320K 187;206;226;250 191;211;231;255 S;S;S 28;48;168 32;52;172 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. L02 cells were harvested after culturing for 24 hrs, then transfected with pCDNA3.1 (-), pCDNA3.1 (-)-LHBs, pCDNA3.1 (-)-N15S, pCDNA3.1 (-)-N123S, pCDNA3.1 (-)-N177S, and pCDNA3.1 (-)-N320K respectively as described in the above methods. 2013 Hepatitis monthly Method HBV N15S;N123S;N177S;N320K 121;140;160;184 125;145;165;189 S 102 106 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The EcoR I-Hind SH-fragment containing the N15S, N123S, N177S and N320K mutations were subcloned into the pCDNA-3.1(-) vector and pEGFP-C1. 2013 Hepatitis monthly Method HBV N15S;N123S;N177S;N320K 43;49;56;66 47;54;61;71 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N123S mutation was introduced with the mutagenic primer 5'- gccatgcagtggagctccaccacattc-3' (nts 355-381). 2013 Hepatitis monthly Method HBV N123S 4 9 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S mutation was introduced with the mutagenic primer 5'-ggcatggggacaagtctttctgttccc-3' (nucleotides (nts) 31-57). 2013 Hepatitis monthly Method HBV N15S 4 8 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N177S mutation was introduced with the mutagenic primer 5'-cgaacatggagagcacaacatcagg-3' (nts 518-542). 2013 Hepatitis monthly Method HBV N177S 4 9 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N320K mutation was introduced with the mutagenic primer 5'-cttcggacggaaagtgcacttgtattc-3' (nts 947-973). 2013 Hepatitis monthly Method HBV N320K 4 9 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The plasmids pEGFP-C1-LHBs (or pEGFP-C1-N15S, pEGFP-C1-N123S, pEGFP-C1-N177S, pEGFP-C1-N320K) and pDS-RED1-N1-CALR were cotransfected into L02 cells. 2013 Hepatitis monthly Method HBV N15S;N123S;N177S;N320K 40;55;71;87 44;60;76;92 S 22 26 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. HBV mutants (MTs) were constructed using fusion-PCR with Primer-Fusion and Primer-rtL180M, -rtM204V/I, -rtQ267H (Table 1) harboring aimed mutations and pBSK-HBV1.3 as template, which is a replication-competent plasmid containing 1.3-folds over-length HBV genome. 2013 Hepatitis monthly Method HBV L180M;M204V;M204I;Q267H 84;94;94;106 89;101;101;111 RT;RT;RT 82;92;104 84;94;106 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Amplicons containing 1.1mer genotype C HBV genome which harbored naturally-occurred rtM204Q, rtM204I, rtA181T, rtA181T+M204Q mutant RT genes or wild-type RT gene from the same patient were constructed for phenotyping of drug resistance based on pTriEx-mod-1.1 vector which was a kind gift by professor Zoulim. 2014 PloS one Method HBV A181T;M204Q;M204I;A181T;M204Q 104;86;95;113;119 109;91;100;118;124 RT;RT;RT;RT;RT;RT 84;93;102;111;132;154 86;95;104;113;134;156 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The sequences of representative HBV RT genes from each rtM204Q-positive patient were submitted to GenBank. 2014 PloS one Method HBV M204Q 57 62 RT;RT 36;55 38;57 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. To construct plasmids encoding truncated preS/S proteins containing 3 nonsense mutations, sL95*, sW182* and sL216*, respectively, site directed mutagenesis experiments were preformed according to a PCR-based method. 2014 PloS one Method HBV L95X;W182X;L216X 90;97;108 95;103;114 PreS;S;S;S;S 41;46;90;97;108 45;47;91;98;109 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. To examine the differences in the major clinicopathological features associated with HBcAg(+) HCC or sW182* mutations, the frequencies and proportions are compared by conventional chi-square association test or Fisher's exact test (when there is at least a cell frequency less than 5). 2014 PloS one Method HBV W182X 101 107 C;S 85;101 90;102 Hepatocellular carcinoma 94 97 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. DNA from clinical sample harboring rtM204I confirmed by sequencing were mixed with wild-type clinical sample in different proportions. 2014 PloS one Method HBV M204I 37 42 RT 35 37 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. LAM-associated mutations including rtL180M and rtM204I/V were identified at the baseline by using the RFMP assay, which was performed using matrix-assisted laser desorption/ionization-time of flight mass spectrometry as described previously. 2015 Gut and liver Method HBV M204I;M204V;L180M 49;49;37 56;56;42 RT;RT 35;47 37;49 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. The wild-type ayw (pSV2A-Neo-(HBV)2) and adr (kindly provided by Dr. 2014 Clinical and molecular hepatology Method HBV P2A;V2A 19;19 24;24 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. About 107 NIH3T3, WT-LHB-NIH3T3 and W4P-LHB-NIH3T3 cells were injected subcutaneously into the right hind legs of 8-week-old nude mice. 2015 Molecular cancer Method HBV W4P 36 39 S;S 21;40 24;43 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. NIH3T3 murine cell lines and Huh7 human HCC cell lines constitutively expressing the WT LHB and W4P variant were established by transfection with pIRES2-WT or pIRES2-W4P, followed by the selection with 500 mug/ml neomycin. 2015 Molecular cancer Method HBV W4P;W4P 96;166 99;169 S 88 91 Hepatocellular carcinoma 40 43 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. One week later, mice were injected with W4P-LHB-NIH3T3 cells subcutaneously together with beta-estradiol (0.5 mg/kg) or PBS injection. 2015 Molecular cancer Method HBV W4P 40 43 S 44 47 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Sequences encoding WT and variant LHBs were amplified from a patient with HBV carrier status and an HCC patient, which were proven without and with W4P/R mutation by a real-time polymerase chain reaction method as described previously. 2015 Molecular cancer Method HBV W4P;W4R 148;148 153;153 S 34 38 Hepatocellular carcinoma 100 103 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Sera from 22 male HCC and liver cirrhosis patients with WT and W4P LHBs were subjected to multiplex cytokine measurement. 2015 Molecular cancer Method HBV W4P 63 66 S 67 71 Hepatocellular carcinoma;Liver cirrhosis 18;26 21;41 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. To examine the secretion of cytokines by macrophages, J774A.1 cells were incubated in the presence or absence of W4P-LHB-expressing tumor homogenate (10 mg) for 48 h with or without 20 mM estrogen. 2015 Molecular cancer Method HBV W4P 113 116 S 117 120 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. After incubation for 24 h, the cells were washed with PBS and treated either with HBc-WT or HBc-R154G in serum-free medium at 37 C for 1 h. 2015 Journal of nanobiotechnology Method HBV R154G 96 101 C;C 82;92 85;95 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Subjects with a single mutation were excluded when assessing A1762T/G1764A double mutations and A1762T/G1764A/G1896A triple mutations. 2015 Virology journal Method HBV G1764A;G1764A;G1896A;A1762T;A1762T 68;103;110;61;96 74;109;116;67;102 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. The following mutation sites were also detected in the included studies: G1613A, C1653T, 1752G, T1754V, T1753V/A1762T/G1764A, T1758C, G1764A/C1766T/T1768A, T1770A, 1773 T, G1775A, C1799V, T1800C, T1803C, G1809T, A1814C, A1837G, A1846G, T1853C, T1858C, G1896A/G1899A, G1896A/G1899A/A1762T/G1764A, C1913V, 1915A/C, T1938C, A1979G, T1961V and T1753V/A1762T/G1764A/G1896A/G1899A, but they were not included in this meta-analysis because the data was insufficient. 2015 Virology journal Method HBV G1899A;A1762T;G1764A;C1766T;T1768A;A1762T;G1764A;G1899A;A1762T;G1764A;G1896A;G1899A;G1613A;C1653T;T1754V;T1758C;G1764A;T1770A;G1775A;C1799V;T1800C;T1803C;G1809T;A1814C;A1837G;A1846G;T1853C;T1858C;G1896A;G1896A;C1913V;T1938C;A1979G;T1961V;T1753V;T1753V 259;111;118;141;148;281;288;274;347;354;361;368;73;81;96;126;134;156;172;180;188;196;204;212;220;228;236;244;252;267;296;313;321;329;104;340 265;117;124;147;154;287;294;280;353;360;367;374;79;87;102;132;140;162;178;186;194;202;210;218;226;234;242;250;258;273;302;319;327;335;110;346 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. We used Stata software (version 12.0; Stata Corp, College Station, TX) to conduct the analysis and to calculate the ACLF summary estimates for the HBV genotype, HBeAg status and T1753V, A1762T, G1764A, A1762T/G1764A, C1766T, T1768A, A1846T, G1862T, G1896A, G1899A and A1762T/G1764A/G1896A mutations for ACLF patients. 2015 Virology journal Method HBV G1764A;G1764A;G1896A;T1753V;A1762T;G1764A;A1762T;C1766T;T1768A;A1846T;G1862T;G1896A;G1899A;A1762T 209;275;282;178;186;194;202;217;225;233;241;249;257;268 215;281;288;184;192;200;208;223;231;239;247;255;263;274 C 161 166 Acute on chronic liver failure;Acute on chronic liver failure 303;116 307;120 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. The YMDD (203tyrosine-methionine-aspartate-aspartate206) RT active site mutants M204A, M204I, M204K, M204L, M204R, M204T, and M204V, were then constructed by PCR-derived mutagenesis. 2015 BMC complementary and alternative medicine Method HBV M204A;M204I;M204K;M204L;M204R;M204T;M204V 80;87;94;101;108;115;126 85;92;99;106;113;120;131 RT;P 57;4 59;8 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. An additional HBV polymerase model was constructed by rtL269I substitution. 2015 PloS one Method HBV L269I 56 61 P;RT 18;54 28;56 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. HBV isolates with WT RT domain or the rtM129L+V173L+M204I+L269I+H337N mutations were derived from patient sera (obtained from tissue bank) and converted to 1.2mer replicon, using the pGEM-4z vector (Promega Corporation, Madison, WI, USA), as previously described. 2015 PloS one Method HBV M129L;H337N;V173L;M204I;L269I 40;64;46;52;58 45;69;51;57;63 RT;RT 21;38 23;40 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Other mutant clones including rtL269I, rtM204I, rtM204I+L269I, rtV173L+M204I, rtV173L+M204I+L269I, rtM129L+V173L+M204I, and rtM129L+V173L+M204I+H337N were generated from the WT HBV 1.2mer by site-directed mutagenesis. 2015 PloS one Method HBV L269I;M204I;M204I;V173L;V173L;M129L;M129L;L269I;M204I;L269I;M204I;M204I;V173L;M204I;V173L;H337N 32;41;50;65;80;101;126;56;71;92;86;113;107;138;132;144 37;46;55;70;85;106;131;61;76;97;91;118;112;143;137;149 RT;RT;RT;RT;RT;RT;RT 30;39;48;63;78;99;124 32;41;50;65;80;101;126 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. To generate the site-directed mutagenesis in 1.2mer replicons, the specific regions of the HBV 1.2mer were amplified by overlapping extension PCR using following primers: for rtM129L, For 5'-GCA CGG GAC CCT GCA AGA CCT GC-3' and Rev 5'-GCA GGT CTT GCA GGG TCC CGT GC-3'; for rtV173L, For 5'-ATT CCT ATG GGA CTG GGC CTC AGT CCG-3' and Rev 5'-CGG ACT GAG GCC CAG TCC CAT AGG AAT-3'; for rtM204I, For 5'-TGG CTT TCA GTT ATA TCG ATG ATG TGG TAT-3' and Rev 5'-ATA CCA CAT CAT CGA TAT AAC TGA AAG CCA-3'; for rtL269I, For 5'-AAC ATA TTG TAC AAA AAA TCA AGC AAT GTT TTC G-3' and Rev 5'-CGA AAA CAT TGC TTG ATT TTT TGT ACA ATA TGT T-3'; for rtH337N, For 5'-TAA ACA ATA TCT GAA CCT TTA CCC CGT TG-3' and Rev 5'-CAA CGG GGT AAA GGT TCA GAT ATT GTT TA-3'. 2015 PloS one Method HBV M129L;V173L;M204I;L269I;H337N 177;277;387;505;635 182;282;392;510;640 RT;RT;RT;RT;RT 175;275;385;503;633 177;277;387;505;635 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. An X-ray diffraction data set for HIV-1 RT Q151M was collected using a PILATUS3 6M detector (Dectris) on beamline BL-17A at the Photon Factory, Tsukuba, Japan at a radiation wavelength of 0.98000 A. 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 43 48 RT 40 42 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Escherichia coli BL21-CodonPlus (DE3)-RIL strain (Novagen) was co-transformed with pET-28_His6-p51 and pCDF_p66_Q151M by electroporation. 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 112 117 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Expression of HIV-1 RT Q151M p66/p51 was induced by adding 0.1 mM isopropyl beta-d-1-thiogalactopyranoside (IPTG) for a further 16 h at 25 C. 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 23 28 RT 20 22 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The HIV-1 RT Q151M crystals belonged to space group P321, with unit-cell parameters a = b = 145.74, c = 118.40 A. 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 13 18 RT 10 12 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The molecular-replacement solutions obtained revealed one p66/p51 heterodimer of HIV-1 RT Q151M in the asymmetric unit. 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 90 95 RT 87 89 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The purified HIV-1 RT Q151M p66/p51 was dialyzed against buffer D (20 mM Tris-HCl pH 8.0, 2 mM MgCl2, 1 mM DTT) and was concentrated to 8 mg ml-1 using a centrifugal filtration device (50 kDa molecular-weight cutoff; Millipore). 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 22 27 RT 19 21 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The Q151M mutation was introduced into the p66 gene of the pCDF-Duet vector (pCDF_p66_Q151M) by inverse PCR according to a previously described method (Hemsley et al., 1989). 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M;Q151M 4;86 9;91 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The structure of HIV-1 RT Q151M was solved by molecular replacement using MOLREP (Vagin & Teplyakov, 2010) in the CCP4 suite (Winn et al., 2011). 2015 Acta crystallographica. Section F, Structural biology communications Method HBV Q151M 26 31 RT 23 25 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. A risk prediction model to classify the HCC cases and controls was constructed according to the following steps: (1) Prediction factor selection: HBV genotype, the 11 independent HCC-related mutations (C1653T, C1673T, T1674C/G, C1730G, A1752G, T1753C, A1762T, G1764A, G1899A, G1915A/C and C1969T), the HLA SNPs (rs9272105 and rs9275319), the HCC-related multiplicative interactions (rs9272105 with the HBV genotype, the HBV mutations C1673T, G1719T, A1726C, C1730G, A1752G and G1799C) and the main effect of the interactions were considered to be the predictive factors by conducting a backwards stepwise logistic regression model, with a significance level of 0.05 for removing the respective variables. 2015 Scientific reports Method HBV T1674G;C1653T;C1673T;T1674C;C1730G;A1752G;T1753C;A1762T;G1764A;G1899A;G1915A;G1915C;C1969T;C1673T;G1719T;A1726C;C1730G;A1752G;G1799C 218;202;210;218;228;236;244;252;260;268;276;276;289;434;442;450;458;466;477 226;208;216;226;234;242;250;258;266;274;284;284;295;440;448;456;464;472;483 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 40;179;342 43;182;345 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. For their generations, rtL180M, rtM204V and rtV173L mutations were introduced into pTmcs-HBV1.3 by site-mutagenesis with the appropriate primers using QuickChange Lightning Site-Directed Mutagenesis Kit (Agilent Technologies) as per the manufacturer s recommendations. 2014 Acta pharmaceutica Sinica. B Method HBV L180M;M204V;V173L 25;34;46 30;39;51 RT;RT;RT;S 23;32;44;251 25;34;46;252 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. In brief, a total of 13.5 mug of pTmcs-HBV1.3, pTmcs-HBV1.3-3TCR or pTmcs-HBV1.3-3TCR-V173L and 4.5 mug of pCMV-SB were co-injected into the tail vein of 6- to 9-week-old NOD/SCID mice in a volume of saline equivalent to 8% of the mouse body weight (e.g., 1.6 mL for mouse of 20 g). 2014 Acta pharmaceutica Sinica. B Method HBV V173L 86 91 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. pTmcs-HBV1.3-3TCR and pTmcs-HBV1.3-3TCR-V173L are two different lamivudine-resistant mutants carrying rtL180M-rtM204V double mutations and rtL180M-rtM204V-rtV173L triple mutations, respectively. 2014 Acta pharmaceutica Sinica. B Method HBV L180M;M204V;M204V;L180M;V173L;V173L 104;112;149;141;157;40 109;117;154;146;162;45 RT;RT;RT;RT;RT 102;110;139;147;155 104;112;141;149;157 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. The primer pairs of 5'-TTGGCTTTCAGTTATGTGGATGATGTGGTATTG-3' and 5'-CAATACCACATCATCCACATAACTGAAAGCCAA-3' were for rtM204V mutation, 5'-GTGGGCCTCAGCCCGTTTCTCATGGCTCAGTTTACTAGTGCC-3' and 5'-GGCACTAGTAAACTGAGCCATGAGAAACGGGCTGAGGCCCAC-3' were for rtL180M mutation, 5'-AAAATTCCTATGGGATTGGGCCTCAGCCCGTTT-3' and 5'-AAACGGGCTGAGGCCCAATCCCATAGGAATTTT-3' were for rtV173L mutation. 2014 Acta pharmaceutica Sinica. B Method HBV M204V;L180M;V173L 115;244;355 120;249;360 RT;RT;RT 113;242;353 115;244;355 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Association of G1986A with few parameters such as HBeAg status, genotype, liver diseases and e-seroconversion rate were statistically determined by chi-square analysis. 2015 Hepatitis monthly Method HBV G1986A 15 21 C 50 55 Liver disease 74 88 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The consensus sequences were then analyzed at the basal core promoter (BCP), precore (PC) and core (C) region and particularly observed for presence of G1986A mutation. 2015 Hepatitis monthly Method HBV G1986A 152 158 BCP;BCP;C;C;Precore;Precore 50;71;100;94;86;77 69;74;101;98;88;84 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In cases with rtA181T mutants, the decreased packaging efficiency of the deficient S protein was coupled with the enhanced activity of the mutated RT enzyme under NA treatment. 2015 Scientific reports Method HBV A181T 16 21 RT;RT;S 14;147;83 16;149;84 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The observed change of rtA181T and rtM204I mutant frequencies in the PVR and VB groups enabled us to assign parameters for the aforementioned dynamic model and further explore the mechanism of HBV dynamics during antiviral therapy (details are presented in Supplementary Text S4). 2015 Scientific reports Method HBV A181T;M204I 25;37 30;42 RT;RT 23;35 25;37 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. We separately specified the total amounts of rtA181T, rtM204I mutants, and drug-sensitive wild-type viruses in the system. 2015 Scientific reports Method HBV A181T;M204I 47;56 52;61 RT;RT 45;54 47;56 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Finally, A1762T/G1764A mutations in BCP region and T1858C, G1862C andG1896A mutations in PC region were analyzed. 2016 PloS one Method HBV G1764A;A1762T;T1858C;G1862C 16;9;51;59 22;15;57;65 BCP;Precore 36;89 39;91 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Using the Mutation Reporter Tool software (http://hvdr.bioinf.wits.ac.za/mrt/), HBV resistance-associated mutations (RAMs) in the pol gene represented by V173L, L180M, A181V, A194T, S202G, M204V/I and N236T were assessed. 2016 PloS one Method HBV V173L;L180M;A181V;A194T;S202G;M204V;M204I;N236T 154;161;168;175;182;189;189;201 159;166;173;180;187;196;196;206 P 130 133 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Of the 557 patients, HBV rtA181T/V mutants were found in 136 patients. 2016 Saudi journal of gastroenterology Method HBV A181T;A181V 27;27 34;34 RT 25 27 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Of these, a total of 30 patients who received ETV (1.0 mg/day) monotherapy or ETV plus ADV (10.0 mg/day) therapy over 48 weeks as rescue therapy against HBV rtA181V/T mutants only without other concomitant mutations were enrolled in this study. 2016 Saudi journal of gastroenterology Method HBV A181V;A181T 159;159 166;166 RT 157 159 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Serum HBV DNA levels, alanine aminotransferase (ALT) levels, and the status of HBeAg at baseline and at 48 weeks of rescue therapy for HBV rtA181V/T mutants were investigated through review of medical records. 2016 Saudi journal of gastroenterology Method HBV A181V;A181T 141;141 148;148 C;RT 79;139 84;141 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Articles that satisfied the following criteria were included: (1) case-control or cohort studies, (2) HCC and control subjects, including ASC, CHB or LC patients, (3) BCP A1762T/G1764A dual mutations (for HBV mutation), (4) HCC outcomes, and (5) available full texts. 2016 Oncotarget Method HBV G1764A;A1762T 178;171 184;177 BCP 167 170 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 102;143;224;150 105;146;227;152 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In our evaluation of the BCP A1762T/G1764A dual mutant, subjects with either a single mutation or a deletion at either site were not included in the analysis. 2016 Oncotarget Method HBV G1764A;A1762T 36;29 42;35 BCP 25 28 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. The following exclusion criteria were applied: (1) studies that included patients who were coinfected with hepatitis A, C, D, E virus or human immunodeficiency virus, had alcohol-related liver diseases, or had previously received antiviral treatments, (2) studies without control subjects, and (3) studies that only investigated A1762T or G1764A single mutations. 2016 Oncotarget Method HBV A1762T;G1764A 329;339 335;345 Liver disease 171 201 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. The following medical subject headings were used: "hepatocellular carcinoma;" "hepatitis B virus X protein;" "mutation;" "basal core promoter;" "A1762T;" "G1764A;" and "variation." Electronic searches were supplemented with manual searches of reference lists used in all retrieved review articles, primary studies, and abstracts from meetings to identify other studies not found in the electronic searches. 2016 Oncotarget Method HBV A1762T;G1764A 144;154 151;161 BCP;X 122;97 141;98 Hepatocellular carcinoma 51 75 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. The sequences were examined for known vaccine escape mutations (sG145R/A, sP142S, sI/T126A/N/I/S, sQ129H/R, sM133L, sD144A/E, sP120S/E, sK141E, sP134I, and sT116N), immunoprophylaxis escape mutations (sI110L, sI126T, sT131N, sM133T, sS143T, sC149R, and sN204S), mutations associated with occult HBV infection (nucleotide changes A233G and G418T), and diagnostic failure mutations (sT123A/N, sK122I, sT131I, and sK141E). 2017 Antiviral therapy Method HBV T126A;T126N;T126I;T126S;G145R;G145A;P142S;I126A;I126N;I126I;I126S;Q129H;Q129R;M133L;D144A;D144E;P120S;P120E;K141E;P134I;T116N;I110L;I126T;T131N;M133T;S143T;C149R;N204S;T123A;T123N;K122I;T131I;K141E;A233G;G418T 82;83;83;83;64;64;74;82;82;82;82;98;98;108;116;116;126;126;136;144;156;201;209;217;225;233;241;253;381;381;391;399;411;329;339 96;96;96;96;72;72;80;96;96;96;96;106;106;114;124;124;134;134;142;150;162;207;215;223;231;239;247;259;389;389;397;405;417;334;344 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 64;74;82;98;108;116;126;136;144;156;201;209;217;225;233;241;253;381;391;399;411 65;75;83;99;109;117;127;137;145;157;202;210;218;226;234;242;254;382;392;400;412 HBV infections 295 308 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. The HBx mutations A1762T (T mutant), G1764A (A mutant), A1762T/G1764A (TA mutant), and T1753A/A1762T/G1764A/T1768A (Combo mutant) were constructed by overlapping extension PCR using pAd-HBx WT as the template, and subcloned into pAdTrack-TO4 (primer sequences are listed in Table S1). 2016 Cancer science Method HBV G1764A;A1762T;G1764A;T1768A;A1762T;G1764A;A1762T;T1753A 63;94;101;108;18;37;56;87 69;100;107;114;24;43;62;93 X;X 4;186 7;189 27538443 Management of Clevudine-Resistant Chronic Hepatitis B: A Multicenter Cohort Study. Eligible patients were identified according to the following inclusion criteria: age over 18 years, HBeAg positive or negative CHB, more than 6 months of CLV therapy, development of virologic breakthrough during CLV therapy with confirmed genotypic resistance to CLV (rtM204I mutation), and rescue therapy for CLV-resistance for more than 12 weeks with either ADV, CLV+ADV, LAM+ADV, or ETV. 2017 Gut and liver Method HBV M204I 270 275 C;RT 100;268 105;270 Chronic Hepatitis B 127 130 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. After several energy minimization steps using GROMACS 43a1 force field, the visualization of the refined model as well as the generation of the G145R mutant were performed by PyMOL software. 2016 Hepatitis monthly Method HBV G145R 144 149 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. At the same time, the wild-type and G145R mutant HBsAg proteins were structurally aligned, and their root mean square deviation (RMSD) and template modeling (TM) scores were computed using the SuperPose and TM-align servers, respectively. 2016 Hepatitis monthly Method HBV G145R 36 41 S 49 54 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. In parallel, the MEMSAT3 and TMpred web tools (http://embnet.vital-it.ch/software/TMPRED_form.html) were also applied to predict the orientation and topology of the transmembrane regions of the G145R mutant compared with the wild-type HBsAg. 2016 Hepatitis monthly Method HBV G145R 194 199 S 235 240 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. MD simulations for both the G145R mutant and the wild-type HBsAg were conducted using GROMACS v5.0.2 package. 2016 Hepatitis monthly Method HBV G145R 28 33 S 59 64 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Predictions regarding the secondary structures of both wild-type (accession numbers: GQ183486) and G145R mutant HBsAg were carried out using three highly accurate secondary structure prediction tools: Jpred 4, PHD, and PSIPRED. 2016 Hepatitis monthly Method HBV G145R 99 104 S 112 117 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. To assess the antigenic potential, both wild-type and G145R mutant HBsAgs were subjected to the antibody epitope prediction server IEDB-AR, which provides multiple tools to predict MHC class I and MHC class II restricted T-cell epitopes as well as linear and discontinuous B-cell epitopes. 2016 Hepatitis monthly Method HBV G145R 54 59 S 67 73 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Introduction of rtD205H mutation resulted in a polymerase-deficient HBV control plasmid, termed tyrosine-methionine-histidine-aspartate (YMHD), which corresponds to the mutated reverse transcriptase (RT) active site tyrosine-methionine-aspartate-aspartate (YMDD). 2017 Journal of hepatology Method HBV D205H 18 23 P;RT;RT;RT;P;P 47;177;16;200;216;257 57;198;18;202;255;261 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Mutants sE2G, sL21R, sG24K, sT47A, sT47K, sC69* sL95W, sL98V, and sG145R were cloned into plasmid pBB4.5 1.2/PC, which contained a 1.2-fold length HBV genome of genotype C with a G1896A mutation in the preC region to facilitate the DNA replication in the in vitro system. 2017 Journal of hepatology Method HBV E2G;L21R;G24K;T47A;T47K;C69X;L95W;L98V;G145R;G1896A 8;14;21;28;35;42;48;55;66;179 12;19;26;33;40;47;53;60;72;185 Precore;S;S;S;S;S;S;S;S;S 202;8;14;21;28;35;42;48;55;66 206;9;15;22;29;36;43;49;56;67 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Plasmids with the human influenza hemagglutinin (HA) tag at the C-terminal of SHB derivatives (WT-HA, sE2G-HA, sC69*-HA, sL95W-HA, sL98V-HA, and sG145R-HA) were cloned into pBB4.5 1.2/PC. 2017 Journal of hepatology Method HBV E2G;C69X;L95W;L98V;G145R 102;111;121;131;145 106;116;126;136;151 S;S;S;S;S;S 102;111;121;131;145;78 103;112;122;132;146;81 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Since the mutant sC69* has a premature stop codon at the SHBs AA position 69, we inserted a HA tag at three different SHBs locations (N terminus, before the stop codon between positions 68 and 69, and after the C terminus of WT SHB sequence). 2017 Journal of hepatology Method HBV C69X 17 22 S;S;S;S 17;228;57;118 18;231;61;122 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The following LNA-based probes (nt 582-591) designed for discrimination between the G145R mutant (nucleotide position at 587: G A) and wild-type were used for real-time PCR: Probe-G (wild-type sequence); 5'-FAM-CGGACGGAAA-IBFQ-3', Probe-A (mutant-type sequence); 5'-HEX-CGGACAGAAA-IBFQ-3' (Integrated DNA Technologies, Coralville, Iowa). 2016 PloS one Method HBV G145R 84 89 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The wild-type and G145R mutant-type DNA extracted from serum were quantified according to the recombinant plasmid wild-type controls and the G145R mutant-type (nucleotide position at 587: G A) controls, respectively. 2016 PloS one Method HBV G145R;G145R 18;141 23;146 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. To validate the LNA-based probe real-time PCR, wild-type and G145R mutant type (nucleotide position at 587: G A) PCR products of the surface region (432bp) were purified and cloned into the pCR4 TOPO vector (Invitrogen, Carlsbad, CA) and transformed into TOP 10 One Shot Escherichia coli bacteria (Invitrogen). 2016 PloS one Method HBV G145R 61 66 Precore;S 191;134 193;141 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Following the same procedure, the resulting plasmid, pTg-sW172*, was the same as pTg-WT except for the presence of target mutation (Figure 1a). 2016 Oncogenesis Method HBV W172X 57 63 S 57 58 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. The sample size used to calculate the incidence of HCC for each line of transgenic mice was selected to ensure that development of HCC in >15% of TgSW172* mice could reach statistical significance. 2016 Oncogenesis Method HBV W172X 148 154 Hepatocellular carcinoma;Hepatocellular carcinoma 51;131 54;134 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Three liver tissues from the noncancerous parts of negative control (Null; non-transgenic), TgWT-H, TgSW172*-H and TgSW172*-L mice were collected for cDNA microarray experiments. 2016 Oncogenesis Method HBV W172X;W172X 102;117 108;123 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. To construct the plasmid encoding the rtA181T/sW172* mutation, site-directed mutagenesis was performed to generate the desired point mutation, G673A, as described previously. 2016 Oncogenesis Method HBV W172X;A181T;G673A 46;40;143 52;45;148 RT;S 38;46 40;47 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. A series of HBsAg eukaryotic expression plasmids(including pcDNA-HBs(sW172L), pcDNA-HBs(sW172*) and pcDNA-HBs(wt)) were also generated when the substituted, truncated and wild-type HBsAg coding genes (1176 bp) were respectively cloned into the eukaryotic expression plasmid pcDNA3.0, by using the corresponding pHBV-rtA181T/sW172L, pHBV-rtA181T/sW172* and pHBV4.1 as the template. 2016 Scientific reports Method HBV W172X;W172L;A181T;A181T;W172X;W172L 345;324;318;339;88;69 351;330;323;344;94;75 S;S;S;S;S;RT;RT;S;S;S;S 65;84;106;12;181;316;337;69;88;324;345 68;87;109;17;186;318;339;70;89;325;346 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. And plasmid pHBV-rtA181T/sW172L could express substituted HBsAg, while pHBV-rtA181T/sW172* could express truncated HBsAg. 2016 Scientific reports Method HBV W172L;W172X;A181T;A181T 25;84;19;78 31;90;24;83 S;S;RT;RT;S;S 58;115;17;76;25;84 63;120;19;78;26;85 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The first part was to compare the DNA replication capacity and viral protein expression among different overlapping S gene mutation (sW172L and sW172*) on rtA181T mutant strain replication and proteins expression in vitro and in vivo HBV replication systems. 2016 Scientific reports Method HBV A181T;W172L;W172X 157;133;144 162;139;150 RT;S;S;S 155;116;133;144 157;117;134;145 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The pHBV-rtA181T/sW172L and pHBV-rtA181T/sW172* mutant plasmids were generated by site-directed mutagenesis using wild-type pHBV4.1 as the template. 2016 Scientific reports Method HBV W172L;W172X;A181T;A181T 17;41;11;35 23;47;16;40 RT;RT;S;S 9;33;17;41 11;35;18;42 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The transfected DNA mixture comprised 5 mug of HBV promoter report gene plasmid (CpLUC or PS1pLUC or SpLUC or XpLUC) and 0.5 mug of HBsAg eukaryotic expression plasmid (pcDNA-HBs(wt) or pcDNA-HBs(sW172*) or pcDNA-HBs(sW172L)) or the negative control plasmid pcDNA3.1. 2016 Scientific reports Method HBV W172X;W172L 196;217 202;223 S;S;S;S;S;S 175;192;213;132;196;217 178;195;216;137;197;218 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. To complete this experiment, the HBsAg eukaryotic expression plasmids of pcDNA-HBs(sW172L), pcDNA-HBs(sW172*) and pcDNA-HBs(wt) were generated, and HBV promoter report gene plasmids and dual-luciferase reporter assay system were also used. 2016 Scientific reports Method HBV W172X;W172L 102;83 108;89 S;S;S;S;S;S 79;98;120;33;83;102 82;101;123;38;84;103 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. To complete this experiment, the pHBV-rtA181T/sW172L and pHBV-rtA181T/sW172* mutant plasmids were generated, and corresponding in vitro and in vivo models of HBV replication were established. 2016 Scientific reports Method HBV W172X;W172L;A181T;A181T 70;46;40;64 76;52;45;69 RT;RT;S;S 38;62;46;70 40;64;47;71 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. To construct HBV replication cell model with above mentioned plasmids (including wild-type pHBV4.1, mutant pHBV-rtA181T/sW172L or pHBV-rtA181T/sW172*), the HepG2 cells were used in this study, which was grown in RPMI-1640 medium supplemented with 10% fetal bovine serumat 37 C in 5% CO2. 2016 Scientific reports Method HBV W172L;W172X;A181T;A181T 120;143;114;137 126;149;119;142 RT;RT;S;S 112;135;120;143 114;137;121;144 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Two other HBs, W1S and W3S cDNA, were cloned from sera used as the panel sera to check the performance of diagnostic machines for HBV infection. 2017 PloS one Method HBV W1S;W3S 15;23 18;26 S 10 13 HBV infections 130 143 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. 17 mg/ml protein of Cp149_Y132A in 20 mM Tris buffer (pH 9.0) and 2 mM DTT was combined with equal volume of crystallization buffer containing 100 mM citrate (pH 5.6), 21% (vol/vol) isopropanol, and 1% (W/V) PEG 10,000. 2017 Scientific reports Method HBV Y132A 26 31 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Accession codes: Atomic coordinates and structure factors of Apo core protein mutant Y132A, Y132A-SBA_R01 and Y132A-HAP_R01 have been deposited in the Protein Data Bank (http://www.pdb.org) with the accession codes 5WTW, 5T2P and 5WRE respectively. 2017 Scientific reports Method HBV Y132A;Y132A;Y132A 85;92;110 90;97;115 C 65 69 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. C-terminal 6XHis-tagged Cp149_Y132A from HBV genotype D strain adyw was constructed as described previously and cloned into pET21a vector. 2017 Scientific reports Method HBV Y132A 30 35 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Cp149_Y132A crystal in P41212 form grew in the well buffer containing 5.4 M ammonium nitrate and 0.1 M Bis-tris propane pH 7.0, within 2 days after setting up the sitting drop at 11.3 mg/ml. 2017 Scientific reports Method HBV Y132A 6 11 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. HBV core variants, T33/N/Q/S, P25A/G/S, and V124F/I, were generated by site directed mutagenesis PCR. 2017 Scientific reports Method HBV P25A;P25G;P25S;V124F;V124I 30;30;30;44;44 38;38;38;51;51 C 4 8 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The datasets were collected on single crystals for Y132A-HAP_R01 or Y132A-SBA_R01 complex structure at BL17U beamline, Shanghai Synchrotron Radiation Facility (SSRF). 2017 Scientific reports Method HBV Y132A;Y132A 51;68 56;73 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Two crystals were averaged for apo Y132A crystal in P41212 space group. 2017 Scientific reports Method HBV Y132A 35 40 28208753 Possible Impact of 190G > A CCR2 and Delta32 CCR5 Mutations on Decrease of the HBV Vaccine Immunogenicity-A Preliminary Report. To assess possible differences in the frequencies of 32 and 190G > A polymorphisms, a control group from the HAPMAP database was used. 2017 International journal of environmental research and public health Method HBV G190A 61 69 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. alphalM0 was derived from alphal by A1896G and A1899G back mutations to restore HBeAg expression. 2017 Virology Method HBV A1896G;A1899G 36;47 42;53 C 80 85 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. The rtH124N mutation identified in this study was introduced in WT-HBV clone (pJET-HBV-wt) by Site-Directed Mutagenesis (Agilent Technologies) with specific mutagenic oligonucleotides (rtH124N_F and rtH124N_R) (Supplementary Table S6) to generate pJET-HBV-mt (rt124N) that was confirmed by sequencing. 2017 Scientific reports Method HBV H124N;H124N 6;201 11;206 RT;RT 4;260 6;262 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Among them, 31 patients developed rtA181T/V mutation strains (rtA181 group), and the other 25 patients developed rtA181T/V and rtN236T mutation strains (rtA181 + rtN236 group). 2017 Virology journal Method HBV A181T;A181V;A181T;A181V;N236T 36;36;115;115;129 43;43;122;122;134 RT;RT;RT;RT;RT;RT 34;62;113;127;153;162 36;64;115;129;155;164 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. They developed rtA181T/V mutation strains during ADV treatment. 2017 Virology journal Method HBV A181T;A181V 17;17 24;24 RT 15 17 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. To investigate the effects of rtS78T/sC69* and preS1/preS2del mutations on replication of HBV, three replication-competent HBV constructs containing the rtS78T/sC69* mutation (M1), the preS1/S2 deletion (preS1/preS2del, M2) with an in frame deletion of the nucleotides 1124 to 1385 as well as the combination of the two, rtS78T/sC69* + preS1/S2del (M3), were generated using site directed mutagenesis and recombination techniques. 2017 Journal of hepatology Method HBV C69X;C69X;C69X;S78T;S78T;S78T 37;160;328;32;155;323 42;165;333;36;159;327 PreS;PreS;PreS1;PreS1;PreS1;PreS1;PreS2;RT;RT;RT;S;S;S 53;210;47;204;336;185;185;30;153;321;37;160;328 57;214;52;209;341;190;191;32;155;323;38;161;329 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. For site-directed mutagenesis, plasmid D-IND 60 was digested by HindIII and EcoO65I, and ligated with the fragments carrying P120T and S143L amino acid mutations to produce the 1.24-fold HBV genome. 2017 World journal of hepatology Method HBV P120T;S143L 125;135 130;140 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. Alternatively, dependent on the scale of antiviral drug treatment received in this population, the therapeutic methods might also partly contribute to selection of mutation G1899A and HBV with higher replication efficiency. 2017 Emerging infectious diseases Method HBV G1899A 173 179 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. However, multivariate analysis that included G1730C, HBeAg, and age showed that the changing prevalence of G1730C was not independent of HBeAg and age (adjusted p = 0.222, 0.049, and 0.027, respectively). 2017 Emerging infectious diseases Method HBV G1730C;G1730C 45;107 51;113 C;C 53;137 58;142 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. In addition, we noted a significant decrease in the prevalence of mutation A1752G over the 5-year period (p = 0.022). 2017 Emerging infectious diseases Method HBV A1752G 75 81 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. In the HBeAg-positive group, we saw a significant increase over time in the prevalence of precore G1899A mutations (p = 0.039) and level of HBV DNA (p = 0.013); however, these 2 factors were independent of each other (adjusted p = 0.009 and 0.003, respectively). 2017 Emerging infectious diseases Method HBV G1899A 98 104 C;Precore 7;90 12;97 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. Multivariate analysis showed that these 3 changes were not independent (adjusted p = 0.062 for age, 0.067 for male sex, and 0.201 for mutation A1752G; data not shown). 2017 Emerging infectious diseases Method HBV A1752G 143 149 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. Three factors were significantly associated with HBeAg status: an increased prevalence of anti-HBe (p = 0.004) and increased prevalence of precore G1896A (p = 0.003) and G1899A (p = 0.019) mutations. 2017 Emerging infectious diseases Method HBV G1896A;G1899A 147;170 153;176 C;C;Precore 95;49;139 98;54;146 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. We noted a mild, but significant, decrease in the prevalence of G1730C mutations (p = 0.034). 2017 Emerging infectious diseases Method HBV G1730C 64 70 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Primers were designed for the mutant gene of HBV polymerase M204I, which were confirmed by the serum samples containing M204I mutation previously detected by sequencing (performed by TIANYI HUIYUAN). 2017 Sensors (Basel, Switzerland) Method HBV M204I;M204I 60;120 65;125 P 49 59 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. QDs-Mediated Fluorescent Method for the Detection of HBV M204I Mutation. 2017 Sensors (Basel, Switzerland) Method HBV M204I 57 62 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. The amplified HBV DNA with a viral load of 106 IU/mL without streptavidin-QDs, the amplified HBV DNA without M204I mutation with a viral load of 106 IU/mL with added streptavidin-QDs, and ultra-pure water were used as the negative controls, respectively. 2017 Sensors (Basel, Switzerland) Method HBV M204I 109 114 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. To start, the amplified HBV DNA, which contains M204I mutation with viral load of 106 IU/mL (the recognized international standard or copies/ml by nucleic acid testing technologies, 1 IU/mL = 5.3 copies/mL, one copy means one virus), were 10-fold serially diluted in a negative serum from 106 IU/mL to 101 IU/mL. 2017 Sensors (Basel, Switzerland) Method HBV M204I 48 53 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. A meta-analysis of the pooled results from case-control and cohort studies investigated the associations between mutation in A1762T, G1764A, and G1896A and the risk of HCC. 2017 Medicine Method HBV A1762T;G1764A;G1896A 125;133;145 131;139;151 Hepatocellular carcinoma 168 171 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Articles that satisfied the following criteria were included: (1) case-control or cohort studies, (2) HCC and control subjects (CHB patients), (3) BCP A1762T, G1764A, and A1762T/G1764A double mutations (for HBV mutation), and precore G1896A, (4) HCC outcomes, and (5) available full texts. 2017 Medicine Method HBV G1764A;A1762T;G1764A;A1762T;G1896A 178;151;159;171;234 184;157;165;177;240 BCP;Precore 147;226 150;233 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma 102;128;246 105;131;249 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. We tested the samples for precore stop codon (G1896A). 2017 Electronic physician Method HBV G1896A 46 52 Precore 26 33 28859616 Molecular characterization of hepatitis B virus in Vietnam. Mutations in the BCP (C1653T, T1674C/G, T1753 V, A1762T, G1764/A, C1766T, and T1768A) and the PC/core region (G1899A, C2002T, A2159G, A2189C, and G2203A/T) associated with HCC were also analyzed. 2017 BMC infectious diseases Method HBV G2203T;C1653T;T1674C;T1674G;T1753V;A1762T;C1766T;T1768A;G1899A;C2002T;A2159G;A2189C;G2203A 146;22;30;30;40;49;66;78;110;118;126;134;146 154;28;38;38;47;55;72;84;116;124;132;140;154 BCP;C;Precore 17;97;94 20;101;96 Hepatocellular carcinoma 172 175 28859616 Molecular characterization of hepatitis B virus in Vietnam. The preS2/S1 sequences were analyzed for preS1 deletion, preS1 mutations (A2962G, C3026A/T, C2964A, and C3116T), preS2 start codon deletion, and preS2 mutations (T31C, T53C, A162G, and T531C/G). 2017 BMC infectious diseases Method HBV C3026T;A2962G;C3026A;C2964A;C3116T;T31C;T53C;A162G;T531C;T531G 82;74;82;92;104;162;168;174;185;185 90;80;90;98;110;166;172;179;192;192 PreS1;PreS1;PreS2;PreS2;PreS2 41;57;4;113;145 46;62;9;118;150 28859616 Molecular characterization of hepatitis B virus in Vietnam. The S gene sequence was analyzed for mutations in the "a" determinant region (T116 N, P120S/T, I/T126S/A, Q129H/R, M133 L/T, K141E, P142S, D144E, and G145R), and other virulence associated mutations (N3S, V184A, and S204R). 2017 BMC infectious diseases Method HBV I126S;I126A;T126S;T126A;N3S;T116N;P120S;P120T;Q129H;Q129R;M133L;M133T;K141E;P142S;D144E;G145R;V184A;S204R 95;95;95;95;200;78;86;86;106;106;115;115;125;132;139;150;205;216 104;104;104;104;203;84;93;93;113;113;123;123;130;137;144;155;210;221 S 4 5 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. HepG2 cells transfected with the pEBMulti expression vector containing WT- or C1485T-HBx were seeded onto a 96-well plate. 2017 Scientific reports Method HBV C1485T 78 84 X 85 88 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Regarding the C1485T mutation in HBx, we used the same primer set as that used for the construction of HBx-mutant Tg mice (see below). 2017 Scientific reports Method HBV C1485T 14 20 X;X 33;103 36;106 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Transfection of the plasmid (control, WT-HBx, C1485T-HBx, empty vector) into HepG2 cells was performed using Fuge-6 (Roche) following the manufacturer's instructions. 2017 Scientific reports Method HBV C1485T 46 52 X;X 41;53 44;56 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Transgenic mice expressing WT- and C1485T-HBx were generated using C57/BL6 mice (Charles River Laboratories Japan, Yokohama, Japan). 2017 Scientific reports Method HBV C1485T 35 41 X 42 45 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The G1896A mutation in PC region and A1762T/G1764A dual mutations in BCP/PC region were analysed in HBV BCP/PC clones of different groups. 2017 Virology journal Method HBV G1764A;G1896A;A1762T 44;4;37 50;10;43 BCP;BCP;Precore;Precore;Precore 69;104;23;73;108 72;107;25;75;110 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. As previously described, we used the Mutation Reporter Tool (MRT) software (http://hvdr.bioinf.wits.ac.za/mrt/) to look for HBV resistance-associated mutations (RAMs) in the Polymerase catalytic domain represented by major RAMs (A181T/V/S, A194T, M204V/I/S and N236T) and compensatory RAMs (I169T, V173L, L180M, S202G/I and M250V. 2018 PloS one Method HBV A181T;A181V;A181S;M204V;M204I;M204S;A194T;N236T;I169T;V173L;L180M;S202G;S202I;M250V 229;229;229;247;247;247;240;261;291;298;305;312;312;324 238;238;238;256;256;256;245;266;296;303;310;319;319;329 P 174 184 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. In addition, we looked for Vaccine Escape Mutants (VEMs) and polymorphic mutations outside (Y100C, Q101H, S117N, T118R and P120S) and within the HBsAg immuno-dominant 'a' determinant (I/T126A/N, A128V, Q129H/R, G130N, M133L/T, K141E, S143L, D144A/H/E and G145R). 2018 PloS one Method HBV T126A;T126N;D144A;D144H;D144E;I126A;I126N;Y100C;Q101H;S117N;T118R;P120S;A128V;Q129H;Q129R;G130N;M133L;M133T;K141E;S143L;G145R 184;184;241;241;241;184;184;92;99;106;113;123;195;202;202;211;218;218;227;234;255 193;193;250;250;250;193;193;97;104;111;118;128;200;209;209;216;225;225;232;239;260 S;S 168;145 182;150 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. During sequences analysis, much emphasis was given for the detection of mutations affecting HBeAg expression at the BCP transcriptional (BCP double mutations; A1762T/G1764A) and translational genes (Kozak sequences mutants, nt1809-1812) and PC initiation (1814-1816), translational stop codon (G1896A with C1858T) and post translational mutant gene (G1862T). 2018 PloS one Method HBV G1764A;A1762T;G1896A;C1858T;G1862T 166;159;294;306;350 172;165;300;312;356 BCP;BCP;C;Precore 116;137;92;241 119;140;97;243 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Finally, the mutant variants detected were compared among the study groups with special emphasis on HIV co-infected patients who were described before as having HBV drug resistance gene mutations at their YMDD RT motif due to rtM204V/I in particular and the rest RT motif of the polymerase gene in general. 2018 PloS one Method HBV M204V;M204I 228;228 235;235 P;RT;RT;RT;P 279;210;226;263;205 289;212;228;265;209 HBV-HIV coinfections 100 115 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. In particular, the HBV-HIV co-infected group was characterized by the YMDD RT associated 3TC/ETV drug resistance gene mutations (rtM204V/I) which appeared as multiple combinations with other mutant variants, such as rtV173L and rtL180M. 2018 PloS one Method HBV M204V;M204I;L180M;V173L 131;131;230;218 138;138;235;223 RT;RT;RT;RT;P 75;129;216;228;70 77;131;218;230;74 HBV-HIV coinfections 23 38 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Generation of the full-length HBV genome construct with the prS1 W4P mutation using site-directed mutagenesis. 2018 World journal of gastroenterology Method HBV W4P 65 68 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Serum HBsAg levels in male and female W4P TG mice and their WT littermates were determined by enzyme-linked immunosorbent assay (ELISA) using a commercial Bioelisa HBsAg color kit (Biokit, Barcelona, Spain) according to the procedures provided by the manufacturer. 2018 World journal of gastroenterology Method HBV W4P 38 41 S;S 6;164 11;169 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. The mutagenesis was performed using the forward primer W4P-F (5'- AACAAGAGCTACGCATGGGAGGTCCGT CATCAAAACCTC-3') and the reverse primer W4P-R (5'-GAGGTTTTGATGACGGACCT CCCATGCTGTAGCTCTTGTT-3') located from 2473 bp and 2513 bp. 2018 World journal of gastroenterology Method HBV W4P;W4P 55;134 58;137 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. The mutant full-length HBV genome construct carrying the W4P mutation in the preS1 region (hereafter, pHY92-W4P) was generated by site-directed mutagenesis of the WT pHBV-1.1x vector (hereafter, pHY92-WT) (Genotype A, GenBank No. 2018 World journal of gastroenterology Method HBV W4P;W4P 57;108 60;111 PreS1 77 82 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. To generate W4P TG mice, fertilized C57BL/6N embryos and HBV full genome with the W4P mutation were co-microinjected into one-cell embryo in accordance with the standard microinjection procedures for TG mouse production (Macrogen, Seoul, Korea). 2018 World journal of gastroenterology Method HBV W4P;W4P 12;82 15;85 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. Distances were calculated using MEGA 6 based on the Kimura-2 parameter (K2P) model. 2018 PloS one Method HBV K2P 72 75 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Mutations creating novel N-linked glycosylation, such as 112NG113, 114NT115, T115N, and G130N, were introduced to the 0.7mer construct by ClonExpress MultiS kit (Vazyme, China). 2018 Virology Method HBV T115N;G130N 77;88 82;93 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Additionally, some of above BALB/c nude mice were also given TGFbeta1(Peprotech, UK) at the dose of 2 ng/ml 20 g via tail vein injection to clarify whether TGF-beta/Smad pathway was involved in the tumorigenicity of HBV-rtA181T/sW172* mutant. 2018 Virology journal Method HBV W172X;A181T 228;222 234;227 RT;S 220;228 222;229 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Additionally, the wild-type, substituted and truncated HBsAg eukaryotic expression plasmids of pcDNA3.1-HBs(sW172L), pcDNA3.1-HBs(sW172*) and pcDNA3.1-HBs(wt) were also constructed and conserved in our laboratory. 2018 Virology journal Method HBV W172X;W172L 130;108 136;114 S;S;S;S;S;S 104;126;151;55;108;130 107;129;154;60;109;131 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, stably transformed L02 cell lines with persistent expression of wild-type HBsAg (pcDNA3.1-HBs(wt) and pHBV4.1-HBs(wt)), substituted mutant HBsAg (pcDNA3.1-HBs(sW172L) and pHBV4.1-HBs(sW172L)), and truncated mutant HBsAg (pcDNA3.1-HBs(sW172*) and pHBV4.1-HBs(sW172*)) were also established and used in vitro and in vivo experiments. 2018 Virology journal Method HBV W172X;W172X;W172L;W172L 252;276;177;201 258;282;183;207 S;S;S;S;S;S;S;S;S;S;S;S;S 108;128;173;197;248;272;92;157;232;177;201;252;276 111;131;176;200;251;275;97;162;237;178;202;253;277 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Plasmid pHBV4.1-HBs(sW172L) could express substituted HBsAg, while pHBV4.1-HBs(sW172*) could express truncated HBsAg. 2018 Virology journal Method HBV W172X;W172L 79;20 85;26 S;S;S;S;S;S 16;75;54;111;20;79 19;78;59;116;21;80 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The first part was to investigate and compare the tumorigenesis of different overlapping S gene mutation (sW172L and sW172*) on rtA181T mutant strain in vitro and in vivo. 2018 Virology journal Method HBV A181T;W172L;W172X 130;106;117 135;112;123 RT;S;S;S 128;89;106;117 130;90;107;118 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The pHBV4.1-HBs(sW172L) and pHBV4.1-HBs(sW172*) mutant plasmids were generated using wild-type pHBV4.1 as the template. 2018 Virology journal Method HBV W172X;W172L 40;16 46;22 S;S;S;S 12;36;16;40 15;39;17;41 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The wild-type pHBV4.1-HBs(wt), pHBV4.1-HBs(sW172L) and pHBV4.1-HBs(sW172*) mutant plasmids were previously constructed. 2018 Virology journal Method HBV W172X;W172L 67;43 73;49 S;S;S;S;S 22;39;63;43;67 25;42;66;44;68 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. According to the sequencing outcome, HBV genotype and mutations (including A1752T/G, T1753C, G1757A, A1762T/G1764A, C1766T, T1768A, A1775G, C1799G, A1846T, T1858C, G1896A, G1898A, G1899A, and Pre S deletion) were confirmed by the BLAST analysis (http://blast.ncbi.nlm.nih.gov/Blast.cgi). 2018 Cancer management and research Method HBV G1764A;A1752T;A1752G;T1753C;G1757A;A1762T;C1766T;T1768A;A1775G;C1799G;A1846T;T1858C;G1896A;G1898A;G1899A 108;75;75;85;93;101;116;124;132;140;148;156;164;172;180 114;83;83;91;99;107;122;130;138;146;154;162;170;178;186 PreS 192 197 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. A systematic review by Zhang et al revealed that the global incidence of rtM204I/V/S is 4.85%. 2018 World journal of gastroenterology Method HBV M204I;M204V;M204S 75;75;75 84;84;84 RT 73 75 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. A total of 26 types of RT mutations, including rtS53N, rtT54N, rtL82M, rtV84M, rtS85A, rtI91L, rtY126C, rtT128I/N, rtN139D, rtW153Q, rtF166L, rtV191I, rtA200V, rtV207I, rtS213T, rtV214A, rtQ215P/S, rtL217R, rtE218D, rtF221Y, rtL229G/V/W, rtI233V, rtP237H, rtN238D/S/T, rtY245H, and rtS/C256G, are considered putative drug resistance mutations (Category 3) (Table 1). 2018 World journal of gastroenterology Method HBV C256G;S53N;T54N;L82M;V84M;S85A;I91L;T128I;T128N;N139D;Q215P;Q215S;L229G;L229V;L229W;N238D;N238S;N238T;S256G;Y126C;W153Q;F166L;V191I;A200V;V207I;S213T;V214A;L217R;E218D;F221Y;I233V;P237H;Y245H 284;49;57;65;73;81;89;106;106;117;189;189;227;227;227;258;258;258;284;97;126;135;144;153;162;171;180;200;209;218;240;249;271 291;53;61;69;77;85;93;113;113;122;196;196;236;236;236;267;267;267;291;102;131;140;149;158;167;176;185;205;214;223;245;254;276 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 23;47;55;63;71;79;87;95;104;115;124;133;142;151;160;169;178;187;198;207;216;225;238;247;256;269;282 25;49;57;65;73;81;89;97;106;117;126;135;144;153;162;171;180;189;200;209;218;227;240;249;258;271;284 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Also, a recent study using direct sequencing of samples from 131 treatment-naive patients infected with genotype C2 reported an overall rate of 12.98% for primary (rtT184A/C/F and rtM204I/V) or compensatory (rtL80I and rtL180M) mutations. 2018 World journal of gastroenterology Method HBV T184A;T184C;T184F;L80I;M204I;M204V;L180M 166;166;166;210;182;182;221 175;175;175;214;189;189;226 RT;RT;RT;RT 164;180;208;219 166;182;210;221 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Another compensatory RT mutation, rtV173L, was also detected in several studies of treatment-naive patients, where Zheng et al, Wang et al, and Mirandola et al reported that it occurred in 0.6%, 0.56%, and 0.39% of their patients, respectively. 2018 World journal of gastroenterology Method HBV V173L 36 41 RT;RT 21;34 23;36 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Another study of 325 genotype D infected treatment-naive patients using direct PCR sequencing reported overall incidence of 15.69% for primary and secondary drug resistance mutations, including L80V/I, L180M, M204I/V, and S213T/N. 2018 World journal of gastroenterology Method HBV L80I;L80V;L180M;M204I;M204V;S213T;S213N 194;194;202;209;209;222;222 200;200;207;216;216;229;229 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. For example, rtL91I and rtY221F were more common in genotype C, compared to genotype B (P < 0.001) (Table 2). 2018 World journal of gastroenterology Method HBV L91I;Y221F 15;26 19;31 RT;RT 13;24 15;26 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. For example, using direct sequencing of samples from treatment-naive patients from the United States, Nguyen et al demonstrated that only four (0.9%) of 472 patients were infected with viruses with primary and secondary mutations (rtA181A/S, rtA194S, and rtM250I). 2018 World journal of gastroenterology Method HBV A181A;A181S;A194S;M250I 233;233;244;257 240;240;249;262 RT;RT;RT 231;242;255 233;244;257 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. For examples, Kobayashi et al, Lee et al, Tuncbilek et al, Fung et al, and Huang et al reported rtM204I/V/S mutation frequencies in Japanese, Taiwanese, Turkish, Canadian, and Chinese treatment-naive patients reached of 27.8%, 57%, 7.8%, 12%, and 26.9%, respectively. 2018 World journal of gastroenterology Method HBV M204I;M204V;M204S 98;98;98 107;107;107 RT 96 98 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Fung et al found a higher rate of baseline RT mutations (12% M204I/V, 10% L180M) by using the INNO-LIPA v.3 assay. 2018 World journal of gastroenterology Method HBV M204I;M204V;L180M 61;61;74 68;68;79 RT 43 45 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Further functional studies are necessary to determine whether the rtD134N mutation can induce HCC via modulation of RT activity or through its effects on HBV replication. 2018 World journal of gastroenterology Method HBV D134N 68 73 RT;RT 66;116 68;118 Hepatocellular carcinoma 94 97 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In addition, a systemic meta-analysis review by Zhang et al showed that rtM204V/I had the highest incidence of 4.89% (95%CI: 4.13%-5.65%) among primary and secondary RT mutations. 2018 World journal of gastroenterology Method HBV M204I;M204V 74;74 81;81 RT;RT 72;166 74;168 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In addition, Li et al and Zheng et al reported that the rtF221Y mutation was strongly related to HCC prognosis after liver resection (hazard ratio, 2.345; P = 0.001). 2018 World journal of gastroenterology Method HBV F221Y 58 63 RT 56 58 Hepatocellular carcinoma 97 100 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In South Africa, rtM204I has been mainly detected in treatment-naive HBV/HIV co-infected individuals with rtM204V in treated HBV mono-infected participants, suggesting HIV co-infection could affect HBV preexisting RT mutation pattern. 2018 World journal of gastroenterology Method HBV M204I;M204V 19;108 24;113 RT;RT;RT 17;106;214 19;108;216 HBV-HIV coinfections;HBV-HIV coinfections 168;73 184;88 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In that study, two of 17 treatment-naive patients had mutations which were detected only by UDPS, but not by direct sequencing; one rtM204I mutation with (1.3% mutant ratio) and the other an rtA181T mutation (1.0% ratio). 2018 World journal of gastroenterology Method HBV A181T;M204I 193;134 198;139 RT;RT 132;191 134;193 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In this study, many patients, most of whom were infected with genotype D, carried rtL180M, rtM204V/I, and rtL80V/I mutations. 2018 World journal of gastroenterology Method HBV M204V;M204I;L80V;L80I;L180M 93;93;108;108;84 100;100;114;114;89 RT;RT;RT 82;91;106 84;93;108 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. In this study, rtD134E/N/C was the most frequently encountered hot spot site among the six A-B inter-domain sites and was mutated in 12/79 patients (15.2%). 2018 World journal of gastroenterology Method HBV D134E;D134N;D134C 17;17;17 26;26;26 RT 15 17 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Interestingly, Kim et al also showed that rtL80I was combined with the rtM204I/V mutation in five of nine rtM204I/V cases, and that patients with L80I had increased HBV replication compared with those without this mutation, suggesting that, together with rtM204I/V, it may contribute to HCC generation in treatment-naive patients by compensating for the defective replication of caused by rtM204I/V. 2018 World journal of gastroenterology Method HBV M204I;M204V;M204I;M204V;M204I;M204V;M204I;M204V;L80I;L80I 73;73;108;108;257;257;391;391;44;146 80;80;115;115;264;264;398;398;48;150 RT;RT;RT;RT;RT 42;71;106;255;389 44;73;108;257;391 Hepatocellular carcinoma 287 290 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Moreover, rtY141F, a genotype C-related SNP, also led to a simultaneous amino acid change in the overlapping 'a' determinant region of HBsAg (sM307T). 2018 World journal of gastroenterology Method HBV Y141F;M307T 12;142 17;148 S;S;RT;S 110;135;10;142 124;140;12;143 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Moreover, some genotype dependent mutations, such as rtM129L, rtD134N, rtM145L, and rtE263H/D/Q, were more frequent in in genotype C than genotype B viruses (P < 0.001). 2018 World journal of gastroenterology Method HBV M129L;D134N;E263H;E263D;E263Q;M145L 55;64;86;86;86;73 60;69;95;95;95;78 RT;RT;RT;RT 53;62;71;84 55;64;73;86 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Moreover, the rtF221Y mutation was also associated with poor overall survival (hazard ratio, 2.557; P = 0.004), suggesting that it is a potential independent risk factor and viral marker for HCC. 2018 World journal of gastroenterology Method HBV F221Y 16 21 RT 14 16 Hepatocellular carcinoma 191 194 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Mutation of rtI169T (0.12%), rtT184G (0.06%), rtA194T (0.07%), and rtM250V/L (0.20%) had a very low pooled incidence (Figure 1). 2018 World journal of gastroenterology Method HBV A194T;M250V;M250L;I169T;T184G 48;69;69;14;31 53;76;76;19;36 RT;RT;RT;RT 12;29;46;67 14;31;48;69 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Notably all the three patients with the rtM204V mutation also had coexisting L180M compensatory mutations, and all were infected with HBV-C genotype viruses, suggesting that naturally occurring LMV-resistant HBV may be more frequent in patients infected with genotype C virus. 2018 World journal of gastroenterology Method HBV M204V;L180M 42;77 47;82 RT 40 42 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Notably, Kim et al reported that rtL80I/V was the most frequently encountered preexisting mutation of secondary drug resistance mutations in South Korea (3.8%, 5/131 patients), even higher than rtL180M frequency (2.3%, 3/131 patients). 2018 World journal of gastroenterology Method HBV L80I;L80V;L180M 35;35;196 41;41;201 RT;RT 33;194 35;196 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Notably, rtN226H/T was the only pretreatment mutation, which is more common in genotype B than genotype C (P < 0.001). 2018 World journal of gastroenterology Method HBV N226H;N226T 11;11 18;18 RT 9 11 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Notably, these authors also found that RT mutations in the A-B interdomain could lead to simultaneous AA substitutions sI126A/N/S/, sG130N, sT131N/P, and sG145R of the overlapped 'a' determinant of HBsAg, including the most frequently described immune-escape mutation sG145R (1/192, 0.52%). 2018 World journal of gastroenterology Method HBV I126A;I126N;I126S;G130N;T131N;T131P;G145R;G145R 120;120;120;132;140;140;154;268 130;130;130;138;148;148;160;274 S;S;RT;S;S;S;S;S 180;198;39;119;132;140;154;268 194;203;41;120;133;141;155;269 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of note, association of the following three mutations, rtM204V, rtL80I, and rtD134N, with disease progression provides a likely explanation for the positive relationship between lamivudine resistance and liver disease progression. 2018 World journal of gastroenterology Method HBV D134N;M204V;L80I 78;57;66 83;62;70 RT;RT;RT 55;64;76 57;66;78 Liver disease 204 217 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of note, the following four putative or pretreatment mutations found in treatment naive patients, rtD134E/N, rtN139D/E/H/K/Q, rtF221Y, and rtI224V, are also reported as associated with progression of severe liver diseases, such as HCC and cirrhosis (described below). 2018 World journal of gastroenterology Method HBV D134E;D134N;N139D;N139E;N139H;N139K;N139Q;F221Y;I224V 100;100;111;111;111;111;111;128;141 107;107;124;124;124;124;124;133;146 RT;RT;RT;RT 98;109;126;139 100;111;128;141 Liver disease;Hepatocellular carcinoma;Liver cirrhosis 207;231;239 221;234;248 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of six positions' mutation in the A-B interdomain, three RT mutations, rtD134E/N, rtN139D/E/H/K/Q, and rtW153E/Q/R, that overlap with HBsAg "a" determinant region are hotspots found most frequently in treatment-naive patients, which could contribute to HBV viral persistence via generation of immune escape "a" determinant mutants proteins. 2018 World journal of gastroenterology Method HBV D134E;D134N;N139D;N139E;N139H;N139K;N139Q;W153E;W153Q;W153R 73;73;84;84;84;84;84;105;105;105 80;80;97;97;97;97;97;114;114;114 S;RT;RT;RT;RT 134;57;71;82;103 139;59;73;84;105 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of the two sites in RT related to HCC outcomes, rtD134N (mutation G529A) was associated with lamivudine resistance, further supporting previous findings of potential correlation between resistance to the anti-HBV nucleoside analog, lamivudine, and HCC prognosis. 2018 World journal of gastroenterology Method HBV D134N;G529A 50;66 55;71 RT;RT 20;48 22;50 Hepatocellular carcinoma;Hepatocellular carcinoma 34;248 37;251 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of these SNPs, rtY141F (Y487F), which is located in the RT region of HBV polymerase was associated with increased viral load and HCC (P = 0.0291). 2018 World journal of gastroenterology Method HBV Y141F;Y487F 17;24 22;29 P;RT;RT 73;15;56 83;17;58 Hepatocellular carcinoma 129 132 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of these, 10 patients had mutations associated with primary resistance or reduced sensitivity, including three cases with a YMDD mutation (rtM204V), three with the mutation, rtM250L/V, which is associated with ETV resistance, and four with the mutation rtI233V, which is associated with reduced sensitivity to ADV. 2018 World journal of gastroenterology Method HBV M204V;M250L;M250V;I233V 141;176;176;255 146;183;183;260 RT;RT;RT;P 139;174;253;124 141;176;255;128 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of these, a RT mutation in the A-B interdomain, rtD134E/N, which also cause a simultaneous sI126N/S mutation of the HBsAg "a" determinant, was found to have the highest frequency in treatment-naive patients (1.70%) (Figure 2). 2018 World journal of gastroenterology Method HBV D134E;D134N;I126N;I126S 50;50;91;91 57;57;99;99 S;RT;RT;S 116;12;48;91 121;14;50;92 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Of these, the YMDD-motif mutation (rtM204I/V) was found in 9 patients of 131 patients (8 HCC and 1 CHB) with the other two types of mutation, rt204I and rt204V, in 8 and 1 patients, respectively. 2018 World journal of gastroenterology Method HBV M204I;M204V 37;37 44;44 RT;RT;RT;P 35;142;153;14 37;144;155;18 Hepatocellular carcinoma;Chronic Hepatitis B 89;99 92;102 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Other amino acid substitutions, which were detected before treatment, but for which the association between their occurrence and drug resistance has not been evaluated, are defined as pretreatment mutations, these include rtT38A, rtY124H, rtD134E/N, rtN139K/H, rtI224V, and rtR242A (Category 4) (Table 1). 2018 World journal of gastroenterology Method HBV T38A;D134E;D134N;N139K;N139H;R242A;Y124H;I224V 224;241;241;252;252;276;232;263 228;248;248;259;259;281;237;268 RT;RT;RT;RT;RT;RT 222;230;239;250;261;274 224;232;241;252;263;276 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Other studies, including Fung et al, Yamani et al, and Mirandola et al reported that the prevalence rates of rtL180M were 10.0%, 2.08%, and 1.18% in Chinese, Indonesian, and Italian HBV carriers, respectively. 2018 World journal of gastroenterology Method HBV L180M 111 116 RT 109 111 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Our literature based incidence data showed that rtL180M had the highest natural incidence (2.96%), which was higher than the pooled mutation rate of rtL80I/V and V173L (incidence:0.46% and 0.15%, respectively) (Figure 1). 2018 World journal of gastroenterology Method HBV L180M;L80I;L80V;V173L 50;151;151;162 55;157;157;167 RT;RT 48;149 50;151 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Our literature based pooled incidence data showed that of primary drug resistance mutations, M204I/V is the most frequently encountered in treatment-naive patients (5.89%), which was far more than the pooled mutation rate of rtA181T/V, rtS202C/G/I and rtN236T (incidence: 1.16%, 0.85% and 0.81%, respectively). 2018 World journal of gastroenterology Method HBV A181T;A181V;S202C;S202G;S202I;N236T;M204I;M204V 227;227;238;238;238;254;93;93 234;234;247;247;247;259;100;100 RT;RT;RT 225;236;252 227;238;254 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Our literature based pooled incidence data showed that several putative or pretreatment mutations, including rtI91L, mutations in 6 positions of A-B interdomain (rtY124H, rtY126C/R/H, rtT128I/N, rtD134E/N, rtN139D/E/H/K/Q and rtW153Q/R/E), rtF221Y and rtI224V, were encountered with high frequency from the treatment naive patients. 2018 World journal of gastroenterology Method HBV I91L;Y126C;Y126R;Y126H;T128I;T128N;D134E;D134N;N139D;N139E;N139H;N139K;N139Q;W153Q;W153R;W153E;Y124H;F221Y;I224V 111;173;173;173;186;186;197;197;208;208;208;208;208;228;228;228;164;242;254 115;182;182;182;193;193;204;204;221;221;221;221;221;237;237;237;169;247;259 RT;RT;RT;RT;RT;RT;RT;RT;RT 109;162;171;184;195;206;226;240;252 111;164;173;186;197;208;228;242;254 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Our literature-based study demonstrated that preexisting RT mutations were also found in treatment-naive patients at 40 of 42 preciously identified NAr RT positions, the two exceptions were rtF242A, a pretreatment mutation and rtF166L, a lamivudine (LMV)-associated putative mutation. 2018 World journal of gastroenterology Method HBV F242A;F166L 192;229 197;234 RT;RT;RT;RT 57;152;190;227 59;154;192;229 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Overall, eight mutations in the RT region, namely rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V, and rtM309K, are significantly related to liver disease progression. 2018 World journal of gastroenterology Method HBV L80I;D134N;N139K;N139T;N139H;Y141F;M204I;M204V;M309K;F221Y;I224V 52;60;69;69;69;82;91;91;124;102;111 56;65;78;78;78;87;98;98;129;107;116 RT;RT;RT;RT;RT;RT;RT;RT;RT 32;50;58;67;80;89;100;109;122 34;52;60;69;82;91;102;111;124 Liver disease 160 173 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Recently, it has been proven through in vitro and in vivo experiments that several putative or pretreatment mutations, including rtL229F, rtS13T, and rtI233V, can also contribute to the development of drug resistance. 2018 World journal of gastroenterology Method HBV S13T;L229F;I233V 140;131;152 144;136;157 RT;RT;RT 129;138;150 131;140;152 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. RT mutations rtN139K/T/H and rtM204I/V also cause simultaneous mutations in the overlapped HBsAg coding sequence (sT131N/P and sI195M, or sW196S/L/Stop). 2018 World journal of gastroenterology Method HBV N139K;N139T;N139H;M204I;M204V;T131N;T131P;I195M;W196S;W196L;W196X 15;15;15;31;31;114;114;127;138;138;138 24;24;24;38;38;122;122;133;151;151;151 S;RT;RT;RT;S;S;S 91;0;13;29;114;127;138 96;2;15;31;115;128;139 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Several other studies have also reported the frequent incidence of rtM204I/V/S in treatment-naive patients. 2018 World journal of gastroenterology Method HBV M204I;M204V;M204S 69;69;69 78;78;78 RT 67 69 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Similarly, Zhang et al reported that the overall frequency of rtL180M mutation is 2.67%. 2018 World journal of gastroenterology Method HBV L180M 64 69 RT 62 64 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Since rtD134N also causes an amino acid change in HBsAg (sI126N/V), it can induce changes in the antigenic properties of HBsAg. 2018 World journal of gastroenterology Method HBV D134N;I126N;I126V 8;57;57 13;65;65 S;S;RT;S 50;121;6;57 55;126;8;58 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Singla et al also showed that rtL91I and rtM129L are more common in samples from genotype C, than genotype D, infected patients. 2018 World journal of gastroenterology Method HBV L91I;M129L 32;43 36;48 RT;RT 30;41 32;43 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. The mutations rtA181T/V, rtM204I, and rtM204V also cause the simultaneous HBsAg mutations, sW172 stop, sW196S/L/Stop, and sI195M, respectively (Table 1). 2018 World journal of gastroenterology Method HBV A181T;A181V;M204I;M204V;W196S;W196L;W196X;I195M;W172X 16;16;27;40;103;103;103;122;91 23;23;32;45;116;116;116;128;101 S;RT;RT;RT;S;S;S 74;14;25;38;91;103;122 79;16;27;40;92;104;123 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. The mutations rtL80I/V, rtV173L, rtL180M are known for secondary resistance mutations. 2018 World journal of gastroenterology Method HBV L80I;L80V;L180M;V173L 16;16;35;26 22;22;40;31 RT;RT;RT 14;24;33 16;26;35 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. The other HCC-related mutation (rtL80I) was first identified as a compensatory mutation associated with LMV resistance. 2018 World journal of gastroenterology Method HBV L80I 34 38 RT 32 34 Hepatocellular carcinoma 10 13 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. The rtL80I/V mutation also occurs frequently in treatment-naive patients. 2018 World journal of gastroenterology Method HBV L80I;L80V 6;6 12;12 RT 4 6 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. These authors also showed that 10 percent, 3 out of 29 patients prior to the initiation of antiretroviral therapy (ART), had drug resistance mutations rtV173L, rtL180M+rtM204V, and rtV214A. 2018 World journal of gastroenterology Method HBV V214A;V173L;L180M;M204V 183;153;162;170 188;158;167;175 RT;RT;RT;RT 151;160;168;181 153;162;170;183 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. These authors found a significantly higher rate of RT mutations in HCC patients than in those with chronic hepatitis (3.17% vs 2.09%, P = 0.003) and also identified a total of three NAr mutations (rtL80I, rtN139K/T/H, and rtM204I/V) significantly associated with HCC progression. 2018 World journal of gastroenterology Method HBV L80I;N139K;N139T;N139H;M204I;M204V 199;207;207;207;224;224 203;216;216;216;231;231 RT;RT;RT;RT 51;197;205;222 53;199;207;224 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma 67;99;263 70;116;266 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. This hypothesis is strongly supported by the recent report of Kim et al of the high frequency of the YMDD mutation, (rtM204V/I) (6.87%, 9/131 patients), in Korean treatment-naive patients with HBV genotype C2 infections. 2018 World journal of gastroenterology Method HBV M204I;M204V 119;119 126;126 RT;P 117;101 119;105 HBV infections 193 219 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Those results were consistent with the report of Li et al, which identified the rtF221Y mutant as an independent risk factor for recurrence of HCC and poor overall survival (P = 0.001 and P = 0.004, respectively). 2018 World journal of gastroenterology Method HBV F221Y 82 87 RT 80 82 Hepatocellular carcinoma 143 146 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Two recent studies reported that genotype A favors the rtM204V mutation, while HBV-B, C, and D select for rtM204I at higher rates, compared with rtM204V. 2018 World journal of gastroenterology Method HBV M204V;M204I;M204V 57;108;147 62;113;152 RT;RT;RT 55;106;145 57;108;147 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Wu et al also investigated preexisting RT mutations potentially related to HCC in Chinese patients and identified rtI224V and rtM309K as significant risk factors for HCC (P = 0.005 and P = 0.007, respectively). 2018 World journal of gastroenterology Method HBV M309K;I224V 128;116 133;121 RT;RT;RT 39;114;126 41;116;128 Hepatocellular carcinoma;Hepatocellular carcinoma 75;166 78;169 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Yamani et al, Kim et al, and Mirandola et al found pre-existing rtL80I/V mutation frequencies of 1.07%, 3.82%, and 0.78%, respectively. 2018 World journal of gastroenterology Method HBV L80I;L80V 66;66 72;72 RT 64 66 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Among them, sP120S/T/A, sT126N/S, sQ129R/N, sT131I/N, sM133I/L, sP142S, sD144A/E, sG145A/R were known to act as vaccine-escape mutations. 2018 BMC infectious diseases Method HBV P120S;P120T;P120A;T126N;T126S;Q129R;Q129N;T131N;M133I;M133L;P142S;D144A;D144E;G145A;G145R;T131I 12;12;12;24;24;34;34;44;54;54;64;72;72;82;82;44 22;22;22;32;32;42;42;52;62;62;70;80;80;90;90;52 S;S;S;S;S;S;S;S 12;24;34;44;54;64;72;82 13;25;35;45;55;65;73;83 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. We also analyzed the prevalence of the NA-induced immune-escape mutations sI195M, sI196S, and sE164D (resulting from drug-resistance mutation rtM204 V, rtM204I, and rtV173L) and stop-codons. 2018 BMC infectious diseases Method HBV M204V;M204I;V173L;I195M;I196S;E164D 144;154;167;74;82;94 150;159;172;80;88;100 RT;RT;RT;S;S;S 142;152;165;74;82;94 144;154;167;75;83;95 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. We determined the prevalence of 29 immune-associated escape mutations (sQ101K, sT114R, sP120S/T/A, sT123A/N, sT126N/S, sP127L, sA128V, sQ129R/N, sG130N/R, sT131I, sM133I/L/T, sY134L, sC138Y, sC139S, sT140S, sP142S, sD144A/E, sG145A/R, sN146S) extensively retrieved from literature and known to affect HBsAg-recognition by antibodies. 2018 BMC infectious diseases Method HBV Q101K;T114R;P120S;P120T;P120A;T123A;T123N;T126N;T126S;P127L;A128V;Q129R;Q129N;G130N;G130R;T131I;M133I;M133L;M133T;Y134L;C138Y;C139S;T140S;P142S;D144A;D144E;G145A;G145R;N146S 71;79;87;87;87;99;99;109;109;119;127;135;135;145;145;155;163;163;163;175;183;191;199;207;215;215;225;225;235 77;85;97;97;97;107;107;117;117;125;133;143;143;153;153;161;173;173;173;181;189;197;205;213;223;223;233;233;241 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 301;71;79;87;99;109;119;127;135;145;155;163;175;183;191;199;207;215;225;235 306;72;80;88;100;110;120;128;136;146;156;164;176;184;192;200;208;216;226;236 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. 1a and 1b schematics are shown to illustrate the hybridisation schemes of the probe to the MT and WT as well as that for the rDNAs to the MT and WT for HBVDM and KRAS G12V, respectively. 2018 Biosensors & bioelectronics Method HBV G12V 167 171 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. In addition to detecting double-stranded synthetic KRAS G12V, detection of human KRAS G12V point mutation in urine was carried out by spiking SW480 DNA fragments in urine. 2018 Biosensors & bioelectronics Method HBV G12V;G12V 56;86 60;90 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. SW480 (ATCC) is a human cell line homozygous for the KRAS G12V point mutation. 2018 Biosensors & bioelectronics Method HBV G12V 58 62 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. The probe for KRAS G12V MT was 17-nt long containing the sense sequence complementary to the targeted antisense strand of the KRAS G12V mutation (Gene ID:3845) centered at the mutation site. 2018 Biosensors & bioelectronics Method HBV G12V;G12V 19;131 23;135 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. The temperature of the detection cell was 35 C for detecting HBVDM and 63 C for detection KRAS G12V. 2018 Biosensors & bioelectronics Method HBV G12V 95 99 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. HBx-S31A or HBx-S31D mutant was generated by specific primers that replaced TCG (a triplet codon of serine) with GCT (a triplet codon of alanine) or GAT (a triplet codon of aspartic acid) and then was inserted into the expression vector. 2018 Cancer medicine Method HBV S31A;S31D 4;16 8;20 X;X 0;12 3;15 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. LCR was performed in the samples, which tested positive for HBV DNA for the detection of wild virus and mutant virus (precore mutant with a point mutation from G-A switch at nucleotide 83 from the precore region). 2018 Saudi journal of biological sciences Method HBV G83A 160 187 Precore;Precore 118;197 125;204 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The LCR was carried out to detect the HBV precore G1896A mutants with the strategy as described by. 2018 Saudi journal of biological sciences Method HBV G1896A 50 56 Precore 42 49 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Furthermore, mutants C18T, G82A, A115C, G120A, A138G, and C189A in SPII were cloned into a plasmid pBlueBac4.5 1.2/PC (p1.2/PC) respectively, which contained a 1.2-fold length HBV genome of genotype C2 with a G1896A mutation in the preC region. 2019 Viruses Method HBV C18T;G82A;A115C;G120A;A138G;C189A;G1896A 21;27;33;40;47;58;209 25;31;38;45;52;63;215 Precore;S promoter II 232;67 236;71 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. These AA sites were sE2, sL21, sR24, sT47, sI68, sC69*, sC76, sL95, sL98, sS117, sR122, sI126, sG145R, sV177, sW182*, sM198, sI218, and sV224. 2019 Viruses Method HBV C69X;G145R;W182X 49;95;110 54;101;116 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 20;25;31;37;43;49;56;62;68;74;81;88;95;103;110;118;125;136 21;26;32;38;44;50;57;63;69;75;82;89;96;104;111;119;126;137 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. To assess the expression of HBsAg affected by mutant SPII, mutation of C18T, G82A, A115C, G120A, A138G, and C189A within SPII was also introduced into an HBsAg expressing plasmid of pBluescript-LMS (pLMS), respectively. 2019 Viruses Method HBV C18T;G82A;A115C;G120A;A138G;C189A 71;77;83;90;97;108 75;81;88;95;102;113 S;S;S promoter II;S promoter II 28;154;53;121 33;159;57;125 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. We constructed 13 such plasmids, i.e., WT, C18T, C44T, A75T, G82A, A115C, T118C, G120A, G129A, T134C, A138G, C189A, and G228A. 2019 Viruses Method HBV C18T;C44T;A75T;G82A;A115C;T118C;G120A;G129A;T134C;A138G;C189A;G228A 43;49;55;61;67;74;81;88;95;102;109;120 47;53;59;65;72;79;86;93;100;107;114;125 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. A QuikChange Lightning site-directed mutagenesis kit (Stratagene, La Jolla, CA, USA) was employed according to manufacturer's instructions to eliminate rtA181C mutation on the rtL180M+A181C+M204V mutant. 2019 Emerging microbes & infections Method HBV A181C;L180M;A181C;M204V 154;178;184;190 159;183;189;195 RT;RT 152;176 154;178 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Because in the serial samples of patients 5, rtL180M+M204V strain was not detected, and also because the need of confirmation of rtA181C' contribution in ETV-resistance by reverse genetic method, site-directed mutagenesis was performed to generate a laboratory rtL180M+M204V strain using clinically derived rtL180M+A181C+M204V strain as the template. 2019 Emerging microbes & infections Method HBV A181C;L180M;L180M;L180M;M204V;M204V;A181C;M204V 131;47;263;309;53;269;315;321 136;52;268;314;58;274;320;326 RT;RT;RT;RT 45;129;261;307 47;131;263;309 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Recombinant vectors that harboured a patient-derived rtL180M+A181C+M204V, rtL180M+A181C+M204V+S202G, rtL180M+A181C+M204V+M250V mutant and wild-type RT genes, as well as another patient-derived rtL180M+S202G+M204V, rtL180M+T184A+M204V, and wild-type RT genes, were constructed for phenotypic analysis based on the pTriEx-mod-1.1 vector. 2019 Emerging microbes & infections Method HBV L180M;L180M;L180M;L180M;L180M;A181C;M204V;A181C;M204V;S202G;A181C;M204V;M250V;M204V;S202G;M204V;T184A 55;76;103;195;216;61;67;82;88;94;109;115;121;207;201;228;222 60;81;108;200;221;66;72;87;93;99;114;120;126;212;206;233;227 RT;RT;RT;RT;RT;RT;RT 53;74;101;148;193;214;249 55;76;103;150;195;216;251 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. To further understand the conformational change of the rtA181C mutant protein, a 2000-picosecond molecular dynamics simulation was performed by NAMD (version 2.13) with a cubic box water model. 2019 Emerging microbes & infections Method HBV A181C 57 62 RT 55 57 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. A stop codon was introduced in the wild-type gene by the site-directed mutagenesis to generate the sW182* construct. 2019 PloS one Method HBV W182X 99 105 S 99 100 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. After overnight the cells on the plate were further transfected with LHBs sW182* and p53 or Smad4/TbetaRI (T204D) constructs as above. 2019 PloS one Method HBV W182X;T204D 74;107 80;112 S;S 69;74 73;75 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Cell lysate was prepared from the transfected HEK293T cells (Flag-LHBs or sW182* mutant) in protein lysis buffer (0.1% Na-deoxtcholate, 10 mM Tris, pH7.8, 1 mM EDTA, 0.2 mM EGTA, 1% Np-40, 140 mM NaCl) supplemented with 1mM DTT, 25 ng/mul RNaseA, 1x cOmplete protease inhibitor cocktail (Merk). 2019 PloS one Method HBV W182X 74 80 S;S 66;74 70;75 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. For co-immunoprecipitation of LHBs and Jab1 protein, 750 mug lysate from HEK293 cells transfected with pCMV2B-Flag-Jab1 and pCDNA6-LHBs-Myc-6xHis or pCDNA6-LHBs (sW182*)-Myc-6xHis was mixed with Myc-agarose beads (Sigma) for 4 h. 2019 PloS one Method HBV W182X 162 168 S;S;S;S 30;131;156;162 34;135;160;163 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. For the p53 analysis, Huh-7 cells (in 12-well plates) were co-transfected with 0.2 mug pCMV5-Flag-p53 and 1 mug pCDNA6-LHBs-myc-His or pCDNA6-LHBs (sW182*)-myc-His using Lipofectamine LTX (Thermo Fisher) following the manufacture's instruction. 2019 PloS one Method HBV W182X 148 154 S;S;S 119;142;148 123;146;149 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. For the Smad4 analysis, the cells were co-transfected with 0.6 mug pCDNA5-DPC4-HA, 25 ng pCMV5-TbetaRI (T204D)-His and 0.6 mug pCDNA6-LHBs-myc-His or pCDNA6-LHBs (sW182*)-myc-His. 2019 PloS one Method HBV W182X;T204D 163;104 169;109 S;S;S 134;157;163 138;161;164 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The core gene point mutations (P5T, S35T, S87G, I97L, Q177K) and the reversion mutations (T5P, T35S, Q79P, D83E, G87S, L97I, K177Q) were individually introduced into pCMVHBV-WT and pCMVHBV-GYF, respectively, by using QuikChange Site-directed Mutagenesis Kit (Stratagene) or Q5 Site-directed Mutagenesis Kit (NEB). 2019 Antiviral research Method HBV P5T;S35T;S87G;I97L;Q177K;T5P;T35S;Q79P;D83E;G87S;L97I;K177Q 31;36;42;48;54;90;95;101;107;113;119;125 34;40;46;52;59;93;99;105;111;117;123;130 C 4 8 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The PCR fragment containing the combined 6 core mutations (P5T/S35T/P79Q/E83D/S87G/Q177K) were amplified from pCMVHBV-GYF-L97I and the PCR product was used as primers to mutate pCMVHBV-WT by Q5 mutagenesis, giving rise to plasmid pCMVHBV-WT-6Cmut. 2019 Antiviral research Method HBV S35T;S87G;Q177K;P79Q;E83D;P5T;L97I 63;78;83;68;73;59;122 67;82;88;72;77;62;126 C 43 47 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. The PCR products of K130M/V131I mutant and wild-type variants of HBx (GOIs) were provided by Dr Nadia Warner. 2019 Molecular cancer research Method HBV V131I;K130M 26;20 31;25 X 65 68 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. The mutation vectors were constructed by the inverse PCR method using primer m5 (G2765A), a sense primer for the G-to-A substitution at the third nucleotide of the Sp1 region, and primer m9 (whole nucleotide mutation), a sense primer for a whole nucleotide mutation of the Sp1 region, and antisense primer mR (Table 1). 2019 Virology journal Method HBV G2765A 81 87 S1 promoter;S1 promoter 164;273 167;276 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Both HepG2-NTCP and HLCs were used for studying the sC69* mutant with WT as a control in vitro. 2019 Frontiers in microbiology Method HBV C69X 52 57 S 52 53 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. HBV replication deficient mutation of YMDD to YMHD for WT-YMHD and sC69*-YMHD were cloned based on the WT and sC69* mutant. 2019 Frontiers in microbiology Method HBV C69X;C69X 67;110 72;115 S;S;P 67;110;38 68;111;42 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Hemagglutinin (HA) tag was inserted into the C terminus of surface protein of the WT and after AA68 of sC69* mutant surface protein as described before. 2019 Frontiers in microbiology Method HBV C69X 103 108 S;S;S 103;59;116 104;66;123 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We cloned the sC69* mutant into plasmid pBB4.5 1.2/PC, which contained a 1.2-fold length HBV genome of genotype C with a G1896A mutation in the precore region. 2019 Frontiers in microbiology Method HBV C69X;G1896A 14;121 19;127 Precore;S 144;14 151;15 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Site directed mutants (SDM) were created for the C1817T and A1838G mutations, both individually and in combination. 2019 Scientific reports Method HBV C1817T;A1838G 49;60 55;66 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. First, we classified 340 genotype C1 strains and 24 Cambodian isolates into 48 patterns by combinations of the following mutations pre-S deletion, G1613A, C1653T, T1753V, and A1762T/G1764A, Pre-C W28 stop codon, and P130 in the core region. 2019 Scientific reports Method HBV G1764A;W28X;G1613A;C1653T;T1753V;A1762T 182;196;147;155;163;175 188;204;153;161;169;181 C;Precore;PreS 228;190;131 232;195;136 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Both WT and D2N/D4N mutant exist as a homodimer Cp1492 in solution. 2018 ACS omega Method HBV D4N;D2N 16;12 19;15 C 48 50 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Furthermore, purified D2N/D4N dimer showed a lower mobility under electronic field due to its four negative charges fewer on each Cp149 dimer (Figure S1C). 2018 ACS omega Method HBV D4N;D2N 26;22 29;25 C 130 132 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The resultant mutant Cp149-D2N/D4N could be expressed to a similar level as the WT protein in E. 2018 ACS omega Method HBV D4N;D2N 31;27 34;30 C 21 23 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. A stop codon mutation was found more frequently in the ALF group (SHB L216*, see Table 3) and was selected for further analysis. 2019 Viruses Method HBV L216X 70 75 S 66 69 Liver disease 55 58 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. In addition, two more variants were used as controls, the SHB D144E which could be found in both groups and the SHB W172*, and its impact on HBsAg secretion has been already described before. 2019 Viruses Method HBV W172X;D144E 116;62 121;67 S;S;S 141;58;112 146;61;115 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. In detail, a Strep-tag HBsAg genotype D was cloned in the pEXPR-IBA 44 (iba-lifesciences) Vector and was subsequently used as a template to generate the HBsAg mutants, D144E, W172* and L216*. 2019 Viruses Method HBV W172X;L216X;D144E 175;185;168 180;190;173 S;S 23;153 28;158 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. A 10-muL reaction mixture was prepared for each sample as follows: 1 mul PCR reaction buffer for Taq (Bioneer E-3150 buffer), 4.25 mM MgCl2, 0.425 mM deoxynucleoside triphosphate mixture (Takara), 0.3 muM forward primer, 1 muM reverse primer, 0.25 muM LNA FAM probe (rtM204I variant), 0.25 muM LNA Hex probe (rtM204I variant), 0.6 U Hot Start Taq (Bioneer E-3150), 1 mg/mL bovine serum albumin (Ambion, Lifetechnologies), 2 muL template DNA, and PCR-grade water (Roche). 2019 World journal of gastroenterology Method HBV M204I;M204I 269;311 274;316 RT;RT 267;309 269;311 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. All the following LNA real-time PCR experiments were done in quadruplicate with positive control DNAs and mixtures of WT and rtM204I at a variety of ratios and concentrations as aforementioned. 2019 World journal of gastroenterology Method HBV M204I 127 132 RT 125 127 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Comparison of LNA real-time PCR and direct sequencing for identification of rtM204I variant and WT DNA. 2019 World journal of gastroenterology Method HBV M204I 78 83 RT 76 78 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. DNAs of a total of 410 human sera were tested for the identification of WT and rtM204I variant of HBV RT gene by LNA real-time PCR in duplicate. 2019 World journal of gastroenterology Method HBV M204I 81 86 RT;RT 79;102 81;104 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Identification of WT and rtM204I variant was determined by comparing their Tm s obtained from their specific channel (FAM for rtM204I, HEX for WT) with their diagnostic Tm ranges obtained from standard assays. 2019 World journal of gastroenterology Method HBV M204I;M204I 27;128 32;133 RT;RT;S 25;126;78 27;128;79 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Logistic regression analyses were performed to identify the independent factors for the presence of naturally occurring rtM204I mutations, or antiviral responsiveness. 2019 World journal of gastroenterology Method HBV M204I 122 127 RT 120 122 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Positive identification of WT and rtM204I variant was recorded only when distinct melting peak formation with their diagnostic Tm is recognized. 2019 World journal of gastroenterology Method HBV M204I 36 41 RT 34 36 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The primer and probe specificity for detection of rtM204I variant was further analyzed using Primer-Blast at NCBI and the Oligo software version 6.5. 2019 World journal of gastroenterology Method HBV M204I 52 57 RT 50 52 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Throughout the real-time PCR assay, two rtM204I positive controls with high copies (2400000) and low copies (2400), two rtM204I positive controls with high copies (2400000) and low copies (2400), and two non-template controls were included in each run to monitor validity of Cqs, Tm s, and cross-contamination for inter-assays. 2019 World journal of gastroenterology Method HBV M204I;M204I 42;122 47;127 RT;RT;S 40;120;283 42;122;284 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Tm, melting peak height, and quantification cycle (Cq) produced by WT- and rtM204I -targeting LNA probes with a sample DNA were measured. 2019 World journal of gastroenterology Method HBV M204I 77 82 RT 75 77 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. We attached two different reporter dyes, FAM to probe for rtM204I variant, and Hex to probe for WT, respectively, to differentially identify rtM204I variant and WT HBV DNA. 2019 World journal of gastroenterology Method HBV M204I;M204I 60;143 65;148 RT;RT 58;141 60;143 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. We designed two different LNA probes for the specific simultaneous detection in a single reaction of wild type (WT) and rtM204I variant of HBV. 2019 World journal of gastroenterology Method HBV M204I 122 127 RT 120 122 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. M0250S New England BioLabs Inc) for 30 mins at 37 C. 2019 Scientific reports Method HBV M0250S 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. N0446S & M0273L) and 0.2 microM each of forward and reverse primers. 2019 Scientific reports Method HBV N0446S;M0273L 0;9 6;15 32084506 7-Deaza-7-fluoro modification confers on 4'-cyano-nucleosides potent activity against entecavir/adefovir-resistant HBV variants and favorable safety. Plasmids carrying the 1.24-fold HBV genomes of a wild-type genotype Ce strain (HBVWTCe), entecavir-resistant strain carrying L180M/S202G/M204V substitutions (HBVETVR), or adefovir-resistant strain carrying A181T/N236T substitutions (HBVADVR) were constructed for in vitro study as previously described. 2020 Antiviral research Method HBV N236T;S202G;M204V;L180M;A181T 212;131;137;125;206 217;136;142;130;211 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Distances were calculated using MEGA 6.1 based on the Kimura-2 parameter (K2P) model. 2020 Viruses Method HBV K2P 74 77 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. The following mutations associated with additional N-linked glycosylation sites were identified: 114N-ins, T115N, T117N, T123N, S113N+T131N+M133T. 2020 Viruses Method HBV T115N;T117N;T123N;S113N;T131N;M133T 107;114;121;128;134;140 112;119;126;133;139;145 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. The newly identified mutations associated with additional N-linked glycosylation sites (114N-ins, T115N, T117N, T123N, S113N+T131N+M133T) were introduced into the Topo.HBV.WT.D plasmid by site-directed mutagenesis. 2020 Viruses Method HBV T115N;T117N;T123N;S113N;T131N;M133T 98;105;112;119;125;131 103;110;117;124;130;136 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Percentage Composition of rtM204I/V in HBV cccDNA, Viral DNA, and RNA. 2021 Hepatology (Baltimore, Md.) Method HBV M204I;M204V 28;28 35;35 RT 26 28 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Percentages of rtM204I/V mutations were calculated using Sequencher software (Gene Codes, Ann Arbor, MI). 2021 Hepatology (Baltimore, Md.) Method HBV M204I;M204V 17;17 24;24 RT 15 17 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. To exclude the potential impact of adefovir on the evolution of drug resistance mutation, only those patients from the MONO group who developed the signature rtM204I/V mutation during LdT monotherapy were included in this study. 2021 Hepatology (Baltimore, Md.) Method HBV M204I;M204V 160;160 167;167 RT 158 160 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. The following mutations were introduced: V190A, V190A + F220L, S204N, S204N + L205P, Y206F, Y206F + S210R, Y206F + V194A, Y206F + S204T, Y206F + M197T, S210N, S210N + F220L. 2020 Emerging microbes & infections Method HBV V190A;V190A;F220L;S204N;S204N;L205P;Y206F;Y206F;S210R;Y206F;V194A;Y206F;S204T;Y206F;M197T;S210N;S210N;F220L 41;48;56;63;70;78;85;92;100;107;115;122;130;137;145;152;159;167 46;53;61;68;75;83;90;97;105;112;120;127;135;142;150;157;164;172 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Dimer (hCp149, hCp149-Y132A, wCp149, and wCp149-Y132A) stocks at 2 mg mL-1 were diluted 1:10 into deuterated reaction buffer (10 mM HEPES, pD 7.5 in D2O). 2020 ACS chemical biology Method HBV Y132A;Y132A 22;48 27;53 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Four expression plasmids, pET11a-hCp149, pET11a-hCp149-Y132A, pET11a-wCp149 and pET11a-wCp149-Y132A, were transformed into E. 2020 ACS chemical biology Method HBV Y132A;Y132A 55;94 60;99 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Specifically, each protein was purified as described: hCp149 , hCp149-Y132A , wCp149 , and wCp149-Y132A . 2020 ACS chemical biology Method HBV Y132A;Y132A 70;98 75;103 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. To determine the thermal stability of hCp149, hCp149-Y132A, wCp149, and wCp149-Y132A differential scanning fluorimetry was used. 2020 ACS chemical biology Method HBV Y132A;Y132A 53;79 58;84 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. All sequences with completely replaced mt were further determined based on an HBV-drug resistance interpretation online tool of Max Planck Institute for Informatics for classical mt, e.g., rtL180M, rtA181V/T, rtT184G/L, rtA194T, rtS202I/G, rtM204I/V, rtN236T, and rtM250I/V, and based on updated references for nonclassical/putative mt, e.g., V207I/M/L, rtS213T, rtL229V, rtI233V, rtP237T, rtN238A/K/T, and rtS256G. 2020 Diagnostics (Basel, Switzerland) Method HBV A181V;A181T;T184G;T184L;S202I;S202G;M204I;M204V;M250I;M250V;N238A;N238K;N238T;L180M;A194T;N236T;S213T;L229V;I233V;P237T;S256G;V207I;V207M;V207L 200;200;211;211;231;231;242;242;266;266;392;392;392;191;222;253;356;365;374;383;409;343;343;343 207;207;218;218;238;238;249;249;273;273;401;401;401;196;227;258;361;370;379;388;414;352;352;352 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 189;198;209;220;229;240;251;264;354;363;372;381;390;407 191;200;211;222;231;242;253;266;356;365;374;383;392;409 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Primers for PCR amplification of nucleotides (nt) 532-929, corresponding to the B, C, D, and E domains and containing major NA-drug resistance mt in HBV RT such as rtV173L, rtL180M, rtA181V/T, rtT184G/L, rtA194T, rtS202I/G, rtM204I/V, rtN236T, and rtM250I/V, were designed as follows. 2020 Diagnostics (Basel, Switzerland) Method HBV V173L;L180M;A181V;A181T;T184G;T184L;A194T;S202I;S202G;M204I;M204V;N236T;M250I;M250V 166;175;184;184;195;195;206;215;215;226;226;237;250;250 171;180;191;191;202;202;211;222;222;233;233;242;257;257 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. The mt controls contained representative mt locating randomly at P1 and P2 fragments: rtA194T (G709A), rtM204I (G741T), and rtN236T (A836C) in pUC19 plasmid (PhuSa Biochem, Can Tho, Vietnam). 2020 Diagnostics (Basel, Switzerland) Method HBV A194T;M204I;N236T;G709A;G741T;A836C 88;105;126;95;112;133 93;110;131;100;117;138 RT;RT;RT 86;103;124 88;105;126 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. The probe sequences were as follows: (G750A probe) 5'-HEX/ATGG+ATGATA+T+A+GT+ATTGG/3'-IABkFQ (nt 739-757); (G750T probe) 5'-HEX/ATGG+ATGATA+T+T+GT+ATTGG/3'-IABkFQ (nt 739-757), where "+" indicates the position of LNA and the underline indicates a mismatched nucleotide. 2020 Diagnostics (Basel, Switzerland) Method HBV G750A;G750T 38;108 43;113 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. The two DNA clinical samples carrying mt rtV207I (G750A) and mt rtV207I (G750T) at low levels of mt/wt were used for detection of the mt by real-time PCR using the Forward-HBV-P1/Reverse-HBV-P1 primers and Lock Nucleic Acid (LNA) fluorescent probes (IDT, IA, USA). 2020 Diagnostics (Basel, Switzerland) Method HBV V207I;V207I;G750A;G750T 43;66;50;73 48;71;55;78 RT;RT 41;64 43;66 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Generation of G1896A and A1762T/G1764A mutants were achieved using the QuikChange II site-directed mutagenesis kit (Agilent Technologies, Santa Clara, United States), as per manufacturer's protocol using the pUC19-HBV.wt and mutagenic primers (Supplementary Table S1). 2020 Frontiers in microbiology Method HBV G1764A;G1896A;A1762T 32;14;25 38;20;31 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Published NGS sequencing data showed the proportion of A1762T, G1764A, and G1896A mutants in the HBV quasi-species population allowed grouping of CHB carriers into three cohorts: predominantly wild-type (<50% of any mutant; n = 4), G1896A (>50% of only G1896A; n = 3), or A1762T/G1764A (>50% of only A1762T and G1764A; n = 4) (Supplementary Table S4). 2020 Frontiers in microbiology Method HBV G1764A;A1762T;G1764A;G1896A;G1896A;G1896A;A1762T;A1762T;G1764A 279;55;63;75;232;253;272;300;311 285;61;69;81;238;259;278;306;317 Chronic Hepatitis B 146 149 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Site-directed mutagenesis was performed to introduce the sW196* (YIDDst, YIDD/S truncation) mutation via a PCR-based method described previously. 2020 International journal of molecular sciences Method HBV W196X 57 63 S;P 57;73 58;77 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. The most conserved regions of S gene sequences were amplified by nest PCR [Prime STAR Max DNA Polymerase (R045A, Takara, Japan)] according to the protocol described. 2020 International journal of medical sciences Method HBV R045A 106 111 P;S 94;30 104;31 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. M6 was modified from M7 by the elimina-tion of the sA159V mutation using the QuikChange Lightning Site-Directed Mutagenesis Kit (Stratagene, La Jolla, CA, United States). 2020 World journal of gastroenterology Method HBV A159V 51 57 S 51 52 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The eight strains were: WT, sA159V (M1), rtM204I (M2), sA159V+rtM204I (M3), rtL180M+rtM204V (M4), sA159V+rtL180M+rtM204V (M5), rtL180M+rtT184L+rtM204V (M6), and sA159V+rtL180M+rtT184L+rtM204V (M7). 2020 World journal of gastroenterology Method HBV M204I;M204I;L180M;M204V;L180M;M204V;L180M;T184L;M204V;L180M;T184L;M204V;A159V;A159V;A159V;A159V 43;64;78;86;107;115;129;137;145;170;178;186;28;55;98;161 48;69;83;91;112;120;134;142;150;175;183;191;34;61;104;167 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S 41;62;76;84;105;113;127;135;143;168;176;184;28;55;98;161 43;64;78;86;107;115;129;137;145;170;178;186;29;56;99;162 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. For control of the assays, a GTA HBeAg-negative genome with precore double mutation G1896A/G1899A, a GTA HBeAg-positive genome. 2020 JCI insight Method HBV G1899A;G1896A 91;84 97;90 C;C;Precore 33;105;60 38;110;67 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. HBV genomes containing A1762T/G1764A and GCAC1809-1812TTCT in different positions in the core promoter and HBx genomic region were commercially synthesized (GenScript; for an overview of analyzed HBV genomes, see Figure 2A). 2020 JCI insight Method HBV G1764A;A1762T 30;23 36;29 Core promoter;X 89;107 102;110 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Three different mutations, rtM204V, rtL229V and rtM204V + rtL229V were introducing into p1.2DNA by site-directed mutagenesis (TransGen Biotech, Beijing, China). 2020 Emerging microbes & infections Method HBV L229V;M204V;M204V;L229V 38;29;50;60 43;34;55;65 RT;RT;RT;RT 27;36;48;58 29;38;50;60 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. To produce HBeAg of various genotypes, a serial of HBV 1.3-fold or CMV-driven 1.1-fold genome plasmids with genotypes A-I (detailed information was shown in supplemental Table 1) or with precore G1896A mutation were transfected into HepG2 cells or Huh7 cells using X-tremeGENE HP DNA Transfection Reagent (Roche). 2021 Emerging microbes & infections Method HBV G1896A 195 201 C;Precore 11;187 16;194 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. According to the most recent clinical practice guidelines of the European Association for the Study of the Liver, the following amino acid substitution profiles for HBV-resistant mutants were used: rtM204V/I (LAM resistance), rtM204I or L180M + rtM204V (LdT resistance), rtA181T/V or rtN236T (ADV resistance), rtL180M + rtM204I/V +- rtT184S/G +- rtS202I/G +- rtM250V (ETV resistance), and rtA181T/V + rtN236T (TDF/TAF-reduced susceptibility). 2020 Frontiers in microbiology Method HBV M204V;M204I;M204I;A181T;A181V;N236T;M204V;T184S;T184G;S202I;S202G;M250V;A181T;A181V;M204V;L180M;M204I;N236T;L180M 200;200;228;273;273;286;322;335;335;348;348;361;391;391;247;312;322;403;237 207;207;233;280;280;291;329;342;342;355;355;366;398;398;252;317;329;408;242 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 198;226;245;271;284;310;320;333;346;359;389;401 200;228;247;273;286;312;322;335;348;361;391;403 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. M0202S and M0203S respectively, both supplied from New England Biolabs) at 30 C for 45 minutes, in order to generate fully dsDNA HBV genomes, as previously described , . 2020 Wellcome open research Method HBV M0202S;M0203S 0;11 6;17 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The rtT301A substitution was introduced to the WT, CYEI, and CYELMVI replicons by NEBuilder HiFi DNA assembly Cloning Kit (New England Biolabs, Ipswich, England) according to the manufacturer's protocol. 2021 International journal of molecular sciences Method HBV T301A 6 11 RT 4 6 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Two clones (CYEI: rtS106C (C) + rtH126Y (Y) + rtD134E (E) + rtL269I (I) and CYELMVI: rtS106C (C) + rtH126Y (Y) + rtD134E (E) + rtV173L (L) + rtL180M (M) + rt204V (V) + rtL269I (I)) have been described in our previous study. 2021 International journal of molecular sciences Method HBV S106C;S106C;H126Y;D134E;L269I;H126Y;D134E;V173L;L180M;L269I 20;87;34;48;62;101;115;129;143;170 25;92;39;53;67;106;120;134;148;175 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 18;32;46;60;85;99;113;127;141;155;168 20;34;48;62;87;101;115;129;143;157;170 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. ETV resistance: Two or more amino acid substitutions are required across the HBV RT protein to confer resistance to ETV which could occur as a combination of M204I/V with one or more of the following substitutions L80I/V, I163V, I169T, V173L, L180M, A181S/T/V, T184X, A186T, S202C/G/I/R, M250I/V and/or C256S/G. 2021 Journal of viral hepatitis Method HBV A181S;A181T;A181V;S202C;S202G;S202I;S202R;C256G;M204I;M204V;L80I;L80V;I163V;I169T;V173L;L180M;T184X;A186T;M250I;M250V;C256S 250;250;250;275;275;275;275;303;158;158;214;214;222;229;236;243;261;268;288;288;303 259;259;259;286;286;286;286;310;165;165;220;220;227;234;241;248;266;273;295;295;310 RT 81 83 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. For this analysis, we considered a total of 12 RAMs (S106C/G, D134E, R153W/Q, V173L, L180M, A181T/V, A194T, A200V, M204I/V, L217R, L229V/W and I269L). 2021 Journal of viral hepatitis Method HBV S106C;S106G;D134E;R153W;R153Q;V173L;L180M;A181T;A181V;A194T;A200V;M204I;M204V;L217R;L229V;L229W;I269L 53;53;62;69;69;78;85;92;92;101;108;115;115;124;131;131;143 60;60;67;76;76;83;90;99;99;106;113;122;122;129;138;138;148 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. K141E/I/R and G145A/R have the strongest evidence base of clinical and in vitro data to support HBV vaccine resistance, while other VEMs are considered putative, as they are supported by less robust data. 2021 Journal of viral hepatitis Method HBV K141E;K141I;K141R;G145A;G145R 0;0;0;14;14 9;9;9;21;21 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. We also considered eight VEMs (C139S, S/T140I, P142S, S/T143L/M, D144A/E/G/N, G145A/E/R, K141A/I/R and C147S) which are located within the epitope region neutralized by the HBV vaccine (aa139-147). 2021 Journal of viral hepatitis Method HBV T140I;S143L;S143M;T143L;T143M;D144A;D144E;D144G;D144N;G145A;G145E;G145R;K141A;K141I;K141R;S140I;C139S;P142S;C147S 38;54;54;54;54;65;65;65;65;78;78;78;89;89;89;38;31;47;103 45;63;63;63;63;76;76;76;76;87;87;87;98;98;98;45;36;52;108 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. We performed phylogenetic dating to estimate the times of emergence of mutations of interest, focused on RAMs V173L, L180M and M204I/V as they are best recognized to cause or contribute (individually or synergistically) resistance to 3TC, ETV and TDF, and VEMs G145A/R and K141E/I/R as they have been best described to cause HBV vaccine resistance. 2021 Journal of viral hepatitis Method HBV K141E;K141I;K141R;V173L;L180M;M204I;M204V;G145A;G145R 273;273;273;110;117;127;127;261;261 282;282;282;115;122;134;134;268;268 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. For HBc-L60V, capsids were selected with "cryolo" using the general neuronal network. 2021 Microorganisms Method HBV L60V 8 12 Capsid;C 14;4 21;7 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. For the model building of P5T-HBc, L60V-HBc and P1/P2 bound to WT-HBc, P5T-HBc, F97L-HBc and L60V-HBc, the pdb model 6HTX was modified and fit into EM maps. 2021 Microorganisms Method HBV P5T;P5T;L60V;F97L;L60V 26;71;35;80;93 29;74;39;84;97 C;C;C;C;C;C 30;40;66;75;85;98 33;43;69;78;88;101 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. For this, the current model of the asymmetric unit of F97L + P1 was fitted into the 3D map using Chimera. 2021 Microorganisms Method HBV F97L 54 58 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. For this, the map of P5T + P1 was chosen as a reference map after B-factor sharpening and low-pass filtering to 3.5 A resolution. 2021 Microorganisms Method HBV P5T 21 24 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. From the re-extracted particles of F97L + P1, we calculated a 3D map ("relion_reconstruct"). 2021 Microorganisms Method HBV F97L 35 39 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Particle images grouping into classes representing intact, centered T = 4 capsids were re-extracted with 440 x 440 Px2 followed by auto-refinement ("relion_refine") with a previously determined map of F97L as start reference and imposing icosahedral symmetry. 2021 Microorganisms Method HBV F97L 201 205 Capsid 74 81 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The purification of HBc-CLPs (genotype D; strain ayw; GenBank: V01460.1.) was performed similarly as outlined before for split-cores with modifications: BL21 (DE3) Star cells were transformed with pRSF-T7-HBcOpt-wt, pRSF-T7-HBcOpt-P5T, pRSF-T7-HBcOpt-F97L and pRSF-T7-HBcOpt-L60V, respectively. 2021 Microorganisms Method HBV P5T;F97L;L60V 231;251;275 234;255;279 C 20 23 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Better probes were selected by subjecting the positive serum, containing the mutant gene of HBV polymerase M204V previously confirmed by Sanger sequencing, to a series of tests. 2021 Journal of clinical and translational hepatology Method HBV M204V 107 112 P 96 106 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. In order to obtain standard curves for the purposes of quantification and estimation of efficacy of the new real-time PCR protocol, a specific plasmid containing the M204V mutation was designed and synthesized by Sinogene Biotech (Beijing, China). 2021 Journal of clinical and translational hepatology Method HBV M204V 166 171 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Primers and probes of M204V. 2021 Journal of clinical and translational hepatology Method HBV M204V 22 27 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Detection with the anti-HBc antibody was confirmed not to be affected by the I97L substitution (data not shown). 2021 Cellular and molecular gastroenterology and hepatology Method HBV I97L 77 81 C 24 27 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBV-dE with I97L was generated by site-directed PCR and fragment swapping using appropriate restriction enzymes. 2021 Cellular and molecular gastroenterology and hepatology Method HBV I97L 12 16 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The I97L substitution was introduced by site-directed PCR and fragment swapping. 2021 Cellular and molecular gastroenterology and hepatology Method HBV I97L 4 8 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. This clone has the amino acid substitution G1896A, which prevents HBeAg production. 2021 Cellular and molecular gastroenterology and hepatology Method HBV G1896A 43 49 C 66 71 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. For all other variants, the final concentration of TX100 was 2 mM and the HBc-monomer concentrations were 700 microM for HBc-P5T and HBc-F97L, and 400 microM for HBc-L60V, which is less soluble. 2021 Viruses Method HBV P5T;F97L;L60V 125;137;166 128;141;170 C;C;C;C 74;121;133;162 77;124;136;165 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. The purification of HBc-CLPs was previously described: In brief, wt HBc and HBc-F97L, HBc-P5T and HBc-L60V were overexpressed in BL21 (DE3) Star cells. 2021 Viruses Method HBV P5T;F97L;L60V 90;80;102 93;84;106 C;C;C;C;C 20;68;76;86;98 23;71;79;89;101 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. For a beta (beta) galactosidase assay, the transfected cells were lysed with 100 microL of Glo Lysis Buffer (Cat# E266A, Promega). 2021 Viruses Method HBV E266A 115 120 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. HBeAg ELISA (HBeAg ELISA kit; Bioneovan, Beijing, China) and preS1 ELISA (Anti-HB Pre-S1 Antigen Quantitative ELISA Kit, Beacle, Kyoto, Japan) were also conducted according to the manufacturer's instructions, since a commercial HBsAg ELISA could not detect W3S sAg. 2021 Viruses Method HBV W3S 257 260 C;C;S;PreS1;PreS1 0;13;228;61;82 5;18;233;66;88 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In the case of pHB-W3S, four 5 mL aliquots (i.e., 20 mL) were used and they were finally combined into one 500 microL TNE solution. 2021 Viruses Method HBV W3S 19 22 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The cells were then transfected with 1 microg of pHB-WT, pHB-W3S or pHB-W3S (N146G). 2021 Viruses Method HBV W3S;W3S;N146G 61;72;77 64;75;82 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The XbaI-SpeI fragments of the pHB-WT were replaced with the region corresponding to W3S and W3S N146G, yielding pHB-W3S and pHB-W3S (N146G). 2021 Viruses Method HBV W3S;W3S;W3S;W3S;N146G;N146G 85;93;117;129;97;134 88;96;120;132;102;139 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Proline substitution mutants W196P, M197P, and M198P, were engineered by introducing a proline into the envelope ORF of the pol-null replicon. 2021 Journal of biomedical science Method HBV W196P;M197P;M198P 29;36;47 34;41;52 S;P 104;124 112;127 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Similarly, envelope mutations W196F, W196S and W196L were introduced into the pol-null replicon plasmid. 2021 Journal of biomedical science Method HBV W196F;W196S;W196L 30;37;47 35;42;52 S;P 11;78 19;81 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Single small loop mutations, W196C, M197T, and M198P, were introduced individually into the envelope ORF in pCHT-9/3091. 2021 Journal of biomedical science Method HBV W196C;M197T;M198P 29;36;47 34;41;52 S 92 100 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. After 45 h of the preliminary cultivation, antigenic stimulation of the PBMC was performed using 20 mug/mL of wild-type rHBsAg (ayw2) or 20 mug/mL of rHBsAg with the escape mutation G145R (ayw2). 2022 Vaccines Method HBV G145R 182 187 S;S 120;150 126;156 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In this case, 1.2 mug/mL of PHA and 20 mug/mL of wild-type rHBsAg (ayw2) or 1.2 mug/mL of PHA and 20 mug/mL of rHBsAg with the G145R escape mutation (ayw2) were added simultaneously to PBMC. 2022 Vaccines Method HBV G145R 127 132 S;S 59;111 65;117 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The studies used wild-type rHBsAg of the ayw2 subtype and rHBsAg with the G145R mutation of the ayw2 subtype, both expressed in the yeast H. 2022 Vaccines Method HBV G145R 74 79 S;S 27;58 33;64 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. Additionally, the 1888 G to A mutation was present in A6 and A9 sequences. 2001 BMC microbiology Result HBV G1888A 18 29 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. As a whole, 10 sequences showed neither common point mutation nor the 1862 G to T point mutation which would explain the anti-HBe phenotype. 2001 BMC microbiology Result HBV G1862T 70 81 C 126 129 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. Finally, the 1899 G to A substitution (codon 29 of the precore), previously shown to enhance the pregenomic RNA transcription, was found in a single isolate (D5). 2001 BMC microbiology Result HBV G1899A 13 24 Precore 55 62 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. For clarity, these mutations will be hereafter called uncommon point mutations in contrast to the A1896 G to A and 1762-1764 AGG to TGA substitutions referred as common point mutations . 2001 BMC microbiology Result HBV A1896G 98 105 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. Further, the 1727 G to A, 1740 C to T, and 1773 T to C changes were predominantly observed among the isolates otherwise mutated at crucial positions 1896 and/or 1762-1764. 2001 BMC microbiology Result HBV G1727A;C1740T;T1773C 13;26;43 24;37;54 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. Table II indicates that only six isolates (A5, A6, D2-D5) showed the double substitution changing AGG to TGA at positions 1762-1764 in the core promoter region, which might explain the anti-HBe seroconversion of the patients infected with isolates not showing the A1896 stop codon mutation. 2001 BMC microbiology Result HBV A1896X 264 274 Core promoter;C 139;190 152;193 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The 1862 G to T point mutation, which has been proposed to contribute to the anti-HBe phenotype, was found in four genotype A sequences, two of them (A5, A6) with common point mutations and the two others (A3, A9) without. 2001 BMC microbiology Result HBV G1862T 4 15 C 82 85 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The following substitutions appeared to be linked to the genotype (although not all the isolates of a determined genotype necessarily showed the mutation): G to A 1721 (found in genotype F), G to A 1757 (D), C to T 1802 (F), G to T 1803 (F), A to T 1850 (D and F), and C to T 1858 (D and F). 2001 BMC microbiology Result HBV G1721A;G1757A;C1802T;G1803T;A1850T;C1858T 156;191;208;225;242;269 167;202;219;236;253;280 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The isolate showing the highest number of mutations, namely D3, displayed the 1766-1768 CTT to TTA double substitution, which has been associated with increased transcription and viral encapsidation of pregenomic RNA, as well as a 1817 C to T change, introducing a stop in codon 2 of the precore. 2001 BMC microbiology Result HBV C1817T 231 242 Precore 288 295 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The seven others (five from genotype D and two from genotype F) showed the 1896 G to A substitution leading to a stable T1858:A1896 base pairing and introducing a stop codon into the ORF of the precore. 2001 BMC microbiology Result HBV G1896A 75 86 Precore 194 201 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. All three clones derived from the sample collected in 1999, during the first lamivudine treatment, showed two lamivudine resistant mutations (L526M and M550V), also detected in the major viral population by direct sequencing. 2004 BMC infectious diseases Result HBV L526M;M550V 142;152 147;157 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Curiously, all HBV sequences obtained during the period without lamivudine treatment (2001) displayed a unique G473E substitution in the polymerase gene. 2004 BMC infectious diseases Result HBV G473E 111 116 P 137 147 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. One clone (1-B57) showed an additional mutation related to drug resistance (V519L) that was not detected by direct sequencing. 2004 BMC infectious diseases Result HBV V519L 76 81 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Two substitutions, H359Y in the polymerase and Y100C in the surface antigen (small S), were observed in all HBV sequences. 2004 BMC infectious diseases Result HBV H359Y;Y100C 19;47 24;52 P;S;S 32;77;60 42;84;67 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. A mutation in the YMDD (tyrosine, methionine, aspartate, aspartate) motif of the viral polymerase (reverse transcriptase [rt]) was noticed as methionine 204 to isoleucine (rtM204I). 2005 Journal of Korean medical science Result HBV M204I;M204I 174;142 179;170 P;RT;RT;RT;P 87;99;122;172;18 97;120;124;174;22 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. Comparing the S gene nucleotide and amino acid sequences of HBV with the published sequence of HBV genotype C subtype adr registered in NCBI AF 286594, the pre-S2 amplification products showed deletion from nucleotide 23 to 55. 2005 Journal of Korean medical science Result HBV del nt23 193 220 PreS2;S 156;14 162;15 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. These changes were consistent with amino acid substitutions at position I126S, T131N, M133T, and S136Y. 2005 Journal of Korean medical science Result HBV I126S;T131N;M133T;S136Y 72;79;86;97 77;84;91;102 15953865 Overlapping gene mutations of hepatitis B virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy. This finding was consistent with the deletion of amino acids 12 to 22 in the pre-S2 region. 2005 Journal of Korean medical science Result HBV del aa12 37 63 PreS2 77 83 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. An interesting fact is that these deletions alter the X open reading frame, changing K130N and introducing an isoleucine in the 131 site and a stop codon in the position135. 2005 Virology journal Result HBV K130N 85 90 X 54 55 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. From group C the T-A mutations were detected in 7 of the 21 sequenced samples, and V131I alone in 3 samples. 2005 Virology journal Result HBV V131I 83 88 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. Group A presented more amino acid or nucleotide variability than the other groups, however, in acute phase samples from group B, 50% of these had common mutations at position 12 (T12A). 2005 Virology journal Result HBV T12A 179 183 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. In a Korean study T-A mutations were found in 32% (13/41) of HBV carriers, and a triple mutation G1714A, C1718T, A1721G was found in 27% (11/41) patients. 2005 Virology journal Result HBV G1714A;C1718T;A1721G 97;105;113 103;111;119 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. In one of the paired samples from this study and in another from reference, the V131I mutation appears in time before the methionine change at position 130. 2005 Virology journal Result HBV V131I 80 85 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. In our study wild type (wt) HBV strain nucleotide were found in the 1714 and 1718 positions, but the mutation A1721G was found in genotype F samples and not in two samples with other genotypes. 2005 Virology journal Result HBV A1721G 110 116 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. In this study, V131I also occurred alone in 5 samples (17%) of the 29 chronic patients; this event has been commonly reported by others; nevertheless M130K alone is very unusual. 2005 Virology journal Result HBV V131I;M130K 15;150 20;155 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. Of 8 chronic patients in group B, the T-A mutations were identified in 5 (62.5%) of the sequenced samples and V131I alone was detected in two. 2005 Virology journal Result HBV V131I 110 115 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. Of the 5 carriers with biopsy classified as KI <= 2, one sample had an 8 bp deletion that included the T-A mutations site and another sample the V131I mutation alone. 2005 Virology journal Result HBV V131I 145 150 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. Table 1 shows the mutation rate of T-A in HBx for M130K and V131I amongst the three study groups. 2005 Virology journal Result HBV M130K;V131I 50;60 55;65 X 42 45 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. Mutations identified in HBV strains from the asymptomatic group were Y100N, T126I, Q129H and N146K; whereas in strains from the symptomatic group identified mutations were F93I and A128V. 2007 Virology journal Result HBV Y100N;T126I;Q129H;N146K;F93I;A128V 69;76;83;93;172;181 74;81;88;98;176;186 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. T113S, S114T, R122K, I126T and P127L were the most frequent in both asymptomatic and symptomatic patients; whereas A159G, R160K, F161Y and V168A were more frequent in symptomatic patients. 2007 Virology journal Result HBV T113S;S114T;R122K;I126T;P127L;A159G;R160K;F161Y;V168A 0;7;14;21;31;115;122;129;139 5;12;19;26;36;120;127;134;144 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. Of the 32 HBV genotype F samples, 31 were adw4, and one, 052-N, had an unusual substitution of isoleucine for leucine at residue 127. 2007 BMC microbiology Result HBV L127I 95 132 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. One (209-CW) displayed the double rtL180M-rtM204V lamivudine-resistance mutation and the other (043-N) showed an additional rtV173L mutation, which is also associated with lamivudine resistance (Table 2). 2007 BMC microbiology Result HBV L180M;M204V;V173L 36;44;126 41;49;131 RT;RT;RT 34;42;124 36;44;126 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. Three HBV genotype A isolates (358-S; 312-SE; 161-CW) were shown to harbor tyrosine to cysteine substitutions in determinant a residue 100 (Y100C), and the T118V-A128V double mutant was found in three genotype D isolates (Table 2). 2007 BMC microbiology Result HBV Y100C;T118V;A128V 140;156;162 145;161;167 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. At last, three patients displayed a single (rtM204I, patient 05-hac) or double (rtL180I/rtM204I, 11-hgg and 01-ufmt) mutation leading to the YIDD motif. 2008 BMC microbiology Result HBV L180I;M204I;M204I 82;46;90 87;51;95 RT;RT;RT;P 44;80;88;141 46;82;90;145 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. Fifteen patients showed the well-known double rtL180M/rtM204V mutation. 2008 BMC microbiology Result HBV L180M;M204V 48;56 53;61 RT;RT 46;54 48;56 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. The last one resulted from the lamivudine resistance mutation at rtL180M position. 2008 BMC microbiology Result HBV L180M 67 72 RT 65 67 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. Two others (03-hgg and 08-hgg) displayed a third mutation (rtV173L) related to lamivudine resistance. 2008 BMC microbiology Result HBV V173L 61 66 RT 59 61 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Among participants with a baseline HBV DNA level of at least 104 copies/mL, those with the precore wild-type G1896 variant had a higher incidence of HCC than those with the G1896A mutant variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9] per 100 000 person-years), and those with the BCP A1762T/G1764A double mutant had a higher incidence of HCC than those with BCP A1762/G1764 wild type (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4] per 100 000 person-years). 2008 Journal of the National Cancer Institute Result HBV G1764A;G1896A;A1762T 321;173;314 327;179;320 BCP;BCP;Precore 310;388;91 313;391;98 Hepatocellular carcinoma;Hepatocellular carcinoma 149;368 152;371 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. By contrast, participants who were infected with HBV genotype B, had the precore G1896A variant, and had the wild-type BCP 1762/1764 variant had the lowest incidence of HCC (173.9 per 100 000 person-years), with an adjusted hazard ratio of 0.20 (95% CI = 0.09 to 0.46, P < .001) relative to participants who were infected with HBV genotype B and wild type for the precore 1896 and BCP 1762/1764 variants. 2008 Journal of the National Cancer Institute Result HBV G1896A 81 87 BCP;BCP;Precore;Precore 119;381;73;364 122;384;80;371 Hepatocellular carcinoma 169 172 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. By contrast, the precore G1896A mutation was associated with a lower risk of HCC than the precore wild type (HRadj = 0.34, 95% CI = 0.21 to 0.57; P < .001). 2008 Journal of the National Cancer Institute Result HBV G1896A 25 31 Precore;Precore 17;90 24;97 Hepatocellular carcinoma 77 80 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Finally, we examined the risk of HCC associated with combinations of HBV genotype, the precore G1896A mutant, and the BCP double mutants. 2008 Journal of the National Cancer Institute Result HBV G1896A 95 101 BCP;Precore 118;87 121;94 Hepatocellular carcinoma 33 36 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Participants who were infected with HBV genotype C, had the wild-type precore 1896 variant, and had the BCP A1762T/G1764A double mutation had the highest incidence of HCC (2254.2 per 100 000 person-years), with an adjusted hazard ratio of 2.99 (95% CI = 1.57 to 5.70, P < .001) relative to participants who were infected with HBV genotype B and wild type for the precore 1896 and BCP 1762/1764 variants (Table 5). 2008 Journal of the National Cancer Institute Result HBV G1764A;A1762T 115;108 121;114 BCP;BCP;Precore;Precore 104;380;70;363 107;383;77;370 Hepatocellular carcinoma 167 170 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The adjusted hazard ratio of HCC for the BCP A1762T/G1764A mutation vs wild type was 1.73 (95% CI = 1.13 to 2.67; P = .013). 2008 Journal of the National Cancer Institute Result HBV G1764A;A1762T 52;45 58;51 BCP 41 44 Hepatocellular carcinoma 29 32 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The prevalence of the BCP A1762T/G1764A double mutant also increased with age (Ptrend = .02 for females and Ptrend = .003 for males). 2008 Journal of the National Cancer Institute Result HBV G1764A;A1762T 33;26 39;32 BCP 22 25 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The prevalence of the BCP A1762T/G1764A double mutant was higher in participants infected with HBV genotype C than in those infected with HBV genotype B (43.0% vs 21.4%; P < .001). 2008 Journal of the National Cancer Institute Result HBV G1764A;A1762T 33;26 39;32 BCP 22 25 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The prevalence of the precore G1869A mutant increased with age in both males and females (Ptrend < .001 for both). 2008 Journal of the National Cancer Institute Result HBV G1869A 30 36 Precore 22 29 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The prevalence of the precore G1896A mutant was higher in participants infected with HBV genotype B than in those infected with HBV genotype C (57.5% vs 25.8%; P < .001). 2008 Journal of the National Cancer Institute Result HBV G1896A 30 36 Precore 22 29 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. A further binding mode study reveals a steric clash in case of M204I HBV due to the unfavorable position and orientation of a methyl group (Figure 13b) of I204 residue. 2008 Antiviral research Result HBV M204I 63 68 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Accordingly, the dual mutation L180M+M204V can cause the removal of two methyl group from the backside hydrophobic pocket, and consequently, clevudine is no longer active in this dual mutant. 2008 Antiviral research Result HBV L180M;M204V 31;37 36;42 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Although LdT does not have any steric clash with 3TC associated mutation M204V, but this mutation alters the backside hydrophobic pocket. 2008 Antiviral research Result HBV M204V 73 78 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. As in the case of L180M, there is absence of a methyl group in the backside hydrophobic pocket (Figure 12b). 2008 Antiviral research Result HBV L180M 18 23 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Due to this fact, M204V mutation may not affect heavily in terms of steric clash (Figure 13a) as it was observed the case of 3TC. 2008 Antiviral research Result HBV M204V 18 23 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Energetic results in Table 4 clearly indicates a significant low binding affinity of 3TC-TP (DeltaE = -346.7 KJ/mol) in comparison to dCTP (DeltaE = -426.5 KJ/mol) in M204I HBV. 2008 Antiviral research Result HBV M204I 167 172 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Figure 9c shows a possible partial steric clash between the exocyclic alkene and the I204 residue, which supports the reduction of potency of ETV in comparison to M204V HBV. 2008 Antiviral research Result HBV M204V 163 168 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Four major mutational patterns (M204V, M204I, L180M-M204V and L180M-M204I) of 3TC-resistant HBV with significant reduced antiviral activity are observed in patients (Table 1), while individuals with L180M mutation show only 1.7 fold resistance. 2008 Antiviral research Result HBV M204V;M204I;M204V;L180M;M204I;L180M;L180M 32;39;52;46;68;62;199 37;44;57;51;73;67;204 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. From above structural studies, it is obvious that the dual mutations L180M+M204V or L180M+M204I won't allow the movement of sugar or the oxathiolane ring backwards and restrict the utilization of hydrophobic pocket for favorable binding of 3TC. 2008 Antiviral research Result HBV M204V;L180M;L180M;M204I 75;69;84;90 80;74;89;95 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Further, the empirical energy calculations (Table 5) reveal that adefovir has better binding affinity in comparison to dATP with the wild type as well as the 3TC-associated mutant HBV (L180 and M204V). 2008 Antiviral research Result HBV M204V 194 199 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. However, it did not provide a quantitative correlation with in-vitro activity of adefovir against M204I and the dual mutant. 2008 Antiviral research Result HBV M204I 98 103 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In addition, the mutant M204V doesn't affect much on the binding mode of ETV as well (Figure 9b). 2008 Antiviral research Result HBV M204V 24 29 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In case of L180M HBV, the resulting M180 is oriented away from the hydrophobic pocket and looses the participation of one methyl group (Figure 6a). 2008 Antiviral research Result HBV L180M 11 16 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In M204V HBV, shifting of oxathiolane ring is disfavored due to bulkiness of branched residue V204 (Figure 6b & 6c), which ultimately leads to an 18 fold resistance (Table 1). 2008 Antiviral research Result HBV M204V 3 8 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In this regard the binding mode of 3TC in dual mutant HBV (L180M+M204I) shown in Figure 7, shows the poor stacking of oxathiolane ring with F88 and steric clash between I204 and 3TC. 2008 Antiviral research Result HBV M204I;L180M 65;59 70;64 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. It's obvious that substitution of M204 to I204 (Isoleucine: more bulky group) will reduce the binding affinity in several folds by enforcing the oxathiolane ring forward to a non-binding mode of 3TC in M204I HBV (Figure 6d). 2008 Antiviral research Result HBV M204I 202 207 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. LdT binding mode in the M204V, M204I and L180M are shown in Figure 11. 2008 Antiviral research Result HBV M204V;M204I;L180M 24;31;41 29;36;46 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Modeling studies of LdT in M204I also clearly shows the significant differences in the binding pocket due to the M204 mutation, in terms of position of the methyl group (Figure 11b) and orientation of the methyl group of I204 residue (Figure 11c). 2008 Antiviral research Result HBV M204I 27 32 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Positional and orientation differences do not support the binding of LdT in the active site of M204I HBV, and this result justifies the several-folds reduced susceptibility of LdT in cell based assays. 2008 Antiviral research Result HBV M204I 95 100 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. The binding mode of LdT in L180M HBV (Figure 11d) and the modeling studies indicate the absence of one methyl group contribution in the back-side hydrophobic pocket causing reduced binding affinity. 2008 Antiviral research Result HBV L180M 27 32 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. The M204V mutation clearly reflects the loss of contribution by one methyl group in the back-side hydrophobic pocket to interact with the sugar ring (Figure 11a). 2008 Antiviral research Result HBV M204V 4 9 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. The mutation of M204 to V204 can result in only partial filling of the small hydrophobic pocket which may be the reason for the reduction of potency of ETV in M204V HBV RT (Table 1). 2008 Antiviral research Result HBV M204V 159 164 RT 169 171 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Therefore, the dual mutation, L180M+M204V, can cause removal of the two methyl group (Figure 11a and Figure 11d) from the backside hydrophobic pocket. 2008 Antiviral research Result HBV L180M;M204V 30;36 35;41 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. These modeling results support the better activity profile of clevudine in comparison to 3TC in M204V. 2008 Antiviral research Result HBV M204V 96 101 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. This could be the reason for the several folds reduced susceptibility of clevudine in M204I as well as in dual mutant L180M/M204I. 2008 Antiviral research Result HBV M204I;M204I;L180M 124;86;118 129;91;123 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. This may be the reason for the modest resistance profile of 3TC (1.7 fold, Table 1) by the L180M mutation. 2008 Antiviral research Result HBV L180M 91 96 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. This result supports the reduced potency of LdT in M204V HBV. 2008 Antiviral research Result HBV M204V 51 56 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Thus, it is obvious that the L180M mutation won't affect on its binding to the active site. 2008 Antiviral research Result HBV L180M 29 34 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Almost all mutations at nt 1653 and nt 1753 are co-incident with the A1762T, G1764A mutations. 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 69;77 75;83 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Mutations at nucleotide (nt) 1653 from C to T and nt 1753 from T to A, G or C (T to V) have been reported to be associated with severe chronic hepatitis B and the development of cirrhosis and HCC. 2008 The American journal of gastroenterology Result HBV C1653T;T1753A 29;53 45;69 Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma 135;178;192 154;187;195 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Of the 2998 recruited initially, 740 were excluded: 638 because the BCP sequences could not be determined at baseline, 13 who were anti-HCV positive and the 89 whose BCP sequences were neither wild type nor had the specific mutations A1762T or G1764A. 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 234;244 240;250 BCP;BCP 68;166 71;169 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Specifically, 93.3% (42/45) of the male cases in the cohort are infected with the mutant type, suggesting that BCP mutations (A1762T, G1764A) may be a good biomarker to identify a subset of male HBsAg carriers at extremely high risk of HCC. 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 126;134 132;140 BCP;S 111;195 114;200 Hepatocellular carcinoma 236 239 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The last group included 69 with the single mutations A1762T or G1764A, 12 with other single or double mutations at these positions, and 8 with deletions of up to 9 nucleotides (Table 2). 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 53;63 59;69 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The nucleotide sequences of the products of both sets of positive PCR reaction were determined (the sequence of 29 samples could not be determined and therefore were grouped as HBV DNA not detected): 1001 were wild type at positions 1762/1764, 1257 had the specific mutations A1762T, G1764A, and 96 had other mutations at these positions or were positive for anti-HCV. 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 276;284 282;290 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The prevalence of the mutations A1762T, G1764A is the same (53.7%) in males and females (Table 2).The prevalence tends to increase up to 35 years of age (Table 3) and parallels a decline in the prevalence of HBeAg and a rise in anti-HBe. 2008 The American journal of gastroenterology Result HBV A1762T;G1764A 32;40 38;46 C;C 233;208 236;213 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The total prevalence of the C1653T mutation from cases and controls is 20% (12/60) and that of T1753V is 28.4% (29/102) (Table 6). 2008 The American journal of gastroenterology Result HBV C1653T;T1753V 28;95 34;101 19077239 Occult hepatitis B infection: an evolutionary scenario. For instance, Hass and coworkers observed that a single G458A mutation prevented splicing from 459 to 1304 or 1384. 2008 Virology journal Result HBV G458A 56 61 19077239 Occult hepatitis B infection: an evolutionary scenario. Replacements typical for d4 HBV are G74V, I80A and Y100C in core and P111S, T123P, T125I, L175S and M197T in surface protein, respectively. 2008 Virology journal Result HBV G74V;I80A;Y100C;P111S;T123P;T125I;L175S;M197T 36;42;51;69;76;83;90;100 40;46;56;74;81;88;95;105 C;S 60;109 64;116 19077239 Occult hepatitis B infection: an evolutionary scenario. Solely, the 7th mutation T173G displayed the ability of changing a grey phenotype (T) into a black one (G) and vice versa. 2008 Virology journal Result HBV T173G 25 30 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. A co-assembly reaction of 11.7 muM Cp149-Y132A with 5 muM wildtype protein at 0.6M NaCl was monitored by SEC over a 24 hour equilibration period and compared to a control experiment with 5 muM wildtype Cp149. 2009 Biochemistry Result HBV Y132A 41 46 C;C 35;202 37;204 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Addition of Cp149-Y132A increased the light scattering by approximately twofold, after accounting for the scattering of free dimer, in good agreement with the results shown in figure 2. 2009 Biochemistry Result HBV Y132A 18 23 C 12 14 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. As Cp149-Y132A co-assembles with Cp149 but does not assemble on its own in HEPES and NaCl, we investigated whether there was a minimum proportion of Cp149 needed to nucleate assembly. 2009 Biochemistry Result HBV Y132A 9 14 C;C;C 3;33;149 5;35;151 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. As the concentration of Cp149-Y132A was increased, we observed small but significant (p < 0.02) increases in the yield of capsid for 0.3, 0.6, and 1.0 M NaCl reactions, though not the great excess suggested by light scattering. 2009 Biochemistry Result HBV Y132A 30 35 Capsid;C 122;24 128;26 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Co-assembling 10muM Cp149 with 20 muM Cp149-Y132A we observed that there was additional light scattering compared to Cp149 alone. 2009 Biochemistry Result HBV Y132A 44 49 C;C;C 20;38;117 22;40;119 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Co-assembly reactions induced by 0.15 M and 0.3 M NaCl showed no significant change in the yield of capsid related to Cp149-Y132A, essentially the same result found when the column was equilibrated with 1 M NaCl buffer. 2009 Biochemistry Result HBV Y132A 124 129 Capsid;C 100;118 106;120 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Micrographs of co-assembly reactions are almost indistinguishable from those of Cp149 reactions except for the background attributable to high concentrations of free protein, in this case Cp149-Y132A. 2009 Biochemistry Result HBV Y132A 194 199 C;C 80;188 82;190 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. More importantly for this experiment, the high NaCl was expected to lead to maximal participation of Cp149-Y132A. 2009 Biochemistry Result HBV Y132A 107 112 C 101 103 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. The difference between results for low and high ionic strength SEC indicates the participation of the Y132A mutant in assembly and its sensitivity to association energy. 2009 Biochemistry Result HBV Y132A 102 107 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. The effect of the Y132A mutation was apparent during purification. 2009 Biochemistry Result HBV Y132A 18 23 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. The phenolic side chain fits into a hydrophobic pocket formed by P20, D22, F23, F122, W125, A137, P138, I139, and L140A of a neighboring subunit. 2009 Biochemistry Result HBV L140A 114 119 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. The Y132A mutant retains the characteristic blue-shifted fluorescence spectrum of Cp149 and the helix-rich circular dichroism spectrum (data not shown), and as demonstrated in this paper, is capable of participating in assembly, all of which indicate that the mutant is properly folded. 2009 Biochemistry Result HBV Y132A 4 9 C 82 84 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. To further investigate the effects of Cp149-Y132A on assembly, we examined the long-term kinetics of assembly over a 24-hour period. 2009 Biochemistry Result HBV Y132A 44 49 C 38 40 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Unlike Cp149, which is isolated from E coli as a capsid, Cp149-Y132A was dimeric based on size exclusion chromatography (SEC). 2009 Biochemistry Result HBV Y132A 63 68 Capsid;C;C 49;7;57 55;9;59 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Using light scattering, we found that purified Cp149-Y132A showed no sign of assembly at concentrations of 200 muM dimer in 1 M NaCl, conditions where wildtype Cp149 which has a pseudo-critical concentration of < 0.5 muM dimer. 2009 Biochemistry Result HBV Y132A 53 58 C;C 47;160 49;162 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. We also noted that high concentrations of Cp149-Y132A did not decrease light scattering, suggesting that the mutant did not poison assembly. 2009 Biochemistry Result HBV Y132A 48 53 C 42 44 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. We reasoned that Cp149-Y132A retained sufficient molecular complementarity that it could participate in assembly with wildtype Cp149. 2009 Biochemistry Result HBV Y132A 23 28 C;C 17;127 19;129 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Among the NRTI-resistance mutations, M204I was detected in 1.3% of the sequence reads in the sample from subject A7; A181T and M204I were present in 1.0% of the sequence reads in the sample from subject E6. 2009 The Journal of infectious diseases Result HBV M204I;A181T;M204I 37;117;127 42;122;132 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Clonal sequencing performed on this sample detected N236T in 2 of 89 clones. 2009 The Journal of infectious diseases Result HBV N236T 52 57 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. For sample A7, M204I was found in 1 of 64 clones sequenced by dideoxynucleotide sequencing; however, that clone had 2 stop codons and G-to-A hypermutation. 2009 The Journal of infectious diseases Result HBV M204I 15 20 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. For the sample from subject E6, A181T and M204I were each found in 1 of 80 molecular clones; the clone with M204I had G-to-A hypermutation and 2 stop codons. 2009 The Journal of infectious diseases Result HBV A181T;M204I;M204I 32;42;108 37;47;113 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Of the mutations reported to be associated with decreased hepatitis B surface antigen immunologic reactivity, only sM133L and sP120T were detected in this study. 2009 The Journal of infectious diseases Result HBV M133L;P120T 115;126 121;132 S;S;S 115;126;70 116;127;77 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. sM133L was present as part of a mixture with wild type in the direct PCR sequence for 2 NRTI-naive patients and as a minor variant detectable only by UDPS for 2 NRTI-naive patients and 1 NRTI-treated patient. 2009 The Journal of infectious diseases Result HBV M133L 0 6 S 0 1 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. sP120T was detected as a minority variant in 1 NRTI-treated patient. 2009 The Journal of infectious diseases Result HBV P120T 0 6 S 0 1 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Table 4 shows the influence of G-to-A hypermutation at the 3 codons at which a G-to-A change is responsible for a drug-resistance mutation (A181T, A194T, and M204I). 2009 The Journal of infectious diseases Result HBV A181T;A194T;M204I 140;147;158 145;152;163 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The 3TC-resistance mutation L80V and the ETV-resistance mutation S202G were detected at prevalences of 1.5% and 9.9%, respectively, in a patient who had received 3TC, ADV, and ETV. 2009 The Journal of infectious diseases Result HBV L80V;S202G 28;65 32;70 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The ADV-resistance mutation N236T was detected at a prevalence of 6.6% in a patient who had received 3TC and ADV but had not been receiving therapy for 19 months at the time the sample was obtained. 2009 The Journal of infectious diseases Result HBV N236T 28 33 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The direct PCR sequences were dominated by 3TC-resistance mutations: L180M and M204V/I in 9 samples; V173L, L180M, and M204V in 5 samples; L180M, A181V (a mutation associated with ADV and 3TC resistance), and M204V in 1 sample; and V173L alone in 1 sample. 2009 The Journal of infectious diseases Result HBV L180M;M204V;M204I;V173L;L180M;M204V;L180M;A181V;M204V;V173L 69;79;79;101;108;119;139;146;209;232 74;86;86;106;113;124;144;151;214;237 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The ETV-resistance mutation T184S was detected at a prevalence of 2%-3% in 2 samples from a 3TC-treated patient for whom the HBV direct PCR sequence contained L180M and M204V. 2009 The Journal of infectious diseases Result HBV T184S;L180M;M204V 28;159;169 33;164;174 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The most common additional mutation was V173L, which was found in 5 samples for which the direct PCR sequence contained L180M and M204V/I. 2009 The Journal of infectious diseases Result HBV V173L;L180M;M204V;M204I 40;120;130;130 45;125;137;137 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Three of the 13 residues with stop codons were always associated with RT amino acid mutations, of which 2 (rtA181T and rtV191I) have previously been reported. 2009 The Journal of infectious diseases Result HBV A181T;V191I 109;121 114;126 RT;RT;RT 70;107;119 72;109;121 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. V173L/M, L180M, A181T, and M204V were detected in a patient who had received 3TC for 52 months but had not been receiving therapy for 27 months at the time the sample was obtained. 2009 The Journal of infectious diseases Result HBV V173M;V173L;L180M;A181T;M204V 0;0;9;16;27 7;7;14;21;32 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. A polyclonal rabbit antibody (Dako) efficiently detects the wild-type core protein, but it is less reactive with the core protein of clone 4B due to an E77Q mutation (Kim K et al., unpublished). 2009 Virology Result HBV E77Q 152 156 C;C 70;117 74;121 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Analysis of site-directed mutants of clone 2A revealed comparable impact of the A1762T/G1764A/C1766T triple mutation (mu 2a), slightly lower effect of the T1753C/A1762T/G1764A triple mutation (mu 4), and least effect of the A1762T/G1764A double mutation (mu 1). 2009 Virology Result HBV G1764A;C1766T;G1764A;A1762T;G1764A;A1762T;T1753C;A1762T 231;94;87;162;169;80;155;224 237;100;93;168;175;86;161;230 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Further study established that the 1570-1813 segment of the 4B genome, which harbors the T1753C, A1762T, G1764A, and C1766T core promoter mutations, up regulated pg RNA but nearly abolished pc RNA (chi9 vs. 2009 Virology Result HBV T1753C;A1762T;G1764A;C1766T 89;97;105;117 95;103;111;123 Core promoter;Precore 124;190 137;192 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The 3' end of the core gene overlaps with the 5' end of the P gene, which is mutated in clone 4B (D16V, T18A) but not 2A. 2009 Virology Result HBV D16V;T18A 98;104 102;108 C;P 18;60 22;61 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. This finding, together with the results of the mapping experiments, establishes that amino acid substitutions at the N-terminus of the 2A core protein (A36Tor G63V) reduce the stringency of virion secretion, whereas amino acid changes at the C-terminus of the 4B core protein (T147A, R151C, D153G, or Q179K) enhance genome maturity of secreted virions. 2009 Virology Result HBV G63V;T147A;R151C;D153G;Q179K 159;277;284;291;301 163;282;289;296;306 C;C 138;263 142;267 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A statistically significant summary odds ratio for A1762T/G1764A was also found for subjects from areas other than Asia. 2009 Journal of the National Cancer Institute Result HBV G1764A;A1762T 58;51 64;57 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A had a sensitivity and specificity of 70.6% (95% CI = 68.7% to 72.5%) and 60.6% (95% CI = 68.7% to 62.0%), respectively, whereas C1653T + T1753V and A1762T/G1764A + C1653T + T1753V had high specificity (92.6% [95% CI = 89.2% to 96.0%] and 93.9% [95% CI = 90.5% to 97.2%], respectively) but low sensitivity (20.6% [95% CI = 14.9% to 26.3%] and 24.3% [95% CI = 17.5% to 31.1%], respectively) (Table 4). 2009 Journal of the National Cancer Institute Result HBV G1764A;G1764A;A1762T;C1653T;T1753V;A1762T;C1653T;T1753V 7;169;0;142;151;162;178;187 13;175;6;148;157;168;184;193 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1653T in HBV subgenotype C2 and T1753V and A1762T/G1764A in HBV subgenotypes C1 and C2 were statistically significantly associated with an increased risk of HCC. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 51;0;33;44 57;6;39;50 Hepatocellular carcinoma 158 161 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Egger's test suggested no statistically significant publication bias for the studies of C1653T, T1753V, A1762T/G1764A, C1858T, and G1896A. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T;C1858T;G1896A 111;88;96;104;119;131 117;94;102;110;125;137 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Finally, we evaluated the frequencies of PreS mutations, C1653T, T1753V, and A1762T/G1764A alone and in combinations using data extracted from all included studies as potential biomarkers for the prediction of HCC. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 84;57;65;77 90;63;71;83 PreS 41 45 Hepatocellular carcinoma 210 213 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1896A and C1858T were not associated with the risk of HCC, regardless of HBeAg status and HBV genotype (data not shown). 2009 Journal of the National Cancer Institute Result HBV G1896A;C1858T 0;11 6;17 C 74 79 Hepatocellular carcinoma 55 58 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. However, C1858T and G1896A were not statistically significantly associated with HCC risk. 2009 Journal of the National Cancer Institute Result HBV C1858T;G1896A 9;20 15;26 Hepatocellular carcinoma 80 83 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Overall, we observed statistically significant associations between PreS mutations (summary OR = 3.77, 95% CI = 2.57 to 5.52), C1653T (summary OR = 2.76, 95% CI = 2.09 to 3.64), T1753V (summary OR = 2.35, 95% CI = 1.63 to 3.40), and A1762T/G1764A (summary OR = 3.79, 95% CI = 2.71 to 5.29), and the risk of HCC in both case-control and cohort studies. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 240;127;178;233 246;133;184;239 PreS 68 72 Hepatocellular carcinoma 307 310 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Statistically significant heterogeneity was found among studies of PreS mutations, T1753V, A1762T/G1764A, C1858T, and G1896A. 2009 Journal of the National Cancer Institute Result HBV G1764A;T1753V;A1762T;C1858T;G1896A 98;83;91;106;118 104;89;97;112;124 PreS 67 71 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The frequencies of A1762T/G1764A-based combined mutations were statistically significantly higher in patients with HCC than in patients without HCC (A1762T/G1764A + C1653T: 43.4% vs 15.8%, P < .001; A1762T/G1764A + T1753V: 51.7% vs 19.6%, P < .001; A1762T/G1764A + PreS mutation: 43.6% vs 20.8%, P = .002; and A1762T/G1764A + C1653T + T1753V: 24.3% vs 6.1%, P < .001). 2009 Journal of the National Cancer Institute Result HBV G1764A;G1764A;G1764A;G1764A;G1764A;A1762T;A1762T;C1653T;A1762T;T1753V;A1762T;A1762T;C1653T;T1753V 26;156;206;256;317;19;149;165;199;215;249;310;326;335 32;162;212;262;323;25;155;171;205;221;255;316;332;341 PreS 265 269 Hepatocellular carcinoma;Hepatocellular carcinoma 115;144 118;147 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The most commonly reported HBV mutations associated with HCC risk were PreS mutations, A1762T/G1764A, G1896A, T1753V, C1653T, and C1858T. 2009 Journal of the National Cancer Institute Result HBV G1764A;A1762T;G1896A;T1753V;C1653T;C1858T 94;87;102;110;118;130 100;93;108;116;124;136 PreS 71 75 Hepatocellular carcinoma 57 60 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The risk estimates of HCC for PreS mutations, C1653T, T1753V, A1762T/G1764A, G1896A, and C1858T in individual case-control and cohort studies and summary estimates are shown in Figure 2. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T;G1896A;C1858T 69;46;54;62;77;89 75;52;60;68;83;95 PreS 30 34 Hepatocellular carcinoma 22 25 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The statistically significant summary odds ratios for PreS mutations, C1653T, T1753V, and A1762T/G1764A were essentially unchanged when we stratified the participants by study location (ie, China, Taiwan, or Hong Kong, Japan, or Korea). 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 97;70;78;90 103;76;84;96 PreS 54 58 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary adjusted odds ratio for PreS mutations from four studies was 6.18 (95% CI = 2.63 to 14.47), for C1653T from five studies was 3.45 (95% CI = 1.12 to 10.65), for T1753V from six studies was 2.56 (95% CI = 1.05 to 6.22), for A1762T/G1764A from 11 studies was 4.87 (95% CI = 2.21 to 10.70), and for G1896A from nine studies was 1.21 (95% CI = 0.72 to 2.03) (Supplementary Figure 1, available online). 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T;G1896A 241;108;172;234;307 247;114;178;240;313 PreS 36 40 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary adjusted relative risks for A1762T/G1764A and G1896A from two cohort studies were 1.93 (95% CI = 1.27 to 2.92) and 1.12 (95% CI = 0.09 to 13.16), respectively (Supplementary Figure 2, available online). 2009 Journal of the National Cancer Institute Result HBV G1764A;A1762T;G1896A 47;40;58 53;46;64 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratio for PreS mutations was higher in subjects with HBV genotype C than in those with HBV genotype B, whereas the opposite was true for A1762T/G1764A, even though both PreS mutations and A1762T/G1764A were statistically significantly associated with the risk of HCC in both HBV genotypes. 2009 Journal of the National Cancer Institute Result HBV G1764A;G1764A;A1762T;A1762T 161;212;154;205 167;218;160;211 PreS;PreS 27;186 31;190 Hepatocellular carcinoma 280 283 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratios for C1653T, T1753V, and A1762T/G1764A in the HBeAg-positive group were higher than the corresponding estimates in the HBeAg-negative group. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 55;28;36;48 61;34;42;54 C;C 69;142 74;147 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratios for C1653T, T1753V, and A1762T/G1764A increased with decreasing study quality score, whereas the summary odds ratios for PreS mutations decreased with decreasing study quality score. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 55;28;36;48 61;34;42;54 PreS 145 149 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratios of HCC for PreS mutations, C1653T, T1753V, and A1762T/G1764A decreased successively when we used asymptomatic HBsAg carriers, patients with chronic hepatitis B, or patients with liver cirrhosis as control subjects (data not shown). 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 78;51;59;71 84;57;65;77 S;PreS 134;35 139;39 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 27;164;202 30;183;217 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratios of HCC for T1753V and A1762T/G1764A were higher for the unmatched groups than for any of the matched groups (Table 3). 2009 Journal of the National Cancer Institute Result HBV G1764A;T1753V;A1762T 53;35;46 59;41;52 Hepatocellular carcinoma 27 30 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Thus, PreS mutations, C1653T, T1753V, and A1762T/G1764A accumulate during the progression of chronic HBV infection. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 49;22;30;42 55;28;36;48 PreS 6 10 Chronic HBV infection 93 114 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. To examine the associations between HBV mutations and the risk of HCC during the progression of HBV chronic infection, we grouped the control subjects into three groups:asymptomatic HBsAg carriers, patients with chronic hepatitis B, and patients with liver cirrhosis:and evaluated the summary risk estimates for PreS mutations, C1653T, T1753V, and A1762T/G1764A in each group. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 355;328;336;348 361;334;342;354 S;PreS 182;312 187;316 Hepatocellular carcinoma;Chronic HBV infection;Chronic Hepatitis B;Liver cirrhosis 66;96;212;251 69;117;231;266 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We also extracted data for HBV mutations in combination from the included studies for the analysis of A1762T/G1764A-based combinations of HBV mutations. 2009 Journal of the National Cancer Institute Result HBV G1764A;A1762T 109;102 115;108 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We found that the frequencies of A1762T/G1764A + C1653T (8.6%), A1762T/G1764A + T1753V (14.6%), A1762T/G1764A + PreS mutation (2.2%), and A1762T/G1764A + C1653T + T1753V (3.2%) were low in asymptomatic HBsAg carriers. 2009 Journal of the National Cancer Institute Result HBV G1764A;G1764A;G1764A;G1764A;A1762T;C1653T;A1762T;T1753V;A1762T;A1762T;C1653T;T1753V 40;71;103;145;33;49;64;80;96;138;154;163 46;77;109;151;39;55;70;86;102;144;160;169 S;PreS 202;112 207;116 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We then summarized the frequencies of PreS mutations, C1653T, T1753V, and A1762T/G1764A in asymptomatic HBsAg carriers, patients with chronic hepatitis B, and patients with liver cirrhosis from all included studies. 2009 Journal of the National Cancer Institute Result HBV G1764A;C1653T;T1753V;A1762T 81;54;62;74 87;60;68;80 S;PreS 104;38 109;42 Chronic Hepatitis B;Liver cirrhosis 134;173 153;188 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. When we excluded the publication(s) with statistically significant heterogeneity and repeated the analysis, the summary estimates for PreS mutations, T1753V, A1762T/G1764A, C1858T, and G1896A did not change statistically significantly. 2009 Journal of the National Cancer Institute Result HBV G1764A;T1753V;A1762T;C1858T;G1896A 165;150;158;173;185 171;156;164;179;191 PreS 134 138 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. Double mutation (A1762T/G1764A), one of significant mutations associated with advanced liver disease including HCC, was only found in 1.96% (2/102) of HBV/B. 2009 Virology journal Result HBV G1764A;A1762T 24;17 30;23 Liver disease;Hepatocellular carcinoma 87;111 100;114 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. However, a G-to-A substitution at nucleotide 1896, which prevents the production of HBeAg by introducing a premature stop codon into the open reading frame of the pre-C region, was found in both strains of HBV/D (data not shown). 2009 Virology journal Result HBV G1896A 11 49 C;Precore 84;163 89;168 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. Double amino acid mutations Ile66 and Ser69 were always accompanied with Glu64Asp and never accompanied with Asn67 (p<0.001). 2009 Journal of clinical virology Result HBV E64D 73 81 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. Substitutions of Ser21 to Thr21 or Ala21 were never accompanied with T1762A1764 core promoter double mutation (p=0.005). 2009 Journal of clinical virology Result HBV S21T 17 31 Core promoter 80 93 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. The Thr12Ser mutation was also found to be correlated with substitutions within CTL epitopes 18-27 (cc=0.43, p=0.0001), and 91-95 (cc=0.40, p=0.0002). 2009 Journal of clinical virology Result HBV T12S 4 12 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. A significantly higher prevalence of the T1753V, A1762T, G1764A, G1896A and G1899A mutations was detected in HB-ACLF than in patients with CHB. 2010 Journal of viral hepatitis Result HBV T1753V;A1762T;G1764A;G1896A;G1899A 41;49;57;65;76 47;55;63;71;82 Chronic Hepatitis B;Acute on chronic liver failure 139;109 142;116 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Genotype B had a significantly lower prevalence of BCP mutations T1753V, A1762T and G1764A but significantly higher prevalence of the G1896A PC mutation in comparison with genotype C. 2010 Journal of viral hepatitis Result HBV T1753V;A1762T;G1764A;G1896A 65;73;84;134 71;79;90;140 BCP;Precore 51;141 54;143 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. In addition, two interesting triple BCP mutations [T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A)] were more frequently detected in HB-ACLF than in patients with CHB (Table 4). 2010 Journal of viral hepatitis Result HBV A1762T;G1764A;G1764A;C1766T;A1762T;T1768A;T1753V 58;65;83;90;76;101;51 64;71;89;96;82;107;57 BCP 36 39 Chronic Hepatitis B;Acute on chronic liver failure 173;143 176;150 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. In genotype B infection, a statistical difference in the mutation occurrence between patients with HB-ACLF and patients with CHB was only observed at the A1762T and G1764A sites. 2010 Journal of viral hepatitis Result HBV A1762T;G1764A 154;165 160;171 Chronic Hepatitis B;Acute on chronic liver failure 125;99 128;106 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. The C1766T and T1768A mutations were not found in the genotype B samples studied. 2010 Journal of viral hepatitis Result HBV C1766T;T1768A 4;15 10;21 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. To simplify data analysis, we defined the A1762T/G1764A and G1896A as the basic BCP and basic PC mutation, respectively, as these were well-known hotspot mutations. 2010 Journal of viral hepatitis Result HBV G1764A;A1762T;G1896A 49;42;60 55;48;66 BCP;Precore 80;94 83;96 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Among the patients in Group P, sW172stop (n=5) and sL173F (n=5) mutations were detected. 2010 Journal of Korean medical science Result HBV L173F;W172X 51;31 57;40 S;S 31;51 32;52 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Among these mutations, only the W172stop/L173F (P<0.001) and A184V (P=0.002) mutation were significantly different between the groups (data not shown). 2010 Journal of Korean medical science Result HBV L173F;W172X;A184V 41;32;61 46;40;66 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. An F46S mutation was observed in Group P (n=2); a Q2K mutation in Groups P (n=1) and C (n=1); an A11T mutation in Groups P (n=2) and C (n=1); and an F22L mutation in Groups P (n=2) and C (n=2). 2010 Journal of Korean medical science Result HBV Q2K;F46S;A11T;F22L 50;3;97;149 53;7;101;153 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. An H51Q mutation was detected in two patients (one case in each group). 2010 Journal of Korean medical science Result HBV H51Q 3 7 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. An L21S mutation was detected in Groups P (n=2) and C (n=2), and R24Q and P203R mutations were found in Groups P (n=1) and C (n=1). 2010 Journal of Korean medical science Result HBV L21S;R24Q;P203R 3;65;74 7;69;79 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. AST (P=0.035) and ALT (P=0.009) levels were significantly lower in patients with W172stop/L173F mutation. 2010 Journal of Korean medical science Result HBV L173F;W172X 90;81 95;89 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Comparison of demographic, biochemical and clinical characteristics between patients with and without the sA184V mutation. 2010 Journal of Korean medical science Result HBV A184V 106 112 S 106 107 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Comparison of demographic, biochemical and clinical characteristics between patients with and without the W172stop/L173F mutation. 2010 Journal of Korean medical science Result HBV L173F;W172X 115;106 120;114 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Eight of 13 patients in Group P and 3 of 9 patients in Group C had a V60A mutation. 2010 Journal of Korean medical science Result HBV V60A 69 73 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. G2A (n=1), G73D (n=1), L74I (n=2), A91T (n=1), and A95T (n=1) mutations were detected in Group P. 2010 Journal of Korean medical science Result HBV G2A;G73D;L74I;A91T;A95T 0;11;23;35;51 3;15;27;39;55 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In Group C, A81T (n=1), T86A (n=2), and A95V (n=1) mutations were detected. 2010 Journal of Korean medical science Result HBV A81T;T86A;A95V 12;24;40 16;28;44 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In Group C, there was one case of each of the following mutations: G10stop, L15V, I28V, W36L, F41S, T47A, Q51L, N59H, C69stop, L87V, F93L, V96G, L97P, G102C, T131P, Y200F, and C221Y. 2010 Journal of Korean medical science Result HBV G10X;L15V;I28V;W36L;F41S;T47A;Q51L;N59H;C69X;L87V;F93L;V96G;L97P;G102C;T131P;Y200F;C221Y 67;76;82;88;94;100;106;112;118;127;133;139;145;151;158;165;176 74;80;86;92;98;104;110;116;125;131;137;143;149;156;163;170;181 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In Group C, there was one case of each of the following mutations: N4K, T7A, H9Q, R16P, R16G, V17P, V17A, R18S, G19S, L20Q, P54Q, nucleotide 418-423 deletion. 2010 Journal of Korean medical science Result HBV N4K;T7A;H9Q;R16P;R16G;V17P;V17A;R18S;G19S;L20Q;P54Q 67;72;77;82;88;94;100;106;112;118;124 70;75;80;86;92;98;104;110;116;122;128 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In Group P, mutations I42T, P54L, and nucleotide 406 deletion. 2010 Journal of Korean medical science Result HBV I42T;P54L 22;28 26;32 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In the S gene, an A184V mutation was found in 9 of 13 patients in Group P. 2010 Journal of Korean medical science Result HBV A184V 18 23 S 7 8 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Only the ALT level was significantly lower in patients with the sA184V mutation (P=0.012). 2010 Journal of Korean medical science Result HBV A184V 64 70 S 64 65 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Other mutations that we detected in the S gene include S3N (Group P=4, Group C=2), I68T (Group P=3, Group C=1), I126T (Group P=4, Group C=1), and L213I (Group P=6, Group C=1). 2010 Journal of Korean medical science Result HBV S3N;I68T;I126T;L213I 55;83;112;146 58;87;117;151 S 40 41 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Similarly, in Group P, there was one case of each of the following mutations: F41C, A45V, P49L, Q54L, P62L, I92T, L98V, T140S, A157V, W182stop, and S204R. 2010 Journal of Korean medical science Result HBV F41C;A45V;P49L;Q54L;P62L;I92T;L98V;T140S;A157V;W182X;S204R 78;84;90;96;102;108;114;120;127;134;148 82;88;94;100;106;112;118;125;132;142;153 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. There was no significant difference, regardless of whether they harbored the rtA181T/V mutation (Table 2). 2010 Journal of Korean medical science Result HBV A181T;A181V 79;79 86;86 RT 77 79 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Three cases of I84T mutations were found in Group C, compared to only one in Group P. 2010 Journal of Korean medical science Result HBV I84T 15 19 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. V32A, I45T, and T49I mutations were detected in the patients with HCC, both groups equally. 2010 Journal of Korean medical science Result HBV V32A;I45T;T49I 0;6;16 4;10;20 Hepatocellular carcinoma 66 69 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. We also compared patients both with and without the W172stop/L173F mutation (Table 3). 2010 Journal of Korean medical science Result HBV L173F;W172X 61;52 66;60 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. We compared patients both with and without the sA184V mutation (Table 4). 2010 Journal of Korean medical science Result HBV A184V 47 53 S 47 48 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. A previously described isolate containing both T184G and S202I substitutions displayed the highest ETVr levels, suggesting that multiple ETVr changes in a LVDr background may have additive or synergistic effects. 2010 PloS one Result HBV T184G;S202I 47;57 52;62 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Additionally, large substitutions S202F/I/Y and small substitutions S202G/A were highly resistant. 2010 PloS one Result HBV S202F;S202I;S202Y;S202A;S202G 34;34;34;68;68 43;43;43;75;75 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Alternatively, in the model of M250V, the valine side chain packs tightly against the dNMP at the +2 position and produces a small hole between M250V/L and Y203 and L66. 2010 PloS one Result HBV M250V;M250V;M250L 31;144;144 36;151;151 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Among those that grew well, both large (T184L/M/F/Q/N) and small (T184A/G/C) residues resulted in ETVr. 2010 PloS one Result HBV T184L;T184A;T184G;T184C;T184M;T184F;T184Q;T184N 40;66;66;66;40;40;40;40 53;75;75;75;53;53;53;53 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Figure 2B shows that introduction of the S202G substitution causes repositioning of the L180M and M204V residues to further restrict the ETV-TP binding site. 2010 PloS one Result HBV S202G;L180M;M204V 41;88;98 46;93;103 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. HBV containing LVDr substitutions M204V+L180M exhibit reduced ETV susceptibility that can lead to virologic breakthrough with additional substitutions at ETVr signature residues T184, S202 or M250. 2010 PloS one Result HBV M204V;L180M 34;40 39;45 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. If experiments were performed using nucleocapsids from cultures without PFA, or if enzyme reactions were extended from the standard 1 hour to 3 hours in duration, both conditions that favored plus-strand DNA synthesis, the cell culture resistance to ETV of the LVDr+M250V virus was not observed enzymatically in vitro (data not shown). 2010 PloS one Result HBV M250V 266 271 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. In contrast, ETVr due to substitutions of M250V or M250L in LVDr HBV was found to be manifested primarily during RNA-directed minus strand DNA synthesis, as the EC50 for the first (minus) strand was increased relative to that for the second (plus) strand. 2010 PloS one Result HBV M250V;M250L 42;51 47;56 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. In response to the M250 mutation, the DNA slightly pivots in the active site to relieve the steric compression between M250V and the +2 dNMP and L66/N65 as they move to fill the hole between M250V and Y203 and L66. 2010 PloS one Result HBV M250V;M250V 119;191 124;196 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Interactions between these structural motifs were first proposed upon the double substitution M204V+L180M encoding LVDr. 2010 PloS one Result HBV M204V;L180M 94;100 99;105 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. M250 substitutions that were smaller than methionine and replicated well, M250A/G/S/T/C/D/E/Q/N/V/L/I, were all resistant. 2010 PloS one Result HBV M250A;M250G;M250S;M250T;M250C;M250D;M250E;M250Q;M250N;M250V;M250L;M250I 74;74;74;74;74;74;74;74;74;74;74;74 101;101;101;101;101;101;101;101;101;101;101;101 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Replication of the singly M250V substituted HBV was 7-fold hypersensitive to LVD in culture (wildtype HBV LVD EC50 = 794 nM, M250V HBV LVD EC50 = 116 nM), suggesting the M250 changes affected the dNTP binding site and not just elongation of the growing DNA. 2010 PloS one Result HBV M250V;M250V 26;125 31;130 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Several different ETVr substitutions have been observed in ETV-treated patients, including T184A/C/F/G/I/L/M/S, S202C/G/I, and M250 I/L/V. 2010 PloS one Result HBV T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M250I;M250L 91;91;91;91;91;91;91;91;112;112;112;127;127 110;110;110;110;110;110;110;110;121;121;121;137;137 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. T184 A and S changes also fit this model. 2010 PloS one Result HBV T184A 0 6 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. T184 I, M, F, substitutions also fit this pattern. 2010 PloS one Result HBV T184I 0 6 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The ETV binding pocket of LVDr HBV (M204V+L180M) is shown in Figure 2A. 2010 PloS one Result HBV M204V;L180M 36;42 41;47 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The larger substitution T184L forces the ETV binding pocket closed as the YMDD loop is repositioned to accommodate the larger amino acid. 2010 PloS one Result HBV T184L 24 29 P 74 78 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The LVDr substitutions M204V and L180M lie juxtaposed in the HBV RT dNTP binding pocket, the M204 positioned within the YMDD active site loop and the L180 residue in the adjacent alpha helix. 2010 PloS one Result HBV M204V;L180M 23;33 28;38 RT;P 65;120 67;124 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The LVDr substitutions M204V+L180M reduced the size of this pocket to exclude the binding of LVD-TP with its larger oxathiolane ring but not the binding of ETV-TP. 2010 PloS one Result HBV M204V;L180M 23;29 28;34 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The M250V substituted HBV RT in the absence of LVDr changes was constructed and tested for susceptibility to LVD, an obligate chain terminator which should not be impacted by the mechanism that could potentially affect ETV chain termination. 2010 PloS one Result HBV M250V 4 9 RT 26 28 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The only exception was the most resistant, quadruple-substituted RT with ETVr T184G+S202I changes in a M204V+L180M LVDr background, where the apparent Km for dGTP was approximately 7-fold less than that for wildtype. 2010 PloS one Result HBV T184G;S202I;M204V;L180M 78;84;103;109 83;89;108;114 RT 65 67 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The results of comprehensive phenotypic analysis of substitutions at positions S202 indicated that S202A/G/C/T/V/N replicated well and S202 I/F/Y replicated poorly, but that other S202 changes did not replicate. 2010 PloS one Result HBV S202A;S202G;S202C;S202T;S202V;S202N;S202I;S202F 99;99;99;99;99;99;135;135 114;114;114;114;114;114;145;145 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The S202G, C or S202I substitutions lose the ability to hydrogen bond with T184 and M204. 2010 PloS one Result HBV S202G;S202I 4;16 9;21 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The S202I change sterically closes the pocket as this region of the loop moves to accommodate the larger side chain. 2010 PloS one Result HBV S202I 4 9 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The smaller T184G substitution (relative to threonine) allows the YMDD loop to be more flexible which dynamically closes the ETV binding pocket. 2010 PloS one Result HBV T184G 12 17 P 66 70 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The smaller, more flexible S202G substitution destabilizes the YMDD loop and closes the ETV binding pocket in the back of the dNTP site. 2010 PloS one Result HBV S202G 27 32 P 63 67 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The T184G substitution was also modeled into the LVDr HBV RT and produced a similar change in the ETV-binding pocket as the S202G change in Figure 2 (not shown). 2010 PloS one Result HBV T184G;S202G 4;124 9;129 RT 58 60 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. These results are consistent with the model in that highly tolerated substitutions were uncharged, similar to serine in size, while resistant residues could be either large or small, which repositioned the YMDD loop closer or further from the stabilizing alpha-helix containing L180M, and could further impact the YMDD loop changes on the ETV-TP binding-pocket. 2010 PloS one Result HBV L180M 278 283 P;P 206;314 210;318 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. This results in an increase in the size of the pocket near M204V and shrinking of the corner of the pocket comprised by the dNMP in the +1 position of the template strand. 2010 PloS one Result HBV M204V 59 64 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Those that were large, replicated and could maintain the positioning of the primer:template, M250F/Y, retained ETV susceptibility. 2010 PloS one Result HBV M250F;M250Y 93;93 100;100 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. Another clone showed otherwise insertion sequence, GGAACAACTCAA, and contained a 3-nt(TCA) deletion from nt491 to nt493(figure 1). 2010 Virology journal Result HBV del nt491-493 91 119 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. C121Y(TGC TAC), T126S/T126A(ACT TCT or ACT GCT), Q129K(CAA AAA), G130R(GGA AGA), G145R(GGA AGA) and other aa substitution compared with consensus sequence in MHR were also showed in figure 2. 2010 Virology journal Result HBV T126A;C121Y;T126S;Q129K;G130R;G145R 22;0;16;49;65;81 27;5;21;54;70;86 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. Compared with consensus sequence of Chinese isolates retrieved from GenBank with same genotype/subtype, clone1-clone11 and clone13-clone15 had KNNT insertion, clone12 ENNT insertion and clone16 RNNS insertion between aa113 and aa114, respectively. 2010 Virology journal Result HBV Ins KNNT;Ins ENNT;Ins RNNS 143;167;194 157;181;208 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. N146D substitution(AAC GAC) occurred in clone5-clon6 at aa146, leading to loss of N-linked glycosylation site at this position. 2010 Virology journal Result HBV N146D 0 5 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. Of 4 clones with wildtype HBsAg, T131N(ACC AAC) and M133T(ATG ACG) substitution occurred in clon17-clone19, also forming a possible N-Linked glycosylation site(figure 2). 2010 Virology journal Result HBV T131N;M133T 33;52 38;57 S 26 31 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. S114T substitution(TCA ACA) occurred in all clones with 4-aa insertion. 2010 Virology journal Result HBV S114T 0 5 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. As some co-infected participants (n=7) were exposed to LMV, we also examined the frequency of polymerase rt L180M and rt M204V (signature LMV resistance mutations. 2010 Virology Result HBV L180M;M204V 108;121 113;126 P;RT;RT 94;105;118 104;107;120 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. In both the co-infected and mono-infected patients, the BCP A1762T and G1764A mutations were the most common mutations (Table 2a) but were significantly more frequent in the mono-infected patients (p=0.02 and 0.01 respectively). 2010 Virology Result HBV A1762T;G1764A 60;71 66;77 BCP 56 59 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. In order to determine whether the differences in frequencies of the BCP A1762T, G1764A, PreS2 deletions and -1G frameshift between the co-infected and mono-infected patients were influenced by genotype, we compared the co-infected and mono-infected patients within each HBV genotype (Table 2b). 2010 Virology Result HBV A1762T;G1764A 72;80 78;86 BCP;PreS2 68;88 71;93 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. The frequency of BCP A1762T and G1764A mutations was significantly higher in HBV mono-infected patients compared to co-infected patients with genotype C, but the frequency was similar in patients with HBV genotype A. 2010 Virology Result HBV A1762T;G1764A 21;32 27;38 BCP 17 20 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. The proportions of G1896A, pol rt M204V, pol rt L180M or PreS1 deletions were similar in both mono and co-infected patients. 2010 Virology Result HBV G1896A;M204V;L180M 19;34;48 25;39;53 P;P;PreS1;RT;RT 27;41;57;31;45 30;44;62;33;47 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. We examined the frequency of the following mutations in the HBV genomes of the mono-infected and co-infected patients: BCP A1762T and G1764A (reduced Precore mRNA transcription), Precore G1896A (W28 stop, failure to synthesize HBeAg), Pre S1 and PreS2 deletions (associated with accelerated disease progression in HBV mono-infection), and the -1G frameshift (associated with HIV co-infection). 2010 Virology Result HBV A1762T;G1764A;G1896A;W28X 123;134;187;195 129;140;193;203 BCP;C;PreS1;Precore;Precore;PreS2 119;227;235;150;179;246 122;232;241;157;186;251 HBV-HIV coinfections;HBV infections 375;314 391;332 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. By contribution of G1776A to HBeAg negativity was further verified in multivariate binary logistic regression analysis G1896A, a common mutation known to introduce a stop codon in e antigen, showed tendency in correlation to HBeAg negativity (P = 0.055; Table 5). 2010 BMC infectious diseases Result HBV G1776A;G1896A 19;119 25;125 C;C;C 180;29;225 189;34;230 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1776A statistically correlated to HBeAg negativity. 2010 BMC infectious diseases Result HBV G1776A 0 6 C 35 40 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1896A mutation in liver disease progression. 2010 BMC infectious diseases Result HBV G1896A 0 6 Liver disease 19 32 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. In univariate binary logistic regression analysis, all the top five high occurrence mutations seemed to relate to ALD, including T1753A/C (OR = 3.2, 95% CI: 1.3-7.9, P = 0.013), A1762T (OR = 3.1, 95% CI: 1.5-6.5, P = 0.003), G1764A (OR = 4.8, 95% CI: 2.1-10.9, P < 0.001), T1803A/G (OR = 5.1, 95% CI: 1-25.4, P = 0.058), and G1896A (OR = 2.4, 95% CI: 1.2-5.0, P = 0.015). 2010 BMC infectious diseases Result HBV T1753C;T1753A;A1762T;G1764A;T1803A;T1803G;G1896A 129;129;178;225;273;273;325 137;137;184;231;281;281;331 Liver disease 114 117 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Indeed subsequent multivariate binary logistic regression analysis indicated that only the mutation G1896A significantly correlated to the disease progression independent of age (P = 0.007, Table 3). 2010 BMC infectious diseases Result HBV G1896A 100 106 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Interestingly, in three previously reported common mutations G1764A, A1762T, and G1896A in this region, the first two types were observed with very high prevalence in these samples (70% and 67%, respectively) (Additional file 1, Table S2). 2010 BMC infectious diseases Result HBV G1764A;A1762T;G1896A 61;69;81 67;75;87 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Moreover, within a recently identified binding site for the transcription factor FXRalpha, G1776A was verified to associate with the HBeAg negativity significantly (P = 0.010). 2010 BMC infectious diseases Result HBV G1776A 91 97 C 133 138 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Patients with the combinations of more than 3 mutations were more likely to have ALD (OR = 3.1, 95% CI: 1.6-6.0, P = 0.001), although only one combination (T1753(A/C)/A1762T/G1764A) was dominant in these patients (FET, P = 0.025). 2010 BMC infectious diseases Result HBV A1762T;G1764A 167;174 173;180 Liver disease 81 84 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Patients with the G1896A (mean age 40 +- 11) had similar average age with those without this mutation (mean age 38 +- 14) but more had ALD (FET, P = 0.005, Table 1). 2010 BMC infectious diseases Result HBV G1896A 18 24 Liver disease 135 138 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. The top three combinations in all 192 patients were the double mutation A1762T/G1764A (36%), the triple mutation A1762T/G1764A/G1896A (11%), and the quadruple mutation T1753(A/C)/A1762T/G1764A/G1896A (8%). 2010 BMC infectious diseases Result HBV G1764A;G1764A;G1896A;A1762T;G1764A;G1896A;A1762T;A1762T 79;120;127;179;186;193;72;113 85;126;133;185;192;199;78;119 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Univariate binary logistic regression analysis showed significant correlation of several substitutions with the HBeAg negativity, including G1776A (OR = 8.1, 95% CI: 1.7-39; P = 0.009), A1846T (OR = 3.8, 95% CI: 1.2-11.8; P = 0.02), G1896A (OR = 3.5, 95% CI: 1.4-8.6; P = 0.007), and the number of individual point mutations >= 3 (OR = 2.8, 95% CI: 1.1-6.8; P = 0.027). 2010 BMC infectious diseases Result HBV G1776A;A1846T;G1896A 140;186;233 146;192;239 C 112 117 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Additionally, nine of the 17 mutations with Q215S had one or more L-nucleoside associated mutations. 2010 Antiviral research Result HBV Q215S 44 49 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Among these ten less well-characterized mutations, three were polymorphic (prevalence >0.5%) in the 2,804 pooled untreated individuals: Q215S (1.1%), I233V (0.7%), and NASH238T (2.8%). 2010 Antiviral research Result HBV Q215S;I233V 136;150 141;155 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. For these mutations, a significant association with L-nucleosides was present for L82M, A200V and Q215S and an association with ANPs was present for S85A (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01). 2010 Antiviral research Result HBV L82M;A200V;Q215S;S85A 82;88;98;149 86;93;103;153 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Supporting these associations were the findings that each of the viruses with L82M or A200V had one or more established L-nucleoside mutation (L180M and/or M204IV) and that each of the viruses with S85A had the ANP mutation N236T. 2010 Antiviral research Result HBV L82M;A200V;L180M;S85A;N236T 78;86;143;198;224 82;91;148;202;229 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Too few sequences from entecavir-treated individuals were available to identify treatment associations for two (I169T and M250V) of the four (I169T, T184SAILFG, S202GI, M250V) entecavir-associated mutation positions. 2010 Antiviral research Result HBV I169T;M250V;I169T;M250V 112;122;142;169 117;127;147;174 20875460 Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery. Twelve mutations at the eight of these 10 positions were significantly associated with N(t)RTI therapy (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01): L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were associated with the L-nucleoside analog lamivudine; A181S/T/V and N236T were associated with the ANP adefovir. 2010 Antiviral research Result HBV A181S;A181T;A181V;L80V;T184S;S202G;L80I;V173L;L180M;A181T;M204I;M204V;N236T 280;280;280;169;198;205;169;177;184;191;215;215;294 289;289;289;175;203;210;175;182;189;196;222;222;299 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Compared to control cells transfected with pCMV-Tag1, MxA mRNA expression induced by IFN-alpha in Huh7 cells transfected with WT and mutated HBc proteins (L60V, I97L and S87G) was decreased to 69.1%, 69.1%, 21.9% and 73.1%, respectively (Figure 1A), suggesting the L60V and S87G mutated proteins have a similar effect to WT (p > 0.05). 2010 Virology journal Result HBV L60V;I97L;S87G;L60V;S87G 155;161;170;265;274 159;165;174;269;278 C 141 144 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In contrast, I97L HBc protein remarkedly decreased the level of MxA mRNA compared to WT (p < 0.01). 2010 Virology journal Result HBV I97L 13 17 C 18 21 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In order to evaluate whether the inhibition of MxA transcription by HBc protein could decrease the inhibitory effect on HBV replication induced by IFN-alpha, pU19-1.24HBV was co-transfected with Renilla luciferase vector into Huh7 cells stably expressing WT HBc protein, L60V, S87G and I97L mutated proteins, respectively. 2010 Virology journal Result HBV L60V;S87G;I97L 271;277;286 275;281;290 C;C 68;258 71;261 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In the stable expression cells after addition of IFN-alpha, the MxA mRNA levels in the WT, L60V, I97L, S87G and pCMV vector only transfected cells were increased by 5.91-fold, 5.33-fold, 1.80-fold, 8.30-fold, and 20-fold respectively compared to those without IFN-alpha (Figure 2A). 2010 Virology journal Result HBV L60V;I97L;S87G 91;97;103 95;101;107 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Our data showed that the promoter activity of MxA gene in the Huh7 cells transfected with WT and mutated HBc proteins (L60V, I97L and S87G) was decreased to 55.2%, 53.3%, 24.1% and 55.9%, respectively (Figure 1B) compared to the control cells transfected with pCMV-Tag1. 2010 Virology journal Result HBV L60V;I97L;S87G 119;125;134 123;129;138 C 105 108 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. This result showed that I97L HBc protein could remarkably decrease the MxA promoter activity induced by IFN-alpha compared to the WT or other two mutated HBc proteins (L60V or S87G) (p < 0.01). 2010 Virology journal Result HBV I97L;L60V;S87G 24;168;176 28;172;180 C;C 29;154 32;157 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. We observed the similar result that WT and hot-spot mutant HBcs inhibitted MxA mRNA expression in stably transfected cells and mutant I97L has most dramatic effect (Fig 2A), this is consistent with our finding in transiently transfected cells (Fig 1). 2010 Virology journal Result HBV I97L 134 138 C 59 63 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In comparison, T123N and M133I/V/T missed in diagnostic assays presented more altered antigenic index profiles, while T143L showed similar if not lesser degree of changes (Table 1). 2010 Virology journal Result HBV M133I;M133V;M133T;T123N;T143L 25;25;25;15;118 34;34;34;20;123 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In contrast, only a small antigenicity change was detected (from -0.2 to -0.05) at the single amino acid site of M133L substitution. 2010 Virology journal Result HBV M133L 113 118 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In pattern T123A, the loop containing the 'a' determinant seemed to shift slightly compared to the reference wild-type. 2010 Virology journal Result HBV T123A 11 16 S 43 57 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In T123A substitution, several amino acids were affected by this single substitution. 2010 Virology journal Result HBV T123A 3 8 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Most significant changes were observed in the T143M substitution. 2010 Virology journal Result HBV T143M 46 51 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Of the four nucleotide substitutions, three single mutation patterns (T123A, M133L and T143M) of HBV surface protein were observed, while A562G was found to be a silent mutation. 2010 Virology journal Result HBV T123A;M133L;T143M;A562G 70;77;87;138 75;82;92;143 S 101 108 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Sequencing of partial HBV surface gene of the clones derived from 25 HBV DNA positive samples showed nucleotide substitutions in 7 samples: A521G in one sample, A551T and A562G in one sample, and C582T in five samples. 2010 Virology journal Result HBV A521G;A551T;A562G;C582T 140;161;171;196 145;166;176;201 S 26 33 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Similar shift in loop structure was observed in pattern M133L, as could be shown in the different orientation of Leu side chain in position 133 compared to Met side chain in the wild-type. 2010 Virology journal Result HBV M133L 56 61 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. The pattern T143M, on the other hand, besides showing differentially-oriented side chain of Met, also showed significant changes in larger part of the loop. 2010 Virology journal Result HBV T143M 12 17 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. These mutation positions corresponded with those of five isolates known to be associated with problem in diagnostic assays and/or escape to vaccine/HBIg therapy: T123N, M133I, M133T, M133V, and T143L (Figure 1). 2010 Virology journal Result HBV T123N;M133I;M133T;M133V;T143L 162;169;176;183;194 167;174;181;188;199 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. Of the remaining eighteen patients in the study, sixteen showed no HBV mutations, whereas one had lamivudine resistant HBV M204V/I mutation and another showed adefovir dipivoxil resistant HBV A181T/V mutation. 2010 Mediators of inflammation Result HBV M204V;M204I;A181T;A181V 123;123;192;192 130;130;199;199 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. Of the two patients with consistently elevated HBV DNA load (Figure 3), one patient had HBV A181T/V mutations that are associated with adefovir dipivoxil resistance and another patient had HBV M204V/I mutations of lamivudine resistance. 2010 Mediators of inflammation Result HBV A181T;A181V;M204V;M204I 92;92;193;193 99;99;200;200 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. Persistently elevated serum ALT and AST were detected in the patient with adefovir dipivoxil resistant HBV A181T/V mutations (Figure 3). 2010 Mediators of inflammation Result HBV A181T;A181V 107;107 114;114 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. The patient with the lamivudine resistant HBV M204V/I mutations showed a similar Th1/Th2 cytokine response with the nonmutation patients; however, the patient with adefovir dipivoxil resistant HBV A181T/V mutations presented with persistent lower levels of Th1/Th2 cytokines producing CD3+CD4+ T-cells. 2010 Mediators of inflammation Result HBV M204V;M204I;A181T;A181V 46;46;197;197 53;53;204;204 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, M250V) that have been reported in the reverse transcriptase regions of HBV polymerase gene in association with the HBV resistance to the treatment of nucleoside and nucleotide analogs. 2010 Mediators of inflammation Result HBV T184G;T184S;T184A;T184C;I169T;V173L;L180M;A181V;A181T;A194T;S202G;S202I;M204V;M204I;N236T;M250V 107;107;107;107;77;84;91;98;98;120;127;127;136;136;145;152 118;118;118;118;82;89;96;105;105;125;134;134;143;143;150;157 P;RT 227;190 237;211 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. A total of four nucleotide mismatches (T36G, A299G, T432C, and C666T) between pcDNA3-Y100C and pcDNA3-SA1 was found along the 681-bp fragment of S gene (not shown). 2011 Hepatitis research and treatment Result HBV T36G;A299G;T432C;C666T;Y100C 39;45;52;63;85 43;50;57;68;90 S 145 146 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. HBsAg levels detected in extracellular medium were about 27-fold and 15-fold higher than that of cells extracts with pcDNA3-SA1 and pcDNA3-Y100C plasmids, respectively. 2011 Hepatitis research and treatment Result HBV Y100C 139 144 S 0 5 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. HBsAg levels detected in medium of transfected cells with pcDNA3-SA1 ranged from 700 to 800 ng/mL (mean and median values of 740 ng/mL (corresponding to 144 IU) and 720 ng/mL (143 IU), resp.), while variation in pcDNA3-Y100C construct ranged from 790 to 1200 ng/mL (mean and median values of 1.013 ng/mL (230 IU) and 1.050 ng/mL (250 IU), resp.). 2011 Hepatitis research and treatment Result HBV Y100C 219 224 S 0 5 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. HBsAg levels of medium and cells extracts of pcDNA3-SA1 and pcDNA3-Y100C constructs, tested in three independent transfection assays, were shown in Figure 2. 2011 Hepatitis research and treatment Result HBV Y100C 67 72 S 0 5 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Nucleotide sequencing of HBV S gene inserted in recombinant expression plasmids pcDNA3-SA1 and pcDNA3-Y100C had confirmed the high similarity between both sequences. 2011 Hepatitis research and treatment Result HBV Y100C 102 107 S 29 30 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Overall, the mean values of extracellular HBsAg of pcDNA3-Y100C plasmid were 1.5-fold higher than those observed when the wild-type plasmid was transfected. 2011 Hepatitis research and treatment Result HBV Y100C 58 63 S 42 47 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. The A299G is the only nonsynonymous substitution changing amino acid Y to C in HBsAg residue 100 of small S protein (Figure 1). 2011 Hepatitis research and treatment Result HBV A299G 4 9 S;S 79;100 84;107 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. The difference between the amount of HBsAg produced by pcDNA3-SA1 and pcDNA3-Y100C was not significant (P = .13). 2011 Hepatitis research and treatment Result HBV Y100C 77 82 S 37 42 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Values of HBsAg detected in cell extracts were much lower than those in medium with both plasmids (pcDNA3-SA1 and pcDNA3-Y100C), indicating that S-HBsAg was secreted well in both cases. 2011 Hepatitis research and treatment Result HBV Y100C 121 126 S;S 10;145 15;152 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. By contrast, rtM204I was more often accompanied by rtL80I (36.5%) than rtM204V (3.9%). 2011 Journal of viral hepatitis Result HBV M204I;L80I;M204V 15;53;73 20;57;78 RT;RT;RT 13;51;71 15;53;73 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Of LAM-resistant mutations, rtM204V was usually concomitant with rtL180M +- V173L. 2011 Journal of viral hepatitis Result HBV M204V;L180M;V173L 30;67;76 35;72;81 RT;RT 28;65 30;67 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Of the resistance mutations detected in patients who received monotherapies, rtM204I (32.2%), rtM204V + L180M +- V173L (32.2%) and rtM204I + L180M +- V173L (21.0%) were dominant patterns for LAM; rtN236T + A181T and/or rtA181V (34.3%), rtN236T (31.4%) and rtA181V (28.6%) were dominant patterns for ADV, and mutations containing rtM204I were dominant patterns for LdT. 2011 Journal of viral hepatitis Result HBV M204I;N236T;A181V;A181V;M204V;M204I;N236T;M204I;L180M;V173L;L180M;V173L;A181T 79;198;221;258;96;133;238;331;104;113;141;150;206 84;203;226;263;101;138;243;336;109;118;146;155;211 RT;RT;RT;RT;RT;RT;RT;RT 77;94;131;196;219;236;256;329 79;96;133;198;221;238;258;331 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Patients harbouring the rtM204I + L180M mutant had higher ALT levels than those harbouring the rtM204I mutant alone [median (Q1, Q3) 41 (28, 69) U/L vs 32 (22, 53) U/L, P < 0.01]. 2011 Journal of viral hepatitis Result HBV M204I;M204I;L180M 26;97;34 31;102;39 RT;RT 24;95 26;97 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Table 4 summarizes the incidence of the purported mutations under different NA treatment schedules, including rtV84M, rtA181T/S (alone), rtV214A, rtQ215S, rtL217R and rtI233V. 2011 Journal of viral hepatitis Result HBV Q215S;L217R;V84M;A181T;A181S;V214A;Q215S;L217R;I233V 148;157;112;120;120;139;148;157;169 153;162;117;128;128;145;154;163;175 RT;RT;RT;RT;RT;RT 110;118;137;146;155;167 112;120;139;148;157;169 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The frequencies of rtM204I with/without rtL180M were significantly different between genotypes C and B (44.6%/55.4%vs 19.4%/80.6%, P < 0.01). 2011 Journal of viral hepatitis Result HBV M204I;L180M 21;42 26;47 RT;RT 19;40 21;42 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The incidence of rtV84M, rtA181T and rtV214A was relatively high, whereas the incidence of rtQ215S, rtL217R and rtI233V was quite low. 2011 Journal of viral hepatitis Result HBV V84M;A181T;I233V;V214A;Q215S;L217R 19;27;114;39;93;102 23;32;119;44;98;107 RT;RT;RT;RT;RT;RT 17;25;37;91;100;112 19;27;39;93;102;114 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The mutation rtA194T with potential resistance to TDF [29] was not detected. 2011 Journal of viral hepatitis Result HBV A194T 15 20 RT 13 15 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The mutational patterns of the two strains were rtL180M + A181V + S202G + M204V + N236T and rtL180M + S202G + M204V + N236T (GenBank accession numbers: GQ402161 and GQ402162), respectively. 2011 Journal of viral hepatitis Result HBV L180M;L180M;A181V;S202G;M204V;N236T;S202G;M204V;N236T 50;94;58;66;74;82;102;110;118 55;99;63;71;79;87;107;115;123 RT;RT 48;92 50;94 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The patterns of rtA181T/S together with signature resistance mutations are presented in 2, 3. 2011 Journal of viral hepatitis Result HBV A181T;A181S 18;18 25;25 RT 16 18 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. Of the 13 patients in the ICP group, only two (15.4%) exhibited CP mutations, including one A1762T/G1764A mutation. 2011 Journal of Korean medical science Result HBV G1764A;A1762T 99;92 105;98 Core promoter 64 66 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. Only one (5.5%) of the 18 ITP patients had the G1764A mutation and 1 had the A1762T/G1764A mutation (Table 2). 2011 Journal of Korean medical science Result HBV G1764A;G1764A;A1762T 84;47;77 90;53;83 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. The distributions of both the precore and CP mutations did not differ significantly (A1762T, P = 0.788; G1764A, P = 0.447; G1896A, P = 0.387, chi-squared test; Table 2). 2011 Journal of Korean medical science Result HBV A1762T;G1764A;G1896A 85;104;123 91;110;129 Core promoter;Precore 42;30 44;37 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations correlated with G1896A variation and the decrease in serum HBV DNA levels. 2011 Virology journal Result HBV A336T;T337C;A336C;G1896A 6;12;0;45 11;17;5;51 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations in HBV core gene were determined with a modified PCR-RFLP assay on total 166 serum samples collected from chronic hepatitis B patients. 2011 Virology journal Result HBV A336T;T337C;A336C 6;12;0 11;17;5 C 36 40 Chronic Hepatitis B 135 154 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations occurred in 26/87 (29.9%) chronic hepatitis B patients with genotype B and 14/79 (17.7%) patients with genotype C, and Chi-square test showed that there was no significant difference in the rate of A336C/A336T/T337C variations between HBV genotype B and C (chi2 = 3.3, P = 0.07, See Table 2). 2011 Virology journal Result HBV A336T;T337C;A336T;T337C;A336C;A336C 6;12;233;239;0;227 11;17;238;244;5;232 Chronic Hepatitis B 55 74 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C/A336T/T337C variations occurred in 40/166(24.1%) chronic hepatitis B patients without any antiviral therapy (See Table 2). 2011 Virology journal Result HBV A336T;T337C;A336C 6;12;0 11;17;5 Chronic Hepatitis B 55 74 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Chi-square test showed C336/T336/C337 variants were more frequent in chronic hepatitis B patients with A1896 variants than those with the wild type G1896 (chi2 = 4.7, P = 0.03), suggesting that A336C/A336T/T337C variations correlated closely with G1896A variation (See Table 2). 2011 Virology journal Result HBV A336T;T337C;A336C;G1896A 200;206;194;247 205;211;199;253 Chronic Hepatitis B 69 88 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Furthermore, Chi-square test also showed that the presence of A1896 variant, age 35 years, HBV genotype B and serum HBV DNA levels <6.0 were also related closely to spontaneous HBeAg loss in chronic hepatitis B patients (See Table 3), therefore, A336C/A336T/T337C variations, serum HBV DNA levels, G1896A variation, age and HBV genotype were entered into a binary logistic regression model to determine which was the independent factor associating with spontaneous HBeAg loss. 2011 Virology journal Result HBV A336T;T337C;A336C;G1896A 253;259;247;299 258;264;252;305 C;C 178;466 183;471 Chronic Hepatitis B 192 211 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. G1896A was the most common variation in precore gene and occurred in 75/166(45.2%) chronic hepatitis B patients in this study. 2011 Virology journal Result HBV G1896A 0 6 Precore 40 47 Chronic Hepatitis B 83 102 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. RFLP patterns and A336C/A336T/T337C variations in chronic hepatitis B patients. 2011 Virology journal Result HBV A336T;T337C;A336C 24;30;18 29;35;23 Chronic Hepatitis B 50 69 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Sequencing also showed that A336C/A336T/T337C variations occurred in serum samples presenting with RFLP patterns G and C/G mixture (A336C/A336T/T337C variations were found in part of HBV DNA from serum samples with RFLP patterns C/G mixture, therefore, serum samples showing RFLP C/G mixture were also considered to be presence of C336/T336/C337 variants). 2011 Virology journal Result HBV A336T;T337C;A336T;T337C;A336C;A336C 34;40;138;144;28;132 39;45;143;149;33;137 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Sequencing of HBV core gene demonstrated complete match between RFLP patterns and SNPs (single nucleotide polymorphisms) A336C/A336T/T337C (data not shown). 2011 Virology journal Result HBV A336T;T337C;A336C 127;133;121 132;138;126 C 18 22 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. A unique melting pattern from a patient sample, showing a mixture of G1899A and G1896A/G1899A, is shown in Figure 5A. 2011 Journal of clinical virology Result HBV G1899A;G1899A;G1896A 87;69;80 93;75;86 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. In the case when G1896A and G1899A were present as a mixture, their "total" titer could be quantified using the probe SPC1. 2011 Journal of clinical virology Result HBV G1896A;G1899A 17;28 23;34 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Mutations at nt 1896-1899 were limited to G1896A, G1899A, G1896A/G1899A or their mixtures, with the exception of 2 cases in which G1898A was detected. 2011 Journal of clinical virology Result HBV G1899A;G1896A;G1899A;G1896A;G1898A 65;42;50;58;130 71;48;56;64;136 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Other patterns (7-9, 11-16) did not possess G1896A or G1899A mutation; they had melting temperatures lower than that of the WT (not shown) thus would not interfere with the quantification of the three target mutations. 2011 Journal of clinical virology Result HBV G1896A;G1899A 44;54 50;60 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Our assay revealed the presence of G1896A in 19/20 patients and G1899A in 16/20 samples. 2011 Journal of clinical virology Result HBV G1896A;G1899A 35;64 41;70 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. SPC1 had higher melting temperatures with the three targeted mutants (G1896A, G1899A and G1896A/G1899A) than with the WT and others. 2011 Journal of clinical virology Result HBV G1899A;G1896A;G1899A;G1896A 96;70;78;89 102;76;84;95 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Ultrasensitive quantification of the precore G1896A and G1899A mutants. 2011 Journal of clinical virology Result HBV G1896A;G1899A 45;56 51;62 Precore 37 44 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. We measured G1896A and/or G1899A mutations in 20 HBeAg-positive patient samples which had no detectable precore mutants by manual sequencing reading. 2011 Journal of clinical virology Result HBV G1896A;G1899A 12;26 18;32 C;Precore 49;104 54;111 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. When small amount of G1896A or G1899A co-existed with the WT, it was difficult to distinguish between G1896A and G1899A by SimpleProbe SPC1. 2011 Journal of clinical virology Result HBV G1896A;G1899A;G1896A;G1899A 21;31;102;113 27;37;108;119 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. In addition to the TA mutant, we studied three HBx mutants in the genotype C background that corresponded to the following core promoter mutations: (1) T1753A, (2) T1768A, (3) combination of T1753A, TA, and T1768A (Combo mutant). 2011 Gastroenterology Result HBV T1753A;T1768A;T1753A;T1768A 152;164;191;207 158;170;197;213 Core promoter;X 123;47 136;50 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. We also constructed plasmids encoding mutant HBx (K130M, V131I) proteins of all three genotypes, corresponding to the core promoter TA mutation. 2011 Gastroenterology Result HBV K130M;V131I 50;57 55;62 Core promoter;X 118;45 131;48 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. A1762T/G1764A double mutation existed in all clones, and G1896A existed in 4 clones obtained from all time points. 2011 Hepatitis research and treatment Result HBV G1764A;A1762T;G1896A 7;0;57 13;6;63 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. Further analysis of the nucleotide sequence at all three time points indicated that nucleotides T361A, C934A, C2351T/A2353T, and C2444T were the mutation been kept in for at least two years' evolution. 2011 Hepatitis research and treatment Result HBV A2353T;T361A;C934A;C2351T;C2444T 117;96;103;110;129 123;101;108;116;135 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. Nucleotides C339T and T770C were the new and major mutation at the 3rd time point, and these mutations caused HBsAg P62L and polymerase (Pol) V560A mutation, respectively (Figure 1). 2011 Hepatitis research and treatment Result HBV C339T;T770C;P62L;V560A 12;22;116;142 17;27;120;147 S;P;P 110;137;125 115;140;135 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. Premature stop codons of S gene (g.200C>T, g.565T>A, g.361T>A, g.455C>T, and g.304_305CC>TT) increased during the course(1/9 versus 3/9 versus 6/8) (Figure 2). 2011 Hepatitis research and treatment Result HBV C200T;T565A;T361A;C455T;C304T;C305T 33;43;53;63;77;77 41;51;61;71;91;91 S 25 26 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. These mutations caused nonsense mutation of preS1 and preCore/Core gene (T361A and C2444T, resp.), missense mutation of precore/core and pol gene (C2351T/A2353T and C934A, resp.). 2011 Hepatitis research and treatment Result HBV A2353T;T361A;C2444T;C2351T;C934A 154;73;83;147;165 160;78;89;153;170 C;C;P;Precore;Precore;PreS1 62;128;137;54;120;44 66;132;140;61;127;49 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. 1611-1619 was shown in Table 2, in which 26% of the NRE sequences contain G1613A mutation. 2011 PloS one Result HBV G1613A 74 80 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Although the discrepancy between sexes is unclear, the analysis suggests that high viral load could be one of the consequences of the G1613A mutation in HBV. 2011 PloS one Result HBV G1613A 134 140 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. As shown in Figure 3C and 3D, the level of intracellular HBV DNA intermediates was not affected whereas the level of extracellular HBV DNA significantly increased in G1613A mutants. 2011 PloS one Result HBV G1613A 166 172 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Association of the prevalence of G1613A mutation to high viral load in chronic HBV carriers. 2011 PloS one Result HBV G1613A 33 39 Chronic Hepatitis B 71 82 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Effect of G1613A mutation on HBV transcripts. 2011 PloS one Result HBV G1613A 10 16 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. G1613A mutation affects nuclear proteins binding on NRE. 2011 PloS one Result HBV G1613A 0 6 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. G1613A mutation drastically suppresses HBeAg secretion and enhances viral DNA production in vitro . 2011 PloS one Result HBV G1613A 0 6 C 39 44 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. G1613A mutation drastically suppresses HBeAg secretion and enhances viral DNA production in vitro. 2011 PloS one Result HBV G1613A 0 6 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In contrast, the G1613A mutation significantly decreased the extracellular HBeAg level by 90% (pA1 vs pG1) and 86% (pA2 vs pG2) (Figure 2D). 2011 PloS one Result HBV G1613A 17 23 C 75 80 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In fact, the G1613A mutation locates within the conserved regions of PRE on HBV RNAs. 2011 PloS one Result HBV G1613A 13 19 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In our previous study, we showed the G1613A mutation is a hotspot mutation in HBV subgenotype Cs in HCC patients. 2011 PloS one Result HBV G1613A 37 43 Hepatocellular carcinoma 100 103 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Intriguingly, the G1613A mutation on the NREgamma site further matches the consensus RFX1 binding sequence, which is consistent to our result that the C2 complex showed higher affinity to mutant than wild-type DNA. 2011 PloS one Result HBV G1613A 18 24 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Moreover, the G1613A mutation can alter the binding of RFX1 binding to NRE, in which that the RFX1 protein favors for the A1613 mutant then the wild-type. 2011 PloS one Result HBV G1613A 14 20 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Moreover, the prevalence of the G1613A mutation is significantly associated to higher viral load in female carriers in a univariate analysis. 2011 PloS one Result HBV G1613A 32 38 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. On the other hand, G1613A mutation significantly increased the level of extracellular HBV DNA by 2 folds (pA1 vs pG1) and 4 folds (pA2 vs pG2) respectively (Figure 3B). 2011 PloS one Result HBV G1613A 19 25 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Our results implied that two different binding mechanisms are involved in NRE in the context of G1613A mutation, and the mutation can modify the binding of two nuclear protein complexes to NRE region. 2011 PloS one Result HBV G1613A 96 102 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. RFX1 protein binds on the NRE and transactivates the core promoter activity corresponds to the G1613A mutation. 2011 PloS one Result HBV G1613A 95 101 Core promoter 53 66 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Since the BCP mutation has high prevalence in HCC patients, it is used (pG1 and pA1) as an independent control to evaluate the effect of G1613A mutation. 2011 PloS one Result HBV G1613A 137 143 BCP 10 13 Hepatocellular carcinoma 46 49 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The higher prevalence of the G1613A mutation in HCC patients. 2011 PloS one Result HBV G1613A 29 35 Hepatocellular carcinoma 48 51 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The level of HBV RNA transcription does not change significantly when compared with HBeAg and HBV DNA levels, suggesting that the G1613A mutation may exert its effect at the posttranscriptional regulation level. 2011 PloS one Result HBV G1613A 130 136 C 84 89 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. These results suggest that RFX1 plays a significant role on regulating HBV core promoter via G1613A mutation on NRE. 2011 PloS one Result HBV G1613A 93 99 Core promoter 75 88 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. These results suggest that the G1613A mutation suppressed the HBeAg secretion and enhance total HBV DNA synthesis. 2011 PloS one Result HBV G1613A 31 37 C 62 67 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. This implied that the RFX1 could possibly be one of the protein complexes which binding to NRE can be modulated by G1613A mutation. 2011 PloS one Result HBV G1613A 115 121 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. To characterize the relationship between the HBV viral load and the G1613A mutation, we quantified the serum viral load in 255 chronic HBV carriers as described in the previous study. 2011 PloS one Result HBV G1613A 68 74 Chronic Hepatitis B 127 138 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. To demonstrate the effect of the mutations on the HBsAg and HBeAg production, 1.3x HBV genomes of subgenotype Cs with the same genetic background but different combination of the G1613A and BCP mutations were constructed (pG1, pA1, pG2 and pA2) and transfected into HuH7 cells. 2011 PloS one Result HBV G1613A 179 185 BCP;C;S 190;60;50 193;65;55 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. To further investigate the functional effect of the G1613A mutation on viral transcription, Northern blot analysis was performed to measure the relative amount of the HBV transcripts after the transfection of the 1.3x HBV genomes (Figure 4). 2011 PloS one Result HBV G1613A 52 58 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. To further investigate the role of the RFX1 on HBV core promoter via G1613A mutation, C-terminally myc-tagged RFX1 protein was overexpressed in HuH7 cells. 2011 PloS one Result HBV G1613A 69 75 Core promoter 51 64 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. To gain insight into the molecular effect of the G1613A mutation, NRE DNA binding with nuclear proteins was studied using EMSA. 2011 PloS one Result HBV G1613A 49 55 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. We showed that the G1613A mutation was found with higher prevalence in HCC patients in all HBV genoytpes (Table 1). 2011 PloS one Result HBV G1613A 19 25 Hepatocellular carcinoma 71 74 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Factors associated with development of rtA181T mutant. 2011 BMC cancer Result HBV A181T 41 46 RT 39 41 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. In these patients, the rtA181T mutation was accompanied by the sW172* mutation in the S reading frame. 2011 BMC cancer Result HBV A181T;W172X 25;63 30;69 RT;S;S 23;63;86 25;64;87 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. It was found that age > 50 years (P = 0.001), the presence of rtA181T mutation (P < 0.001), BCP A1762T/G1764A mutations (P = 0.002) and liver cirrhosis (P < 0.001) were significantly associated with severe liver consequences. 2011 BMC cancer Result HBV G1764A;A181T;A1762T 103;64;96 109;69;102 BCP;RT 92;62 95;64 Liver cirrhosis 136 151 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. It was found that only age > 50 years (P = 0.001), the presence of rtA181T mutation (P < 0.001), and liver cirrhosis (P < 0.001) were significantly associated with occurrence of HCC (Figure 2). 2011 BMC cancer Result HBV A181T 69 74 RT 67 69 Liver cirrhosis;Hepatocellular carcinoma 101;178 116;181 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. It was found that only older age was significantly associated with development of rtA181T mutant (OR, 1.144; 95%CI, 1.056-1.240; P = 0.001). 2011 BMC cancer Result HBV A181T 84 89 RT 82 84 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Multivariate Cox proportional hazards regression analysis using the forward stepwise model showed rtA181T to be the only variable that remained in the equation as an independent predictor (Hazard Ratio, 13.091; 95% CI, 3.255 to 52.653; P < 0.001). 2011 BMC cancer Result HBV A181T 100 105 RT 98 100 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Multivariate Cox proportional hazards regression analysis using the forward stepwise model showed rtA181T to be the only variable that remained in the equation as an independent predictor (Hazard Ratio, 21.443; 95% CI, 3.556 to 129.302; P = 0.001). 2011 BMC cancer Result HBV A181T 100 105 RT 98 100 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Notably, in the three patients with rtA181T mutants (patients-1 to 3), a relatively high level of HBV-DNA (> 104 copies/mL) persisted for at least 10 months. 2011 BMC cancer Result HBV A181T 38 43 RT 36 38 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Since rtA181T mutation was identified as an independent predictor for severe consequences of liver disease including HCC and liver failure, linear regression analysis was performed to identify factors associated with emergence of rtA181T mutation (Table 3). 2011 BMC cancer Result HBV A181T;A181T 8;232 13;237 RT;RT 6;230 8;232 Liver disease;Hepatocellular carcinoma 93;117 106;120 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The difference in the prevalence of BCP A1762T/G1764A mutation between genotype B and C HBV was statistically significant (P < 0.001; Table 1). 2011 BMC cancer Result HBV G1764A;A1762T 47;40 53;46 BCP 36 39 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The rtA181T mutation was detected in 10 patients. 2011 BMC cancer Result HBV A181T 6 11 RT 4 6 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. It is obvious that the pattern of rtM204I alone was dominantly observed (36.26%), followed by rtM204V + rtL180M (23.08%), while other mutation patterns were rare. 2011 Medical science monitor Result HBV M204I;M204V;L180M 36;96;106 41;101;111 RT;RT;RT 34;94;104 36;96;106 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A C-to-T mutation at nucleotide 1653 occurred in 45% of HCC group 1 and 19% of non-HCC group 1 (p < 0.05). 2011 BMC cancer Result HBV C1653T 2 36 Hepatocellular carcinoma;Hepatocellular carcinoma 56;83 59;86 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A G-to-A mutation at nucleotide 1613 occurred in 38% of HCC group 1 and 10% of non-HCC group 1 (p < 0.008). 2011 BMC cancer Result HBV G1613A 2 36 Hepatocellular carcinoma;Hepatocellular carcinoma 56;83 59;86 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. However, the BCP mutation was frequently found in conjunction with the G1613A mutation or the C1653T mutation. 2011 BMC cancer Result HBV G1613A;C1653T 71;94 77;100 BCP 13 16 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. Statistical analysis revealed that G1613A and C1653T mutations were dependent on each other. 2011 BMC cancer Result HBV G1613A;C1653T 35;46 41;52 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The A1762T/G1764A BCP mutation rate was not different between HCC group 1 and non-HCC group 1 (75% vs. 2011 BMC cancer Result HBV G1764A;A1762T 11;4 17;10 BCP 18 21 Hepatocellular carcinoma;Hepatocellular carcinoma 62;82 65;85 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The C1653T mutation was found in 27% of HBeAg-positive patients and in 31% of HBeAg-negative patients (N.S.). 2011 BMC cancer Result HBV C1653T 4 10 C;C 40;78 45;83 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The following characteristics, which were proven to be statistically significant with univariate analysis, were used for multiple logistic regression analysis: age >=45 years, male, and the G1613A mutation. 2011 BMC cancer Result HBV G1613A 190 196 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The following characteristics, which were proven to be statistically significant with univariate analysis, were used for multiple logistic regression analysis: age >=45, Plt (x104/mul) <=14, ALT (>=70), and the presence of G1613A and C1653T. 2011 BMC cancer Result HBV G1613A;C1653T 223;234 229;240 X 175 176 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The G1613A and/or the C1653T mutations were found at a significantly lower frequency in the non-HCC group 2. 2011 BMC cancer Result HBV G1613A;C1653T 4;22 10;28 Hepatocellular carcinoma 96 99 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The G1613A mutation was found in 32% of HBeAg-positive patients and 24% of HBeAg-negative patients (N.S. 2011 BMC cancer Result HBV G1613A 4 10 C;C 40;75 45;80 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The odds ratio of the BCP mutation was 8.2 in the G1613A mutant and 4.62 in the C1653T mutant as compared to wild type (p < 0.05). 2011 BMC cancer Result HBV G1613A;C1653T 50;80 56;86 BCP 22 25 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The presence of the G1613A mutation was significantly higher in the group that later developed HCC. 2011 BMC cancer Result HBV G1613A 20 26 Hepatocellular carcinoma 95 98 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The rate of the G1613A and C1653T mutations was 50% and 50% in HCC group 2, while each of these mutations was found in only 12% of the non-HCC group 2 (p < 0.05). 2011 BMC cancer Result HBV G1613A;C1653T 16;27 22;33 Hepatocellular carcinoma;Hepatocellular carcinoma 63;139 66;142 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The rate of the G1613A and C1653T mutations were significantly higher in patients with HCC (Table 4). 2011 BMC cancer Result HBV G1613A;C1653T 16;27 22;33 Hepatocellular carcinoma 87 90 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The rate of the G1613A mutation was significantly higher in isolates with the C1653T mutation as compared to isolates without the C1653T mutation (65% vs. 2011 BMC cancer Result HBV G1613A;C1653T;C1653T 16;78;130 22;84;136 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. To evaluate the effect of the mutations on the development of HCC, multiple logistic regression analysis was performed with the clinical features and the G1613A and C1653T mutations (Table 6). 2011 BMC cancer Result HBV G1613A;C1653T 154;165 160;171 Hepatocellular carcinoma 62 65 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. A 10th patient was excluded because the patient's virus had the M204I mutation at the initiation of HAART and further investigation revealed that this patient had previously been on zidovudine AZT/3TC dual therapy when the mutation was likely to have emerged. 2011 BMC research notes Result HBV M204I 64 69 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. The M204V mutation was always accompanied by the mutation L180M. 2011 BMC research notes Result HBV M204V;L180M 4;58 9;63 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. The virus from patient 12 had an S219A mutation, which reverted to the wild-type when 3TC resistance mutations V173L, L180M and M204V were acquired. 2011 BMC research notes Result HBV S219A;V173L;L180M;M204V 33;111;118;128 38;116;123;133 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Four different LAM resistance patterns were identified in 84 out of 194 patients (43%): baseline primary mutation (rtM204I/V, n = 26), primary mutation with the compensatory mutations rtL80I/V (n = 16) or rtL180M (n = 24), triple mutant (rtM204I/V + rtV173L + rtL180M or rtA194G, n = 12), and the single mutation rtL180M (n = 6). 2011 Hepatitis monthly Result HBV M204I;M204V;L80I;L80V;L180M;M204I;M204V;V173L;L180M;A194G;L180M 117;117;186;186;207;240;240;252;262;273;315 124;124;192;192;212;247;247;257;267;278;320 RT;RT;RT;RT;RT;RT;RT;RT 115;184;205;238;250;260;271;313 117;186;207;240;252;262;273;315 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. N236T) were most frequently detected. 2011 Hepatitis monthly Result HBV N236T 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Single compensatory mutations were not detected in the switch therapy group; however, rtQ215H/P/S +- rtV214A/P mutations were found in 12 out of 88 patients (14%) in the add-on therapy group, and this difference was significant (P < 0.01). 2011 Hepatitis monthly Result HBV Q215H;Q215P;Q215S;V214A;V214P 88;88;88;103;103 97;97;97;110;110 RT;RT 86;101 88;103 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The ETV-resistance mutation rtM204I/V + rtL180M + rtT184A/I/S or rtS202C was found in 10 out of 194 patients (5%). 2011 Hepatitis monthly Result HBV M204I;M204V;T184A;T184I;T184S;L180M;S202C 32;32;56;56;56;46;71 39;39;65;65;65;51;76 RT;RT;RT;RT 30;44;54;69 32;46;56;71 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The ADV-associated mutations rtA181T/V, rtN236T, and rtA181T + rtN236T were detected in 6, 8, and 2 patients, respectively (for a total of 16 out of 194 patients, or 8%). 2011 Hepatitis monthly Result HBV A181T;A181V;A181T;N236T;N236T 31;31;55;42;65 38;38;60;47;70 RT;RT;RT;RT 29;40;53;63 31;42;55;65 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The most frequent mutations detected in response to LAM treatment were rtM204I/V and rtL180M Table 2. 2011 Hepatitis monthly Result HBV M204I;M204V;L180M 73;73;87 80;80;92 RT;RT 71;85 73;87 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The observed patterns of LdT resistance included baseline primary mutations (rtM204I, n = 24) associated with the compensatory mutations rtL80I/V or rtL180M (n = 28) and triple mutants (rtM204I + rtV173L + rtL180M or rtL80I/V, n = 8; Table 1). 2011 Hepatitis monthly Result HBV L80I;L80V;L80I;L80V;M204I;L180M;M204I;V173L;L180M 139;139;219;219;79;151;188;198;208 145;145;225;225;84;156;193;203;213 RT;RT;RT;RT;RT;RT;RT 77;137;149;186;196;206;217 79;139;151;188;198;208;219 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Two patients in the add-on therapy group had sC137G amino acid substitutions (with rtL80M + rtM204I mutations), 2 patients in the switch therapy group had sG145R mutations (with rtN236T mutations), and 4 patients in the switch therapy group had sD144E mutations (1 patient with rtL80M + rtM204V mutations and 3 patients with rtQ215S mutations). 2011 Hepatitis monthly Result HBV L80M;Q215S;M204I;N236T;L80M;M204V;C137G;G145R;D144E 89;339;98;188;292;301;49;162;256 93;344;103;193;296;306;55;168;262 RT;RT;RT;RT;RT;RT;S;S;S 87;96;186;290;299;337;49;162;256 89;98;188;292;301;339;50;163;257 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Although the girl with failure of immunoprophylaxis was positive for the mutant 1 probe, the G145R mutant was not detected as a predominant strain in any patients (Table 2). 2012 BMC research notes Result HBV G145R 93 98 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Although the mutant primer detected a weak signal of wild-type HBV DNA, these findings suggested that the mutant primer could clearly identify the mutant with a point mutation at nt 587 G to A if the mutant was the predominant strain. 2012 BMC research notes Result HBV G587A 182 192 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. As a predominant strain, I/T126S mutant was detected in one (5.6%) of the 18 children with failure of prophylaxis. 2012 BMC research notes Result HBV T126S;I126S 25;25 32;32 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. At the 1:100 ratio, there was no difference in the Ct values or in the shape of the amplification curves among these mutant-specific probes, and it was impossible to identify the mutant with a point mutation at nt 587 G to A (wild-type: Ct values = 24.74 and 24.91; mutant 1: Ct values = 27.65 and 27.75; mutant 2: Ct values = 28.04 and 28.12; mutant 3: Ct values = 26.95 and 27.17) (Figure 1D). 2012 BMC research notes Result HBV G587A 214 224 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Consistent with the results of the mutant-specific real-time PCR, her electropherogram indicated that the wild-type HBV was the predominant strain and the G145R mutant was a minor strain. 2012 BMC research notes Result HBV G145R 155 160 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Constructed plasmid mutant-type (a point mutation at nt 587 G to A) DNA and wild-type DNA were mixed. 2012 BMC research notes Result HBV G587A 56 66 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Detection of G145R mutant by cloning of PCR products. 2012 BMC research notes Result HBV G145R 13 18 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. HBV DNA from clinical serum samples in which we had confirmed a mutation with G145R (at nt 587 G to A, genotype C, the levels of HBV DNA: 5.7 log copies/mL) was amplified using the mutant-specific real-time PCR in duplicate. 2012 BMC research notes Result HBV G145R;G587A 78;91 83;101 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. In addition to the G145R mutant, the a determinant (aa 124-147) was evaluated using the direct sequencing. 2012 BMC research notes Result HBV G145R 19 24 S 37 50 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. In addition, I/T126S (n = 4), I/T126V (n = 1), Q129L (n = 1), T131P (n = 2), M133T + T140I (n = 1), and S136Y (n = 1) mutants were detected as a predominant strain in 10 (9.3%) of the 107 HBV carriers who had not received the HB vaccine or HBIG. 2012 BMC research notes Result HBV T126S;T126V;I126S;I126V;Q129L;T131P;M133T;T140I;S136Y 13;30;13;30;47;62;77;85;104 20;37;20;37;52;67;82;90;109 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Next, we assessed whether the specific probe could distinguish the G145R mutant as a minor strain from the predominant wild-type strain (Figure 1B-C). 2012 BMC research notes Result HBV G145R 67 72 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 11 patients, 6 (CHB-26, -62, -67, -73, -94, and -104) had the G145R mutant as the minor strain (Table 3). 2012 BMC research notes Result HBV G145R 69 74 Chronic Hepatitis B 23 26 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 20 clones, 5 (25.0%) were G145R mutants (Figure 2A, lower) by PCR cloning technique. 2012 BMC research notes Result HBV G145R 33 38 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 7 HBV carriers with the G145R mutant, including the girl with failure of immunoprophylaxis (F-16), 6 were positive for HBeAg (Table 3, upper). 2012 BMC research notes Result HBV G145R 31 36 C 126 131 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. PCR cloning revealed that 6 (33.3%) of 18 clones were G145R mutants (Figure 2B, lower). 2012 BMC research notes Result HBV G145R 54 59 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The amplification curves of this girl indicated that the G145R mutant strain and wild-type strain were coexisting (Figure 2A, upper, the serum sample was taken in May 2007). 2012 BMC research notes Result HBV G145R 57 62 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The amplification signals were detected for HBV DNA from serum with mutant G145R in the wild probe and the mutant probe. 2012 BMC research notes Result HBV G145R 75 80 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The mutant-specific real-time PCR (mutant 1 probe) could detect the G145R mutant in a child with failure of immunoprophylaxis. 2012 BMC research notes Result HBV G145R 68 73 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The remaining 5 patients (CHB-2, -5, -30, -42, and -100), who had overlapped peaks at nt 587 by sequencing, did not have the G145R mutant as a minor strain (Table 3, lower). 2012 BMC research notes Result HBV G145R 125 130 Chronic Hepatitis B 26 29 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The result of the PCR cloning for the G145R mutant in the girl with failure of immunoprophylaxis raised a question. 2012 BMC research notes Result HBV G145R 38 43 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. These findings suggested that the mutant probe could detect the G145R mutant representing as little as 10% of the wild-type population. 2012 BMC research notes Result HBV G145R 64 69 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. All of these 14 patients had mutations at the same position (G 1896A). 2010 Hepatitis monthly Result HBV G1896A 61 68 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. Class 1 included 3 patients (6.8%) with a PC mutation at (G1896A) and a BCP mutation at (A1762/A1764). 2010 Hepatitis monthly Result HBV G1896A 58 64 BCP;Precore 72;42 75;44 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. Class 2 included 8 (18.2%) patients with a PC mutation at (G1896A) and a BCP mutation at (T1762/A1764). 2010 Hepatitis monthly Result HBV G1896A 59 65 BCP;Precore 73;43 76;45 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. Finally Class 4 consisted of 3 patients (6.8%) with a PC mutation at (G1896A) and a BCP mutation at (T1762/G1764; Table 2). 2010 Hepatitis monthly Result HBV G1896A 70 76 BCP;Precore 84;54 87;56 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Besides G145R, there were different types of aa substitutions in the MHR that were associated with lower reactivity in HBsAg assays reported in previous studies: i.e. 2012 Virology journal Result HBV G145R 8 13 S 119 124 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. D99N, Q101R/H, L109I, I110N, T115S, S117T, P120S, K122R, S126T/A, P127H, A128V, Q129R/H/L, G130E, T131N/A, M133T/L/S, F134R/I/L, T143M, A159V, F161Y, W163G, E164G, V168A. 2012 Virology journal Result HBV Q129R;Q129H;Q129L;M133T;M133L;M133S;F134R;F134I;F134L;D99N;Q101R;Q101H;L109I;I110N;T115S;S117T;P120S;K122R;S126T;S126A;P127H;A128V;G130E;T131N;T131A;T143M;A159V;F161Y;W163G;E164G;V168A 80;80;80;107;107;107;118;118;118;0;6;6;15;22;29;36;43;50;57;57;66;73;91;98;98;129;136;143;150;157;164 89;89;89;116;116;116;127;127;127;4;13;13;20;27;34;41;48;55;64;64;71;78;96;105;105;134;141;148;155;162;169 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. D99N, Y100F, Q101R/H, L110I, T113S, S114T, S117T, T118M, I126T/V, W165L, and V168A, which may be associated with antigenicity of HBsAg. 2012 Virology journal Result HBV D99N;Y100F;Q101R;Q101H;L110I;T113S;S114T;S117T;T118M;I126T;I126V;W165L;V168A 0;6;13;13;22;29;36;43;50;57;57;66;77 4;11;20;20;27;34;41;48;55;64;64;71;82 S 129 134 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. G145R substitution, however, was not observed. 2012 Virology journal Result HBV G145R 0 5 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. In the genotype B group, 29 sequences belonged to serotype adw2 (122 K + 160 K + 127P), samples 564014 and 560744 were from ayw1 (122R + 160 K + 127P + 159A), but the sample 522082 (122 K + 160 K + 127H) could not be classified into serotype adw2, adw3 or adw4 for the mutation P127H. 2012 Virology journal Result HBV P127H 278 283 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. In the sequences 502019 and 565200, mutations were clustered before but not within the MHR: L91S, I92P, F93C/G, L94W, L95R, V96A, L97Y, and L98Q. 2012 Virology journal Result HBV L91S;I92P;F93C;F93G;L94W;L95R;V96A;L97Y;L98Q 92;98;104;104;112;118;124;130;140 96;102;110;110;116;122;128;134;144 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Phe at position 93 was replaced with cysteine residue (F93C) in the sequence 502019 from genotype B and sequence 513357 from genotype C. 2012 Virology journal Result HBV F93C;F93C 55;0 59;45 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Similar with sequences 502019 and 565200 from genotype B, sequence 513357 from genotype C showed mutations clustered before the MHR: L91S, I92P, F93C, L94W, V96W, and L97F. 2012 Virology journal Result HBV L91S;I92P;F93C;L94W;V96W;L97F 133;139;145;151;157;167 137;143;149;155;161;171 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. The well-known G145R substitution was found in the 5 sequences, i.e., 531355, 546227, 563060, 506519, 525706, all of which were from B2/adw2. 2012 Virology journal Result HBV G145R 15 20 22510694 Convergence and coevolution of hepatitis B virus drug resistance. 1) harboured additional substitution rtA181T that also confers decreased susceptibility to lamivudine and adefovir. 2012 Nature communications Result HBV A181T 39 44 RT 37 39 22510694 Convergence and coevolution of hepatitis B virus drug resistance. All the HBV variants in Patients 5 and 6 contained rtM204I or rtM204V, respectively. 2012 Nature communications Result HBV M204I;M204V 53;64 58;69 RT;RT 51;62 53;64 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Among 44 HBV variants identified in Patient 3, 43 contained rtM204I, while 1 variant contained rtM204V. 2012 Nature communications Result HBV M204I;M204V 62;97 67;102 RT;RT 60;95 62;97 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Besides the sites for the primary (rtM204V/I) and secondary (rtL180M) lamivudine-resistance mutations identified in five patients, only one additional site with significant changes in intra-host populations was shared by HBV in three patients and four sites by HBV in two patients. 2012 Nature communications Result HBV M204V;M204I;L180M 37;37;63 44;44;68 RT;RT 35;61 37;63 22510694 Convergence and coevolution of hepatitis B virus drug resistance. both containing the rtM204I substitution. 2012 Nature communications Result HBV M204I 22 27 RT 20 22 22510694 Convergence and coevolution of hepatitis B virus drug resistance. For example, the HBV genotype A variants in Patient 1 contained the rtM204V substitution, whereas variants of genotype G in the same patient contained rtM204I. 2012 Nature communications Result HBV M204V;M204I 70;153 75;158 RT;RT 68;151 70;153 22510694 Convergence and coevolution of hepatitis B virus drug resistance. In Patient 10, 23% of all variants contained the rtM204I substitution, whereas the remainder contained rtM204V. 2012 Nature communications Result HBV M204I;M204V 51;105 56;110 RT;RT 49;103 51;105 22510694 Convergence and coevolution of hepatitis B virus drug resistance. In Patient 6, one major post-treatment HBV variant differed from the major pre-treatment variant by only rtM204V and rtL180M. 2012 Nature communications Result HBV L180M;M204V 119;107 124;112 RT;RT 105;117 107;119 22510694 Convergence and coevolution of hepatitis B virus drug resistance. In Patients 6 and 9, the rtM204I substitution was identified in a single clone of pre-treatment HBV populations but these clones were not present in their post-treatment populations (Table 1). 2012 Nature communications Result HBV M204I 27 32 RT 25 27 22510694 Convergence and coevolution of hepatitis B virus drug resistance. One branch represents a cluster of closely related sequences that contain the rtM204I substitution whereas the other four branches contain rtM204V. 2012 Nature communications Result HBV M204V;M204I 141;80 146;85 RT;RT 78;139 80;141 22510694 Convergence and coevolution of hepatitis B virus drug resistance. One variant of this cluster is wild type, suggesting that it represents the pre-treatment minority HBV subpopulation, which served as a source for subsequent resistant variants containing rtM204I. 2012 Nature communications Result HBV M204I 190 195 RT 188 190 22510694 Convergence and coevolution of hepatitis B virus drug resistance. Strikingly, the major variants in each population differed from each other by the same substitution at the same position, rtP1S, and between populations by four substitutions at the same positions, with two of these substitutions being rtM204V and rtL180M. 2012 Nature communications Result HBV P1S;L180M;M204V 124;250;238 127;255;243 RT;RT;RT 122;236;248 124;238;250 22510694 Convergence and coevolution of hepatitis B virus drug resistance. The finding is surprising because the genotype G subpopulation contained a variant manifesting rtM204I. 2012 Nature communications Result HBV M204I 97 102 RT 95 97 22510694 Convergence and coevolution of hepatitis B virus drug resistance. The rtM204I/V substitution was detected in all patients except Patient 9. 2012 Nature communications Result HBV M204I;M204V 6;6 13;13 RT 4 6 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Consistent with the findings obtained by ultra-deep sequencing, quantitative real-time PCR revealed that entecavir administration significantly reduced the proportion of the G1896A pre-C mutant in 13 of 14 cases (92.9%) irrespective of their HBeAg serostatus, while the G1896A pre-C mutant were detectable in substantial proportion before treatment in all cases (Figure 2A, 2B and 2C; p = 0.001). 2012 PloS one Result HBV G1896A;G1896A 174;270 180;276 C;Precore;Precore 242;181;277 247;186;282 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Emergence of G1896A mutation in the pre-C region, and A1762T and G1764A mutations in the core-promoter region is well known to be associated with HBe-seroconversion. 2012 PloS one Result HBV G1896A;A1762T;G1764A 13;54;65 19;60;71 Core promoter;C;Precore 89;146;36 102;149;41 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. High sensitivity of the G1896A pre-C mutant to nucleos(t)ide analogues. 2012 PloS one Result HBV G1896A 24 30 Precore 31 36 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Importantly, however, 4 of 8 HBeAg-negative cases showed a relatively low prevalence of the G1896A pre-C mutant (Liver #8, #12, #13, #14), and all but one case (Liver #10) showed a high prevalence of the A1762T and G1764A mutations, irrespective of HBe serologic status and NA treatment history (Table 3). 2012 PloS one Result HBV G1896A;A1762T;G1764A 92;204;215 98;210;221 C;C;Precore 249;29;99 252;34;104 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Notably, liver tissues of all but one (Liver #17) chronic-NA cases showed extremely low levels of the G1896A pre-C mutant (0.0, 0.0, 0.1, and 1.1%), suggesting the high sensitivity of the G1896A pre-C mutant to NA (Table 3). 2012 PloS one Result HBV G1896A;G1896A 102;188 108;194 Precore;Precore 109;195 114;200 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Other mutations resistant to adefovir were detected in 7 (50.0%) and 3 (21.4%) cases at A181TV and N236T, respectively (Table 4). 2012 PloS one Result HBV N236T 99 104 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. The mean prevalence of the G1896A pre-C mutant in HBeAg-positive cases was lower than that in the HBeAg-negative cases (27.4% and 46.5%, respectively). 2012 PloS one Result HBV G1896A 27 33 C;C;Precore 50;98;34 55;103;39 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. These findings suggested that other mutations except G1896A, A1762T and G1764A were also involved in the HBeAg seroconversion status. 2012 PloS one Result HBV G1896A;A1762T;G1764A 53;61;72 59;67;78 C 105 110 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. These results further support the findings that HBV clones comprising the G1896A mutation were more sensitive to NA than those with wild-type sequences. 2012 PloS one Result HBV G1896A 74 80 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. To confirm the difference of the sensitivity to NA between the wild-type and the G1896A pre-C mutant, we examined the dynamic changes of the relative proportion of the G1896A pre-C mutant in the serum of 14 treatment-naive patients before and after entecavir administration. 2012 PloS one Result HBV G1896A;G1896A 81;168 87;174 Precore;Precore 88;175 93;180 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Among them, combined variants carrying only LMV resistant mutations, such as rtV173L-rtL180M-rtM204V and rtL180M-rtM204V, increased in frequency from LMV to ETV VBK (from 0.6% to 1.3% and from 0.3% to 3.2%, respectively) (Table 5 and Figure 5). 2012 PloS one Result HBV L180M;L180M;V173L;M204V;M204V 87;107;79;95;115 92;112;84;100;120 RT;RT;RT;RT;RT 77;85;93;105;113 79;87;95;107;115 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. As observed in the baseline quasispecies, a significant portion of the 20 most frequent variants (highest average substitution frequencies in the 5 samples) led to stop codons (sW156*, sW172*, sW182*, sW191*, sW196* and sW199*), especially at LMV VBK and at the end of ADV, mainly due to mutation sW172*, related to rtA181T, (71.7% and 64%, respectively) and sW182*, related to rtV191I, (5.8% and 8%, respectively). 2012 PloS one Result HBV A181T;V191I;W156X;W172X;W182X;W191X;W196X;W199X;W172X;W182X 318;380;177;185;193;201;209;220;297;359 323;385;183;191;199;207;215;226;303;365 RT;RT;S;S;S;S;S;S;S;S 316;378;177;185;193;201;209;220;297;359 318;380;178;186;194;202;210;221;298;360 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. At ETV VBK (sample 4E), two variants previously detected by LiPA at LMV VBK were strongly selected, rtL180M (99.3%) and rtM204V (99.4%) (Table 3 and Figure 4). 2012 PloS one Result HBV L180M;M204V 102;122 107;127 RT;RT 100;120 102;122 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. At the end of ADV (sample 4D), rtA181T, which was detected by LiPA, remained as the major variant (64%) (Table 3 and Figure 4), whereas rtV191I (8%) continued increasing. 2012 PloS one Result HBV A181T;V191I 33;138 38;143 RT;RT 31;136 33;138 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. At the time of LMV VBK (sample 4C), percentages of rtA181T (71.7%), rtM204V (5.6%), and rtL180M (5%) notably increased relative to baseline samples, as did other LMV resistance substitutions, particularly rtV191I (5.8%), rtV207I (3.9%), and rtV173L (1.4%), although to a lesser extent. 2012 PloS one Result HBV A181T;M204V;L180M;V207I;V173L;V191I 53;70;90;223;243;207 58;75;95;228;248;212 RT;RT;RT;RT;RT;RT 51;68;88;205;221;241 53;70;90;207;223;243 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Four of these 8 stop codons affected RT positions associated with NA resistance (sW172* related to rtA181T, sW182* to rtV191I, sW196* to rtM204I, and sW199* to rtV207I), at frequencies of 0.20% to 0.30%, significantly higher than the artifactual error (0.03%). 2012 PloS one Result HBV A181T;V191I;M204I;V207I;W172X;W182X;W196X;W199X 101;120;139;162;81;108;127;150 106;125;144;167;87;114;133;156 RT;RT;RT;RT;RT;S;S;S;S 37;99;118;137;160;81;108;127;150 39;101;120;139;162;82;109;128;151 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Furthermore, rtL180M and rtM204V, which were present in frequencies below the mismatch error (0.03%) at pre-treatment, accounted for around 5% of the quasispecies at LMV VBK (sample 4C in Table 3). 2012 PloS one Result HBV L180M;M204V 15;27 20;32 RT;RT 13;25 15;27 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In addition, other NA-resistant variants related with resistance to ETV and detected by Sanger sequencing also increased significantly at ETV VBK: rtV173L (18.2%), which was detectable by LiPA, rtS202G (80.9%) and rtI169T (17.3%), inconsistently observed by Sanger (Table 3 and Figure 4). 2012 PloS one Result HBV S202G;I169T;V173L 196;216;149 201;221;154 RT;RT;RT 147;194;214 149;196;216 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In addition, substitutions rtD205N and rtD206N, both of which affect essential residues from the YMDD catalytic motif, showed frequencies of 0.26% and 0.13%, respectively. 2012 PloS one Result HBV D205N;D206N 29;41 34;46 RT;RT;P 27;39;97 29;41;101 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In contrast, rtR153Q and rtA194T, also associated with NA resistance, were less variable (positions 25 and 26 in Table 3). 2012 PloS one Result HBV A194T;R153Q 27;15 32;20 RT;RT 13;25 15;27 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In order to confirm whether the association of rtV207I and rtM204V was specific to this patient or a more general phenomenon, results from a first-generation LiPA strip (which included NA resistance-related substitutions in codons rt204 and rt207) of 50 patients who had failed LMV treatment were retrospectively checked. 2012 PloS one Result HBV V207I;M204V 49;61 54;66 RT;RT;RT;RT 47;59;231;241 49;61;233;243 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In patient 4, rtA181T and rtM204I were the most prevalent aa substitutions at pre-treatment according to UDPS results; however only rtA181T was detected by LiPA (INNO-LiPA HBV DR v2 assay) and direct sequencing at LMV VBK (Table 2). 2012 PloS one Result HBV A181T;A181T;M204I 16;134;28 21;139;33 RT;RT;RT 14;26;132 16;28;134 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In patients 2 and 3, LMV resistance was associated with predominant selection of rtL180M and rtM204V, despite the fact that higher percentages of rtA181T and/or rtM204I were detected by UDPS at baseline (Table 2). 2012 PloS one Result HBV A181T;L180M;M204V;M204I 148;83;95;163 153;88;100;168 RT;RT;RT;RT 81;93;146;161 83;95;148;163 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In the "a determinant", only substitution sG145R (0.11%), the main HBsAg immune escape variant, was present at >0.1%. 2012 PloS one Result HBV G145R 42 48 S;S;S 8;67;42 21;72;43 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Interestingly, immediately after these well known NA-resistant variants, in positions 11 and 12, we found the rare variants rtA181S and rtA200V, which are associated with ADV and L-nucleoside analogue (LMV and LdT) resistance, respectively. 2012 PloS one Result HBV A181S;A200V 126;138 131;143 RT;RT 124;136 126;138 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Linkage analysis yielded two main findings: First, the 10 most variable aa substitutions were mainly present in variant combinations, the only exception being rtA181T, which was the single substitution in 64.1% of sequences at LMV VBK and 56.5% at the end of ADV (Table 5). 2012 PloS one Result HBV A181T 161 166 RT 159 161 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Of note, a substantial part of these substitutions (4 out of 9) resulted in stop codons (*) (sW156*, sW163*, sW165* and sW172*), giving rise to proteins with significant aa deletions. 2012 PloS one Result HBV W156X;W163X;W165X;W172X 93;101;109;120 99;107;115;126 S;S;S;S 93;101;109;120 94;102;110;121 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. On calculation of the average percentage of each aa change in the 4 baseline populations, 13 changes were found at average frequencies of >=0.1% (Table S1), and 4 of them are known to confer NA resistance: rtA181T (0.10%), rtV191I (0.23%), rtA194T (0.11%), and rtM204I (0.15%). 2012 PloS one Result HBV A181T;V191I;A194T;M204I 208;225;242;263 213;230;247;268 RT;RT;RT;RT 206;223;240;261 208;225;242;263 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Patient 1 had detectable percentages of rtA181T and rtM204V/I by UDPS in the baseline quasispecies, but neither was selected during LMV treatment (Table 2). 2012 PloS one Result HBV A181T;M204V;M204I 42;54;54 47;61;61 RT;RT 40;52 42;54 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Second, at ETV VBK, rtI169T and/or rtS202G, which are typically associated with ETV resistance, always appeared linked to the LMV resistance signature (rtL180M-rtM204V), in keeping with previous reports (Table 5), whereas rtV207I, which has not been previously associated with ETV resistance, unexpectedly appeared in most of the highly frequent combinations and always together with other variants, especially rtM204V (Table 5). 2012 PloS one Result HBV I169T;M204V;S202G;L180M;V207I;M204V 22;162;37;154;224;413 27;167;42;159;229;418 RT;RT;RT;RT;RT;RT 20;35;152;160;222;411 22;37;154;162;224;413 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The 10 most variable RT substitutions observed during sequential NA treatment, blindly selected after SD sorting and all associated with NA resistance (rtL180M, rtM204V, rtS202G, rtV207I, rtA181T, rtL173V, rtI169T, rtV191I, rtM204I, and rtT184A) (Table 3), were included in the linkage analysis. 2012 PloS one Result HBV T184A;L180M;M204V;S202G;V207I;A181T;L173V;I169T;V191I;M204I 239;154;163;172;181;190;199;208;217;226 244;159;168;177;186;195;204;213;222;231 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 21;152;161;170;179;188;197;206;215;224;237 23;154;163;172;181;190;199;208;217;226;239 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The 10 most variable substitutions (highest SD value), rtL180M, rtM204V, rtS202G, rtV207I, rtA181T, rtV173L, rtI169T, rtV191I, rtM204I and rtT184A, are known to be associated with NA resistance. 2012 PloS one Result HBV T184A;L180M;M204V;S202G;V207I;A181T;V173L;I169T;V191I;M204I 141;57;66;75;84;93;102;111;120;129 146;62;71;80;89;98;107;116;125;134 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 55;64;73;82;91;100;109;118;127;139 57;66;75;84;93;102;111;120;129;141 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The consensus sequence was identical in both samples and the variants showed low comparative changes in frequency, except for rtV191I, which increased from 0.6% (4A) to 1.1% (4B) (Table 3). 2012 PloS one Result HBV V191I 128 133 RT 126 128 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The dominant sequence in patient 2 was accompanied by around 5% of sequences carrying substitutions rtH148Y, rtR153W, rtI187L and rtL199V (Figure 2). 2012 PloS one Result HBV L199V;H148Y;R153W;I187L 132;102;111;120 137;107;116;125 RT;RT;RT;RT 100;109;118;130 102;111;120;132 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The ETV-associated substitution rtS202G also increased slightly (0.15%) (Table 3). 2012 PloS one Result HBV S202G 34 39 RT 32 34 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The most variable positions were those that overlapped RT residues associated with NA resistance, particularly sI195M, related to rtM204V, present in 5.6% and 99% of sequences at LMV VBK and ETV VBK, respectively. 2012 PloS one Result HBV M204V;I195M 132;111 137;117 RT;RT;S 55;130;111 57;132;112 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. These 20 variants did not include the immune escape variant sG145R, detected in relatively high frequencies at pre-treatment, but otherwise included the variants sS167L, sW172C, and sW172*, located at the minimal recognized sequence (positions s165 to s172) of the TH-s156/s175 epitope; among these, sS167L showed a continuous percentage increase from pre-treatment to ETV-VBK (sample 4A: 0.2%, 4B: 0.7%, 4C: 1.1%, 4D: 1.3%, 4E: 4%). 2012 PloS one Result HBV G145R;S167L;W172C;W172X;S167L 60;162;170;182;300 66;168;176;188;306 S;S;S;S;S;S;S;S;S 60;162;170;182;244;252;268;273;300 61;163;171;183;245;253;269;274;301 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Thirty-nine percent of them showed rtV207I and rtM204V/I (data not shown). 2012 PloS one Result HBV M204I;V207I;M204V 49;37;49 56;42;56 RT;RT 35;47 37;49 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. This substitution was also found in combination with rtV191I in a significant percentage of variants (4.4% at LMV VBK and 6.6% at ADV end) (Table 5). 2012 PloS one Result HBV V191I 55 60 RT 53 55 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Three patients carrying rtM204V and rtV207I had been subsequently treated with ETV, and two of them had rapid VBK after an initial ETV response. 2012 PloS one Result HBV M204V;V207I 26;38 31;43 RT;RT 24;36 26;38 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. We also observed an increase in other NA-resistant variants that have not been previously related to ETV resistance, such as rtV207I (80.9%), detected by Sanger sequencing, and the rare substitution, rtA200V (0.38%) (Table 3 and Figure 4). 2012 PloS one Result HBV A200V;V207I 202;127 207;132 RT;RT 125;200 127;202 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. Interestingly, all but two individuals whose major virus population was composed of WT isolates and a small percentage of resistant variants detected by pyrosequencing had a YIDD variant as a minor subpopulation, suggesting that the rtM204I mutation may naturally occur more often and replicate more efficiently than YVDD variants in environments with little or no selection pressures. 2012 BMC microbiology Result HBV M204I 235 240 RT;P;P 233;174;317 235;178;321 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Finally, 85 case-control studies were included, among which, 43 case-control studies focused on G1896A, 56 studies on A1762T/G1764A, 24 studies on Pre-S mutation, 27 studies on T1753V and 23 studies on C1653T. 2012 PloS one Result HBV G1764A;G1896A;A1762T;T1753V;C1653T 125;96;118;177;202 131;102;124;183;208 PreS 147 152 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For another new mutation G1899A in Precore region, 11 studies including 693 cases and 953 controls were included. 2012 PloS one Result HBV G1899A 25 31 Precore 35 42 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For the controversial Precore mutation G1896A, 43 studies were included in the meta-analysis. 2012 PloS one Result HBV G1896A 39 45 Precore 22 29 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For these mutations, statistically significant heterogeneity was observed for BCP double mutation (I2 = 76.1%, p<0.001), T1753V (I2 = 71.4%, p<0.001) and C1653T (I2 = 60.8%, p<0.001). 2012 PloS one Result HBV T1753V;C1653T 121;154 127;160 BCP 78 81 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In our study, we appraised the correlation between the other common mutations like BCP double mutation, C1653T etc. 2012 PloS one Result HBV C1653T 104 110 BCP 83 86 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In subgroup analysis by ethnicity, a significant association was found to exist between G1899A and HCC in Asians (OR = 3.22, 95%CI = 2.42-4.28). 2012 PloS one Result HBV G1899A 88 94 Hepatocellular carcinoma 99 102 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In subgroup analysis by ethnicity, all the mutations correlated with the risk of HCC in Asians (For A1762T/G1764A, OR = 4.20, p<0.001; T1753V, OR = 2.19, p<0.001; C1653T, OR = 2.61, p<0.001). 2012 PloS one Result HBV G1764A;A1762T;T1753V;C1653T 107;100;135;163 113;106;141;169 Hepatocellular carcinoma 81 84 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In subgroup analysis by genotype, A1762T/G1764A in HBV genotype B and C, T1753V in HBV genotype C and D, C1653T in genotype C patients significantly correlated with the increased risk of HCC. 2012 PloS one Result HBV G1764A;A1762T;T1753V;C1653T 41;34;73;105 47;40;79;111 Hepatocellular carcinoma 187 190 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In the subgroup analysis by ethnicity, the results indicated that G1896A correlated with an increased risk among the Asians (OR = 1.47, 95% CI = 1.16-1.92,) and even after adjustment for heterogeneity (OR = 1.33, 95% CI = 1.14-1.54), while no such correlation was found in Caucasians and Africans (See Table 1). 2012 PloS one Result HBV G1896A 66 72 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Moreover, we still observed significant correlation between G1896A and the progressive disease group with an OR = 1.85 (95%CI = 1.27-2.70) (See Table S2). 2012 PloS one Result HBV G1896A 60 66 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Results showed that BCP double mutation A1762T/G1764A strongly correlated with the occurrence of HCC (OR = 3.98, 95%CI = 3.19-4.95) (See Figure S1); T1753V associated with a 2.23-fold risk (95% CI = 1.69-2.93) (See Figure S2), and C1653T with a 2.55-fold increased risk of HCC (95%CI = 1.95-3.35) (See Table S2, Figure S3). 2012 PloS one Result HBV G1764A;A1762T;T1753V;C1653T 47;40;149;231 53;46;155;237 BCP 20 23 Hepatocellular carcinoma;Hepatocellular carcinoma 97;273 100;276 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Results showed that G1899A correlated with an increased risk of HCC (OR = 3.13, 95%CI = 2.38-4.13) (See Figure 4). 2012 PloS one Result HBV G1899A 20 26 Hepatocellular carcinoma 64 67 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Significant correlation was found between G1896A and the occurrence of HCC (summary OR = 1.46; 95%CI = 1.15-1.84) (See Figure 2A). 2012 PloS one Result HBV G1896A 42 48 Hepatocellular carcinoma 71 74 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. The odds ratio for T1753V was 2.77 (95%CI = 1.92-4.01), for C1653T was 2.59 (95%CI = 1.53-4.37). 2012 PloS one Result HBV T1753V;C1653T 19;60 25;66 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. While for C1653T, a higher risk susceptible to HCC could be seen in the negative group (See Table S2). 2012 PloS one Result HBV C1653T 10 16 Hepatocellular carcinoma 47 50 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. While in HBeAg subgroup, BCP A1762T/G1764A was associated with the increased risk of HCC irrespective of the HBeAg status. 2012 PloS one Result HBV G1764A;A1762T 36;29 42;35 BCP;C;C 25;9;109 28;14;114 Hepatocellular carcinoma 85 88 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. 35% of all specimens had the precore stop mutation G1896A which abrogates HBeAg production; however, this was detected in 41% of genotype B compared to only 3% of genotype C viruses (p<0.0001; Figure 4). 2012 PloS one Result HBV G1896A 51 57 C;Precore 74;29 79;36 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. 78.9% (n = 15/19) of these individuals had undetectable HBV viral loads and, of the 4 patients on HAART with a detectable HBV viral load, one - a HIV/HBV/HCV coinfected IDU - had drug resistance associated mutations, L180M and M204V in the pol gene conferring resistance to lamivudine and possible resistance to telbivudine. 2012 PloS one Result HBV L180M;M204V 217;227 222;232 P 240 243 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Evaluation of fragments for which there was an available corresponding S gene sequence also identified a difference in mutational patterns at the subgenotype level: B2 viruses compared to B4 for both G1896A (20%, n = 1/5 vs 40.2%, n = 53/132) and A1762T/G1764A (40%, n = 2/5 vs 19.7%, n = 26/132). 2012 PloS one Result HBV G1764A;G1896A;A1762T 254;200;247 260;206;253 S 71 72 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. In the preS2 region, 5.5% of specimens had a point mutation in the start codon which changed the amino acid to I (3.3%), V (1.7%) or T (0.55%), and 5.3% had a mutation at F22L with either a single or dual point mutation at this site. 2012 PloS one Result HBV F22L 171 175 PreS2 7 12 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Mutations associated with immune escape were identified in 23.5% (n = 45/187) samples and included the following residues Y100C (n = 6), T118K (n = 1), P120L/Q/S/T (n = 10), T123A/N (n = 2), I126N/S (n = 8), P127S (n = 2), Q129R (n = 2), G130D/N/R (n = 1), T131I (n = 4), M133L/T (n = 18), G144E (n = 1) and G145A/R (n = 4). 2012 PloS one Result HBV P120L;P120Q;P120S;P120T;G130D;G130N;G130R;M133T;Y100C;T118K;T123A;T123N;I126N;I126S;P127S;Q129R;T131I;M133L;G144E;G145A;G145R 152;152;152;152;238;238;238;272;122;137;174;174;191;191;208;223;257;272;290;308;308 163;163;163;163;247;247;247;279;127;142;181;181;198;198;213;228;262;279;295;315;315 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Sixty-four specimens had mutations in the T cell epitope (including N40N/S, L42L/P, G44D/E/G, A45T, P46H, T47A/E/K/T). 2012 PloS one Result HBV G44D;G44E;G44G;T47A;N40S;T47E;T47K;T47T;N40N;L42L;L42P;A45T;P46H 84;84;84;106;68;106;106;106;68;76;76;94;100 92;92;92;116;74;116;116;116;74;82;82;98;104 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. A1993T and T2077C mutations were only found in FHF cases (Table 1). 2012 PloS one Result HBV A1993T;T2077C 0;11 6;17 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Amino acid mapping reveals that the S region was relatively conserved; however, an important substitution of P120T/S was observed in 7.8% (9/115) of AVH and 11.2% (13/116) in CH patients. 2012 PloS one Result HBV P120T;P120S 109;109 116;116 S 36 37 Acute Hepatitis B;Chronic Hepatitis B 149;175 152;177 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Among the patients of LC, SW172stop (6.4%) and SL173F (4.2%) mutations were also detected. 2012 PloS one Result HBV W172X;L173F 26;47 35;53 Liver cirrhosis 22 24 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Further, the C1914G core gene mutation was associated with the HCC cases (32.2%) compared to ASC (5.0%), CHB (7.8%) and LC (10.3%), respectively. 2012 PloS one Result HBV C1914G 13 19 C 20 24 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 63;105;120 66;108;122 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. In the S gene, an A184V mutation was found in 17.9% of the cirrhotic and 24.6% HCC patients included in this study, respectively. 2012 PloS one Result HBV A184V 18 23 S 7 8 Hepatocellular carcinoma;Liver cirrhosis 79;59 82;68 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. No G145R substitution was identified in any of the isolates. 2012 PloS one Result HBV G145R 3 8 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Other precore mutations were G1899A and C1914G which were comparable in AVH and FHF patients. 2012 PloS one Result HBV G1899A;C1914G 29;40 35;46 Precore 6 13 Acute Hepatitis B 72 75 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Some substitutions such as P127T, V128A and D144N were observed in the immunologic domain of the "a determinant" region. 2012 PloS one Result HBV P127T;V128A;D144N 27;34;44 32;39;49 S 98 111 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. In the 3 other patients, the viral breakthrough was not associated with the detection of HBV resistance mutations; however the M204V mutation was detected later during the follow-up in 2 patients, (i) at 42 months, along the compensatory resistance mutations rtV173L+L180M in one patient, and (ii) at 78 months with rtL180M mutation in one patient. 2012 PloS one Result HBV V173L;L180M;M204V;L180M 261;318;127;267 266;323;132;272 RT;RT 259;316 261;318 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. Late HBV breakthrough occurred in 3 patients and was associated with the emergence of 3TC-resistance mutations: rtV173L+L180M+M204I, rtL180M+M204V and rtL180M+M204I. 2012 PloS one Result HBV V173L;L180M;L180M;L180M;M204I;M204V;M204I 114;135;153;120;126;141;159 119;140;158;125;131;146;164 RT;RT;RT 112;133;151 114;135;153 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. One patients had the HBV mutation ntG741A (G to A nucleotide at position 741), resulting in the known 3TC-associated resistance mutation rtM204I. 2012 PloS one Result HBV M204I;G741A;G741A 139;35;43 144;41;76 RT 137 139 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. The ntT843G mutation of unknown significance was also observed and resulted in the change from asparagine to lysine in the reverse transcriptase protein (rtN238K). 2012 PloS one Result HBV N238K;T843G 156;5 161;11 RT;RT 123;154 144;156 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. This mutation led to the concomitant substitution of tryptophan to stop codon at position 196 (sW196stop) in the surface protein. 2012 PloS one Result HBV W196X;W196X 95;53 104;93 S;S 95;113 96;120 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. A significant portion of patients with rtS106C mutations were detected in the CHB group (14/100, 14.0%) or cirrhosis group (14/100, 14.0%) when compared to those in the HCC group (4/100, 4.0%, P=0.013). 2012 Liver international Result HBV S106C 41 46 RT 39 41 Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma 78;107;169 81;116;172 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Additionally, A significant portion of patients with rtD134E/G/N/S mutations were detected in the CHB group (22/100, 22.0%) or cirrhosis group (21/100, 21.0%) when compared to those in the HCC group (10/100, 10.0%, P=0.021 and P=0.032, respectively). 2012 Liver international Result HBV D134E;D134G;D134N;D134S 55;55;55;55 66;66;66;66 RT 53 55 Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma 98;127;189 101;136;192 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Among patients with adefovir related resistance mutations, five had rtA181T/V, one had rtN236T and eightteen had rtV214A/E/I. 2012 Liver international Result HBV A181T;A181V;V214A;V214E;V214I;N236T 70;70;115;115;115;89 77;77;124;124;124;94 RT;RT;RT 68;87;113 70;89;115 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Among patients with lamivudine related resistance mutations, eleven had rtM204I/V/S (four with rtM204I, six with rtM204V and one with rtM204S), nine had rtL180M and three had rtV173L mutation. 2012 Liver international Result HBV M204I;M204V;M204S;M204V;M204I;M204S;L180M;V173L 74;74;74;115;97;136;155;177 83;83;83;120;102;141;160;182 RT;RT;RT;RT;RT;RT 72;95;113;134;153;175 74;97;115;136;155;177 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Eight patients had double mutations of rtM204V/I+rtL180M and one patient with triple mutations of rtM204V+rtL180M+rtV173L. 2012 Liver international Result HBV M204I;L180M;M204V;M204V;L180M;V173L 41;51;41;100;108;116 48;56;46;105;113;121 RT;RT;RT;RT;RT 39;49;98;106;114 41;51;100;108;116 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Other related resistance mutations were found in two patients with rtI169L/T/N and one patient with rtS202I. 2012 Liver international Result HBV I169L;I169T;I169N;S202I 69;69;69;102 78;78;78;107 RT;RT 67;100 69;102 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. All nucleotides sequences corresponding to genotypes D had a thymidine "T" at nt 1858, whereas all genotype A sequences had a cytosine "C" at nt 1858, except four cases harboring G1896A, in which concomitant C1858T mutation occurred. 2012 PloS one Result HBV G1896A;C1858T 179;208 185;214 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. As shown in Figure 1, G1896A and G1899A were more common in genotype D than in genotype A strains (p<0.001, p = 0.03, respectively) while A1762T/G1764A was more frequent in genotype A than in genotype D strains (p = 0.003). 2012 PloS one Result HBV G1764A;G1896A;G1899A;A1762T 145;22;33;138 151;28;39;144 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Both elevated ALT and high HBV-DNA levels were significantly associated with the presence of T1753V, A1762T/G1764 and C1766T/T1768A mutations (p<0.001). 2012 PloS one Result HBV T1768A;T1753V;A1762T;C1766T 125;93;101;118 131;99;107;124 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1766T/T1768A was found only among ACH and AdLD groups, with a significantly higher prevalence in AdLD group (p = 0.014). 2012 PloS one Result HBV T1768A;C1766T 7;0 13;6 Aggressive Hepatitis and advanced liver disease;Chronic active Hepatitis;Aggressive Hepatitis and advanced liver disease 98;35;43 102;38;47 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Further combined analysis of common pre-C (G1896A) and CP (A1762T/G1764A) mutations was performed in all patients. 2012 PloS one Result HBV G1764A;G1896A;A1762T 66;43;59 72;49;65 Core promoter;Precore 55;36 57;41 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1764A and A1762T were frequently found together in 55 patients (29.5%). 2012 PloS one Result HBV G1764A;A1762T 0;11 6;17 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1896A mutation occurred significantly more frequently in non-AdLD group than in AdLD group (p = 0.04). 2012 PloS one Result HBV G1896A 0 6 Aggressive Hepatitis and advanced liver disease;Aggressive Hepatitis and advanced liver disease 81;62 85;66 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1899A mutation was also frequent (52.7%) and was mostly accompanied by G1896A in 87 patients (46.8%). 2012 PloS one Result HBV G1899A;G1896A 0;72 6;78 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In addition, patients harboring strains with G1899A, C1653T, T1753V, A1762T/G1764A and C1766T/T1768A mutations were significantly older than those without these mutations (p<=0.01). 2012 PloS one Result HBV G1764A;T1768A;G1899A;C1653T;T1753V;A1762T;C1766T 76;94;45;53;61;69;87 82;100;51;59;67;75;93 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the BCP, G1764A was the most frequent (72/186, 38.7%), followed by A1762T (59/186, 31.7%), T1753V (28.5%), A1757G (21.5%), C1766G (48/186, 26%), C1766T (41/186, 22%), G1764T (35/186, 18.8%) and T1768A (29/186, 15.6%). 2012 PloS one Result HBV G1764A;A1762T;T1753V;A1757G;C1766G;C1766T;G1764T;T1768A 12;70;94;110;126;148;170;197 18;76;100;116;132;154;176;203 BCP 7 10 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the CP region, eleven frequent mutations were found: C1653T was the most common in the URR (14%) followed by C1637A (11.3%) and T1636G (9.7%). 2012 PloS one Result HBV C1653T;C1637A;T1636G 56;112;131 62;118;137 Core promoter 7 9 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the pre-C region, G1896A mutation occurred the most frequently (83.9%). 2012 PloS one Result HBV G1896A 21 27 Precore 7 12 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. It was found that older age (>=40 years), male sex, high serum HBV-DNA level (>4.3 log10 IU/mL) and the presence of mutations C1653T, T1753V, A1762T/G1764A and C1766T/T1768A were independent risk factors predictor of AdLD development, whereas G1896A was associated with a decreased risk of AdLD development (Table 4). 2012 PloS one Result HBV G1764A;T1768A;C1653T;T1753V;A1762T;C1766T;G1896A 149;167;126;134;142;160;243 155;173;132;140;148;166;249 Aggressive Hepatitis and advanced liver disease;Aggressive Hepatitis and advanced liver disease 290;217 294;221 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Likewise, T1768A was frequently present in association with C1766T in 24 (12.4%) patients. 2012 PloS one Result HBV T1768A;C1766T 10;60 16;66 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Moreover, no significant difference was observed between genotype A and D regarding the prevalence of mutations C1637A (p = 0.946), C1653T (p = 0.102), T1753V (p = 0.809), and C1766T/T1768A (p = 0.744). 2012 PloS one Result HBV T1768A;C1637A;C1653T;T1753V;C1766T 183;112;132;152;176 189;118;138;158;182 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Mutations affecting the initiation of translation of pre-C gene (TIM) were found in 7 (3.8%) patients, including A1814C (three ICs), T1815C (one IC), T1815A (one patient with ACH) and C1817T (two ICs). 2012 PloS one Result HBV A1814C;T1815C;T1815A;C1817T 113;133;150;184 119;139;156;190 Precore 53 58 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. No patients with TIM had concomitant G1896A mutation. 2012 PloS one Result HBV G1896A 37 43 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The mutations T1636G, A1757G and G1764T/C1766G were exclusively found in genotype D strains. 2012 PloS one Result HBV C1766G;T1636G;A1757G;G1764T 40;14;22;33 46;20;28;39 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The prevalence of C1653T was significantly higher in AdLD group than in IC (p<0.0001) and ACH group (p = 0.0005). 2012 PloS one Result HBV C1653T 18 24 Aggressive Hepatitis and advanced liver disease;Chronic active Hepatitis 53;90 57;93 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The prevalence of G1899A mutation was significantly higher in AdLD group than in ICs (p = 0.03). 2012 PloS one Result HBV G1899A 18 24 Aggressive Hepatitis and advanced liver disease 62 66 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The prevalence of T1753V and A1762T/G1764A increased significantly with disease progression (IC vs. 2012 PloS one Result HBV G1764A;T1753V;A1762T 36;18;29 42;24;35 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. There were no significant differences between patients with and without G1896A regarding mean age (p = 0.56) and HBV-DNA level (p = 0.84), but compared to patients infected with the wild-type virus, patients carrying G1896A mutation had a lower ALT level although the difference did not reach statistical significance (p = 0.06). 2012 PloS one Result HBV G1896A;G1896A 72;217 78;223 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Therefore, we investigated the frequency of the combination of the six CP mutations independently associated with AdLD (C1653T, T1753V, A1762T, G1764A, C1766T, and T1768A) in the 3 clinical groups (Figure 3). 2012 PloS one Result HBV C1653T;T1753V;A1762T;G1764A;C1766T;T1768A 120;128;136;144;152;164 126;134;142;150;158;170 Core promoter 71 73 Aggressive Hepatitis and advanced liver disease 114 118 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Thus, G1764A/A1762T and C1766T/T1768A were considered as mutational patterns. 2012 PloS one Result HBV A1762T;T1768A;G1764A;C1766T 13;31;6;24 19;37;12;30 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Triple mutations were found in 14 ACH and 6 AdLD patients, with T1753V/A1762T/G1764A, the most frequent. 2012 PloS one Result HBV A1762T;G1764A;T1753V 71;78;64 77;84;70 Chronic active Hepatitis;Aggressive Hepatitis and advanced liver disease 34;44 37;48 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. With regard to the CP mutations, six were associated with the clinical status of patients: C1653T, G1764A, A1762T, T1753V, C1766T and T1768A. 2012 PloS one Result HBV C1653T;G1764A;A1762T;T1753V;C1766T;T1768A 91;99;107;115;123;134 97;105;113;121;129;140 Core promoter 19 21 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. As expected, the frequencies of C1653T, T1753V, A1762T/G1764A mutations in these 'free' HBV DNAs from both tumor derived and non-tumor derived samples were at the same level as that for the serum derived samples of the LC group and HCC group (Table 2). 2012 PloS one Result HBV G1764A;C1653T;T1753V;A1762T 55;32;40;48 61;38;46;54 Hepatocellular carcinoma;Liver cirrhosis 232;219 235;221 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. It is worth noting that the frequency of either C1653T or A1762T/G1764A mutations seen was significantly higher than that found for the integrated group (C1653T, 9% vs. 2012 PloS one Result HBV G1764A;C1653T;A1762T;C1653T 65;48;58;154 71;54;64;160 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. Meta-analysis of previously published data, both our own and that of others, has shown that the number of mutations of the HBV genome (C1653T, T1753V and A1762T/G1764A) gradually increased with disease progression and correlated with hepatocarcinogenesis (Table 2). 2012 PloS one Result HBV G1764A;C1653T;T1753V;A1762T 161;135;143;154 167;141;149;160 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. The frequencies of C1653T, T1753V and A1762T/G1764A mutations found were at the same level as that seen in the serum derived samples of the CHB group (Table 2), and were significantly lower than that in the LC and HCC group (Table 2). 2012 PloS one Result HBV G1764A;C1653T;T1753V;A1762T 45;19;27;38 51;25;33;44 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 140;214;207 143;217;209 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. The frequencies of C1653T, T1753V and A1762T/G1764A point mutations in the X gene of the inserted HBV viral sequences were the same as that found for serum derived samples i.e.: 'free' non integrated viral DNA in CHB group (Table 2). 2012 PloS one Result HBV G1764A;C1653T;T1753V;A1762T 45;19;27;38 51;25;33;44 X 75 76 Chronic Hepatitis B 213 216 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. HBsAg expression was also assessed for the M103I, K122R, or G145A mutations. 2012 Journal of viral hepatitis Result HBV M103I;K122R;G145A 43;50;60 48;55;65 S 0 5 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. However, overall HBsAg levels were higher in the supernatant, while lysate HBsAg levels were lower, indicating increased HBsAg secretion with the second C-HBV backbone, presumably due to the 2 amino acid mutations (G164E and S212F) that differentiate the C-HBV sequences. 2012 Journal of viral hepatitis Result HBV G164E;S212F 215;225 220;230 S;S;S 17;75;121 22;80;126 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In contrast, combinations of mutations containing G145A resulted in significantly lower HBsAg levels - some below detectable limits. 2012 Journal of viral hepatitis Result HBV G145A 50 55 S 88 93 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In contrast, the G145A mutation resulted in significantly lower HBsAg levels in both cell supernatants and lysates. 2012 Journal of viral hepatitis Result HBV G145A 17 22 S 64 69 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In lysates, HBsAg levels were slightly lower for expression vectors containing the M103I and K122R mutations compared to wild-type (Figures 1B,D). 2012 Journal of viral hepatitis Result HBV M103I;K122R 83;93 88;98 S 12 17 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Similar results were observed in HepG2 cells, in which the only constructs with ratios >1 were those containing the G145A mutation alone or in combination. 2012 Journal of viral hepatitis Result HBV G145A 116 121 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Supernatant levels of HBsAg were similar between wild-type, M103I, and K122R in both Huh7 and HepG2 cells (Figures 1A,C). 2012 Journal of viral hepatitis Result HBV M103I;K122R 60;71 65;76 S 22 27 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The G145A, M103I+G145A, K122R+G145A, and M103I+K122R+G145A vectors continued to have higher intracellular HBsAg levels at all time points in Huh7 cells, when above the detection limit. 2012 Journal of viral hepatitis Result HBV G145A;M103I;G145A;G145A;K122R;M103I;G145A;K122R 4;11;17;30;24;41;53;47 9;16;22;35;29;46;58;52 S 106 111 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The most pronounced reductions in HBsAg synthesis was observed with M103I+K122R+G145A (Figure 2, Supplemental Figure 3). 2012 Journal of viral hepatitis Result HBV M103I;K122R;G145A 68;74;80 73;79;85 S 34 39 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. When examining the combined effects of these mutations, M103I+K122R resulted in decreased HBsAg levels in both supernatants (Figures 2A,C) and lysates (Figures 2B,D), but remained well above the ELISA detection limit. 2012 Journal of viral hepatitis Result HBV M103I;K122R 56;62 61;67 S 90 95 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. An unusual mutation, T1884C, was detected in three HBV isolates (SHH0187, SHH219 and SHH246). 2012 PloS one Result HBV T1884C 21 27 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Analysis of 457 sequences from GenBank revealed that the rtE1D mutation was found in genotype B and G isolates from Asian countries. 2012 PloS one Result HBV E1D 59 62 RT 57 59 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. In the polymerase region, the following mutations occurred significantly more frequently in HBV isolated from HIV-co-infected individuals than in isolates of the same cluster on the phylogenetic tree: spQ23K, spL28P, spS91I, spP132Q, spQ125E and rtE1D (p<0.05). 2012 PloS one Result HBV E1D;Q23K;L28P;S91I;P132Q;Q125E 248;202;210;218;226;235 251;207;215;223;232;241 P;RT 7;246 17;248 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. In the pre-S1, ps1I48V/T occurred more frequently in females than males (p<0.05). 2012 PloS one Result HBV I48V;I48T 19;19 24;24 PreS1;PreS1 7;15 13;18 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Isolates with sV168A occurred more frequently in participants with viral loads greater than 200 IU per ml (p<0.05). 2012 PloS one Result HBV V168A 14 20 S 14 15 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Mutations 1762T/1764A known to down-regulate HBeAg expression at the transcriptional level occurred in eight isolates (SHH009, SHH061, SHH148, SHH180, SHH184, SHH221 and SHH264, SHH274), in five cases occurring together with the T1753C. 2012 PloS one Result HBV T1753C 229 235 C 45 50 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. sQ129R was the only mutation detected in the only isolate sequenced from a true occult HBV infection (SHH107, viral load <200 IU/ml). 2012 PloS one Result HBV Q129R 0 6 S 0 1 HBV infections 87 100 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The classical G1896A mutation occurred in five isolates and in four cases it occurred together with C1858T. 2012 PloS one Result HBV G1896A;C1858T 14;100 20;106 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The following mutations occurred significantly more frequently in HBV isolated from HIV-co-infected individuals in this study than in strains of the same cluster of the phylogenetic tree: in the pre-S1, ps1F25L, ps1V88L/A; in the pre-S2, ps2Q10R, ps2 R48K/T, ps2A53V and in the S region sQ129R/H, sQ164A/V/G/D, sV168A and sS174N (p<0.05). 2012 PloS one Result HBV V88A;V88L;F25L;Q10R;A53V;Q129R;Q129H;Q164A;Q164V;Q164G;Q164D;V168A;S174N;R48K;R48T 215;215;206;241;262;287;287;297;297;297;297;311;322;251;251 221;221;210;245;266;295;295;309;309;309;309;317;328;257;257 PreS1;PreS2;PreS1;PreS1;PreS2;PreS2;PreS2;S;S;S;S;S 195;230;203;212;238;247;259;278;287;297;311;322 201;236;206;215;241;250;262;279;288;298;312;323 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The G1862T, which interferes with post-translational modification of the HBeAg-precursor and affects HBeAg expression occurred in isolates from 7 HBeAg-ve sera. 2012 PloS one Result HBV G1862T 4 10 C;C;C 73;101;146 78;106;151 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The unusual start codon mutation, rtE1D, was seen in eight isolates, which grouped in the "Asian" cluster following phylogenetic analysis. 2012 PloS one Result HBV E1D 36 39 RT 34 36 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. There was no difference in the frequency of the various BCP/PC mutations between the HBsAg+ve and HBsAg-ve groups, except for G1862T, which occurred in HBV from one third of HBsAg-ve participants (7/21), but in none of the isolates from 18 HBsAg+ve participants (p<0.05). 2012 PloS one Result HBV G1862T 126 132 BCP;S;S;S;S;Precore 56;85;98;174;240;60 59;90;103;179;245;62 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. This mutation occurred together with rtS105T+rtH122N in 7 isolates and with rtQ125E in three isolates. 2012 PloS one Result HBV H122N;S105T;Q125E 47;39;78 52;44;83 RT;RT;RT 37;45;76 39;47;78 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Three isolates had drug resistant mutations: SHH011 had rtV214A, SHH074 had rtL180M+rtM204V and SHH130 had rtV173L. 2012 PloS one Result HBV V214A;L180M;M204V;V173L 58;78;86;109 63;83;91;114 RT;RT;RT;RT 56;76;84;107 58;78;86;109 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. When comparing the frequency of mutations in HBsAg+ve and HBsAg-ve individuals, only sS174N occurred more frequently in HBsAg-ve individuals (p<0.05). 2012 PloS one Result HBV S174N 85 91 S;S;S;S 45;58;120;85 50;63;125;86 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. A comparison of the clinical data between patients with or without C-I97F/L showed that this mutation was related to old age (57.4 vs. 2012 PloS one Result HBV I97L;I97F 69;69 75;75 C 67 68 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Among 6 HCC-related preC/C mutations, C-I97F/L, previously known to lead to defects in the HBcAg assembly, was found the most frequently in HCC patients (17 HCC patients). 2012 PloS one Result HBV I97L;I97F 40;40 46;46 C;C;Precore;C 38;91;20;25 39;96;24;26 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 8;140;157 11;143;160 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. As expected, mutation in the 28th codon (tryptophan to stop, designated preC-W28*), previously known as the "mutational hot spot" (1896 preC mutation) leading to the inhibition of HBeAg production and related to the progression of liver diseases, was found most frequently in the preC region (17 patients, 24.3%). 2012 PloS one Result HBV W28X 77 81 C;Precore;Precore;Precore 180;72;136;280 185;76;140;284 Liver disease 231 245 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Five mutations in the C region (C-D32N/H, C-E43K, C-P50A/H/Y, C-A131G/N/P and C-S181H/P) and two in preC (preC-W28* and preC-G29D) were found to affect the HBeAg serostatus. 2012 PloS one Result HBV P50A;A131G;D32H;P50H;P50Y;A131N;A131P;W28X;D32N;E43K;S181H;S181P;G29D 52;64;34;52;52;64;64;111;34;44;80;80;125 60;73;40;60;60;73;73;115;40;48;87;87;129 C;C;C;C;C;C;C;Precore;Precore;Precore 22;32;42;50;62;78;156;100;106;120 23;33;43;51;63;79;161;104;110;124 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Five mutations in the C region (C-P5H/L/T, C-E83D, C-I97F/L, C-L100I and C-Q182K/*) and one in preC (preC-W28*) were found to be related to HCC patients compared to patients at other stages of the disease, such as LC and CH, respectively. 2012 PloS one Result HBV P5H;P5L;P5T;I97L;W28X;E83D;I97F;L100I;Q182K 34;34;34;53;106;45;53;63;75 41;41;41;59;110;49;59;68;82 C;C;C;C;C;C;Precore;Precore 22;32;43;51;61;73;95;101 23;33;44;52;62;74;99;105 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 140;221;214 143;223;216 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. However, the predominance of preC-W28* in HCC patients did not reach a statistically relevant level (p = 0.093). 2012 PloS one Result HBV W28X 34 38 Precore 29 33 Hepatocellular carcinoma 42 45 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. I97F/L (76.5%), p = 0.024] (Table S2). 2012 PloS one Result HBV I97L;I97F 0;0 6;6 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. In the C region, mutation in the 101st codon (leucine to tryptophan or serine, designated C-L101W/S) was found the most frequently (22 patients, 31.4%). 2012 PloS one Result HBV L101W;L101S 92;92 99;99 C;C 7;90 8;91 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Interestingly, the two negatively related HBeAg mutations in the C region (C-P50A/H/Y and C-A131G/N/P) were located at M2RR. 2012 PloS one Result HBV P50A;A131G;P50H;P50Y;A131N;A131P 77;92;77;77;92;92 85;101;85;85;101;101 C;C;C;C 65;75;90;42 66;76;91;47 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Notably, the following 4 of 5 HCC-related C mutations, C-P5H/L/T, C-E83D, C-I97F/L and C-L100I, were located at M2RR (one at aa 1-20 and three at aa 81-105. 2012 PloS one Result HBV P5H;P5L;P5T;I97L;E83D;I97F;L100I 57;57;57;76;68;76;89 64;64;64;82;72;82;94 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Of these, the frequencies of five mutations (preC-W28*, C-E43K, C-P50A/H/Y, C-A131G/N/P and C-S181H/P), but not two others (C-G29D and C-D32N/H), reached a statistically significant level. 2012 PloS one Result HBV P50A;A131G;W28X;P50H;P50Y;A131N;A131P;D32H;E43K;S181H;S181P;G29D;D32N 66;78;50;66;66;78;78;137;58;94;94;126;137 74;87;54;74;74;87;87;143;62;101;101;130;143 C;C;C;C;C;C;Precore 56;64;76;92;124;135;45 57;65;77;93;125;136;49 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Of those, two mutations (C-D32N/H, C-E43K) and five other mutations (preC-W28*, C-G29D, C-P50A/H/Y, C-A131G/N/P and C-S181H/P) were found to be related to the HBeAg-positive and HBeAg-negative serostatus, respectively. 2012 PloS one Result HBV P50A;A131G;D32H;W28X;P50H;P50Y;A131N;A131P;D32N;E43K;G29D;S181H;S181P 90;102;27;74;90;90;102;102;27;37;82;118;118 98;111;33;78;98;98;111;111;33;41;86;125;125 C;C;C;C;C;C;C;C;Precore 25;35;80;88;100;116;159;178;69 26;36;81;89;101;117;164;183;73 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. Patients with any genomic change in HBV (G1896A in precore region, A1762T/G1764A in BCP region, C1653T and T1753V in X region, or pre-S2 deletion) did not exhibit different survival periods from those without such changes (Table 3). 2013 Annals of surgical oncology Result HBV G1764A;G1896A;A1762T;C1653T;T1753V 74;41;67;96;107 80;47;73;102;113 BCP;Precore;PreS2;X 84;51;130;117 87;58;136;118 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. Point mutation of C1653T and T1753V in the X region was found in 24 % and 16 % of the patients, respectively. 2013 Annals of surgical oncology Result HBV C1653T;T1753V 18;29 24;35 X 43 44 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. Presence of BCP double mutations at A1762T/G1764A was found in 80 % of the subjects. 2013 Annals of surgical oncology Result HBV G1764A;A1762T 43;36 49;42 BCP 12 15 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The G1896A mutation in the PC region was detected in 51 % of patients with HBV-associated HCC. 2013 Annals of surgical oncology Result HBV G1896A 4 10 Precore 27 29 Hepatocellular carcinoma 90 93 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The presence of mutants such as G1896A in the precore region, A1762T/G1764A in the BCP region, and C1653T and T1753V in the X gene of HBV were not associated with postoperative recurrence of HCC in patients with HBV-associated HCC treated with curative surgical resection. 2013 Annals of surgical oncology Result HBV G1764A;G1896A;A1762T;C1653T;T1753V 69;32;62;99;110 75;38;68;105;116 BCP;Precore;X 83;46;124 86;53;125 Hepatocellular carcinoma;Hepatocellular carcinoma 191;227 194;230 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. After injection of the wild type (pHBV4.1) or the mutant (pHBVrtA181T/sW172*) plamids, the level of serum HBsAg in mice injected with the wild type plasmid was very high (OD>2.4) on day 1, 3, and 5, and became low (OD<0.2) since day 7. 2012 Virology journal Result HBV W172X 70 76 S;S 106;70 111;71 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Compared to wild type HBV, the rtA181T mutant remained sensitive to ETV, but had a reduced susceptibility to LAM, ADV and LdT, as the inhibition effects decreased about 2.36-fold, 1.77-fold and 1.74-fold (Figure 5). 2012 Virology journal Result HBV A181T 33 38 RT 31 33 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Compared to wild type, the rtA181T/sW172* mutant strain showed an approximately 0.8 log reduction on day 1, 2.6 log reduction on day 3, 1.5 log reduction on day 5, and 0.7 log reduction on day 7 in serum HBV DNA titers. 2012 Virology journal Result HBV W172X;A181T 35;29 41;34 RT;S 27;35 29;36 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. However, the HBV DNA replication intermediates levels of the HBV mutant rtA181T/sW172* were detectable from day 1 to day 15 and peaked on day 3 and day 5 (Figure 3B). 2012 Virology journal Result HBV W172X;A181T 80;74 86;79 RT;S 72;80 74;81 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. In order to investigate the transcriptional character of the HBV rtA181T/sW172* mutant strain, HBV RNA levels in mouse liver were evaluated by northern blotting analysis (Figure 2A, B) and qPCR (Figure 2C, D). 2012 Virology journal Result HBV W172X;A181T 73;67 79;72 RT;S 65;73 67;74 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. To analyze the effects of the HBV rtA181T/sW172* mutation on antiviral drug resistance, the inhibitory effects of four anti-HBV drugs on replication of the wild type and mutant HBV were compared. 2012 Virology journal Result HBV W172X;A181T 42;36 48;41 RT;S 34;42 36;43 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. A1762T/G1764A mutations, HBV subgenotypes and serum HBeAg status. 2012 Iranian journal of public health Result HBV G1764A;A1762T 7;0 13;6 C 52 57 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. CHB; respectively) and A1762T/G1764A mutations (57.33% vs. 2012 Iranian journal of public health Result HBV G1764A;A1762T 30;23 36;29 Chronic Hepatitis B 0 3 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV subgenotypes, A1762T/G1764A mutations and clinicopathological characteristics in HCC patients. 2012 Iranian journal of public health Result HBV G1764A;A1762T 25;18 31;24 Hepatocellular carcinoma 85 88 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Serological markers, HBV DNA, HBV genotypes/subgenotypes and A1762T/G1764A mutations in 466 patients. 2012 Iranian journal of public health Result HBV G1764A;A1762T 68;61 74;67 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. The results of serological tests, HBV genotypes/subgenotypes and A1762T/G1764A mutations in subjects with CHB (n=160), LC (n=150) and HCC (n=156) were listed in Table 1. 2012 Iranian journal of public health Result HBV G1764A;A1762T 72;65 78;71 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 106;134;119 109;137;121 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. To investigate whether HBV subgenotypes and A1762T/G1764A mutations were responsible to clinicopathological characteristics in HCC patients, we gathered four important clinicopathological parameters from 156 HCC patients which could represent for clinical behaviors of tumor. 2012 Iranian journal of public health Result HBV G1764A;A1762T 51;44 57;50 Hepatocellular carcinoma;Hepatocellular carcinoma 127;208 130;211 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. We focused on the relationship of serum HBeAg status, HBV genotypes/subgenotypes and A1762T/G1764A mutations. 2012 Iranian journal of public health Result HBV G1764A;A1762T 92;85 98;91 C 40 45 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. Furthermore, the prevalence of the T1753V mutation in the Minangkabau ethnic group was significantly higher than in the non-Minangkabau ethnic group (50.0% vs 19.2%, P=0.015) (Table 1). 2013 Virology journal Result HBV T1753V 35 41 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The mutations A1762T/G1764A and T1753V were found in high prevalence, 35/58 (60.3%) and 21/58 (36.2%) respectively. 2013 Virology journal Result HBV G1764A;A1762T;T1753V 21;14;32 27;20;38 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The T1753V mutation was found in 51.9% and 27.4% of the Minangkabau and Javanese ethnic groups (P=0.007), whilst the A1762T/G1764A mutation was detected in 71.2% and 41.9% of the Minangkabau and Javanese ethnic groups (P=0.002) (Table 2). 2013 Virology journal Result HBV G1764A;T1753V;A1762T 124;4;117 130;10;123 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. All observed strains who carried mutations at nt 1726 (C to A), nt 1727 (T to A or G) and nt 1730 (G to C) in EnhII region, had BCP mutation at position 1802C-1803G. 2012 Hepatitis monthly Result HBV C1726A;T1727A;G1730C 49;67;93 62;80;106 BCP;Enh II 128;110 131;115 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. All of them had C to T change at nt 1858. 2012 Hepatitis monthly Result HBV C1858T 16 40 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. Of limited number of 1858C variant virus examined in this study, none of them was found to have 1896A mutation when mutant G1896A was associated with double mutation A1850T and C1858T. 2012 Hepatitis monthly Result HBV G1896A;A1850T;C1858T 123;166;177 129;172;183 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. Only 20 isolates out of 34 HBeAg-negative cases were found to have G to A mutation at nt 1896. 2012 Hepatitis monthly Result HBV G1896A 67 93 C 27 32 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. The samples of 39 patients containing wild-type strain at position 1721, had G1719T, C1726A, T1727A and G1730C mutations. 2012 Hepatitis monthly Result HBV G1719T;C1726A;T1727A;G1730C 77;85;93;104 83;91;99;110 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. The wild-type strain for nt 1703 present in 18 samples, had the wild-type at the positions 1701, 1702, 1721, 1728 and 1740, but had mutant-type at nt 1719 (G to T), nt 1726 (C to A), nt 1727 (T to A) and nt 1730 (G to C). 2012 Hepatitis monthly Result HBV G1719T;C1726A;T1727A;G1730C 150;168;186;207 163;181;199;220 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Another point mutation, the T1753V in the X region did not show significant difference in prevalence between patients with HCC and CHB [17% (49/284) vs 14% (29/210), P > 0.05]. 2013 Journal of viral hepatitis Result HBV T1753V 28 34 X 42 43 Hepatocellular carcinoma;Chronic Hepatitis B 123;131 126;134 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. However, combinations of A1762T/G1764A and T1753V or pre-S deletions did not differ significantly between the two groups. 2013 Journal of viral hepatitis Result HBV G1764A;A1762T;T1753V 32;25;43 38;31;49 PreS 53 58 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. In addition, coexistence of two X gene mutations such as C1653T and T1753V was more frequent in the HCC than in the CHB group [n = 17 (6%) vs n = 4 (2%), P = 0.025]. 2013 Journal of viral hepatitis Result HBV C1653T;T1753V 57;68 63;74 X 32 33 Hepatocellular carcinoma;Chronic Hepatitis B 100;116 103;119 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Moreover, the coexistence of A1762T/G1764A and C1653T was another risk factor for HCC, which had an OR of 5.396 (95% CI, 1.106-26.319, P = 0.037). 2013 Journal of viral hepatitis Result HBV G1764A;A1762T;C1653T 36;29;47 42;35;53 Hepatocellular carcinoma 82 85 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. On the other hand, other combinations of mutations such as G1896A and pre-S deletion, pre-S deletion and C1653T, and pre-S deletion and T1753V did not show significant differences between groups. 2013 Journal of viral hepatitis Result HBV G1896A;C1653T;T1753V 59;105;136 65;111;142 PreS;PreS;PreS 70;86;117 75;91;122 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Similarly, combination of the G1896A and T1753V in the X region was associated more frequently with HCC rather than CHB [n = 23 (8%) vs n = 7 (3%), P = 0.035]. 2013 Journal of viral hepatitis Result HBV G1896A;T1753V 30;41 36;47 X 55 56 Hepatocellular carcinoma;Chronic Hepatitis B 100;116 103;119 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The BCP double mutation A1762T/G1764A was found in 73% (202/278) of patients with HCC and 65% (132/204) of patients with CHB, but this difference was not statistically significant (P = 0.072). 2013 Journal of viral hepatitis Result HBV G1764A;A1762T 31;24 37;30 BCP 4 7 Hepatocellular carcinoma;Chronic Hepatitis B 82;121 85;124 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The C1653T mutation in the X region was found in 22% (62/281) and 11% (24/210) of the HCC and CHB groups, respectively (P = 0.003). 2013 Journal of viral hepatitis Result HBV C1653T 4 10 X 27 28 Hepatocellular carcinoma;Chronic Hepatitis B 86;94 89;97 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The combination of G1896A and C1653T was observed in 12% of the HCC group and in just 2% of the control group. 2013 Journal of viral hepatitis Result HBV G1896A;C1653T 19;30 25;36 Hepatocellular carcinoma 64 67 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The combination of the BCP double mutation, A1762T/G1764A and C1653T in the X region, tended to occur more frequently in patients with HCC compared with the controls [n = 44 (16%) vs n = 21 (10%), P = 0.08]. 2013 Journal of viral hepatitis Result HBV G1764A;A1762T;C1653T 51;44;62 57;50;68 BCP;X 23;76 26;77 Hepatocellular carcinoma 135 138 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The combined BCP double mutation, A1762T/G1764A and the G1896A in the PC region, were more common in the HCC group compared with the CHB group [n = 102 (37%) vs n = 26 (13%), P < 0.001]. 2013 Journal of viral hepatitis Result HBV G1764A;A1762T;G1896A 41;34;56 47;40;62 BCP;Precore 13;70 16;72 Hepatocellular carcinoma;Chronic Hepatitis B 105;133 108;136 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The G1896A mutation in the PC region was more frequently seen in patients with HCC than in patients with CHB [50% (142/282) vs 23% (48/210), P < 0.001]. 2013 Journal of viral hepatitis Result HBV G1896A 4 10 Precore 27 29 Hepatocellular carcinoma;Chronic Hepatitis B 79;105 82;108 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The presence of C1653T in the X region (OR, 5.278; 95% CI, 1.182-23.575; P = 0.029) and older age (OR, 1.094; 95% CI, 1.069-1.120; P < 0.001) were also significant risk factors for HCC development. 2013 Journal of viral hepatitis Result HBV C1653T 16 22 X 30 31 Hepatocellular carcinoma 181 184 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The presence of the G1896A in the PC region was independently associated with the development of HCC [odds ratio (OR), 2.725; 95% confidence interval (CI), 1.260- 5.894; P = 0.011]. 2013 Journal of viral hepatitis Result HBV G1896A 20 26 Precore 34 36 Hepatocellular carcinoma 97 100 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. All the isolates having rtI91L were associated with rtV103I. 2013 Virology journal Result HBV I91L;V103I 26;54 30;59 RT;RT 24;52 26;54 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Among the treated patients no primary antiviral drug resistant mutations, confirmed by in vitro studies as associated with resistance to NA (rtL80I/V-rtI169T-rtV173LrtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-rtM204V/I-rtN236T-rtM250V) were found. 2013 Virology journal Result HBV L80I;L80V;I169T;A181T;A181V;A181S;T184A;T184S;T184G;T184C;A194T;S202C;S202G;S202I;M204V;M204I;N236T;M250V 143;143;152;175;175;175;187;187;187;187;201;209;209;209;221;221;231;239 149;149;157;184;184;184;198;198;198;198;206;218;218;218;228;228;236;244 RT;RT;RT;RT;RT;RT;RT;RT;RT 141;150;173;185;199;207;219;229;237 143;152;175;187;201;209;221;231;239 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Analysis of pol gene mutations with respect to the genotype distributation showed that rtI91L and rtV103I was found among the HBV/A and HBV/D but not in HBV/C. 2013 Virology journal Result HBV I91L;V103I 89;100 93;105 P;RT;RT 12;87;98 15;89;100 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. The known lamivudine (LMV) resistant mutation rtI187L was found in two therapy naive patients. 2013 Virology journal Result HBV I187L 48 53 RT 46 48 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. The prevalence of rtI91L was 80% (24/30) among them. 2013 Virology journal Result HBV I91L 20 24 RT 18 20 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Two stop codon mutations were identified at position rtS106* and rtY111* in HBV/D genotype and both was found to be present as unique viral variant. 2013 Virology journal Result HBV S106X;Y111X 55;67 60;72 RT;RT 53;65 55;67 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Effect of rtI233V mutation and adefovir action: Molecular modeling and docking analysis. 2013 Bioinformation Result HBV I233V 12 17 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Furthermore, two subjects with pre-existing rtI233V mutation at baseline (treatment-naive) responded to lamivudine and entecavir subsequently in our center (unpublished data). 2013 Bioinformation Result HBV I233V 46 51 RT 44 46 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. It was further attempted to study whether rtI233V substitution would alter the relative positions of neighbouring residues and alter the conformation. 2013 Bioinformation Result HBV I233V 44 49 RT 42 44 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The wild type model exhibited the best docking energy of -5.97 Kcal/mol and the rtI233V mutation decreased the docking score to less than 1 Kcal/mol (-5.19 Kcal/mol; Table 1 (see supplementary material). 2013 Bioinformation Result HBV I233V 82 87 RT 80 82 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Therefore rtI233V mutation does not show any significant changes in the binding of adefovir. 2013 Bioinformation Result HBV I233V 12 17 RT 10 12 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Therefore, it was predicted that rtI233V substitution in the reverse transcriptase domain may not affect the antiviral action of adefovir and dNTP binding. 2013 Bioinformation Result HBV I233V 35 40 RT;RT 61;33 82;35 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. This again shows that rtI233V mutation does not alter the antiviral efficacy to any of these drugs. 2013 Bioinformation Result HBV I233V 24 29 RT 22 24 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. By electron microscopy of concentrated Huh7 cell medium 22 h after infection we could confirm that the G2S variant was released as 22 nm subviral particles with an accessible preS1 antigen on the surface as shown by binding of MAb MA18/7 and subsequent anti-mouse IgG conjugated with 5 nm gold particles (Figure 2) according to the method of Louro and Lesemann. 2013 Virology journal Result HBV G2S 103 106 PreS1;S 175;196 180;203 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Its variant with Gly 2 substituted to Ser (pSFV1-G2S 1-48preS/S) (Figure 1A) was generated by amplification of the corresponding gene from the plasmid pFD Pr[13-59]S (kindly provided by K. 2013 Virology journal Result HBV G2S;G2S 49;17 52;41 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Sasnauskas) by forward primer 5' GACACAGATCTGCCGCCACCATGTCTCAGAATCTTTCCAC 3'; the G2A variant (pSFV1-G2A 1-48preS/S) (Figure 1A) was generated by forward primer 5' GACACAGATCTGCCGCCACCATGGCCCAGAATCTTTCCAC 3' from plasmid pFD GlyPr[13-59] (gift from K. 2013 Virology journal Result HBV G2A;G2A 82;101 85;104 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. The glycosylation pattern of the in-frame co-expressed S protein was not affected, S protein could be detected in single glycosylated and unglycosylated form for the G2A and G2S 1-48preS/S mutants. 2013 Virology journal Result HBV G2S;G2A 174;166 177;169 S;S 55;83 56;84 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. To examine how mutation of the myristoylation site affects the subcellular localization of L protein deletion variants, BHK-21 cells were infected with rSFV encoding 1-48preS1/S, G2S and G2A mutants and were analyzed by confocal immunofluorescence microscopy. 2013 Virology journal Result HBV G2S;G2A 179;187 182;190 S 91 100 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. We observed a slightly but significantly reduced secretion of the 1-48preS/S variant with an inactivated myristoylation site (G2A or G2S) compared to the unmodified variant, although the intracellular expression level of the wt and the G2S mutant was equal (Table 1). 2013 Virology journal Result HBV G2S;G2S;G2A 133;236;126 136;239;129 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. A minor groove binding modification was used to enhance the specificity of the probe designed to bind the rtL180M T to A mutation, which lies between the rt173 and rt204 mutations (Figure 1). 2013 Journal of virological methods Result HBV L180M 108 113 RT;RT;RT 106;154;164 108;156;166 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Additional specificity testing was performed on single mutant templates (rtL180M, rtM204V, or rtV173L) and the double mutant template rtM204V and L180M, the most common clinically relevant double mutant. 2013 Journal of virological methods Result HBV L180M;M204V;V173L;M204V;L180M 75;84;96;136;146 80;89;101;141;151 RT;RT;RT;RT 73;82;94;134 75;84;96;136 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Previous consensus sequencing characterized the sample as containing HBV genotype A with the rtM204V mutation, but the additional rtV173L and rtL180M mutations were not detected (data not shown). 2013 Journal of virological methods Result HBV M204V;V173L;L180M 95;132;144 100;137;149 RT;RT;RT 93;130;142 95;132;144 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Subsequently, an allele-specific rtL180M probe was designed to have a compatible Tm for use with the LNA primers in a TaqMan probe-based qPCR. 2013 Journal of virological methods Result HBV L180M 35 40 RT 33 35 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. The sensitivity of the quantitative triple mutant assay was determined using 3microL per reaction of serial 10 fold dilutions, plus an extra point at 50 copies/microL, of rtV173L+rtL180M+rtM204V triple mutant plasmid DNA. 2013 Journal of virological methods Result HBV V173L;M204V;L180M 173;189;181 178;194;186 RT;RT;RT 171;179;187 173;181;189 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. There was also no amplification of the rtM204V+rtL180M double mutant at concentrations of 3x104 or 3x105 copies (Figure 2E-F). 2013 Journal of virological methods Result HBV L180M;M204V 49;41 54;46 RT;RT 39;47 41;49 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. There was no amplification at 3x108 copies of the single mutants rtL180M, rtM204V, or rtV173L (Figure 2B-D). 2013 Journal of virological methods Result HBV L180M;M204V;V173L 67;76;88 72;81;93 RT;RT;RT 65;74;86 67;76;88 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. After alignment of protein coding sequences, the rtN236T mutation was observed in two (6.6%) patients. 2013 Iranian journal of microbiology Result HBV N236T 51 56 RT 49 51 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. LAM resistance analysis using RFLP method identified the type of YMDD mutations; 24(80%) patients had the rtM204I mutation, 2 (6.6%) had the rtM204V and 4(13.3%) had both. 2013 Iranian journal of microbiology Result HBV M204I;M204V 108;143 113;148 RT;RT;P 106;141;65 108;143;69 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. while twenty eight others had neither rtN236T, nor rtA181V/T mutation (Table 2.) Genetic distance was estimated using the Kimura two-parameter matrix and phylogenetic tree was constructed by the neighbor-joining (NJ) method. 2013 Iranian journal of microbiology Result HBV A181V;A181T;N236T 53;53;40 60;60;45 RT;RT 38;51 40;53 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. ADV resistance rtA181T associated mutations were detected in 5 (2.2%) cases; among those, 3 had never received ADV. 2013 Virology journal Result HBV A181T 17 22 RT 15 17 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Amino-acid change rtM180L was found in 87.5% of the cases associated with rtM204I or V but was found as an isolated mutation in 8 remaining cases. 2013 Virology journal Result HBV M204I;M180L 76;20 81;25 RT;RT 18;74 20;76 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Amino-acid change sG145R was found in only one patient but sG145A, less frequently described, was detected in 5 sequences (2%). 2013 Virology journal Result HBV G145R;G145A 18;59 24;65 S;S 18;59 19;60 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Overall, only 1 patient who had never received 3TC or FTC for HBV- or HIV-infection presented M204V and L180M mutations. 2013 Virology journal Result HBV M204V;L180M 94;104 99;109 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. rtV173L, rtL180M, rtA181V/T, rtT184G, rtS202I, rtM204V/I, rtN236T and rtM250V were first studied and then, others residues with changes present in at least two patients were further considered. 2013 Virology journal Result HBV L180M;A181V;A181T;M204V;M204I;M250V;V173L;T184G;S202I;N236T 11;20;20;49;49;72;2;31;40;60 16;27;27;56;56;77;7;36;45;65 RT;RT;RT;RT;RT;RT;RT;RT 0;9;18;29;38;47;58;70 2;11;20;31;40;49;60;72 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. The most prevalent resistant mutations were rtL180M (28.7%; 64/223) and rtM204V/I (26%; 58/223). 2013 Virology journal Result HBV M204V;M204I;L180M 74;74;46 81;81;51 RT;RT 44;72 46;74 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. In the study subjects with the data of HBV mutations in the EnhII/BCP/PC region, pri-miR-34b/c rs4938723 in dominant genetic model was significantly associated with an increased risk of HCC whereas its interaction with C1730G, a HBV mutation inversely associated with HCC risk, was significantly associated with a reduced risk of HCC; the interaction of pre-miR-196a2 rs11614913 TC genotype with G1896A was significantly associated with an increased risk of HCC (Table 4). 2013 PloS one Result HBV C1730G;G1896A 219;396 225;402 BCP;Enh II;Precore 66;60;70 69;65;72 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 186;268;330;458 189;271;333;461 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. In those with the data of HBV mutations in the preS region, pri-miR-34b/c rs4938723 in dominant genetic model was significantly associated with an increased risk of HCC whereas its interactions with viral mutations were not significantly associated with HCC risk; the interaction of pre-miR-196a2 rs11614913 TC genotype with A3120G/T was significantly associated with a reduced risk of HCC, although A3120G/T was a risk factor of HCC (Table 5). 2013 PloS one Result HBV A3120T;A3120G;A3120G;A3120T 325;325;400;400 333;333;408;408 PreS 47 51 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 165;254;386;430 168;257;389;433 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. It was found that pri-miR-34b/c rs4938723 CC genotype was significantly associated with increased frequency of T1674C/G, while pre-miR-196a2 rs11614913 TC genotype was significantly associated with increased frequency of G1896A (Table 3). 2013 PloS one Result HBV T1674C;T1674G;G1896A 111;111;221 119;119;227 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. The HBV mutations including T1674C/G, A1762T/G1764A, T1753V, C1653T, and G1896A in the EnhII/BCP/PC as well as preS deletion, preS1 start codon mutation, preS2 start codon mutation, C2875A, A3120G/T, C7A, and C76A in the preS region were significantly associated with an increased risk of HCC, while C1730G and C1799G were inversely associated with HCC risk. 2013 PloS one Result HBV G1764A;T1674G;A3120T;C7A;T1674C;A1762T;T1753V;C1653T;G1896A;C2875A;A3120G;C76A;C1730G;C1799G 45;28;190;200;28;38;53;61;73;182;190;209;300;311 51;36;198;203;36;44;59;67;79;188;198;213;306;317 BCP;Enh II;Precore;PreS;PreS;PreS1;PreS2 93;87;97;111;221;126;154 96;92;99;115;225;131;159 Hepatocellular carcinoma;Hepatocellular carcinoma 289;349 292;352 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Common and frequent lamivudine-related amino acid substitutions were found in this study including N53K 3.68% (12/325), L80V/I 3.07% (each 5/325), L82M1.22% (4/325) L91I 7.06% (23/325), T128I 1,53% (5/325), L180M3.37% (11/325), and M204I2.76%(9/325) M204V 1.23% (4/325) see Figure 1. 2013 Hepatitis monthly Result HBV L80I;N53K;L80V;L91I;T128I;M204V 120;99;120;165;186;250 126;103;126;169;191;255 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Cross-resistance mutations to lamivudine and entecavirwere: M204I 2.76% (9/325) and M204V/I + L180M 2.45% (8/325) (Figure 1). 2013 Hepatitis monthly Result HBV M204I;M204I;M204V;L180M 84;60;84;94 91;65;91;99 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Cross-resistance mutations to lamivudineand telbivudinewere: M204I 2.76% (9/325), M204V 1.23% (4/325), M204V/I + L180M 2.45% (8/325), and L80I + M204I 1.23% (4/325). 2013 Hepatitis monthly Result HBV M204V;M204I;M204V;M204I;L180M;L80I;M204I 82;61;103;103;113;138;145 87;66;110;110;118;142;150 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. RT sequence changes implicated in adefovir-resistance were detected, including S213T 5.83% (19/325), S213N 0.9% (3/325), V214E 0.61% (2/325), V214A 0.61% (2/325), Q215P 2.75% (9/325), Q215S 7.06% (23/325), Q215H1.53% (5/325), and F221Y 2.76% (9/325) of isolations that previously reported adefovir-resistance mutation (Figure 1). 2013 Hepatitis monthly Result HBV S213T;S213N;V214E;V214A;Q215P;Q215S;F221Y 79;101;121;142;163;184;230 84;106;126;147;168;189;235 RT 0 2 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. In the present study, we found two patterns of basal core promoter mutations included A1762A/G1764T and A1762T/G1764A. 2013 Hepatitis monthly Result HBV G1764T;G1764A;A1762A;A1762T 93;111;86;104 99;117;92;110 BCP 47 66 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. We did not observe the mutation pattern of A1762A/G1764A in the promoter core. 2013 Hepatitis monthly Result HBV G1764A;A1762A 50;43 56;49 C 73 77 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Among six patients with LAM failure, cloning and sequencing data on the RT region of HBV revealed that LAM resistance mutation, L180M or M204V/I substitutions, pre-existed in patient 1, 2, 5, and 6, albeit a small percentage (1% to 2%). 2013 Gut and liver Result HBV L180M;M204V;M204I 128;137;137 133;144;144 RT 72 74 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. At 6 months of LAM therapy, quasispecies variants bearing LAM resistance mutations, M204V/I+L180M, appeared in all six patients. 2013 Gut and liver Result HBV M204V;M204I;L180M 84;84;92 91;91;97 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. At baseline, some colonies contained LAM or ETV resistant mutations such as L80V/I, L180M, M204V/I, A181V, and N236H. 2013 Gut and liver Result HBV L80I;L80V;L180M;M204V;M204I;A181V;N236H 76;76;84;91;91;100;111 82;82;89;98;98;105;116 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 1, 23 of 100 clones (23%) contained T38A+H55A, which was followed by T38A (21%), and E271Q (20%). 2013 Gut and liver Result HBV T38A;H55A;T38A;E271Q 47;52;80;96 51;56;84;101 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 1, 3, and 4, I169L substitution was also detected. 2013 Gut and liver Result HBV I169L 24 29 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 1, ADV-associated variant N236H newly emerged in conjunction with M204I substitution. 2013 Gut and liver Result HBV N236H;M204I 37;77 42;82 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 1, changes of the P gene, rtW153Q, rtI169L, rtV173L, rtA181V, and rtM204V, corresponded to change of the S gene, rtG145R, rtF161H, rtE164D, and rtI195M, respectively (Table 4). 2013 Gut and liver Result HBV A181V;W153Q;I169L;V173L;M204V;G145R;F161H;E164D;I195M 66;39;48;57;79;126;135;144;157 71;44;53;62;84;131;140;149;162 P;RT;RT;RT;RT;RT;RT;RT;RT;RT;S 29;37;46;55;64;77;124;133;142;155;116 30;39;48;57;66;79;126;135;144;157;117 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 2, rtW153Q and rtW196L change, a termination codon caused by rtM204, was detected. 2013 Gut and liver Result HBV W153Q;W196L 16;28 21;33 RT;RT;RT 14;26;72 16;28;74 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In patient 3 and 4, ADV related changes, N236H and A181T, became undetectable at this time point. 2013 Gut and liver Result HBV N236H;A181T 41;51 46;56 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Interestingly, the colonies of patient 3 contained S202G, which is known as ETV signature resistance, in conjunction with I169L. 2013 Gut and liver Result HBV S202G;I169L 51;122 56;127 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Moreover, 1% of the clones in patient 1 and 4 harbored ADV resistance mutations, A181V. 2013 Gut and liver Result HBV A181V 81 86 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Neither L180M nor A181V mutation was detected in the six responders (Table 2). 2013 Gut and liver Result HBV L180M;A181V 8;18 13;23 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The ADV resistance mutation, rtA181V resulted in a concomitant change of rtL173F in patient 4. 2013 Gut and liver Result HBV A181V;L173F 31;75 36;80 RT;RT 29;73 31;75 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The predominant HBV quasispecies in patient 2 was R242A (36%), and the remaining were N76D+D134E (20%), D134E+R242A (17%), and D134E (13%). 2013 Gut and liver Result HBV R242A;N76D;D134E;R242A;D134E;D134E 50;86;91;110;104;127 55;90;96;115;109;132 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Whereas, only M204V/I substitution was identified in 1% of the clones in one patient who responded to LAM therapy. 2013 Gut and liver Result HBV M204V;M204I 14;14 21;21 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. While ETV-related mutations became undetectable in patient 1, 3, and 4, I169L+L180M+M204V was detected in patient 6. 2013 Gut and liver Result HBV L180M;I169L;M204V 78;72;84 83;77;89 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. Of 24 cases with the rtM204I mutation, three had co-dominant rtM204I and rtL180M mutations. 2013 Hepatitis monthly Result HBV M204I;M204I;L180M 23;63;75 28;68;80 RT;RT;RT 21;61;73 23;63;75 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. One patient had a mixed pattern of rtM204I/V and rtL180M mutations. 2013 Hepatitis monthly Result HBV M204V;M204I;L180M 37;37;51 44;44;56 RT;RT 35;49 37;51 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. The rtM204I mutation in the HBV polymerase gene was detected in 24 patients; the remaining patients had wild-type rt204 and rt180. 2013 Hepatitis monthly Result HBV M204I 6 11 P;RT;RT;RT 32;4;114;124 42;6;116;126 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. The genotypic characteristics of these 51 HBVCI patients were also assayed, including genotype, precore stop codon G1896A mutation, BCP A1762T/G1764A mutation, pre-S deletion mutation and sequence analysis of the whole S coding region (Table 5). 2013 PloS one Result HBV G1764A;G1896A;A1762T 143;115;136 149;121;142 BCP;Precore;PreS;S 132;96;160;219 135;103;165;220 HBV-HCV coinfections 42 47 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. A1762T/G1764A was found in 11 G1896A mutants and in one T1815C mutant. 2013 BMC infectious diseases Result HBV G1764A;A1762T;G1896A;T1815C 7;0;30;56 13;6;36;62 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. In 22/49 HBeAg-negative sera, the absence of HBeAg was as a result of missense mutations affecting the translation of the HBeAg precursor: 18 had the classical stop codon mutation G1896A (p< 0.05, when comparing isolates from HBeAg-negative and -positive sera) and 4 had initiation codon mutations, 2 A1814T and 2 T1815C. 2013 BMC infectious diseases Result HBV G1896A;A1814T;T1815C 180;301;314 186;307;320 C;C;C;C 9;45;122;226 14;50;127;231 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. In the reverse transcriptase domain of the polymerase, the following mutations were detected: rtA194T in SDAC049 (genotype D), rtV207M in SDAC020 (genotype D), rtS213T in SDAC063 and SDAC098 (genotype D), SDAC002, SDAC121 and SDAC004 (genotype E), rtV214A in SDAC059 (genotype E) and rtS215Q in SDAC049 and SDAC090 (genotype D). 2013 BMC infectious diseases Result HBV A194T;V214A;V207M;S213T;S215Q 96;250;129;162;286 101;255;134;167;291 P;RT;RT;RT;RT;RT;RT 43;7;94;127;160;248;284 53;28;96;129;162;250;286 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. One genotype A isolate from a HBeAg-positive patient, (SDAC108) had A1762T/G1764A. 2013 BMC infectious diseases Result HBV G1764A;A1762T 75;68 81;74 C 30 35 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. One isolate had wild-type BCP/PC region, two had A1762T/G1764A, one with G1862T and the fourth isolate had G1862T alone. 2013 BMC infectious diseases Result HBV G1764A;A1762T;G1862T;G1862T 56;49;73;107 62;55;79;113 BCP;Precore 26;30 29;32 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. SDAC031 (D6) showed preS2I42T, spV59F and rtT237P. 2013 BMC infectious diseases Result HBV T237P;I42T;V59F 44;25;32 49;29;37 PreS2;RT 20;42 25;44 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. SDAC085 (D6) had spV59S. 2013 BMC infectious diseases Result HBV V59S 18 23 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. SDAC107 (D6) had preS2I42T and rtT237P. 2013 BMC infectious diseases Result HBV T237P;I42T 33;22 38;26 PreS2;RT 17;31 22;33 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Seven of 8 genotype D or E isolates from HBeAg-positive patients had wild-type BCP/PC, and one (SDAC118) had G1764T. 2013 BMC infectious diseases Result HBV G1764T 109 115 BCP;C;Precore 79;41;83 82;46;85 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Six isolates from HBeAg-negative sera had A1762T/G1764A alone. 2013 BMC infectious diseases Result HBV G1764A;A1762T 49;42 55;48 C 18 23 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. The vaccine escape mutation, sM133T, was observed in genotype E isolates, SDAC022, SDAC067 and SDAC088. 2013 BMC infectious diseases Result HBV M133T 29 35 S 29 30 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Three cis-acting elements mutations were found: C1092T in the Enhancer I in one isolate, C1155T in the Enhancer I in 6 isolates and T3109G S2 promoter in 2 isolates. 2013 BMC infectious diseases Result HBV C1092T;C1155T;T3109G 48;89;132 54;95;138 Enh I;Enh I;S2 promoter 62;103;139 72;113;150 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Each of the combined mutations detected in this study included the A1762T and/or the G1764A variant. 2013 Brazilian journal of medical and biological research Result HBV A1762T;G1764A 67;85 73;91 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Four mutation patterns (C1810T, A1846T, G1862T, and G1896A) close to the precore region were more prevalent in the patients with the B2 than with the C2 subgenotype (P<0.001; Table 5). 2013 Brazilian journal of medical and biological research Result HBV C1810T;A1846T;G1862T;G1896A 24;32;40;52 30;38;46;58 Precore 73 80 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Seven mutation patterns (C1653T, G1719T, G1730C, T1753C, A1762T, G1764A, and G1799C) in the CP region were more prevalent in the patients with the C2 than with the B2 subgenotype (P<0.05). 2013 Brazilian journal of medical and biological research Result HBV C1653T;G1719T;G1730C;T1753C;A1762T;G1764A;G1799C 25;33;41;49;57;65;77 31;39;47;55;63;71;83 Core promoter 92 94 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The A1762T/G1764A double mutation was highly prevalent, occurring in 36.9% of CHB patients, 63.6% of LC patients, and 60.0% of HCC patients. 2013 Brazilian journal of medical and biological research Result HBV G1764A;A1762T 11;4 17;10 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 78;127;101 81;130;103 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The frequencies of 10 mutation patterns (C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, and G1896A) were higher in HCC patients than in CHB patients (P<0.05). 2013 Brazilian journal of medical and biological research Result HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A 41;49;57;65;73;81;89;97;105;117 47;55;63;71;79;87;95;103;111;123 Hepatocellular carcinoma;Chronic Hepatitis B 140;161 143;164 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The frequencies of four mutation patterns close to the precore region (C1810T, A1846T, G1862T, and G1896A) were higher in HCC patients than in LC patients (P<0.05; Table 4). 2013 Brazilian journal of medical and biological research Result HBV C1810T;A1846T;G1862T;G1896A 71;79;87;99 77;85;93;105 Precore 55 62 Hepatocellular carcinoma;Liver cirrhosis 122;143 125;145 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The frequencies of six mutation patterns in the CP region (C1653T, G1730C, T1753C, A1762T, G1764A, and G1799C) were higher in LC patients than in CHB patients (P<0.05). 2013 Brazilian journal of medical and biological research Result HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C 59;67;75;83;91;103 65;73;81;89;97;109 Core promoter 48 50 Chronic Hepatitis B;Liver cirrhosis 146;126 149;128 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. To analyze the independent risk factors for the progression of chronic liver disease, the multiple variants were evaluated by multivariate regression, including HBeAg status, HBV subgenotype, and the presence of C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, or G1896A mutations (Table 7). 2013 Brazilian journal of medical and biological research Result HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A 212;220;228;236;244;252;260;268;276;287 218;226;234;242;250;258;266;274;282;293 C 161 166 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. When CHB patients were the control, HBV subgenotype C2 infection and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) in the CP region were independent risk factors for LC or C2 infection, and eight mutation patterns (C1653T, T1753C, A1762T, G1764A, C1810T, A1846T, G1862T, and G1896A) were independent risk factors for HCC. 2013 Brazilian journal of medical and biological research Result HBV C1653T;T1753C;A1762T;G1764A;C1653T;T1753C;A1762T;G1764A;C1810T;A1846T;G1862T;G1896A 102;110;118;130;238;246;254;262;270;278;286;298 108;116;124;136;244;252;260;268;276;284;292;304 Core promoter 145 147 Chronic Hepatitis B;Hepatocellular carcinoma 5;340 8;343 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. When LC patients were the control, HBV subgenotype B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) close to the precore region were independent risk factors for HCC. 2013 Brazilian journal of medical and biological research Result HBV C1810T;A1846T;G1862T;G1896A 84;92;100;112 90;98;106;118 Precore 133 140 Hepatocellular carcinoma;Liver cirrhosis 182;5 185;7 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. The analysis of mutations in the Enh II, PC and BCP regions of the 10 samples revealed the following results: the mutation G1613A was identified in two samples (20%), two samples (20%) had the mutation pair A1762T/G1764A and one sample carried both G1896A and the A1762T/G1764A double mutation. 2013 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;G1764A;G1613A;A1762T;G1896A;A1762T 214;271;123;207;249;264 220;277;129;213;255;270 BCP;Enh II;Precore 48;33;41 51;39;43 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. The analysis of the MHR mutations revealed a change in residue Q129H in two samples (11%). 2013 Memorias do Instituto Oswaldo Cruz Result HBV Q129H 63 68 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. Two secondary mutations that were potentially associated with resistance, rtV207L and rtN238T, were identified in one (6%) and five (33%) of the analysed samples, respectively. 2013 Memorias do Instituto Oswaldo Cruz Result HBV V207L;N238T 76;88 81;93 RT;RT 74;86 76;88 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. None of the study sequences had a G1896A stop codon mutation. 2013 Journal of medical virology Result HBV G1896A 34 40 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. Six (24%) of the study sequences had preC start codon mutations: three (3321, T033, and N60) had A1814C, two (3354 and 3658) had A1814T, and one (3269) had G1816T. 2013 Journal of medical virology Result HBV A1814C;A1814T;G1816T 97;129;156 103;135;162 Precore 37 41 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. In the pre-S2 region, V39A and L54P were observed in 6 and 4 isolates, respectively. 2013 PloS one Result HBV V39A;L54P 22;31 26;35 PreS2 7 13 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. In the S region, P70H and S143L were found in 2 and 4 isolates, respectively. 2013 PloS one Result HBV P70H;S143L 17;26 21;31 S 7 8 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. Mutation S143L was found in four sequences of genotype C/D in the "a" determinant, which is also related to vaccine escape. 2013 PloS one Result HBV S143L 9 14 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. P130T in the C region and A90V/S in the pre-S1 regions were observed in 2 and 6 isolates, respectively. 2013 PloS one Result HBV P130T;A90V;A90S 0;26;26 5;32;32 C;PreS1 13;40 14;46 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. As with the recently identified T118M mutation in the 'a' determinant of HBsAg , the occurrence of sG145K or sG145R mutants are well reported , and they therefore may have a more significant role in infection diagnosis. 2013 Virology journal Result HBV T118M;G145K;G145R 32;99;109 37;105;115 S;S;S;S 55;73;99;109 69;78;100;110 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Decrease in the antigenicity of sG145R-rtM204I/V HBsAg mutant. 2013 Virology journal Result HBV M204I;M204V;G145R 41;41;32 48;48;38 S;RT;S 49;39;32 54;41;33 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. However, the rtM204V (sW196S) mutation, failed to cause a reduction in avidity in the five ELISA kits tested (Figure 3). 2013 Virology journal Result HBV M204V;W196S 15;22 20;28 RT;S 13;22 15;23 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Interestingly, rtM204V (sW196S) mutation also decreased the antigenicity of sG145R HBsAg but only for the WT and BN ELISA kits (Figure 4). 2013 Virology journal Result HBV M204V;W196S;G145R 17;24;76 22;30;82 S;RT;S;S 83;15;24;76 88;17;25;77 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Negligible decline in the antigenicity of sT118M-rtM204I or sT118M-rtM204V mutant. 2013 Virology journal Result HBV M204I;M204V;T118M;T118M 51;69;42;60 56;74;48;66 RT;RT;S;S 49;67;42;60 51;69;43;61 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Of the five commercial HBsAg ELISA kits used in this study, four kits (LZ, WT, GBT, and BN) recognized the sT118M immune-escaped mutant and recombinant sT118M-rtM204I (sT118M-sI195M) mutant, yielding similar titration curves, and indicating that rtM204I may contribute marginally to the antigenicity of sT118M HBsAg. 2013 Virology journal Result HBV M204I;M204I;T118M;T118M;T118M;T118M;I195M 161;248;107;152;168;303;175 166;253;113;158;174;309;181 S;S;RT;RT;S;S;S;S;S 23;310;159;246;107;152;168;175;303 28;315;161;248;108;153;169;176;304 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Significant reduction in the antigenicity of sG145K-rtM204I HBsAg mutant. 2013 Virology journal Result HBV M204I;G145K 54;45 59;51 S;RT;S 60;52;45 65;54;46 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Similarly, the differences in avidity (as determined by the slope of the curve) was indistinguishable between the sT118M mutant and sT118M-rtM204V (sT118M- sW196S) mutant for all five assays, suggesting that drug-resistant YMDD mutants caused a negligible loss in antigenicity for immune-escaped sT118M HBsAg (Figure 2). 2013 Virology journal Result HBV M204V;T118M;W196S;T118M;T118M;T118M 141;114;156;296;132;148 146;120;162;302;138;154 S;RT;S;S;S;S;S;P 303;139;114;132;148;156;296;223 308;141;115;133;149;157;297;227 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The antigenicity profile also decreased for sG145R HBsAg when coupled with mutation rtM204I (sI195M) for all of the ELISA kits. 2013 Virology journal Result HBV M204I;G145R;I195M 86;44;93 91;50;99 S;RT;S;S 51;84;44;93 56;86;45;94 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. These results suggest that unlike sT118M HBsAg, rtM204I (sI195M) may cause a considerable reduction in the antigenicity of sG145K mutant HBsAg. 2013 Virology journal Result HBV M204I;T118M;I195M;G145K 50;34;57;123 55;40;63;129 S;S;RT;S;S;S 41;137;48;34;57;123 46;142;50;35;58;124 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. With the rtM204I (sI195M) mutation on the backbone of the immune escape mutant sG145K, avidity was reduced significantly for four of the ELISA kits. 2013 Virology journal Result HBV M204I;I195M;G145K 11;18;79 16;24;85 RT;S;S 9;18;79 11;19;80 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Additionally, among LAM/LdT-based monotherapy, 50% of patients who (4/8) received ADV add-on also detected rtN236T mutations. 2013 Virology journal Result HBV N236T 109 114 RT 107 109 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Among ADV-based treatment (n=46), the rtN236T mutations were detected in 78% (32/41), 66.7% (2/3) and 50% (1/2) of patients receiving ADV monotherapy, LAM add-on, or ETV switch-to therapies, respectively. 2013 Virology journal Result HBV N236T 40 45 RT 38 40 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Among those rtM204 mutations, a total of 14 types of rtM204 containing mutant patterns were observed, and rtM204I/V+rtL180M (78/106, 73.6%) and rtM204 I/V+rtL80I/V (48/106, 45.3%) were the two most common mutation patterns (Table 1). 2013 Virology journal Result HBV M204I;M204V;L180M;M204I;M204V;L80I;L80V 108;108;118;146;146;157;157 115;115;123;154;154;163;163 RT;RT;RT;RT;RT;RT 12;53;106;116;144;155 14;55;108;118;146;157 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. And among those rtM204 mutations, rtM204I, rtM204V and rtM204I/V accounted for 60.4% (64/106), 31.1% (33/106) and 8.5% (9/106), respectively. 2013 Virology journal Result HBV M204I;M204V;M204V;M204I 36;57;45;57 41;64;50;64 RT;RT;RT;RT 16;34;43;55 18;36;45;57 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. By contrast, all rtM204V mutants were found to be coexistent with rtL180M mutations, which was significantly higher than that of rtM204I mutants [rtM204V+rtL180M (100%, 33/33) vs. 2013 Virology journal Result HBV M204V;L180M;M204I;M204V;L180M 19;68;131;148;156 24;73;136;153;161 RT;RT;RT;RT;RT 17;66;129;146;154 19;68;131;148;156 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Compared with the rtM204V mutants, the rtM204I mutants were preferentially accompanied by the rtL80I/V mutations with a statistically significant difference [rtM204I+rtL80I/V (50.0%, 32/64) vs. 2013 Virology journal Result HBV L80I;L80V;L80I;L80V;M204V;M204I;M204I 168;168;96;96;20;41;160 174;174;102;102;25;46;165 RT;RT;RT;RT;RT 18;39;94;158;166 20;41;96;160;168 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. In this cohort, HBV rtA181T/V mutation was observed in 19.3% (22/114) of patients with LAM/LdT-based therapies and 23.9% (11/46) of patients with ADV-based therapies. 2013 Virology journal Result HBV A181T;A181V 22;22 29;29 RT 20 22 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Our findings suggested that rtA181T/V mutations were common among patients with NAs resistance, and it should be regularly monitored in real clinical practice. 2013 Virology journal Result HBV A181T;A181V 30;30 37;37 RT 28 30 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Recently, HBV rtA181T/V mutations had been widely concerned and it was regarded to be a multidrug resistance which not only could result in resistance to ADV but also reduce sensitivity to LAM and LdT. 2013 Virology journal Result HBV A181T;A181V 16;16 23;23 RT 14 16 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. rtM204V+rtL80I/V (27.3%, 9/33), P=0.032]. 2013 Virology journal Result HBV L80I;L80V;M204V 10;10;2 16;16;7 RT;RT 0;8 2;10 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Thus, our finding further confirms that rtM204 should be considered as an important primary LAM/LdT-resistance mutation position in real clinical practice, and rtM204I mutation is the most common type. 2013 Virology journal Result HBV M204I 162 167 RT;RT 40;160 42;162 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. Among the 13 subjects from Sao Paulo, we detected only the rtS219A + sS210R mutations. 2013 Virology journal Result HBV S219A;S210R 61;69 66;75 RT;S 59;69 61;70 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. Modifications within the POL gene were observed in 9 out of 34 samples (26.47%); we found only one case with the rtM204V mutation, which caused complete resistance to LAM, along with the compensatory mutation rtL180M (2.94%). 2013 Virology journal Result HBV M204V;L180M 115;211 120;216 P;RT;RT 25;113;209 28;115;211 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. The other samples showed only the compensatory mutations rtL80F (5.88%), rtL80V (2.94%), rtL82V + rtV207L (2.94%), rtT128P (5.88%), rtT128N/S (2.94%) and rtS219A (5.88%). 2013 Virology journal Result HBV L80F;L80V;L82V;T128P;T128N;T128S;V207L;S219A 59;75;91;117;134;134;100;156 63;79;95;122;141;141;105;161 RT;RT;RT;RT;RT;RT;RT 57;73;89;98;115;132;154 59;75;91;100;117;134;156 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. When the genes were analyzed together, 9 of the 34 samples had mutations in both genes, and we found the following combinations: sM133L + sI195T with rtL80F + rtT128P, sI195M with rtL180M + rtM204V, sP120T with rtT128N, sY100F with rtT128S + rtL80V, sY100S with rtL80F, sY100C + sI/T126P + sQ129P with rtT128P, sM198I + sF183C with rtL82V + rtV207L and sS210R with rtS219A (in two samples), as shown in Table 1. 2013 Virology journal Result HBV T126P;L80F;T128N;L80V;L80F;L82V;T128P;L180M;M204V;T128S;T128P;V207L;S219A;M133L;I195T;I195M;P120T;Y100F;Y100S;Y100C;I126P;Q129P;M198I;F183C;S210R 280;152;213;244;264;334;161;182;192;234;304;343;367;129;138;168;199;220;250;270;279;290;311;320;353 287;156;218;248;268;338;166;187;197;239;309;348;372;135;144;174;205;226;256;276;287;296;317;326;359 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S;S;S;S;S;S;S;S;S 150;159;180;190;211;232;242;262;302;332;341;365;129;138;168;199;220;250;270;279;290;311;320;353 152;161;182;192;213;234;244;264;304;334;343;367;130;139;169;200;221;251;271;280;291;312;321;354 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Clinical Significance of G1896A Precore Mutation and Serum TLR2. 2013 Advances in virology Result HBV G1896A 25 31 Precore 32 39 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Demographic characteristics and frequency of the G1896A precore mutation along with the clinical and biochemical profiles of study subjects are summarized in Table 1. 2013 Advances in virology Result HBV G1896A 49 55 Precore 56 63 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Patients infected with the wild-type HBV revealed similar mean of viral load compared to G1896A precore mutant patients (3.54 +- 1.02 versus 3.41 +- 1.1 log copies/mL). 2013 Advances in virology Result HBV G1896A 89 95 Precore 96 103 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Serum TLR2 and ALT had significant correlation (r = 0.46; P = 0.01) which was more pronounced in patients with G1896A mutation (r = 0.48; P = 0.008) (Figure 1). 2013 Advances in virology Result HBV G1896A 111 117 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. The concentration of serum TLR2 was higher in G1896A precore mutants than wild-type infected patients (4.8 +- 2.9 versus 3.4 +- 2.2 ng/mL, P = 0.032) (Table 1). 2013 Advances in virology Result HBV G1896A 46 52 Precore 53 60 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. The quantification of HBV DNA was reported in log copies/mL with a mean value of 3.46 +- 1.06 and 29 (57%) patients that showed the G1896A precore mutation. 2013 Advances in virology Result HBV G1896A 132 138 Precore 139 146 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. There was no significant relationship between G1896A mutation variants with neither age nor sex. 2013 Advances in virology Result HBV G1896A 46 52 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. The C1858T and G1757A substitutions were found in 226/228 (99.1%) and 189/228 patients (82.8%) respectively. 2013 PloS one Result HBV C1858T;G1757A 4;15 10;21 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. As shown in Figure 4B, LHBs and its four mutations were N-glycoproteins, and the N123S may be not the key sites N-linked glycosylation modification of LHBs. 2013 Hepatitis monthly Result HBV N123S 81 86 S;S 23;151 27;155 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. As shown in Supplement 2, incorporation of BrdU into the control, accumulation of mitotic L02 cells was delayed by LHBs and its mutations, especially in N320K (Figure 3B). 2013 Hepatitis monthly Result HBV N320K 153 158 S 115 119 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. Because LHBs protein is localized in ER, we further determined whether the mutation protein of LHBs at N15S, N123S, N177S and N320K was associated with ER stress. 2013 Hepatitis monthly Result HBV N15S;N123S;N177S;N320K 103;109;116;126 107;114;121;131 S;S 8;95 12;99 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. But, the expression of GADD34 and GRp78 was significantly down-regulated in L02 cells transfected with N177S mutation compared to those of transfected with LHBs and other mutations. 2013 Hepatitis monthly Result HBV N177S 103 108 S 156 160 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. In contrast to the markers of ER stress, the expression of GADD34 and GRp78 was significantly upregulated in L02 cells transfected with LHBs and its mutations compared to control, especially N320K mutation (Figure 1A). 2013 Hepatitis monthly Result HBV N320K 191 196 S 136 140 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. It confirmed that LHBs and it four mutated proteins contained p62-derived UBA domain, especially in N15S, N123S and N320K mutations, but not hHR23B-derived UBA2 domain, NBR1-derived UBA domain and NUB1/NUB1L UBA domain. 2013 Hepatitis monthly Result HBV N15S;N123S;N320K 100;106;116 104;111;121 S 18 22 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. LHBs and its mutations induced an increase in G1 phase and inhibition of S phase, especially in N320K (Supplement 2A). 2013 Hepatitis monthly Result HBV N320K 96 101 S 0 4 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. Our results showed that the N15S, N123S and N177S mutated LHBs proteins could induce overexpression of cyclinA in L02 cells. 2013 Hepatitis monthly Result HBV N15S;N123S;N177S 28;34;44 32;39;49 S 58 62 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. Our results showed that the N15S, N123S and N177S mutated LHBs proteins could induce overexpression of EDEM in L02 cells (Figure 1B). 2013 Hepatitis monthly Result HBV N15S;N123S;N177S 28;34;44 32;39;49 S 58 62 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. PNGase F converted especially gp42 to the nonglycosylated p39 form of the N320K mutation LHBs (Figure 4D). 2013 Hepatitis monthly Result HBV N320K 74 79 S 89 93 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The LHBs and N123S, N177S, N320K LHBs mutation proteins could induce overexpression of cyclin B1 in L02 cells, especially in LHBs. 2013 Hepatitis monthly Result HBV N123S;N177S;N320K 13;20;27 18;25;32 S;S;S 4;33;125 8;37;129 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S and N123S mutations of LHBs contained fucosylated modification sites by Lectin array (Figure 4C). 2013 Hepatitis monthly Result HBV N15S;N123S 4;13 8;18 S 32 36 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S, N123S and N177S LHBs mutation proteins could induce overexpression of cyclin D1 in L02 cells, especially in N15S and N123S LHBs mutations. 2013 Hepatitis monthly Result HBV N15S;N123S;N177S;N15S;N123S 4;10;20;118;127 8;15;25;122;132 S;S 26;133 30;137 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S, N123S, N177S and N320K LHBs mutation proteins could interact with EDEM protein in L02 cells, especially N177S, but not LHBs (Figure 1C). 2013 Hepatitis monthly Result HBV N15S;N123S;N177S;N320K;N177S 4;10;17;27;114 8;15;22;32;119 S;S 33;129 37;133 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S, N123S, N177S and N320K LHBs mutation were determined by nucleotide and amino acid sequences analysis (Supplement 1). 2013 Hepatitis monthly Result HBV N15S;N123S;N177S;N320K 4;10;17;27 8;15;22;32 S 33 37 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N320K LHBs mutation proteins could induce overexpression of cyclin E (Figure 2). 2013 Hepatitis monthly Result HBV N320K 4 9 S 10 14 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The subcellular localization of LHBs was similar to its mutations (Supplement 2A-2E, A; LHBs; B: N15S; C: N123S; D: N177S; E: N320K). 2013 Hepatitis monthly Result HBV N15S;N123S;N177S;N320K 97;106;116;126 101;111;121;131 S;S 32;88 36;92 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. These data demonstrated that N-glycosylation modification sites of LHBs were related to ER stress, especially in N177S and N320K N-glycosylation (Figure 1A). 2013 Hepatitis monthly Result HBV N177S;N320K 113;123 118;128 S 67 71 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Furthermore, ACLF-LC patients had significantly higher frequency (P < 0.05) of BCP mutations at T1753V, A1762T, and G1764A than ACLF-CHB patients. 2013 Hepatitis monthly Result HBV T1753V;A1762T;G1764A 96;104;116 102;110;122 BCP 79 82 Chronic Hepatitis B;Liver cirrhosis 133;18 136;20 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. HBV genotypes, HBeAg status, and frequencies of the BCP/PC/C mutations (T1753V, A1762T, G1764T, A1846T, G1899A, and C1913A/G) were included in the study. 2013 Hepatitis monthly Result HBV C1913G;T1753V;A1762T;G1764T;A1846T;G1899A;C1913A 116;72;80;88;96;104;116 124;78;86;94;102;110;124 BCP;C;Precore 52;15;56 55;20;58 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. However there were no significant differences in previous reported hotspot mutations (T1753V, A1762T, G1764T, G1896A, and G1899A) between either CHB and ACLF-CHB patients or LC and ACLF-LC patients. 2013 Hepatitis monthly Result HBV T1753V;A1762T;G1764T;G1896A;G1899A 86;94;102;110;122 92;100;108;116;128 Chronic Hepatitis B;Chronic Hepatitis B;Acute on chronic liver failure;Liver cirrhosis;Liver cirrhosis 145;158;181;174;186 148;161;185;176;188 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In addition, since BCP/PC mutations of T1754G, T1758C, C1766T, T1768A, G1862T, and T1858C were observed only in 7, 5, 7, 4, 1, and 4 of ACLF patients, respectively, these mutations were not included in further analysis. 2013 Hepatitis monthly Result HBV T1754G;T1758C;C1766T;T1768A;G1862T;T1858C 39;47;55;63;71;83 45;53;61;69;77;89 BCP;Precore 19;23 22;25 Acute on chronic liver failure 136 140 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In genotype B infected patients, a significantly higher prevalence of A1846T and C1913A/G mutations was observed in the HBV isolates of ACLF-CHB patients in comparison with those of CHB patients (71.4% vs. 2013 Hepatitis monthly Result HBV C1913G;A1846T;C1913A 81;70;81 89;76;89 Chronic Hepatitis B;Chronic Hepatitis B;Acute on chronic liver failure 141;182;136 144;185;140 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In genotype C infection, a statistically higher prevalence (P < 0.05) in the occurrence of mutations was observed at A1846T and C1913A/G in patients with ACLF-CHB and ACLF-LC than those with CHB and LC, respectively. 2013 Hepatitis monthly Result HBV C1913G;A1846T;C1913A 128;117;128 136;123;136 HBV infections;Chronic Hepatitis B;Acute on chronic liver failure;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 3;191;167;159;172;199 23;194;171;162;174;201 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Meanwhile the C1913A/G mutation in HBV C region was significantly increased in patients with ACLF-CHB, and ACLF-LC than those with CHB and LC, respectively (P < 0.001). 2013 Hepatitis monthly Result HBV C1913G;C1913A 14;14 22;22 C 39 40 Chronic Hepatitis B;Chronic Hepatitis B;Acute on chronic liver failure;Liver cirrhosis;Liver cirrhosis 98;131;93;112;139 101;134;97;114;141 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. The presence of A1846T in PC region (OR: 2.86, 95% CI: 1.58-5.19, P < 0.01) and the C1913A/G in the C region (OR: 5.93; 95% CI: 2.260-6.894; P < 0.001) were independently associated with the development of ACLF, suggesting that A1846T and C1913A/G were independent risk factors for ACLF. 2013 Hepatitis monthly Result HBV C1913G;C1913G;A1846T;C1913A;A1846T;C1913A 84;239;16;84;228;239 92;247;22;92;234;247 C;Precore 100;26 101;28 Acute on chronic liver failure;Acute on chronic liver failure 206;282 210;286 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. The prevalence of the A1846T mutation in HBV PC region was 65.5%, and 56.9% in patients with ACLF-CHB and ACLF-LC, respectively, which was significantly higher than those in CHB, and LC patients (P < 0.05). 2013 Hepatitis monthly Result HBV A1846T 22 28 Precore 45 47 Chronic Hepatitis B;Chronic Hepatitis B;Acute on chronic liver failure;Liver cirrhosis;Liver cirrhosis 98;174;93;111;183 101;177;97;113;185 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. At least 4 different genotype/subgenotype unrelated aa mutations are observed: V96A (1/47; 2.13%), L98V (1/47; 2.13%), Y100C (1/47; 2.13%), and I1110L (3/47; 6.38%) (data not shown). 2013 TheScientificWorldJournal Result HBV V96A;L98V;Y100C;I1110L 79;99;119;144 83;103;124;150 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. In one case, A159G and R160K amino acid changes were found, and in the other, I68T amino acid substitution was observed. 2013 TheScientificWorldJournal Result HBV A159G;R160K;I68T 13;23;78 18;28;82 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Multiple mutations were found in the A-B interdomain region, such as rtI91L, rtL93P, rtS106C, rtR110G, rtN118T, rtS119T, rtY126H, rtG127W/R, rtC136R, and rtY158H (data not shown). 2013 TheScientificWorldJournal Result HBV I91L;L93P;G127W;G127R;S106C;R110G;N118T;S119T;Y126H;C136R;Y158H 71;79;132;132;87;96;105;114;123;143;156 75;83;139;139;92;101;110;119;128;148;161 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 69;77;85;94;103;112;121;130;141;154 71;79;87;96;105;114;123;132;143;156 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Some novel (rtS119T, rtY126H, rtG127W/R, rtC136R, and rtY158H) and nonclassical putative (rtI91L) mutations were found. 2013 TheScientificWorldJournal Result HBV G127W;G127R;I91L;S119T;Y126H;C136R;Y158H 32;32;92;14;23;43;56 39;39;96;19;28;48;61 RT;RT;RT;RT;RT;RT 12;21;30;41;54;90 14;23;32;43;56;92 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. As described above, most of HBx point mutants retained the ability to upregulate HIF-1alpha, and especially the dual mutations K130M/V131I enhanced this function. 2014 British journal of cancer Result HBV V131I;K130M 133;127 138;132 X 28 31 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Dual point mutations K130M/V131I upregulate HIF-1alpha. 2014 British journal of cancer Result HBV V131I;K130M 27;21 32;26 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Especially, the mutant HA-K130M/V131I-HBx induced the highest expression of them, compared with wild-type HBx and the other five HBx mutants (Figure 1B). 2014 British journal of cancer Result HBV V131I;K130M 32;26 37;31 X;X;X 38;106;129 41;109;132 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Furthermore, the mutant HA-K130M/V131I-HBx has been demonstrated to possess the ability to enhance the transcriptional activity of HIF-1alpha, compared with wild-type HBx and the other mutants (P<0.05). 2014 British journal of cancer Result HBV V131I;K130M 33;27 38;32 X;X 39;167 42;170 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. It was particularly interested to find that mutants A1630G and G1721A always appeared concurrently and that mutant A1762T constantly accompanied mutant G1764A. 2014 British journal of cancer Result HBV A1630G;G1721A;A1762T;G1764A 52;63;115;152 58;69;121;158 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Of the double mutations A1630G/G1721A, the mutation G1721A does not lead to the alteration of HBx codon, and thus the double mutations affect only the codon 86 of the X protein (H86Y). 2014 British journal of cancer Result HBV G1721A;A1630G;G1721A;H86Y 31;24;52;178 37;30;58;182 X;X 94;167 97;168 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. The dual mutations at nucleotides A1762T/G1764A affected the codons of HBx, resulting in a lysine to methionine change at codon 130 and a valine to isoleucine change at codon 131 (K130M/V131I). 2014 British journal of cancer Result HBV G1764A;V131I;A1762T;K130M;K130M;V131I 41;186;34;180;91;138 47;191;40;185;131;178 X 71 74 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. The dual point mutations K130M/V131I in this region enhanced the properties of HBx to regulate HIF-1alpha, whereas the truncations of this region abrogated this effect. 2014 British journal of cancer Result HBV V131I;K130M 31;25 36;30 X 79 82 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Therefore, these findings indicated that the dual point mutations A1762T/G1764A, which result in mutated K130M/V131I HBx proteins, enhanced the activity of HBx to regulate HIF-1alpha expression. 2014 British journal of cancer Result HBV G1764A;V131I;A1762T;K130M 73;111;66;105 79;116;72;110 X;X 117;156 120;159 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Therefore, we would like to focus on the mutants with deletion of seven amino acids from codon 128 to codon 135 of HBx. 2014 British journal of cancer Result HBV del aa128 54 98 X 115 118 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. To this end, six artificial HBx mutants have been established, including HA-A12T-HBx, HA-V44I-HBx, HA-A66T-HBx, HA-H86Y-HBx, HA-E109D-HBx and HA-K130M/V131I-HBx (Figure 1A). 2014 British journal of cancer Result HBV V131I;A12T;A66T;V44I;H86Y;E109D;K130M 151;76;102;89;115;128;145 156;80;106;93;119;133;150 X;X;X;X;X;X;X 28;81;94;107;120;134;157 31;84;97;110;123;137;160 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Together, these results revealed that HBx point mutants retained the functionality in upregulating the expression and activity of HIF-1alpha, and that among these HBx point mutants, HA-K130M/V131I-HBx possesses the greatest effect on HIF-1alpha. 2014 British journal of cancer Result HBV V131I;K130M 191;185 196;190 X;X;X 38;163;197 41;166;200 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. After LMV treatment, interestingly a novel mutation, rtQ267H was found, except rtM204V and/or rtL180M emerged as described in previous reports, in all of the ten patients, and took place in five of them in high-frequency, as shown in Figure 1. 2013 Hepatitis monthly Result HBV M204V;Q267H;L180M 81;55;96 86;60;101 RT;RT;RT 53;79;94 55;81;96 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. As shown in Figure 3 A, LMV inhibited the replication of WT HBV in a dose-dependent manner, while the susceptibility of pHBV1.3-rtQ267H, -rtM204V/Q267H, -rtL180M/M204V and -rtL180M/M204V/Q267H to LMV and LdT was greatly reduced. 2013 Hepatitis monthly Result HBV Q267H;M204V;M204V;Q267H;Q267H;M204V;L180M;L180M 146;162;181;187;130;140;156;175 151;167;186;192;135;145;161;180 RT;RT;RT;RT 128;138;154;173 130;140;156;175 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. As shown in Figure 4, the half maximal effective concentration (EC50) of pHBV1.3-WT, -rtQ267H, -rtQ267H/M204V, -rtL180M/M204V and -rtL180M/M204V/Q267H to LMV were about 1.08, 1.89, 39.44, 36.75. 2013 Hepatitis monthly Result HBV M204V;M204V;M204V;Q267H;Q267H;Q267H;L180M;L180M 104;120;139;145;88;98;114;133 109;125;144;150;93;103;119;138 RT;RT;RT;RT 86;96;112;131 88;98;114;133 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. For LdT, similar to LMV, the EC50 of pHBV1.3-WT, -rtQ267H, -rtQ267H/M204V, -rtL180M/M204V and -rtL180M/M204V/Q267H to LdT were about 11.50, 21.40, 83.80, 82.50, and 102.70 muM, respectively. 2013 Hepatitis monthly Result HBV M204V;M204V;M204V;Q267H;Q267H;Q267H;L180M;L180M 68;84;103;109;52;62;78;97 73;89;108;114;57;67;83;102 RT;RT;RT;RT 50;60;76;95 52;62;78;97 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Huh7 cells were transfected with WT pHBV1.3, pHBV-rtQ267H, -rtQ267H/M204V, -rtL180M/M204V and -rtL180M/M204V/Q267H, then treated with indicated concentrations of ADV, ETV and TDF. 2013 Hepatitis monthly Result HBV M204V;M204V;M204V;Q267H;Q267H;L180M;L180M;Q267H 68;84;103;109;52;78;97;62 73;89;108;114;57;83;102;67 RT;RT;RT;RT 50;60;76;95 52;62;78;97 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. It follows that rtQ267H could not only reduce the anti-HBV effect of LMV, but also enhance HBV replication which was attenuated by LMV resistant mutation, such as rtM204V/I. 2013 Hepatitis monthly Result HBV M204I;Q267H;M204V 165;18;165 172;23;172 RT;RT 16;163 18;165 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Mutations rtM204V/I weaken HBV replication, while rtL180M could restore the impaired replication capacity, in accordance with previous report. 2013 Hepatitis monthly Result HBV M204I;L180M;M204V 12;52;12 19;57;19 RT;RT 10;50 12;52 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. rtQ267H, rtQ267H/M204V, rtL180M/M204V, and rtL180M/M204V/Q267H substitutions reduced the anti-HBV effect of LMV and LdT. 2013 Hepatitis monthly Result HBV M204V;M204V;Q267H;M204V;Q267H;Q267H;L180M;L180M 17;32;57;51;2;11;26;45 22;37;62;56;7;16;31;50 RT;RT;RT;RT 0;9;24;43 2;11;26;45 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Southern blotting and subsequent densitometry analysis (Figure 2 A) revealed that rtQ267H enhances HBV replication with or without a background of rtM204V or rtL180M/M204V significantly. 2013 Hepatitis monthly Result HBV M204V;L180M;Q267H;M204V 166;160;84;149 171;165;89;154 RT;RT;RT 82;147;158 84;149;160 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtQ267H is involved in Reduced Susceptibility to LMV, Aggravated Existing LMV/LdT Resistance Degree of rtM204V. 2013 Hepatitis monthly Result HBV Q267H;M204V 15;118 20;123 RT;RT 13;116 15;118 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtQ267H Maintained Normal Susceptibility to Other NAs, Except for LMV and LdT. 2013 Hepatitis monthly Result HBV Q267H 15 20 RT 13 15 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtQ267H was Related With LMV Therapy from Sequence Analysis. 2013 Hepatitis monthly Result HBV Q267H 15 20 RT 13 15 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The relative level of LMV's anti-HBV effect is shown as a percentage of the control by gray analysis (lower panel), and the EC50 of pHBV1.3-WT, -rtQ267H, -rtM204V/Q267H, -rtL180M/M204V and -rtL180M/M204V/Q267H HBV to LMV was calculated by gray analysis were 1.15, 1.97, 34.24, 32.39, 41.63 muM, respectively. 2013 Hepatitis monthly Result HBV Q267H;M204V;M204V;Q267H;Q267H;M204V;L180M;L180M 163;179;198;204;147;157;173;192 168;184;203;209;152;162;178;197 RT;RT;RT;RT 145;155;171;190 147;157;173;192 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The results indicated that rtL180M and/or rtM204V/I and/or rtQ267H had no influence on HBsAg and HBeAg expression comparing to that of WT HBV, in spite of the fact that rtM204V and rtM204I led to sI195M and sW196S in S ORF, due to overlapping between S and P gene. 2013 Hepatitis monthly Result HBV L180M;M204V;M204I;Q267H;M204V;M204I;I195M;W196S 29;44;44;61;171;183;196;207 34;51;51;66;176;188;202;213 C;S;P;RT;RT;RT;RT;RT;S;S;S;S 97;87;257;27;42;59;169;181;196;207;217;251 102;92;258;29;44;61;171;183;197;208;218;252 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. The results indicated that rtQ267H, rtQ267H/M204V, rtL180M/M204V, and rtL180M/M204V/Q267H decreased the susceptibility of HBV to LMV and LdT, but they were still susceptible to ADV, ETV, and TDF in vitro. 2013 Hepatitis monthly Result HBV M204V;M204V;Q267H;M204V;Q267H;Q267H;L180M;L180M 44;59;84;78;29;38;53;72 49;64;89;83;34;43;58;77 RT;RT;RT;RT 27;36;51;70 29;38;53;72 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. To determine whether rtQ267H influenced HBV susceptibility to LMV and others NAs, Huh7 cells were transfected with MT or WT HBV plasmids, then exposed to the indicated NA concentrations and the HBV core-associated DNA was analyzed by Southern blot. 2013 Hepatitis monthly Result HBV Q267H 23 28 C;RT 198;21 202;23 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. To further analyze the influence of the rtQ267H on HBV replication and sensitivity to LMV, MT HBV replication-competent plasmids, pHBV-rtQ267H, -rtL180M, -rtM204V, -rtM204I, -rtL180M/M204V, -rtL180M/Q267H, -rtM204V/Q267H, -rtL180M/M204V/Q267H were constructed based on pHBV1.3. 2013 Hepatitis monthly Result HBV M204V;Q267H;Q267H;Q267H;M204V;Q267H;Q267H;L180M;M204V;L180M;L180M;L180M;M204I;M204V 183;199;215;237;231;42;137;147;157;177;193;225;167;209 188;204;220;242;236;47;142;152;162;182;198;230;172;214 RT;RT;RT;RT;RT;RT;RT;RT;RT 40;135;145;155;165;175;191;207;223 42;137;147;157;167;177;193;209;225 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Amino acid alignment showed that four children (Y1-Y4) were infected with serotype adw having a lysine (K) at aa 160 and one (Y5) was infected with serotype adr having an arginine (R) at aa 160 (Table 1). 2013 TheScientificWorldJournal Result HBV K160K;R160R 95;170 117;194 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Fifteen substitutions outside the B- and T-cell epitopes (Q10 K, M12T, N15S, N20S, A54E, H56N, V60A, S62A, T68I, Q82S, L84I, L85F, A90V, V172A, and L173P) were found. 2013 TheScientificWorldJournal Result HBV Q10K;M12T;N15S;N20S;A54E;H56N;V60A;S62A;T68I;Q82S;L84I;L85F;A90V;V172A;L173P 58;65;71;77;83;89;95;101;107;113;119;125;131;137;148 63;69;75;81;87;93;99;105;111;117;123;129;135;142;153 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Four replacements (S45T/A, N131T, I194V, and S207N) within the immune epitopes were observed in all isolates. 2013 TheScientificWorldJournal Result HBV S45T;S45A;N131T;I194V;S207N 19;19;27;34;45 25;25;32;39;50 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Nucleotide analysis showed that several nucleotide substitutions were detected and two (T586C and A748G) of them were found in Y1-Y4 (Table 2). 2013 TheScientificWorldJournal Result HBV T586C;A748G 88;98 93;103 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Within the "a" determinant, one (N131T) substitution was detected in all isolates and three additional variants (T126I, T143S, and G145A) were found in subject Y5 (Table 3). 2013 TheScientificWorldJournal Result HBV N131T;T126I;T143S;G145A 33;113;120;131 38;118;125;136 24444423 Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies. More aa substitutions were found, including I103T, M133I, F134V, D144E, V164E and L175S in the HBsAg (Table 2) and T45S, N122D, V133G/N and W144G in the HBV RT sequence (Table 3). 2014 Virology journal Result HBV I103T;M133I;F134V;D144E;V164E;L175S;T45S;N122D;V133G;V133N;W144G 44;51;58;65;72;82;115;121;128;128;140 49;56;63;70;77;87;119;126;135;135;145 S;RT 95;157 100;159 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Analysis of the HBV P gene sequence of patient 630304 showed presence of two significant mutations which were L180M and M204I, indicating possible multi-drug resistance to lamivudine, emtricitabine, famciclovir, and telbivudine. 2014 Hepatitis monthly Result HBV L180M;M204I 110;120 115;125 P 20 21 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Based on genome analysis, Patient 155693 possessed mutation A181T, which was responsible to cause resistance to lamivudine. 2014 Hepatitis monthly Result HBV A181T 60 65 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Based on sequence analysis, patient 839920, a 76-year-old male, showed the presence of L180V, M204I, and V173L mutations in P gene sequence of HBV DNA. 2014 Hepatitis monthly Result HBV L180V;M204I;V173L 87;94;105 92;99;110 P 124 125 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Patient 247131 was found to have mutations L180M, M204I, T184G, and M250V, which were associated with resistance to lamivudine, entecavir, emitricitabine, famciclovir, and telbivudine. 2014 Hepatitis monthly Result HBV L180M;M204I;T184G;M250V 43;50;57;68 48;55;62;73 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Patient 830757 also had multiple mutations in HBV P gene, which were S202I, N236T, and M250L. 2014 Hepatitis monthly Result HBV S202I;N236T;M250L 69;76;87 74;81;92 P 50 51 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. All patients detected with rtM204Q were infected with genotype C, serotype adr HBV and had a moderate to high level of HBV viral load (DNA >104 IU/mL) when antiviral therapy initiated. 2014 PloS one Result HBV M204Q 29 34 RT 27 29 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. By contrast, rtM204I/rtM204V was detected in 2,502 patients with an incidence of 25.5% (2,502/9,830). 2014 PloS one Result HBV M204I;M204V 15;23 20;28 RT;RT 13;21 15;23 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clinical course and clonal analysis of three rtM204Q-positive patients during antiviral treatment. 2014 PloS one Result HBV M204Q 47 52 RT 45 47 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing (28 clones) of the sample at this point (Sb2) showed predominance of rtM204Q strain (64%) concomitant with rtA181T+M204Q (14%), rtA181T (7%), rtA181V (7%) and wild-type (7%) strains in the viral pool. 2014 PloS one Result HBV A181T;A181T;A181V;M204Q;M204Q 127;148;162;89;133 132;153;167;94;138 RT;RT;RT;RT 87;125;146;160 89;127;148;162 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing (35 clones) of the sample at month 29 (Sa4) showed 91% wild-type strain and 9% rtA181T mutant in the viral pool. 2014 PloS one Result HBV A181T 99 104 RT 97 99 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing (35 clones) of the sample at months 24 (Sa3) showed that rtM204Q, rtA181T, rtM204I, rtA181T+M204Q and wild-type strains occupied 14%, 14%, 3%, 0%, and 69%, respectively. 2014 PloS one Result HBV A181T;A181T;M204Q;M204I;M204Q 86;104;77;95;110 91;109;82;100;115 RT;RT;RT;RT 75;84;93;102 77;86;95;104 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing (37 clones) of the sample at this point (Sa2) showed coexistence of rtM204Q (30%), rtA181T (27%), rtM204I (5%), rtA181T+M204Q (3%) and wild-type (35%) strains in the viral pool. 2014 PloS one Result HBV A181T;A181T;M204Q;M204I;M204Q 103;132;88;118;138 108;137;93;123;143 RT;RT;RT;RT 86;101;116;130 88;103;118;132 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Clonal sequencing (44 clones) of the sample at this point (Sc2) showed predominance of rtM204Q strain (52%) concomitant with rtL180M+A181V (16%), rtA181T (16%), rtV173L+L180M+A181V (9%), rtA181V (5%) and wild-type (2%) strains in the viral pool. 2014 PloS one Result HBV A181T;M204Q;L180M;V173L;A181V;A181V;L180M;A181V 148;89;127;163;189;133;169;175 153;94;132;168;194;138;174;180 RT;RT;RT;RT;RT 87;125;146;161;187 89;127;148;163;189 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Fourteen representative HBV RT sequences from each rtM204Q-positive patient were deposited in GenBank (accession number KJ011529 through KJ011542). 2014 PloS one Result HBV M204Q 53 58 RT;RT 28;51 30;53 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Phenotypic analysis of drug resistance showed that rtM204Q and rtM204I mutants had 76-fold and 1396-fold increased LAM EC50 of the wild-type strain respectively, and both of the mutants remained susceptible to ADV, ETV and TDF compared to the wild-type strain. 2014 PloS one Result HBV M204Q;M204I 53;65 58;70 RT;RT 51;63 53;65 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Replication capacity and drug resistance of rtM204Q. 2014 PloS one Result HBV M204Q 46 51 RT 44 46 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. rtM204Q mutant was predominantly detected in the patients' samples collected at the time-point of virologic breakthrough. 2014 PloS one Result HBV M204Q 2 7 RT 0 2 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The results showed that rtM204Q mutant had a replication capacity intermediate to that of rtM204I mutant and wild-type HBV, while rtA181T+M204Q had the lowest natural replication capacity among the wild-type HBV and the four tested mutants (Figure 2). 2014 PloS one Result HBV A181T;M204Q;M204I;M204Q 132;26;92;138 137;31;97;143 RT;RT;RT 24;90;130 26;92;132 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204Q emerged either alone or in concomitance with other mutations (rtM204I/V, rtA181T, rtL180M, rtT184I) by direct sequencing. 2014 PloS one Result HBV M204V;M204Q;M204I;A181T;L180M;T184I 76;6;76;87;96;105 83;11;83;92;101;110 RT;RT;RT;RT;RT 4;74;85;94;103 6;76;87;96;105 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204Q mutation of RT domain was detected in seven LAM-refractory and three LdT-refractory patients by direct sequencing, and the detection rate of rtM204Q among the chronically HBV-infected patients in Beijing 302 Hospital was 0.1% (10/9,830). 2014 PloS one Result HBV M204Q;M204Q 6;155 11;160 RT;RT;RT 4;24;153 6;26;155 HBV infections 183 195 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Again, sW182* was the most frequently found mutations, being found in 4 tumors. 2014 PloS one Result HBV W182X 7 13 S 7 8 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Among the three mutants, sW182* had the highest colony counts (Figure S3C). 2014 PloS one Result HBV W182X 25 31 S 25 26 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Among them, sW182* was found in two tumors and also identified in one of the paired non-tumor liver tissue. 2014 PloS one Result HBV W182X 12 18 S 12 13 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Colonies of 4 stable clones: the Mock, Wt, sL95*, sL216*, and sW182*, in soft agar were visualized by 0.1% p-iodonitro tetrazolium violet (INT) staining. 2014 PloS one Result HBV L95X;L216X;W182X 43;50;62 48;56;68 S;S;S 43;50;62 44;51;63 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. In contrast, almost all of the injected cells of the Wt and control (vector-only) still stayed in the yolk at 3 dpi (Figure S6C and S6D). 2014 PloS one Result HBV S6D 132 135 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Only the W182-1 (100%) and W182-2 clones (100%) had significant higher tumor growth rate compared with Mock, and the tumor sizes of sW182* clones were also the largest compared with Wt and the other two mutants (Figure S4). 2014 PloS one Result HBV W182X 132 138 S 132 133 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Phosphorylation profile of signaling molecules in 3 stable clones: Wt, vector only and sW182* mutant, were evaluated for 7 proteins: (a) ERK. 2014 PloS one Result HBV W182X 87 93 S 87 88 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. sW182* mutants showed higher phosphorylation level than Mock and Wt in most of the proteins except ERK and Stat1 (Figure S7 A to G). 2014 PloS one Result HBV W182X 0 6 S 0 1 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. The HBV surface antigen expression was lowest in the tumors derived from sL216*. 2014 PloS one Result HBV L216X 73 79 S;S 73;8 74;15 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. The proliferation assay of the 4 stable clones: wild type (Wt), sL95*, sW182* and sL216*, indicated that all three nonsense mutations of S gene could enhance the cell growth compared with Wt and Mock (Figure S3A). 2014 PloS one Result HBV L95X;W182X;L216X 64;71;82 69;77;88 S;S;S;S 64;71;82;137 65;72;83;138 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Three nonsense mutations of S gene were identified (sL95*, sW182*, and sL216*) in the HCC tumor tissue of 4 patients. 2014 PloS one Result HBV L95X;W182X;L216X 52;59;71 57;65;77 S;S;S;S 28;52;59;71 29;53;60;72 Hepatocellular carcinoma 86 89 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. W182 exhibited significantly higher migration ability compared to Wt or vector-only (Figure S6E). 2014 PloS one Result HBV S6E 92 95 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. As indicated in Table 2, RT-AS-LNA-qPCR could detect rtM204I at a proportion as low as 0.01% (detection limit) of the total population, whereas sequencing analysis only detect at a proportion of 10%. 2014 PloS one Result HBV M204I 55 60 RT;RT 25;53 27;55 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. Clinical samples containing different proportions (50%, 25%, 20%, 10%, 5%, 1%, 0.5%, 0.05%~0.01%) of rtM204I were used to compare the sensitivity of RT-AS-LNA-qPCR with sequencing. 2014 PloS one Result HBV M204I 103 108 RT;RT 101;149 103;151 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. A total of 8 isolates (8/59, 13.6%) harbored the BCP (A1762T/G1764A) double mutations. 2014 PloS one Result HBV G1764A;A1762T 61;54 67;60 BCP 49 52 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Additionally, two premature stop codon mutations, the C69* and the W182* mutation, were observed outside the MHL region in two isolates. 2014 PloS one Result HBV C69X;W182X 54;67 58;72 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Furthermore, the G1862T mutation was found in 33.9% (20/59) of the study subjects. 2014 PloS one Result HBV G1862T 17 23 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. In 4 cases it occurred together with the T1753C mutation whereas in 5 cases the BCP mutations were accompanied by the G1896A precore mutation. 2014 PloS one Result HBV T1753C;G1896A 41;118 47;124 BCP;Precore 80;125 83;132 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. In addition, other mutations such as Y100D, Q101R/H, M103V/I, D144E and G145S was also found within the major hydrophilic loop (MHL) of the S gene. 2014 PloS one Result HBV Y100D;Q101R;Q101H;M103V;M103I;D144E;G145S 37;44;44;53;53;62;72 42;51;51;60;60;67;77 S 140 141 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Interestingly, all the subjects with PreS1 or PreS2 deletion had A1762T/G1764A mutation in their BCP region whereas the G1896A PC mutation was found in two of the isolates. 2014 PloS one Result HBV G1764A;A1762T;G1896A 72;65;120 78;71;126 BCP;Precore;PreS1;PreS2 97;127;37;46 100;129;42;51 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Moreover, 93.3% of the HBV/D2 strains had T118V (14/15) whereas all the HBV/D2 isolates were associated with A128V. 2014 PloS one Result HBV T118V;A128V 42;109 47;114 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Several amino acid substitutions were found within the immune-active region of the HBV core gene including the T12S (9/57, 15.8%) and T67N (7/57, 12.3%) mutation in the MHC class II restricted T-cell epitope of HBV core protein and the V27I (6/57, 10.5%) mutation in the MHC class I restricted T-cell epitope. 2014 PloS one Result HBV T12S;T67N;V27I 111;134;236 115;138;240 C;C 87;215 91;219 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Similarly, the A1814C precore start codon mutation was found in two isolates. 2014 PloS one Result HBV A1814C 15 21 Precore 22 29 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Similarly, the precore stop codon mutation (G1896A) occurred in 13 isolates (13/59, 22%) with all harboring the C1858T mutation and in 4 cases it occurred along with G1899A mutation. 2014 PloS one Result HBV G1896A;C1858T;G1899A 44;112;166 50;118;172 Precore 15 22 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The Kozak sequence mutation (nt 1809-1812 from EcoRI site) was found in only one HBV/A isolate harboring the A1811C mutation. 2014 PloS one Result HBV A1811C 109 115 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Very few amino acid substitutions were found within the hepatocyte binding site including the G27S and G35R mutation in only one HBV/C isolate and A39S/R mutation in 3 HBV/D isolates. 2014 PloS one Result HBV A39R;G27S;G35R;A39S 147;94;103;147 153;98;107;153 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. At all, mutations disrupting T- or B-cell epitopes, including deletions in the pre-S2 region, substitution R34K in the pre-S1 region, and R to K substitutions at positions 16 and 18 in the pre-S2 region, were observed in 8/12 (67%) samples with concurrent HBsAg and anti-HBs but in none of the 18 samples without anti-HBs antibodies. 2014 PloS one Result HBV R34K;R16K 107;138 111;174 S;S;S;PreS1;PreS2;PreS2 271;318;256;119;79;189 274;321;261;125;85;195 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. Furthermore, pre-S2 R16K and/or R18K mutations were observed in five HBV isolates derived from individuals with concurrent HBsAg/anti-HBs (LDA067, LDA232, LDA423, LDA470 and LDA494). 2014 PloS one Result HBV R16K;R18K 20;32 24;36 S;S;PreS2 134;123;13 137;128;19 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. HBV isolate LDA265 showed the lamivudine resistance substitution rtL180M associated to the adefovir resistance mutation rtA181V (not shown). 2014 PloS one Result HBV A181V;L180M 122;67 127;72 RT;RT 65;120 67;122 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. Otherwise, the Q129H escape mutation in determinant 'a' was observed in two isolates (LDA265 and LDA339; Table 3). 2014 PloS one Result HBV Q129H 15 20 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. Strains derived from four subjects with concurrent HBsAg/anti-HBs (LDA265, LDA423, LDA481 and LDA494) showed an R34K substitution in the pre-S1 region. 2014 PloS one Result HBV R34K 112 116 S;S;PreS1 62;51;137 65;56;143 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. The common variations A1762T-G1764A in the basal core promoter and G1896A and G1899A in the precore region were identified in three, four and two isolates, respectively. 2014 PloS one Result HBV A1762T;G1764A;G1896A;G1899A 22;29;67;78 28;35;73;84 BCP;Precore 43;92 62;99 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. The two others, LDA173 and LDA339, displayed the lamivudine resistance triple mutation rtV173L, rtL180M, rtM204V/I which causes the concomitant amino acid substitutions E164D/G and I195M in the small S protein (Table 3). 2014 PloS one Result HBV M204V;M204I;V173L;L180M;E164D;E164G;I195M 107;107;89;98;169;169;181 114;114;94;103;176;176;186 RT;RT;RT;S 87;96;105;194 89;98;107;201 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Interesting to note that T127P surface peptide mutation was documented in 54.5% of the Genotype D isolates in comparison to 6.1% of Genotype A. 2014 PloS one Result HBV T127P 25 30 S 31 38 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Precore promoter mutation (G1896A) was also observed in 46% (56/121) of HBV Genotype D and 25% (17/66) of HBV Genotype A patients. 2014 PloS one Result HBV G1896A 27 33 Precore 0 7 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A799G and T1055A are missense mutations resulting in aa substitutions of I224V and M309K, and A987G is a synonymous mutation. 2014 PloS one Result HBV A799G;T1055A;I224V;M309K;A987G 0;10;73;83;94 5;16;78;88;99 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. After adjustments for HBeAg status, serum ALT level, and HBV-DNA level, A799G, A987G, and T1055A were associated with a 5.53-fold (95% CI: 1.69-18.10, P = 0.005), 4.20-fold (95% CI: 1.15-15.35, P = 0.030), and 3.78-fold (95% CI: 1.45-9.86, P = 0.007) increased risk of HCC, respectively (Table 4). 2014 PloS one Result HBV A799G;A987G;T1055A 72;79;90 77;84;96 C 22 27 Hepatocellular carcinoma 269 272 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. And the negative predictive values of A799G, A987G, and T1055A were 0.526, 0.517, and 0.535, respectively. 2014 PloS one Result HBV A799G;A987G;T1055A 38;45;56 43;50;62 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. As shown in Figure 3, patients infected with the T1055A mutant had a significantly lower level of HBV DNA in their blood than those who were infected with prototype (4.69+-1.19 vs. 2014 PloS one Result HBV T1055A 49 55 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. As shown in聽Table 3, the mutation rate of A799G (14.3% vs. 5.7%,聽P鈥=鈥0.038) and T1055A (12.4% vs. 3.8%,聽P鈥=鈥0.023) were again significantly higher in the HCC patients than the non-HCC controls, with respective crude ORs of 2.75 (95% CI: 1.02鈥7.39) and 3.57 (95% CI: 1.12鈥11.33) 2014 PloS one Result HBV T1055A;A799G 80;42 86;47 Hepatocellular carcinoma;Hepatocellular carcinoma 154;180 157;183 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Because the residues from rt304 to rt311 have been reported to be critical for RT activity, we analyzed the relationship between the rtM309K mutation and HBV DNA load. 2014 PloS one Result HBV M309K 135 140 RT;RT;RT;RT 26;35;79;133 28;37;81;135 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Because this study aimed to investigate the effect of RT mutations on HCC, we then selected 11 mutations (A799G, T843C, T870C, T895A, T906R, C936T, A942S, A987G, T1055A, T1069A, and T1071C) that did not affect HBsAg function as candidates for further validation assays. 2014 PloS one Result HBV A799G;T843C;T870C;T895A;T906R;C936T;A942S;A987G;T1055A;T1069A;T1071C 106;113;120;127;134;141;148;155;162;170;182 111;118;125;132;139;146;153;160;168;176;188 S;RT 210;54 215;56 Hepatocellular carcinoma 70 73 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Except for T906R and A942S, all of the mutations occurred with a higher frequency in the HCC patients than the non-HCC controls. 2014 PloS one Result HBV T906R;A942S 11;21 16;26 Hepatocellular carcinoma;Hepatocellular carcinoma 89;115 92;118 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. however, A987G failed to show a significant difference between the HCC and non-HCC patients (P = 0.210). 2014 PloS one Result HBV A987G 9 14 Hepatocellular carcinoma;Hepatocellular carcinoma 67;79 70;82 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Impact of T1055A and A799G Mutations on the HBV DNA Load. 2014 PloS one Result HBV T1055A;A799G 10;21 16;26 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. In contrast, the A799G mutation, a missense mutation that results in an isoleucine to valine substitution at the rt224 position did not affect the HBV DNA load in either the HCC or non-HCC patients (both P>0.050). 2014 PloS one Result HBV A799G 17 22 RT 113 115 Hepatocellular carcinoma;Hepatocellular carcinoma 174;185 177;188 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. It is worth noting that we did not observe any of the common NA-related resistance mutations including rtM204V/I, rtS202C/G/I, rtL180M, rtA181T/V, rtT184A/I/L/G/C/M, rtA194T, rtI169T, rtV173L, rtL80I, rtN236T, and rtM250I/V, suggesting that these variants were either absent or present at a very low frequency in our study subjects. 2014 PloS one Result HBV M204V;M204I;S202C;S202G;S202I;A181T;A181V;T184A;T184I;T184L;T184G;T184C;T184M;L80I;M250I;M250V;L180M;A194T;I169T;V173L;N236T 105;105;116;116;116;138;138;149;149;149;149;149;149;195;216;216;129;168;177;186;203 112;112;125;125;125;145;145;164;164;164;164;164;164;199;223;223;134;173;182;191;208 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 103;114;127;136;147;166;175;184;193;201;214 105;116;129;138;149;168;177;186;195;203;216 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The combined data analysis indicated that the A799G, A987G, and T1055A mutations were independent factors significantly associated with HCC. 2014 PloS one Result HBV A799G;A987G;T1055A 46;53;64 51;58;70 Hepatocellular carcinoma 136 139 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The crude ORs for A799G, A987G and T1055A were 3.37 (95% CI: 1.17-9.67), 6.08 (95%CI: 1.31-28.19) and 4.45 (95% CI: 1.72-11.54), respectively. 2014 PloS one Result HBV A799G;A987G;T1055A 18;25;35 23;30;41 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The linkage disequilibrium between A799G, A987G, and T1055A was analyzed by Haploview software (www.broad.mit.edu/mpg/haploview) according to the method described previously. 2014 PloS one Result HBV A799G;A987G;T1055A 35;42;53 40;47;59 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The positive predictive values of A799G, A987G, and T1055A were 0.732, 0.842, and 0.778, respectively. 2014 PloS one Result HBV A799G;A987G;T1055A 34;41;52 39;46;58 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The T1055A mutation causes a methionine to lysine substitution at rt309. 2014 PloS one Result HBV T1055A 4 10 RT 66 68 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. These results suggested that impaired viral replication could be a consequence of the T1055A mutation, but not of the A799G mutation. 2014 PloS one Result HBV T1055A;A799G 86;118 92;123 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Three mutations, A799G (15.5% in HCC vs. 5.2% in non-HCC,聽P鈥=鈥0.018), A987G (11.3% in HCC vs. 2.1% in non-HCC,聽P鈥=鈥0.010) and T1055A (22.7% in HCC vs. 6.2% in non-HCC,聽P鈥=鈥0.001) 2014 PloS one Result HBV A799G;A987G;T1055A 17;70;126 22;76;132 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 33;86;143;53;106;163 36;89;146;56;109;166 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. The rtM204I/V mutation (50.2%) was most frequently detected, followed by rtL180M (39.2%) and rtA181V/T (19.6%) mutations. 2014 Annals of laboratory medicine Result HBV M204I;M204V;L180M;A181V;A181T 6;6;75;95;95 13;13;80;102;102 RT;RT;RT 4;73;93 6;75;95 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. There was no statistical difference of HBeAg positive rates among rtM204V, rtL180M, and rtM204I mutant groups. 2014 Annals of laboratory medicine Result HBV M204V;L180M;M204I 68;77;90 73;82;95 C;RT;RT;RT 39;66;75;88 44;68;77;90 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. When the rtM204V and rtM204I mutation groups were compared, all 72 cases of rtM204V mutation had a simultaneous rtL180M mutation, while in 79 cases of rtM204I mutation, 43 cases (54.4%) had a simultaneous rtL180M mutation, 33 cases (41.8%) had the rtM204I mutation alone, and the remaining 3 cases (3.8%) showed a simultaneous rtV173L mutation. 2014 Annals of laboratory medicine Result HBV M204I;M204V;M204V;L180M;M204I;L180M;M204I;V173L 23;11;78;114;153;207;250;329 28;16;83;119;158;212;255;334 RT;RT;RT;RT;RT;RT;RT;RT 9;21;76;112;151;205;248;327 11;23;78;114;153;207;250;329 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Among them seven patients had lamivudine resistance mutations (LAM) and one had the adefovir resistance mutation (ADV; S85A of patient #155). 2014 PloS one Result HBV S85A 119 123 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. However, the well-described vaccine escape mutation P120T was found in two sequences of HBsAg-positive patients (samples 43 and 88) while both of them could be related to HBV genotype D. 2014 PloS one Result HBV P120T 52 57 S 88 93 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Notably, one patient (patient #069) showed four mutations (L80V, L180M, M204V, and Q215S) and patient #049 three mutations (L80V, L180M, and M204V). 2014 PloS one Result HBV L80V;L180M;M204V;Q215S;L80V;L180M;M204V 59;65;72;83;124;130;141 63;70;77;88;128;135;146 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Other possible vaccine escape mutations were detected at positions T126 (T126S) and M133 (M133T); however, their impact on vaccine escape is under discussion. 2014 PloS one Result HBV T126S;M133T 73;90 78;95 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. The classical diagnostic/vaccine escape mutations, G145R and D144E, could not be detected. 2014 PloS one Result HBV G145R;D144E 51;61 56;66 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. The N236T adefovir dipivoxil resistance mutation and other previously described resistance mutations against other antiviral drugs (e.g. 2014 PloS one Result HBV N236T 4 9 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. Among these nine hot spot mutations, pre-S deletions, pre-S start codon mutations, T31C, and T53C mutations were significantly associated with HCC, showing adjusted ORs from 0.524 to 3.199 (Table 2). 2014 PloS one Result HBV T31C;T53C 83;93 87;97 PreS;PreS 37;54 42;59 Hepatocellular carcinoma 143 146 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. These included well-studied mutations (e.g., the pre-S2 start codon mutation and pre-S deletion) and less well-defined mutations (e.g., C3026A or T in pre-S1, T31C and T53C in pre-S2, A162G, T531C or G, A706C, and T766A in S). 2014 PloS one Result HBV C3026A;T31C;T53C;A162G;T531C;A706C;T766A 136;159;168;184;191;203;214 142;163;172;189;196;208;219 PreS;PreS1;PreS2;PreS2;S 81;151;49;176;223 86;157;55;182;224 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. Among 9 patients on ART, one patient had the [L180M, M204V] mutations conferring resistance to lamivudine. 2014 PloS one Result HBV L180M;M204V 46;53 51;58 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. The [V173L] mutation was found in the patient from Guinea-Conakry infected with HBV genotype D. 2014 PloS one Result HBV V173L 5 10 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. Baseline mutation profiles, rtL180M (p=0.051), rtM204I (p=0.992), and rtM204I/V (p=0.177) were not correlated with cumulative virological response (Table 2). 2015 Gut and liver Result HBV M204I;M204V;L180M;M204I 49;72;30;72 54;79;35;79 RT;RT;RT 28;47;70 30;49;72 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. However, none of these four patients who developed the rtA181T mutation showed virological breakthrough during 96 weeks of LAM-ADV combination therapy. 2015 Gut and liver Result HBV A181T 57 62 RT 55 57 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. LAM-resistant (rtL180M and rtM204I/V) and ADV-resistant (rtA181V/T and rtN236T) mutation profiles were followed through RFMP assay at weeks 48 and 96 of the combination therapy. 2015 Gut and liver Result HBV M204I;M204V;A181V;A181T;L180M;N236T 29;29;59;59;17;73 36;36;66;66;22;78 RT;RT;RT;RT 15;27;57;71 17;29;59;73 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The ADV-resistant mutation, rtN236T was not found in 12 patients at 48 and 96 weeks of rescue therapy; however, rtA181T mutants emerged as a minor population in two and four patients at weeks 48 and 96, respectively. 2015 Gut and liver Result HBV A181T;N236T 114;30 119;35 RT;RT 28;112 30;114 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The rtL180M mutation was detected in 51 patients (68%) (Table 1). 2015 Gut and liver Result HBV L180M 6 11 RT 4 6 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The rtM204I mutation was identified in 37 (49%), rtM204V in 27 (36%), and both mutations in 11 patients (15%). 2015 Gut and liver Result HBV M204V;M204I 51;6 56;11 RT;RT 4;49 6;51 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. Thirty-three patients (87%) with rtM204V mutation and 24 patients (50%) with rtM204I mutation were accompanied with rtL180M mutation. 2015 Gut and liver Result HBV M204V;M204I;L180M 35;79;118 40;84;123 RT;RT;RT 33;77;116 35;79;118 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. 2A suggests that C139R (clone 22) and D144E (clone 21) are the likely mutations responsible for impaired HBsAg recognition, whereas deletion of Y225 (clone 24) may have reduced HBsAg secretion. 2014 Clinical and molecular hepatology Result HBV C139R;D144E 17;38 22;43 S;S 105;177 110;182 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Deletion of residue 225 in the C-terminus of HBsAg (Y225del) was found in an interferon-treated patient. 2014 Clinical and molecular hepatology Result HBV Y225del 52 59 S 45 50 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Four out of 19 patients (21%) harbored rare mutations inside the 'a'-determinant: M125I, M125N, C139R, and D144E. 2014 Clinical and molecular hepatology Result HBV M125I;M125N;C139R;D144E 82;89;96;107 87;94;101;112 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Of the three individuals for whom HBV sequences before and after HBsAg loss were available, only one patient had a specific mutation after HBsAg loss (T123S, patient 6). 2014 Clinical and molecular hepatology Result HBV T123S 151 156 S;S 65;139 70;144 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Taking the entire MHR region into consideration, three additional patients contained amino acid substitutions: T123S, V177A, L192F, and W196L. 2014 Clinical and molecular hepatology Result HBV T123S;V177A;L192F;W196L 111;118;125;136 116;123;130;141 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. The A1762T and G1764A core promoter mutations were found only in the lamivudine-treated patient. 2014 Clinical and molecular hepatology Result HBV A1762T;G1764A 4;15 10;21 Core promoter 22 35 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. 15% (3/20), p = 0.01)] found in HBeAg positive patients whereas A1762T/G1764A with A1053G in enhancer-I region [54% (7/13) vs. 2014 PloS one Result HBV G1764A;A1762T;A1053G 71;64;83 77;70;89 Enh I;C 93;32 103;37 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A1762T/G1764A with T147C in core region [56% (5/9) vs. 2014 PloS one Result HBV G1764A;A1762T;T147C 7;0;19 13;6;24 C 28 32 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Additionally, a single point mutation L213I in C-terminal region of surface was encountered at a high frequency in LC (45%) and HCC (50%) patients but was statistically insignificant (p = 0.085). 2014 PloS one Result HBV L213I 38 43 S 68 75 Hepatocellular carcinoma;Liver cirrhosis 128;115 131;117 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Although the prevalence of A1053G was extremely high in both LC (50%) and HCC (50%), it was only 6% in nLF and 11% in LF (p = 0.081) whereas, T1050G/A and their combination T1050G/A+A1053G showed significant escalating trend over the course of infection from nLF (18%, 0%) to HCC (54%, 32%) through LF (22%, 11%) and LC (35%, 25%) (p = 0.035, 0.008 respectively). 2014 PloS one Result HBV T1050G;T1050A;A1053G;T1050G;T1050A;A1053G 173;173;27;142;142;182 181;181;33;150;150;188 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 74;276;61;317 77;279;63;319 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. and A1762T/G1764A with L213I in surface region [67% (6/9) vs. 2014 PloS one Result HBV G1764A;A1762T;L213I 11;4;23 17;10;28 S 32 39 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. As shown in Figure 1, age was an associated risk factor for HCC development (p<0.01) but the common A1762T/G1764A dual mutation in BCP failed to show significant correlation in both HBeAg positive [89% (8/9)] and negative HCC [69% (9/13)] compared to non-HCC [60% (12/20); p = 0.2 and 42% (10/24); p = 0.17 in HBeAg positive and negative cases respectively]. 2014 PloS one Result HBV G1764A;A1762T 107;100 113;106 BCP;C;C 131;182;310 134;187;315 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 60;222;255 63;225;258 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Few other mutations E113Q (36%), I116L (50%) and P130Q (32%) in B cell epitope were observed with high frequency in HCC but the differences were insignificant. 2014 PloS one Result HBV E113Q;I116L;P130Q 20;33;49 25;38;54 Hepatocellular carcinoma 116 119 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. immune epitopes of HBx ORF was significantly altered with progression of CHB to HCC, except the changes in BCP region, which induce mutations in overlapping HBx ORF such as T1753C to I127T, A1762T and G1764A to K130M and V131I. 2014 PloS one Result HBV T1753C;I127T;A1762T;G1764A;K130M;V131I 173;183;190;201;211;221 179;188;196;207;216;226 BCP;X;X 107;19;157 110;22;160 Chronic Hepatitis B;Hepatocellular carcinoma 73;80 76;83 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Interestingly, two mutations in "a determinant region" of surface T125M and T127L were noted inversely correlated with each other. 2014 PloS one Result HBV T125M;T127L 66;76 71;81 S;S 33;58 46;65 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Mutation C1653T in enhancer-II and T1753C in BCP, which were reported previously as risk factor for HCC in HBV-genotype C, were not observed with significantly enhancing frequencies from nLF to HCC through LF and LC in HBV-genotype D infection (p = 0.079, 0.14 respectively). 2014 PloS one Result HBV C1653T;T1753C 9;35 15;41 BCP;Enh II 45;19 48;30 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 100;194;213 103;197;215 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Older age and the presence of T147C [OR 14.58, 95% CI (1.17-181.76), p = 0.037] in CTL epitope and P130Q [OR 20.71, 95% CI (1.64-261.77), p = 0.019] on B-cell epitope were identified as independent predictor of HCC in HBeAg positive and negative patients respectively (Table 4). 2014 PloS one Result HBV T147C;P130Q 30;99 35;104 C 218 223 Hepatocellular carcinoma 211 214 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Other two precore mutations G1862T and G1896A, which were frequently found in HBeAg negative patients, were noted exclusively in the advanced stages such as LC and HCC (10%, 0% and 18%, 27%; p = 0.05 and 0.225 respectively) (Table 3). 2014 PloS one Result HBV G1862T;G1896A 28;39 34;45 C;Precore 78;10 83;17 Hepatocellular carcinoma;Liver cirrhosis 164;157 167;159 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Overall three mutations in Th epitope (T12S, S35T, T67N) and one in CTL epitope (T147C) of core showed significant association with HCC (p<0.05) (Table 3). 2014 PloS one Result HBV T12S;S35T;T67N;T147C 39;45;51;81 43;49;55;86 C 91 95 Hepatocellular carcinoma 132 135 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Patients harbouring T1753C in BCP, T147C in CTL epitope of core and L213I mutation in surface were found more in HBeAg positive HCC than non-HCC cases (67% vs. 2014 PloS one Result HBV T1753C;T147C;L213I 20;35;68 26;40;73 BCP;C;C;S 30;59;113;86 33;63;118;93 Hepatocellular carcinoma;Hepatocellular carcinoma 128;141 131;144 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T1050G/A and A1053G were noticed first time in HBV-genotype D. 2014 PloS one Result HBV T1050A;T1050G;A1053G 0;0;13 8;6;19 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T125M was found with high frequency (>52%) in nLF, LF and LC but low in HCC (32%) whereas T127L was noted only in LC (20%) and HCC (41%). 2014 PloS one Result HBV T125M;T127L 0;90 5;95 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 72;127;58;114 75;130;60;116 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The L213I mutation (TTA to ATG) in surface leads to F221Y and A222T dual mutations in reverse transcriptase (RT) domain of HBV polymerase resulting a change in polymerase activity or viral replication whereas the mutation S98T in pre S1 (L12V in Polymerase) lies in the non-essential spacer region of the polymerase. 2014 PloS one Result HBV L213I;F221Y;A222T;S98T;L12V 4;52;62;222;238 9;57;67;226;242 P;P;P;P;PreS1;RT;RT;S 127;160;246;305;230;86;109;35 137;170;256;315;236;107;111;42 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The most common mutation in BCP (nt.1751-1769) A1762T and G1764A, which reduce the expression of HBeAg were always detected in combination with extremely high frequency in each of the disease stages, 35% in nLF, 44% in LF, 65% in LC and 77% in HCC (p = 0.01). 2014 PloS one Result HBV A1762T;G1764A 47;58 53;64 BCP;C 28;97 31;102 Hepatocellular carcinoma;Liver cirrhosis 244;230 247;232 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The most notable amino acid substitution observed in overlapping B and T cell epitopes of pre S1 region was S98T, which showed significant association with disease progression from LF (11%) to HCC (32%) through LC (20%) (p = 0.001) and was undetected in nLF. 2014 PloS one Result HBV S98T 108 112 PreS1 90 96 Hepatocellular carcinoma;Liver fibrosis;Liver cirrhosis 193;181;211 196;183;213 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The occurrence of precore mutation, T1858C was noticed with an increasing frequencies of 5.88% in nLF, 11% in LF, 15% in LC and 36% in HCC (p = 0.08). 2014 PloS one Result HBV T1858C 36 42 Precore 18 25 Hepatocellular carcinoma;Liver cirrhosis 135;121 138;123 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The odds ratios (OR) of these three mutations for HCC risk were significant at 7.3 [95% CI (1.037-67.9), p = 0.032] for both T1753C and L213I and 10.1 [95% CI (1.334 106.5), p = 0.01] for T147C (Table S1). 2014 PloS one Result HBV T1753C;L213I;T147C 125;136;188 131;141;193 Hepatocellular carcinoma 50 53 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The prevalence of those combinations were significantly more in HCC than non-HCC, such as A1762T/G1764A with T1753C in enhancer II [67% (6/9) vs. 2014 PloS one Result HBV G1764A;A1762T;T1753C 97;90;109 103;96;115 Enh II 119 130 Hepatocellular carcinoma;Hepatocellular carcinoma 64;77 67;80 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. While the prevalence of T1858C in precore, two mutations in B cell epitopes of core I116L and P130Q and S98T in pre S1 were predominant in HBeAg negative HCC (38% vs. 2014 PloS one Result HBV T1858C;I116L;P130Q;S98T 24;84;94;104 30;89;99;108 C;C;PreS1;Precore 79;139;112;34 83;144;118;41 Hepatocellular carcinoma 154 157 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. There were three patients with four amino acid substitutions in the MHR (Q101H; C149R; L158G; G159R). 2014 PloS one Result HBV Q101H;C149R;L158G;G159R 73;80;87;94 78;85;92;99 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Additionally, rtR192C, rtI187V and rtT150S substitutions were observed in samples 024, 038 and 123, respectively (Figure 4). 2014 Virology journal Result HBV R192C;I187V;T150S 16;25;37 21;30;42 RT;RT;RT 14;23;35 16;25;37 25471066 Occult hepatitis B virus infection among blood donors in Colombia. In the coding region of HBsAg, three amino acid substitutions were identified, sY100H, sV184A and sK141N in samples 001, 024 and 038, respectively (Figure 3); these changes correspond to the mutations T1387C, T1640C and A1512T (Table 4). 2014 Virology journal Result HBV Y100H;V184A;K141N;T1387C;T1640C;A1512T 79;87;98;201;209;220 85;93;104;207;215;226 S;S;S;S 24;79;87;98 29;80;88;99 25471066 Occult hepatitis B virus infection among blood donors in Colombia. In the RT domain of the polymerase we identified three amino acid substitutions in sample 001 (rtL108P, rtR110G and rtL180M). 2014 Virology journal Result HBV L108P;R110G;L180M 97;106;118 102;111;123 P;RT;RT;RT;RT 24;7;95;104;116 34;9;97;106;118 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. BCP A1762T, G1764A and PC G1896A were significantly associated with HCC-tissue HBV sequencing (75.3%). 2014 Hepatitis monthly Result HBV A1762T;G1764A;G1896A 4;12;26 10;18;32 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. Characteristics of chronic carriers + VHD were high level of DNA-HBV, predominance of PC G1896A mutation and highest percent of genotype D presence. 2014 Hepatitis monthly Result HBV G1896A 89 95 Precore 86 88 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. D genotype was mainly associated with presence of PC G1896A (50.1% from D-patients present PC G1896A or BCP A1762T, G1764A-PC G1896); . 2014 Hepatitis monthly Result HBV G1896A;G1896A;A1762T;G1764A 53;94;108;116 59;100;114;122 BCP;Precore;Precore;Precore 104;50;91;123 107;52;93;125 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. D genotype was mainly associated with presence of PC G1896A (50.1% from D-patients present PC G1896A or BCP A1762T, G1764A-PC G1896). 2014 Hepatitis monthly Result HBV G1896A;G1896A;A1762T;G1764A 53;94;108;116 59;100;114;122 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. Indeed, for serum sequencing PC G1896A was predominant, while for tissue sequencing BCP A1762T/G1764A and PC G1896A were predominant. 2014 Hepatitis monthly Result HBV G1764A;G1896A;A1762T;G1896A 95;32;88;109 101;38;94;115 BCP;Precore;Precore 84;29;106 87;31;108 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. PC G1896A was mainly associated with HCC-serum HBV sequencing and chronic carriers + HDV (66.7% and respectively 73.3% of patients had PC G1896A). 2014 Hepatitis monthly Result HBV G1896A;G1896A 3;138 9;144 Precore;Precore 0;135 2;137 Hepatocellular carcinoma 37 40 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. We detected significantly higher level of HBV DNA in serum of patients with both BCP A1762T/G1764A , PC G1896A mutation (15.23) and BCP A1762T/G1764A mutations (14.44) compared to patients with PC G1896A mutation alone (12.75) and patients with WT sequence (8.99); P < 0.001. 2014 Hepatitis monthly Result HBV G1764A;G1764A;A1762T;G1896A;A1762T;G1896A 92;143;85;104;136;197 98;149;91;110;142;203 BCP;BCP;Precore;Precore 81;132;101;194 84;135;103;196 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. C619T (L169) was the most common synonymous mutation, occurring in four samples (Table 6). 2014 PloS one Result HBV C619T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. However, the F122I mutation was caused by three different nucleotide substitutions at position 493. 2014 PloS one Result HBV F122I 13 18 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L209V was the only amino acid exchange detected in the S gene of the three A2 Palestinian genotypes, due to T779G point mutation. 2014 PloS one Result HBV L209V;T779G 0;108 5;113 S 55 56 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Non-synonymous mutations L217R and I253V and synonymous mutations Y252, G258, and K268 were present in all A2 samples. 2014 PloS one Result HBV L217R;I253V 25;35 30;40 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Three further mutations; H124Y, S219P and I266K were caused by two different nucleotide substitutions at positions 499, 784 and 926 respectively (Table 5). 2014 PloS one Result HBV H124Y;S219P;I266K 25;32;42 30;37;47 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Two synonymous mutations were found in one of the three samples at position C406T (L84) and A436G (L94). 2014 PloS one Result HBV C406T;A436G 76;92 81;97 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. A total of seven variations between the WT and W4P variant LHB sequences were found. 2015 Molecular cancer Result HBV W4P 47 50 S 59 62 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Although there was no significant difference in tumor incidence between male and female mice, surprisingly, the tumor volume in the W4P-cell-injected male mice was significantly larger than in the female mice (Figure 2C). 2015 Molecular cancer Result HBV W4P 132 135 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Although treatment with JSI-124 reduced the proliferation of both WT- and W4P-LHB-expressing cells, reduction of W4P-LHB-expressing cells was much greater than that of WT-LHB-expressing cells (Figure 4B). 2015 Molecular cancer Result HBV W4P;W4P 74;113 77;116 S;S;S 78;117;171 81;120;174 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. An increase in the well-known proliferation marker proliferating cell nuclear antigen (PCNA) by W4P LHB supported the higher cell-proliferating activity of W4P LHB (Figure 1D). 2015 Molecular cancer Result HBV W4P;W4P 96;156 99;159 S;S 100;160 103;163 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. As shown in Figure 1A, both WT and W4P LHBs significantly facilitated cell proliferation. 2015 Molecular cancer Result HBV W4P 35 38 S 39 43 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Co-cultivation of the murine macrophage cell line J774A with W4P-LHB-NIH3T3 cells resulted in increased production of IL-6, which was reduced by treatment with estradiol (Figure 5B). 2015 Molecular cancer Result HBV W4P 61 64 S 65 68 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Compared with NIH3T3 cells, the colony numbers in WT and W4P increased by about 1.9 and 4.6 times, respectively, suggesting that W4P LHB regulates the cell cycle and has a strong transforming effect on NIH3T3 cells (Figure 2A). 2015 Molecular cancer Result HBV W4P;W4P 57;129 60;132 S 133 136 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Consistent with the in vivo data, W4P-LHB-NIH3T3 cells produced a significant amount of IL-6, while the WT-LHB-NIH3T3 and NIH3T3 cells did not produce a detectable amount of IL-6 (Figure 5A). 2015 Molecular cancer Result HBV W4P 34 37 S;S 38;107 41;110 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Consistent with the previous data showing the crucial role of IL-6-JAK2-stat3 signaling pathway, treatment with beta-estradiol completely abolished the effect of W4P LHB on cell growth (Figure 5D). 2015 Molecular cancer Result HBV W4P 162 165 S 166 169 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Expression of WT and W4P LHB induced 33.5% and 52% increases in the percentages of cells in S and G2/M phases, respectively (Figure 1C). 2015 Molecular cancer Result HBV W4P 21 24 S;S 25;92 28;93 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. IL-6 is significantly related to gender disparity in hepatocarcinogenesis; thus, we attempted to determine whether IL-6 was also related to gender disparity in the tumorigenicity in our W4P-injected mouse model. 2015 Molecular cancer Result HBV W4P 186 189 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. IL-6 signaling pathway was necessary for cell proliferating and transforming activities of W4P LHB. 2015 Molecular cancer Result HBV W4P 91 94 S 95 98 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. In addition, beta-estradiol treatment suppressed phosphorylation of stat3 in W4P LHB-expressing cells, further supporting the hypothesis that W4P LHB induced higher cell proliferation and tumorigenesis (Figure 5E). 2015 Molecular cancer Result HBV W4P;W4P 77;142 80;145 S;S 81;146 84;149 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. In line with the mouse data, HCC patients with the W4P variant had significantly higher serum IL-6 levels than those carrying WT LHB (Figure 3D), while there was no significant difference in the level of TNF-alpha (Figure 3E). 2015 Molecular cancer Result HBV W4P 51 54 S 129 132 Hepatocellular carcinoma 29 32 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. LHB variant with W4P mutation showed enhanced cell proliferating activity and facilitated cell cycle progression. 2015 Molecular cancer Result HBV W4P 17 20 S 0 3 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Notably, W4P LHB showed significantly greater enhancement of cell growth than WT LHB showed. 2015 Molecular cancer Result HBV W4P 9 12 S;S 13;81 16;84 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Secretion of IL-6 by J774 was significantly enhanced by treatment of W4P tumor lysates but not WT tumor lysate, and the level was lowered by estradiol, suggesting that IL-6 is produced by W4P-LHB-expressing cells and neighboring macrophages (Figure 5C). 2015 Molecular cancer Result HBV W4P;W4P 69;188 72;191 S 192 195 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Serum IL-6 level in the W4P-injected mice was significantly higher than in mice injected with NIH3T3 or WT (Figure 3A), whereas there was no significant difference in the level of tumor necrosis factor (TNF)-alpha (Figure 3B). 2015 Molecular cancer Result HBV W4P 24 27 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Serum IL-6 level of W4P-LHB-NIH3T3-injected mice was significantly higher in male than in female mice, suggesting the involvement of IL-6 in gender disparity of W4P-induced tumor growth (Figure 3A). 2015 Molecular cancer Result HBV W4P;W4P 20;161 23;164 S 24 27 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Similar results were obtained from the experiment using Huh7 human HCC cell lines expressing vector, WT and W4P LHBs. 2015 Molecular cancer Result HBV W4P 108 111 S 112 116 Hepatocellular carcinoma 67 70 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Similarly, W4P-LHB-expressing Huh7 cells lines formed increased numbers of colonies compared with vector cells or WT-LHB-expressing cells, suggesting that W4P LHB facilitates growth of HCC cells (Additional file 3: Figure S3). 2015 Molecular cancer Result HBV W4P;W4P 11;155 14;158 S;S;S 15;117;159 18;120;162 Hepatocellular carcinoma 185 188 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Suppression of the JAK2-stat3 signaling axis by siRNAs targeting JAK2 or stat3 resulted in significant suppression of W4P-LHB-expressing cell growth (Figure 4D, 4E). 2015 Molecular cancer Result HBV W4P 118 121 S 122 125 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Surprisingly, 19 (10 male and 9 female) of the 20 mice injected with W4P cells developed tumors, whereas no tumors were noted in the groups injected with WT-LHB-NIH3T3 and the control NIH3T3 cells during the 4 weeks observation period, indicating that LHB gained oncogenic potential by W4P mutation (Figure 2B). 2015 Molecular cancer Result HBV W4P;W4P 69;286 72;289 S;S 157;252 160;255 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Taken together, our data strongly suggest that IL-6 plays a pivotal role in tumorigenicity and growth of W4P-expressing cells, and estrogen is capable of suppressing W4P-LHB-mediated tumorigenicity and tumor growth. 2015 Molecular cancer Result HBV W4P;W4P 105;166 108;169 S 170 173 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The cell transforming activity of W4P was also suppressed by treatment with JSI-124, and there was no significant difference in the transforming activities of WT- and W4P-LHB-expressing cells after treatment with JSI-124 (Figure 4C). 2015 Molecular cancer Result HBV W4P;W4P 34;167 37;170 S 171 174 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The levels of cyclin-dependent kinase (CDK)2, CDK4, cyclin A, and cyclin D, which are known to be involved in G1/S transition, were higher in W4P expressing cells than WT and NIH3T3 cell lines (Figure 1D). 2015 Molecular cancer Result HBV W4P 142 145 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The levels of p53 and p21 proteins, which are associated with the G1/S checkpoint, were reduced by expression of LHBs, and W4P exerted a stronger effect than WT (Figure 1D). 2015 Molecular cancer Result HBV W4P 123 126 S 113 117 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The W4P variation was related to HCC; therefore, we examined whether the variation was implicated in cell growth using mouse NIH3T3 cell lines constitutively expressing WT LHB (WT-LHB-NIH3T3) and W4P variant LHB (W4P-LHB-NIH3T3) (Additional file 2: Figure S2). 2015 Molecular cancer Result HBV W4P;W4P;W4P 4;196;213 7;199;216 S;S;S;S 172;180;208;217 175;183;211;220 Hepatocellular carcinoma 33 36 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. These results suggest that LHBs, especially W4P LHB, regulate cell cycle progression, and LHBs may affect G1/S transition. 2015 Molecular cancer Result HBV W4P 44 47 S;S;S 48;27;90 51;31;94 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. To test further whether W4P variation was involved in tumorigenicity and gender disparity of HCC, we grafted the cell lines into nude mice. 2015 Molecular cancer Result HBV W4P 24 27 Hepatocellular carcinoma 93 96 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. To understand the physiological role of W4P mutation of HBV genotype C, LHB sequences from a carrier (WT) and a variant LHB sequence with W4P mutation (W4P) from an HCC patient were cloned. 2015 Molecular cancer Result HBV W4P;W4P;W4P 40;138;152 43;141;155 S;S 72;120 75;123 Hepatocellular carcinoma 165 168 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Treatment of male mice with beta-estradiol drastically reduced the W4P-LHB-expressing tumor incidence. 2015 Molecular cancer Result HBV W4P 67 70 S 71 74 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Treatment with beta-estradiol of the W4P-LHB-NIH3T3 cells resulted in a significant decrease of IL-6 production (Figure 5A). 2015 Molecular cancer Result HBV W4P 37 40 S 41 44 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-expressing cells had oncogenic potential to form tumor masses in a mouse model and tumor growth showed gender disparity. 2015 Molecular cancer Result HBV W4P 0 3 S 4 7 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-expressing cells induced production of high levels of IL-6, especially in male mice. 2015 Molecular cancer Result HBV W4P 0 3 S 4 7 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-expressing NIH3T3 and Huh7 cells displayed higher phosphorylation of stat3 than WT-LHB-expressing cells and parental cells (Figure 4A and Additional file 4: Figure S4). 2015 Molecular cancer Result HBV W4P 0 3 S;S 4;91 7;94 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-induced tumor showed a typical fasciculated proliferating pattern with an interstitial collagen matrix (Figure 2D). 2015 Molecular cancer Result HBV W4P 0 3 S 4 7 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-mediated IL-6 production and tumor growth were downregulated by estrogen. 2015 Molecular cancer Result HBV W4P 0 3 S 4 7 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-mediated production of IL-6 is involved in tumor growth and IL-6 production was significantly lower in female mice; therefore, we tested the hypothesis that estrogen signaling may suppress IL-6 production and inhibit IL-6-mediated tumor growth. 2015 Molecular cancer Result HBV W4P 0 3 S 4 7 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P-LHB-NIH3T3 cells showed a significantly higher colony forming ability than WT-LHB-NIH3T3 and NIH3T3 cells. 2015 Molecular cancer Result HBV W4P 0 3 S;S 4;82 7;85 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. We examined whether W4P mutation was involved in cell transformation. 2015 Molecular cancer Result HBV W4P 20 23 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. We investigated the effect of estrogen on W4P-induced tumor growth in male mice (Figure 6A). 2015 Molecular cancer Result HBV W4P 42 45 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Among the basal core promoter mutations, A1762T-G1764A double mutation was present in 26.9%, C1653T in 8.6%, A1752G in 10.8% and C1766T in 2.2% of the isolates. 2014 Hepatitis monthly Result HBV A1762T;G1764A;C1653T;A1752G;C1766T 41;48;93;109;129 47;54;99;115;135 BCP 10 29 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Another identified precore mutation was G1896A with the occurrence of 25.8%. 2014 Hepatitis monthly Result HBV G1896A 40 46 Precore 19 26 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Case Report of W182 Stop Codon Mutation. 2014 Hepatitis monthly Result HBV W182X 15 24 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The characteristics of the two patients with W182* mutation were summarized in Table 3. 2014 Hepatitis monthly Result HBV W182X 45 50 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The most common mutation observed was precore mutation C1858 T which comprised 64.5% of the sequencedisolates. 2014 Hepatitis monthly Result HBV C1858T 55 62 Precore 38 45 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The position of W182* and pre-S1 deletion were shown in Figure 6. 2014 Hepatitis monthly Result HBV W182X 16 21 PreS1 26 32 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The W182 stop codon (W182*) and deletion at open reading frame (ORF) of pre-S1 were present with the frequencies of 2.2% (2.93) and 5.4% (5.93), respectively. 2014 Hepatitis monthly Result HBV W182X;W182X 21;4 26;13 PreS1 72 78 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. Combined mutation characteristics were also found in other hotspot mutation positions from genotype C sequences of children, such as G1721A (G1721A/A1775G/T1858C, 16/18) and A1775G mutations (G1721A/A1775G/T1858C, 16/19). 2015 Hepatitis monthly Result HBV T1858C;A1775G;T1858C;A1775G;G1721A;G1721A;A1775G;G1721A 155;148;206;199;133;141;174;192 161;154;212;205;139;147;180;198 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. For example, the frequency of T1858C mutation in genotype C sequences from children was 31.5% (17/54). 2015 Hepatitis monthly Result HBV T1858C 30 36 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. However, the frequency of G1721A mutation in genotype C strains was higher than genotype B (31.5% vs 0.5%, P < 0.001). 2015 Hepatitis monthly Result HBV G1721A 26 32 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. Most combined mutations had no correlation with clinical phenotypes, with exception to the G1721A/A1775G/T1858C triple mutation. 2015 Hepatitis monthly Result HBV A1775G;T1858C;G1721A 98;105;91 104;111;97 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. Similarly, most of the C1856T mutations from genotype C sequences of the HBV-infected children were also detected in combined mutation forms (G1721A/A1775G/C1856T/T1858C, 8/9, 88.9%). 2015 Hepatitis monthly Result HBV C1856T;T1858C;A1775G;C1856T;G1721A 156;163;149;23;142 162;169;155;29;148 HBV infections 73 85 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. The age of children containing G1721A/A1775G/T1858C triple-mutation strains was significantly lower than that of triple-mutation-free patients (4.56 +- 2.45 vs 6.56 +- 4.12, P = 0.012, Table 4). 2015 Hepatitis monthly Result HBV A1775G;T1858C;G1721A 38;45;31 44;51;37 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. This mutation was detected in combination with other mutations, as exemplified by the G1721A/A1775G/T1858C triple-mutation (16/17, 94.1%). 2015 Hepatitis monthly Result HBV T1858C;A1775G;G1721A 100;93;86 106;99;92 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. In comparison, the frequencies of the A1762T/G1764A double mutation and T1753V mutation increased in genotype C infected children patients (P< 0.05). 2015 PloS one Result HBV G1764A;A1762T;T1753V 45;38;72 51;44;78 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. In HBeAg-positive adult CHB patients, the A1762T/G1764A double mutation was significantly correlated with a low viral load (log107.39+-1.36 vs log106.15+-1.59,wild type group vs double mutation group, P = 0.0077) but not with ALT level (89.6+-101.8 vs 317.5+-229.8, wild type group vs double mutation group, respectively, P = 0.0681), which differs from previous findings. 2015 PloS one Result HBV G1764A;A1762T 49;42 55;48 C 3 8 Chronic Hepatitis B 24 27 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Most mutations had no correlation with the clinical phenotypes, except the A1762T/G1764A double mutation, which was significantly correlated with a low viral DNA load and high ALT levels in HBeAg-positive child patients (viral load log108.10+-1.17 vs log107.51+-0.97, P = 0.006 and ALT 59.3+-114.7 vs 129.7+-242.4, P = 0.006 for wildtype group vs double mutation group, respectively), but this correlation was not present in the HBeAg-negative child patient group. 2015 PloS one Result HBV G1764A;A1762T 82;75 88;81 C;C 190;429 195;434 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Notably, the frequency of the G1896A mutation in the HBeAg-negative child patients was significantly lower than in the HBeAg-negative adult patients (41.1% vs 91.7%, P < 0.001), and similar results were also observed for other BCP/precore mutations such as A1846T (17.8% vs 37.5%, P = 0.010) and the G1899A substitution (7.8% vs 20.8%, P = 0.026). 2015 PloS one Result HBV G1896A;A1846T;G1899A 30;257;300 36;263;306 BCP;C;C;Precore 227;53;119;231 230;58;124;238 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Notably, the higher mutation ratio in the adult patients than in the child patients for these combined mutations (G1896A/A1846T: 35.4%vs12.2%, P<0.001; G1896A/G1899A: 18.8%vs4.6%, P = 0.015; G1896A/A1762T/G1764A: 35.4%vs12.2%, P<0.001) implied that combined mutations in the BCP/precore regions were less correlated with HBeAg seroconversion in child patients than adult patients. 2015 PloS one Result HBV A1846T;G1899A;A1762T;G1764A;G1896A;G1896A;G1896A 121;159;198;205;114;152;191 127;165;204;211;120;158;197 BCP;C;Precore 275;321;279 278;326;286 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The frequency of the A1752G mutation was higher in genotype B than genotype C HBV (46.1% vs 5.6% in children, 53.0% vs 3.8% in adults, P<0.001 for both). 2015 PloS one Result HBV A1752G 21 27 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The ratio of three combined mutations(G1896A/A1762T/G1764A, G1896A/A1846T and G1896A/A1752G)was obviously higher in HBeAg-negative patients than in the HBeAg-positive patient groups, suggesting that these combined mutation types could distinguish the HBeAg seroconverted patients with CHB. 2015 PloS one Result HBV A1846T;A1752G;A1762T;G1764A;G1896A;G1896A;G1896A 67;85;45;52;38;60;78 73;91;51;58;44;66;84 C;C;C 116;152;251 121;157;256 Chronic Hepatitis B 285 288 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In brief, those patients infected with sgF4 and gD mutated G1896A more frequently than A1762T/G1764A (p = 0.007 and p<0.001 respectively), whereas those patients carrying sgF1b and sgA2 had the opposite mutation pattern, showing higher rates of mutations in positions 1762 and 1764 than in 1896 (p = 0.013 and p = 0.010 respectively). 2015 PloS one Result HBV G1764A;G1896A;A1762T 94;59;87 100;65;93 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In order to assess the role of 1727, 1740 and 1773 polymorphisms in the mutation pattern of 1896 position, the frequency of G1896A mutation was determined in those samples carrying 1858T. 2015 PloS one Result HBV G1896A 124 130 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In spite of the low prevalence of mutations in AHB infections (25.7%), those subgenotypes more frequently observed in this stage, sgA2 and sgF1b, had the double mutation A1762T/G1764A, while gD and sgF4 did not mutate these positions (Table 3). 2015 PloS one Result HBV G1764A;A1762T 177;170 183;176 HBV-HIV coinfections 47 61 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In the preCore region, G1896A was the most common mutation (55.2%), whereas other mutations that prevent HBeAg synthesis, such as those affecting the preCore initiation codon (nt 1814-1816), mutations (C1817T, G1897A), insertions and deletions that create a premature stop codon, were observed in a lower frequency (33.3%). 2015 PloS one Result HBV G1896A;C1817T;G1897A 23;202;210 29;208;216 C;Precore;Precore 105;7;150 110;14;157 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In the preCore region, gD and sgF4 had higher frequencies of G1896A mutation (81.0 and 72.7%, respectively) compared to sgA2 and sgF1b (0.0 and 31.3%). 2015 PloS one Result HBV G1896A 61 67 Precore 7 14 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. It is widely accepted that the G1896A mutation rate is closely related to the viral genotype. 2015 PloS one Result HBV G1896A 31 37 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. Samples with 1727A, 1740T and 1773C (D and F4) were more prone to select G1896A mutation than those with 1727G, 1740C and 1773T (F1b) (p<0.05) (Table 4). 2015 PloS one Result HBV G1896A 73 79 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. The double mutation A1762T/G1764A was more frequently found in sgF1b infections (75.0%) than in sgA2, gD and sgF4 (40.0, 33.3 and 31.8%, respectively). 2015 PloS one Result HBV G1764A;A1762T 27;20 33;26 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. The G1896A mutation rate observed in sgF1b (carrying 1858T) was unexpectedly low, displaying a mutation pattern more similar to genotype A (1858C) than genotypes D and F4 (1858T). 2015 PloS one Result HBV G1896A 4 10 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. One of the samples with G1896A mutation was registered in NCBI under the accession number: KC928094. 2015 Jundishapur journal of microbiology Result HBV G1896A 24 30 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. Our results showed that G1896A was detected as the most prevalent mutation in 44 patients, out of which 41 (93.18%) were HBeAg negative. 2015 Jundishapur journal of microbiology Result HBV G1896A 24 30 C 121 126 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. Sex and age specific prevalence of G1896A mutants showed no significant difference between sexes and ages. 2015 Jundishapur journal of microbiology Result HBV G1896A 35 41 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. Substitutions at position G1896A were seen in 44 (36.66%), leading to the creation of stop codon in the 28th amino acid of the PC region in 39 (32.50%) of these patients. 2015 Jundishapur journal of microbiology Result HBV G1896A 26 32 Precore 127 129 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. As compared with non-ACLF cases, T216C, G285A, A1846T/G, G1896A, C1913A/G, A2159G/C, A2189T/C in genotype B and G285A, A1846T/G, G1896A, C1913A/G and A2159G/C in genotype C were significantly associated with an increased risk of ACLF(see Table 5). 2015 PloS one Result HBV C1913G;A2159C;T216C;G285A;A1846T;A1846G;G1896A;C1913A;A2159G;A2189T;A2189C;G285A;A1846T;A1846G;G1896A;C1913A;C1913G;A2159G;A2159C 65;75;33;40;47;47;57;65;75;85;85;112;119;119;129;137;137;150;150 73;83;38;45;55;55;63;73;83;93;93;117;127;127;135;145;145;158;158 Acute on chronic liver failure 229 233 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. In ACLF group, the mutations at seven sites (T216C, G285A, A1846T, G1896A, C1913A/G, A2159G and A2189C) were frequently found, and there were significant differences in the mutation frequencies at these sites between the ACLF and CHB-M groups (P<0.05 or P<0.01). 2015 PloS one Result HBV C1913G;T216C;G285A;A1846T;G1896A;C1913A;A2159G;A2189C 75;45;52;59;67;75;85;96 83;50;57;65;73;83;91;102 Acute on chronic liver failure;Chronic Hepatitis B 3;230 7;233 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. In ACLF patients with genotype B virus, the substitution rates of T216C, G285A, A1846T/G, G1896A, C1913A/G, A2159G/C, and A2189T/C were 70.6%, 60.3%, 66.2%, 76.5%, 63.2%, 47.1%, and 50.0%, respectively; while in ACLF patients with genotype C virus, the substitution rates were 8.3%, 13.9%, 44.4%, 63.9%, 41.7%, 41.7%, 47.2%, respectively. 2015 PloS one Result HBV C1913G;A2159C;T216C;G285A;A1846T;A1846G;G1896A;C1913A;A2159G;A2189T;A2189C 98;108;66;73;80;80;90;98;108;122;122 106;116;71;78;88;88;96;106;116;130;130 Acute on chronic liver failure;Acute on chronic liver failure 3;212 7;216 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. It was found that the old age, genotype B, T216C, G1896A, C1913A/G and A2159G/C mutations were risk factors independently associated with ACLF, as compared with non-ACLF (P < 0.05 or P < 0.01). 2015 PloS one Result HBV A2159C;T216C;G1896A;C1913A;C1913G;A2159G 71;43;50;58;58;71 79;48;56;66;66;79 Acute on chronic liver failure 138 142 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Rather than a single mutation, combinations with any 2 or more of T216C, G1896A, C1913A/G and A2159G/C were significantly associated with the development of ACLF compared with non-ACLF (78.8% vs. 2015 PloS one Result HBV A2159C;T216C;G1896A;C1913A;C1913G;A2159G 94;66;73;81;81;94 102;71;79;89;89;102 Acute on chronic liver failure 157 161 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. After stratifying by gender, it was found that the interaction between the polymorphism of rs2299939 GT+TT and C3116T significantly reduced the risk of HCC in male HBV-infected subjects (AOR = 0.27, 95% CI = 0.13-0.57). 2015 Chinese medical journal Result HBV C3116T 111 117 Hepatocellular carcinoma;HBV infections 152;164 155;176 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. Although the variant genotype of rs2299939 was significantly associated with a reduced risk of HCC, the interaction of rs2299939 variant genotypes with A3054T was significantly associated with an increased risk of HCC. 2015 Chinese medical journal Result HBV A3054T 152 158 Hepatocellular carcinoma;Hepatocellular carcinoma 95;214 98;217 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. HBV C3116T mutation was a significant risk factor of HCC; however, its interaction with rs2299939 variant genotypes was significantly associated with a reduced risk of HCC. 2015 Chinese medical journal Result HBV C3116T 4 10 Hepatocellular carcinoma;Hepatocellular carcinoma 53;168 56;171 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. It was found that the variant genotype (TC) of rs1234220 was significantly associated with increased frequencies of HBV mutations A1652G (AOR = 4.16, 95% CI = 1.64-10.55), C1673T (AOR = 2.40, 95% CI = 1.02-5.66), and C1730G (AOR = 2.34, 95% CI = 1.02-5.39) in genotype B HBV-infected subjects. 2015 Chinese medical journal Result HBV A1652G;C1673T;C1730G 130;172;217 136;178;223 HBV infections 271 283 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. Similarly, the interaction between rs1234213 CT+TT and C3116T also significantly increased HCC risk in male HBV-infected subjects (AOR = 3.61, 95% CI = 1.54-8.42) after stratifying by gender. 2015 Chinese medical journal Result HBV C3116T 55 61 Hepatocellular carcinoma;HBV infections 91;108 94;120 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. There were significant interactions between PTEN polymorphisms and A3054T or C3116T, important HBV mutations in the preS region [Table 6]. 2015 Chinese medical journal Result HBV A3054T;C3116T 67;77 73;83 PreS 116 120 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. We also found that the interaction of rs1234213 variant genotypes with HBV C3116T mutation significantly increased the risk of HCC in the HBV-infected subjects. 2015 Chinese medical journal Result HBV C3116T 75 81 Hepatocellular carcinoma;HBV infections 127;138 130;150 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. Among them, the R154G mutation of HBc was the most effective in decreasing the cell binding ability to all three cell types, while its potency was fairly close to those of R150G, R151G and R152G. 2015 Journal of nanobiotechnology Result HBV R154G;R150G;R151G;R152G 16;172;179;189 21;177;184;194 C 34 37 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. In contrast, the green fluorescence of HBc-R154G particles was little observed in any three cell types. 2015 Journal of nanobiotechnology Result HBV R154G 43 48 C 39 42 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The binding curve of the HBc-R154G particle was lower than that of wild-type HBc particles, which agreed with the results found using a flow cytometer. 2015 Journal of nanobiotechnology Result HBV R154G 29 34 C;C 25;77 28;80 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The mutations of R residues at aa 150, 151, 152 and 154 (R150G, R151G, R152G and R154G) in HBc considerably decreased the cell binding ability. 2015 Journal of nanobiotechnology Result HBV R150G;R151G;R152G;R154G 57;64;71;81 62;69;76;86 C 91 94 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The replacement of the R residues at aa 157, 158 and 159 (R157G, R158G and R159G) showed a comparatively higher cell binding ability compared with other HBc mutants. 2015 Journal of nanobiotechnology Result HBV R157G;R158G;R159G 58;65;75 63;70;80 C 153 156 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The value of ka showed a 1.5-fold difference between WT-HBc (1.45 x 107) and HBc-R154G (9.44 x 106) particles. 2015 Journal of nanobiotechnology Result HBV R154G 81 86 C;C 56;77 59;80 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. This result indicated that the HBc-R154G particles showed the decrease of the non-specific cellular uptake ability for three different cell types. 2015 Journal of nanobiotechnology Result HBV R154G 35 40 C 31 34 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. Thus, the R154 residue and its peripheral R residues (aa 150-152) in the arginine-rich domain are critical to the cell binding ability of HBc particles, and the HBc-R154G particles would be useful in the development of an engineered HBc particles for the targeted cell-specific delivery of nucleic acids. 2015 Journal of nanobiotechnology Result HBV R154G 165 170 C;C;C 138;161;233 141;164;236 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. To evaluate the effect of R154G mutation on cellular uptake, HeLa, NuE and A431 cells were treated with HBc-WT and HBc-R154G particles labelled with Alexa Fluor 488. 2015 Journal of nanobiotechnology Result HBV R154G;R154G 26;119 31;124 C;C 104;115 107;118 25942596 The characteristic changes in hepatitis B virus x region for hepatocellular carcinoma: a comprehensive analysis based on global data. Five positions in HCC group (A1383C, R1479Y, C1485T, C1653T, and G1719T) showed elevating mutant ratios more than 10% toward Non-HCC group and A1383C single mutation showed a relatively low mutant ratio (26%) in genotype C Non-HCC but elevated to more than 50% in genotype C HCC group. 2015 PloS one Result HBV A1383C;R1479Y;C1485T;C1653T;G1719T;A1383C 29;37;45;53;65;143 35;43;51;59;71;149 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 18;275;129;227 21;278;132;230 25942596 The characteristic changes in hepatitis B virus x region for hepatocellular carcinoma: a comprehensive analysis based on global data. Here, how those seven genotype C HBx risk mutations, A1383C, R1479C/T, C1485T, C1631T, C1653T, G1719T, and T1800C, are distributed among genotype C HCC patients from different countries is an intriguing question. 2015 PloS one Result HBV A1383C;C1485T;C1631T;C1653T;G1719T;T1800C;R1479C 53;71;79;87;95;107;61 59;77;85;93;101;113;69 X 33 36 Hepatocellular carcinoma 148 151 25942596 The characteristic changes in hepatitis B virus x region for hepatocellular carcinoma: a comprehensive analysis based on global data. Logistic regression showed that mutations A1383C (OR: 2.32, 95% CI: 1.34-4.01), R1479C/T (OR: 1.96, 95% CI: 1.05-3.64; OR: 5.15, 95% CI: 2.53-10.48), C1485T (OR: 2.40, 95% CI: 1.41-4.08), C1631T (OR: 4.09, 95% CI: 1.41-11.85), C1653T (OR: 2.58, 95% CI: 1.59-4.19), G1719T (OR: 2.11, 95% CI: 1.19-3.73), and T1800C (OR: 23.59, 95% CI: 2.25-247.65) were independent risk factors for genotype C HBV-related HCC (Table 4), where Stepwise Forward (Conditional) method for logistic regression was used and those variates with insignificant p values (P > 0.05) were not analyzed further for OR calculation. 2015 PloS one Result HBV A1383C;C1485T;C1631T;C1653T;G1719T;T1800C;R1479C 42;150;188;227;265;307;80 48;156;194;233;271;313;88 Hepatocellular carcinoma 404 407 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. After 21-24 months of combination treatment, ADV-resistant variants rtA181V and rtN236T gradually decreased to undetectable levels. 2015 International journal of medical sciences Result HBV A181V;N236T 70;82 75;87 RT;RT 68;80 70;82 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. During 27-36 months of combination treatment, no LAM-resistant variants (rtM204I/V with or without rtL180M) or ETV-resistant variants (rtT184, rtS202, or rtM250) were detected in the viral population. 2015 International journal of medical sciences Result HBV M204I;M204V;L180M 75;75;101 82;82;106 RT;RT;RT;RT;RT 73;99;135;143;154 75;101;137;145;156 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. In contrast to patient 1, the virus with the single rtN236T variant was responsible for virological breakthrough. 2015 International journal of medical sciences Result HBV N236T 54 59 RT 52 54 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. In patient 1, the proportion of the virus harboring rtN236T gradually increased for 6 months before virological breakthrough (defined as an increase in the HBV DNA level of more than 1 log10 copies/mL compared to the nadir HBV DNA level during therapy). 2015 International journal of medical sciences Result HBV N236T 54 59 RT 52 54 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. In patient 3, the dynamics was characterized by outgrowth of the virus with rtN236T within the background of the virus harboring rtA181V and was predominant. 2015 International journal of medical sciences Result HBV A181V;N236T 131;78 136;83 RT;RT 76;129 78;131 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. The emergence of ADV-resistant variants, such as rtA181V and/or rtN236T, was found in all these patients during the 24 - 33 months of ADV monotherapy. 2015 International journal of medical sciences Result HBV A181V;N236T 51;66 56;71 RT;RT 49;64 51;66 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. The replication of ADV-resistant variants (rtA181V and/or rtN236T) was inhibited after ETV was added to the ongoing ADV monotherapy. 2015 International journal of medical sciences Result HBV A181V;N236T 45;60 50;65 RT;RT 43;58 45;60 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. The virus harboring rtA181V emerged at month 36 and was predominant at month 42, while the wild-type virus was profoundly inhibited. 2015 International journal of medical sciences Result HBV A181V 22 27 RT 20 22 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. The virus harboring rtN236T was predominant and was responsible for virological breakthrough. 2015 International journal of medical sciences Result HBV N236T 22 27 RT 20 22 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. Three resistant viral populations were found during ADV administration in these three patients, including rtN236T alone (patient 1), rtA181V alone (patient 2), and both rtA181V and rtN236T (patient 3). 2015 International journal of medical sciences Result HBV N236T;A181V;A181V;N236T 108;135;171;183 113;140;176;188 RT;RT;RT;RT 106;133;169;181 108;135;171;183 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. In contrast, a new amino acid substitution (rtD263E) was found exclusively in 60% (30/50) of patients treated with TDF, while this mutation was only observed in 12% (6/50) of patients prior to initiation of TDF therapy. 2015 Hepatitis monthly Result HBV D263E 46 51 RT 44 46 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. Moreover, a comparison between baseline and post-baseline samples from these patients showed that the presence of rtL91I, rtN238H/T/S, rtC256G, rtN53S/T and rtY54N mutations reduced significantly after the initiation of TDF treatment (P < 0.05) (Table 4). 2015 Hepatitis monthly Result HBV L91I;N238H;N238T;N238S;N53S;N53T;Y54N;C256G 116;124;124;124;146;146;159;137 120;133;133;133;152;152;163;142 RT;RT;RT;RT;RT 114;122;135;144;157 116;124;137;146;159 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. No patient harbored previously described amino acid substitutions, including substitutions that could be associated with reduced TDF susceptibility (rtA181V/T, rtN236T or rtA194T). 2015 Hepatitis monthly Result HBV A181V;A181T;N236T;A194T 151;151;162;173 158;158;167;178 RT;RT;RT 149;160;171 151;162;173 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Except for those with G1764A and G1896A/A1762T/G1764A, we did not observe any publication bias with T1753V, A1762T, A1762T/G1764A, C1766T, T1768A, A1846T, G1862T, G1896A or G1899A, (Table 5 and. 2015 Virology journal Result HBV G1764A;G1764A;A1762T;G1764A;G1896A;T1753V;A1762T;A1762T;C1766T;T1768A;A1846T;G1862T;G1896A;G1899A 123;47;40;22;33;100;108;116;131;139;147;155;163;173 129;53;46;28;39;106;114;122;137;145;153;161;169;179 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1764A showed a high positive prediction value (PPV; 80.1 %, 95 % CI, 77.7-82.4; Table 4). 2015 Virology journal Result HBV G1764A 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1862T was not significantly associated with ACLF risk, but when we removed the study conducted by Xiaoqiang Ren, statistical significance was achieved (summary OR = 2.579 [1.510-4.405], p = 0.001). 2015 Virology journal Result HBV G1862T 0 6 Acute on chronic liver failure 45 49 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Most of the mutation sites showed low sensitivity and relatively high specificity, except A1762T, which had a sensitivity of 74.5 % (95 % CI = 71.9-76.9 %) and specificity of 45.8 % (95 % CI = 43.7-47.9 %). 2015 Virology journal Result HBV A1762T 90 96 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Overall, the following mutations were found to be meaningfully related to ACLF risk (shown as summary OR and 95 % [CI]): T1753V (1.919 [1.414-2.606]), A1762T (2.685 [2.264-3.185]), G1764A (2.901 [2.041-4.122]), A1762T/G1764A double mutation (2.376 [1.548-3.648]), C1766T (1.849 [1.403-2.437]), T1768A (2.199 [1.563-3.094]), A1846T (3.163 [2.157-4.639]), G1896A (2.181 [1.800-2.642]), G1899A (3.525 [2.882-4.312]) and G1896A/A1762T/G1764A triple mutation (1.575 [1.172-2.116]). 2015 Virology journal Result HBV G1764A;A1762T;G1764A;T1753V;A1762T;G1764A;A1762T;C1766T;T1768A;A1846T;G1896A;G1899A;G1896A 218;424;431;121;151;181;211;264;294;324;354;384;417 224;430;437;127;157;187;217;270;300;330;360;390;423 Acute on chronic liver failure 74 78 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. The most common mutations in the BCP/PC regions that were associated with ACLF progression were T1753V, A1762T/G1764A, A1762T, G1764A, C1766T, T1768A, A1846T, G1862T, G1896A, G1899A and G1896A/A1762T/G1764A (Table 1). 2015 Virology journal Result HBV G1764A;A1762T;G1764A;T1753V;A1762T;A1762T;G1764A;C1766T;T1768A;A1846T;G1862T;G1896A;G1899A;G1896A 111;193;200;96;104;119;127;135;143;151;159;167;175;186 117;199;206;102;110;125;133;141;149;157;165;173;181;192 BCP;Precore 33;37 36;39 Acute on chronic liver failure 74 78 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. The summary OR of ACLF risk for several variations was lower in matched subgroups than that in unmatched subgroups, such as T1753V, A1762T, G1764A, C1766T, G1896A, G1899A and A1846T, while an opposite result was observed for A1762T/G1764A and T1768A (Table 3). 2015 Virology journal Result HBV G1764A;T1753V;A1762T;G1764A;C1766T;G1896A;G1899A;A1846T;A1762T;T1768A 232;124;132;140;148;156;164;175;225;243 238;130;138;146;154;162;170;181;231;249 Acute on chronic liver failure 18 22 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. There was a large amount of heterogeneity between different trials for T1753V, G1764A, A1846T, G1862T, G1896A and A1762T/G1764A. 2015 Virology journal Result HBV G1764A;T1753V;G1764A;A1846T;G1862T;G1896A;A1762T 121;71;79;87;95;103;114 127;77;85;93;101;109;120 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. We therefore conducted a sensitivity analysis using a "leave one out" approach and Egger's testing, and found that these mutations were not influential, except for G1862T. 2015 Virology journal Result HBV G1862T 164 170 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. As expected, ETV at 1 to 1,000 nM concentrations failed to block HBVETV-RL180M/S202G/M204V replication; even the highest concentration (1,000 nM) of ETV failed to achieve 50% signal reduction as shown in. 2015 Hepatology (Baltimore, Md.) Result HBV S202G;M204V 79;85 84;90 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. By contrast, both CAdA and CdG significantly blocked HBVETV-RL180M/S202G/M204V replication in a dose-response fashion. 2015 Hepatology (Baltimore, Md.) Result HBV S202G;M204V 67;73 72;78 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. CAdA and CdG block HBVETV-RL180M/S202G/M204V and HBVADV-RA181T/N236T replication. 2015 Hepatology (Baltimore, Md.) Result HBV N236T;S202G;M204V 63;33;39 68;38;44 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. ETV, at a dose of 0.02 mg/kg/day, showed essentially no reduction in HBVETV-RL180M/S202G/M204V viremia levels (lower panel. 2015 Hepatology (Baltimore, Md.) Result HBV M204V;S202G 89;83 94;88 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. HBVETV-RL180M/S202G/M204V-infected mice treated with ETV, CAdA, or CdG also had a gradual decrease in their h-albumin levels; however, there was no significant difference observed between the three groups. 2015 Hepatology (Baltimore, Md.) Result HBV M204V;S202G 20;14 25;19 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. In 8 weeks following inoculation of the hu-liver-chimeric-uPA+/+/SCID+/+ mice with an HBVETV-RL180M/S202G/M204V, the viremia levels had reached 8.6 x 105 - 7.7 x 106 (lower panels in. 2015 Hepatology (Baltimore, Md.) Result HBV S202G;M204V 100;106 105;111 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. S2, both CAdA and CdG were active against HBVADV-RA181T/N236T with IC50s of 0.09 and 0.04 muM, respectively, although ADV had a significantly greater IC50 value of 39.5 muM. 2015 Hepatology (Baltimore, Md.) Result HBV N236T 56 61 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. The average fold-reductions of the potency of CAdA and CdG against HBVETV-RL180M/S202G/M204V were only 9.7 and 4.3, respectively, compared with their IC50 values against HBVWT (Table 2). 2015 Hepatology (Baltimore, Md.) Result HBV S202G;M204V 81;87 86;92 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. The data clearly indicate that HBVETV-RL180M/S202G/M204V is highly susceptible to both CAdA and CdG. 2015 Hepatology (Baltimore, Md.) Result HBV S202G;M204V 45;51 50;56 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. We also determined the activity of CAdA and CdG against HBVADV-RA181T/N236T. 2015 Hepatology (Baltimore, Md.) Result HBV N236T 70 75 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. We subsequently asked whether CAdA and CdG blocked the replication of ETV-resistant HBV (HBVETV-RL180M/S202G/M204V) and ADV-resistant HBV (HBVADV-RA181T/N236T). 2015 Hepatology (Baltimore, Md.) Result HBV N236T;S202G;M204V 153;103;109 158;108;114 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. A less frequently observed mutation following LMV treatment is M204S, although additional mutations can be found in different RT regions. 2015 BMC complementary and alternative medicine Result HBV M204S 63 68 RT 126 128 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. indicating that an additional L180M mutation in the P gene might confer LMV resistance. 2015 BMC complementary and alternative medicine Result HBV L180M 30 35 P 52 53 26220282 Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro. M204V or M204I are the most frequently observed mutations in this region, and confer resistance to LMV, LdT, and ETV. 2015 BMC complementary and alternative medicine Result HBV M204V;M204I 0;9 5;14 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. As a rare case, natural mutation of S202I, responsible for resistance to ENC, occurred before starting drug consumption (in patient SH1). 2015 Hepatitis monthly Result HBV S202I 36 41 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. As expected, in all the 6 subjects, M204I point mutation, responsible for complete resistance to LAM or telbivudine (TEB) and intermediate resistance to entecavir (ENC), was detected as dominant mutation. 2015 Hepatitis monthly Result HBV M204I 36 41 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. The obtained results demonstrated three types of escape mutations (Y134N, I110V, G145R) in four subjects with drug resistance mutations and higher viral load (Table 4) as well. 2015 Hepatitis monthly Result HBV Y134N;I110V;G145R 67;74;81 72;79;86 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. A sequence analysis revealed that almost all patients (13 out of 14 "difficult-to-treat" patients) expressed the rtL269I substitution during the follow-up time (Table 2). 2015 PloS one Result HBV L269I 115 120 RT 113 115 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Although the rtM129L+V173L+M204I+H337N mutant displayed enhanced replication than the M204I single mutant, the replication efficiency remained less than 10% of the quintuple mutant. 2015 PloS one Result HBV M129L;M204I;H337N;V173L;M204I 15;27;33;21;86 20;32;38;26;91 RT 13 15 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Altogether, these results support the in vivo relevance of rtL269I substitution as a compensatory mutation in multi-drug resistant HBV. 2015 PloS one Result HBV L269I 61 66 RT 59 61 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Among the four patients treated with CLV, one patient (patient 22) harbored the rtL269I mutation prior to therapy. 2015 PloS one Result HBV L269I 82 87 RT 80 82 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Among these 16 patients, 7 (43.8%) displayed the rtL269I substitution (Table 1). 2015 PloS one Result HBV L269I 51 56 RT 49 51 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. As expected, replication of the rtM204I mutant was barely detectable (less than 10% of the WT). 2015 PloS one Result HBV M204I 34 39 RT 32 34 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. As the quintuple mutant was resistant to LMV and ETV (Fig 1C), the effect of rtL269I on LMV (Fig 3) and ETV (Fig 4) resistance was determined using all artificial mutants. 2015 PloS one Result HBV L269I 79 84 RT 77 79 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Based on the biochemical results obtained above, it is suggested that the rtL269I substitution locates the primer strand in such a way that the polymerase forms a more efficient ternary complex with the incoming dNTP substrate, which eventually leads to the enhanced activity of rtI269-HBV polymerase in both WT and YMDD mutant. 2015 PloS one Result HBV L269I 76 81 P;P;RT;RT;P 144;290;74;279;316 154;300;76;281;320 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Co-emergence of rtL269I substitution and YMDD mutation in CHB patients experiencing treatment failure. 2015 PloS one Result HBV L269I 18 23 RT;P 16;41 18;45 Chronic Hepatitis B 58 61 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Consistent with previous report, rtV173L facilitated replication of the rtM204I mutant. 2015 PloS one Result HBV V173L;M204I 35;74 40;79 RT;RT 33;72 35;74 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Due to the overlap of the polymerase gene with the surface gene, these mutations are accompanied by two mutations in the surface gene; sE164D and sW196L (Fig 1A). 2015 PloS one Result HBV E164D;W196L 135;146 141;152 P;S;S;S;S 26;135;146;51;121 36;136;147;58;128 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. First, the effect of the rtM129L, rtV173L, and rtH337N mutations on the replication of the rtM204I YMDD mutant was tested. 2015 PloS one Result HBV H337N;M204I;M129L;V173L 49;93;27;36 54;98;32;41 RT;RT;RT;RT;P 25;34;47;91;99 27;36;49;93;103 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In order to determine the molecular basis whereby the rtL269I substitution enhances HBV polymerase activity in WT and rtM204I YMDD drug-resistant mutant backbone, a three-dimensional structure of the HBV polymerase was modeled via a comparative modeling study (Fig 5A). 2015 PloS one Result HBV M204I;L269I 120;56 125;61 P;P;RT;RT;P 88;204;54;118;126 98;214;56;120;130 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In the presence of LMV (Fig 3C) or ETV (Fig 4C), the rtL269I substitution enhanced replication by approximately 2.5- to 5-fold only when M204I mutation was also present. 2015 PloS one Result HBV L269I;M204I 55;137 60;142 RT 53 55 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. None of the treatment-naive patients harbored HBV with the rtL269I substitution (Table 1). 2015 PloS one Result HBV L269I 61 66 RT 59 61 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. On the other hand, rtM129L and rtH337N did not increase replication of the YMDD mutant (Fig 2B). 2015 PloS one Result HBV M129L;H337N 21;33 26;38 RT;RT;P 19;31;75 21;33;79 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. rtL269I substitution enhances replication of WT virus and especially drug-resistant HBV. 2015 PloS one Result HBV L269I 2 7 RT 0 2 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Since the YMDD mutant M204I is replication defective, the 2-fold higher replication ability of the quintuple mutant (harboring the M204I mutation) than the WT led us to investigate the compensatory mutation(s) that rescue DNA replication. 2015 PloS one Result HBV M204I;M204I 22;131 27;136 P 10 14 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Southern blot analysis of four mutants (rtM204I, rtV173L+M204I, rtM129L+V173L+M204I, and rtM129L+V173L+M204I+H337N) was performed to determine the replicative capacity of each clone compared to the WT virus (Fig 2B). 2015 PloS one Result HBV M204I;V173L;M129L;M129L;H337N;M204I;V173L;M204I;V173L;M204I 42;51;66;91;109;57;72;78;97;103 47;56;71;96;114;62;77;83;102;108 RT;RT;RT;RT 40;49;64;89 42;51;66;91 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Taken together, our data demonstrated that the substitution at rtL269 is associated with marked rescue of the replication capacity of the multi-drug resistant M204I mutant. 2015 PloS one Result HBV M204I 159 164 RT 63 65 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Taken together, these results demonstrated that rtL269I is a compensatory mutation for multi-drug resistant YMDD HBV mutants, rather than a drug-resistant mutation. 2015 PloS one Result HBV L269I 50 55 RT;P 48;108 50;112 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The effect of rtL269I substitution on drug resistance was then investigated. 2015 PloS one Result HBV L269I 16 21 RT 14 16 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The effect of rtL269I was much higher in the mutant backbones and was in the order rtM129L+V173L+M204I+H337N > rtV173L+M204I > rtM204I > WT (approximately 7-fold vs 4-fold vs 3-fold vs 2-fold, respectively). 2015 PloS one Result HBV L269I;M129L;V173L;M204I;H337N;V173L;M204I;M204I 16;85;113;129;103;91;97;119 21;90;118;134;108;96;102;124 RT;RT;RT;RT 14;83;111;127 16;85;113;129 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The in vitro experiments demonstrated that the rtL269I substitution strongly restored HBV polymerase activity of the YMDD mutant. 2015 PloS one Result HBV L269I 49 54 P;RT;P 90;47;117 100;49;121 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtL269I single mutant was susceptible to LMV and ETV treatment, similar to the WT HBV. 2015 PloS one Result HBV L269I 6 11 RT 4 6 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtL269I substitution does not confer drug resistance. 2015 PloS one Result HBV L269I 6 11 RT 4 6 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtL269I substitution may increase polymerase activity through structural change. 2015 PloS one Result HBV L269I 6 11 P;RT 38;4 48;6 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Therefore, mutants containing rtL269I (Fig 2A) were constructed, and the effect of rtL269I on the replication of all artificial mutants was determined (Fig 2C).Remarkably, rtL269I substitution resulted in 2- to 7-fold higher replication ability (Fig 2D). 2015 PloS one Result HBV L269I;L269I;L269I 32;85;174 37;90;179 RT;RT;RT 30;83;172 32;85;174 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Therefore, our clinical data suggest that the rtL269I substitution gradually emerged during treatments, as the genotypic resistance becomes more complex, and that rtL269I is associated with sustained viral replication when subjected to antiviral treatment. 2015 PloS one Result HBV L269I;L269I 48;165 53;170 RT;RT 46;163 48;165 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Thus, our molecular modeling study suggests that the rtL269I substitution causes a conformational change in both RT region and the primer strand. 2015 PloS one Result HBV L269I 55 60 RT;RT 53;113 55;115 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. We have previously reported a multi-drug resistant HBV mutant (clone 50-2), which harbored the quintuple rtM129L+V173L+M204I+L269I+H337N mutations in the RT domain. 2015 PloS one Result HBV M129L;V173L;M204I;L269I;H337N 107;113;119;125;131 112;118;124;130;136 RT;RT 105;154 107;156 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. When the rtL269I mutation was added to the YMDD mutants, the relative replication levels (no drug vs LMV or ETV treatment) of none of the artificial mutants were significantly altered by LMV (Fig 3A and 3B) or ETV treatment (Fig 4A and 4B). 2015 PloS one Result HBV L269I 11 16 RT;P 9;43 11;47 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. Case #3B also carried the classic HBV vaccine escape variant (i.e, G145R) in the CD4+ and CD56+ compartment at ~2-4% of the total population. 2015 PloS one Result HBV G145R 67 72 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. In the CD56+ sample of Case #3B, the G145R variant was found in greater frequency in the plasmid control NGS data compared to the percentage of mutation in the matching sample. 2015 PloS one Result HBV G145R 37 42 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. However, Q129R was observed more frequently in anti-HBc+/anti-HBs + group (3/5, 60 %) than in anti-HBc+/anti-HBs- group (1/5, 20 %), but this difference did not reach statistical significance. 2015 Virology journal Result HBV Q129R 9 14 C;C;S;S 52;99;62;109 55;102;65;112 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M and Q129R amino acid substitutions were significantly more frequent in cases with occult HBV infection than in overt HBV infection (2 and 4 of 10 vs. 2015 Virology journal Result HBV T125M;Q129R 0;10 5;15 HBV infections;HBV infections 95;123 108;136 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M and Q129R amino acid substitutions were significantly more frequent in cases with occult HBV infection than in overt HBV infection (P = 0.01 for each) (Table 1). 2015 Virology journal Result HBV T125M;Q129R 0;10 5;15 HBV infections;HBV infections 95;123 108;136 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M and Q129R substitutions were simultaneously present in only one subject positive for anti-HBs (OCU 18) (Table 3. 2015 Virology journal Result HBV T125M;Q129R 0;10 5;15 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M was detected in one case in the anti-HBc+/anti-HBs + group (sample ID, OCU 18) and in one case in the anti-HBc+/anti-HBs- group (sample ID, OCU 158). 2015 Virology journal Result HBV T125M 0 5 C;C;S;S 43;113;53;123 46;116;56;126 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The most frequent one was Q129R in 4 (40 %) of the retrieved sequences, followed by T125M in 2 (20 %) and P127T in one (10 %) sample. 2015 Virology journal Result HBV Q129R;T125M;P127T 26;84;106 31;89;111 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The most frequent one was Q129R in 40 % (4/10) of the retrieved sequences, followed by T125M in 20 % and P127T in one sample. 2015 Virology journal Result HBV Q129R;T125M;P127T 26;87;105 31;92;110 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The most prevalent variant was S143L/T detected in 12 (16.2 %) of sequences, followed by T115S in 7 (9.5 %), Q129R in 5 (5.8 %), P120T/S in 2 (2.7 %), and K141R in one (1.4 %). 2015 Virology journal Result HBV S143L;S143T;T115S;Q129R;P120T;P120S;K141R 31;31;89;109;129;129;155 38;38;94;114;136;136;160 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The most prevalent variant was S143L/T detected in 16.2 % of sequences, followed by T115S in 9.5 %, Q129R in 5.8 %, P120T/S in 2.7 %, and K141R in 1.4 %. 2015 Virology journal Result HBV S143L;S143T;T115S;Q129R;P120T;P120S;K141R 31;31;84;100;116;116;138 38;38;89;105;123;123;143 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The T125M HBsAg variant in the MHR was detected in one sample negative for anti-HBs (OCU158), while Q129R alone was detected in a further 3 samples. 2015 Virology journal Result HBV T125M;Q129R 4;100 9;105 S;S 80;10 83;15 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The well-known G145A/R variant was not observed in either the overt infection or occult infection group. 2015 Virology journal Result HBV G145A;G145R 15;15 22;22 Occult Hepatitis B 81 97 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. All of the nine clones from the son have the same amino acid substitution pattern (T118K, T123N and G145A) as seen in his father. 2015 PloS one Result HBV T118K;T123N;G145A 83;90;100 88;95;105 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Amino acid substitution mutations in the major hydrophilic region predicted from eleven clones of HBV from the mother's sample include D99N, T131N, F161S and V168A. 2015 PloS one Result HBV D99N;T131N;F161S;V168A 135;141;148;158 139;146;153;163 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Amino acid substitutions in mother include T16I, R41S, V44A,N53S, H55R, W58R, N76D, S81T, V103I, G107E, N121I, I122L, N123D, Q125K, H126Y, N134D, N139H, N139Q, Y158H, I163V, F178L, S185N, V207M, Q215L,Y221F, A222T, I224V, G232R. 2015 PloS one Result HBV T16I;R41S;V44A;N53S;H55R;W58R;N76D;S81T;V103I;G107E;N121I;I122L;N123D;Q125K;H126Y;N134D;N139H;N139Q;Y158H;I163V;F178L;S185N;V207M;Q215L;Y221F;A222T;I224V;G232R 43;49;55;60;66;72;78;84;90;97;104;111;118;125;132;139;146;153;160;167;174;181;188;195;201;208;215;222 47;53;59;64;70;76;82;88;95;102;109;116;123;130;137;144;151;158;165;172;179;186;193;200;206;213;220;227 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Amino acid substitutions in the major hydrophilic region predicted from nine clones of HBV from the son's sample include L104S, T118K, T123N, S143L and G145A. 2015 PloS one Result HBV L104S;T118K;T123N;S143L;G145A 121;128;135;142;152 126;133;140;147;157 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Amino acid substitutions in the major hydrophilic region predicted from twelve clones of HBV from the father's sample include T115I, T116A, S117G, T118K, 123N, Q129L, T131N, M133L, M133S, F134L, G145A and I152V. 2015 PloS one Result HBV T115I;T116A;S117G;T118K;Q129L;T131N;M133L;M133S;F134L;G145A;I152V 126;133;140;147;160;167;174;181;188;195;205 131;138;145;152;165;172;179;186;193;200;210 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Except for L104S, all are escape substitutions. 2015 PloS one Result HBV L104S 11 16 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Five of the twelve substitutions, including T118K, T123N, T131N, M133L and N 145A, are associated with antibody escape. 2015 PloS one Result HBV T118K;T123N;T131N;M133L;N145A 44;51;58;65;75 49;56;63;70;81 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. In this study, there are eleven amino acid substitutions in the overlapping polymerase in all clones from the son's sample, including R15L, V23I, T38A, T38K, H55Q, S57F, L72P, L77S, H126Q, V191I and H197R. 2015 PloS one Result HBV R15L;V23I;T38A;T38K;H55Q;S57F;L72P;L77S;H126Q;V191I;H197R 134;140;146;152;158;164;170;176;182;189;199 138;144;150;156;162;168;174;180;187;194;204 P 76 86 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Only the T131N mutation causes detection failure and this mutation could be seen in one clone only (Fig 2). 2015 PloS one Result HBV T131N 9 14 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Seven clones have the same amino acid substitution pattern as that in the son: T118K, T123N and N145A. 2015 PloS one Result HBV T118K;T123N;N145A 79;86;96 84;91;101 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. T118K and T123N may result in failure to detect of HBsAg. 2015 PloS one Result HBV T118K;T123N 0;10 5;15 S 51 56 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. The T118K and N145A substitutions may result in vaccine escape. 2015 PloS one Result HBV T118K;N145A 4;14 9;19 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. There are twenty-one amino acid substitutions in the overlapping polymerase in all clones from father's sample, including F46S, R51K, H55Q, H55R, S57F, P109S, N118T, N124R, Y124H, Q125R, H126Q, 127R, N134D, C136R, N139K, Y141F, S143T, H160R, A211T, S213T and Q215H. 2015 PloS one Result HBV F46S;R51K;H55Q;H55R;S57F;P109S;N118T;N124R;Y124H;Q125R;H126Q;N134D;C136R;N139K;Y141F;S143T;H160R;A211T;S213T;Q215H 122;128;134;140;146;152;159;166;173;180;187;200;207;214;221;228;235;242;249;259 126;132;138;144;150;157;164;171;178;185;192;205;212;219;226;233;240;247;254;264 P 65 75 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. Two clones have T118K and N145A substitutions, two other clones have T131N and the final clone has M133L (Fig 2). 2015 PloS one Result HBV T118K;N145A;T131N;M133L 16;26;69;99 21;31;74;104 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. HIV-1 RT Q151M was crystallized in the trigonal space group P321, with one p66/p51 heterodimer in the asymmetric unit. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 9 14 RT 6 8 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. HIV-1 RT with a Q151M mutation is known to exhibit NRTI resistance (Shirasaka et al., 1993, 1995), while it remains sensitive to tenofovir and lamivudine (Iversen et al., 1996; Mbisa et al., 2011). 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 16 21 RT 6 8 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. In contrast, the relative orientations of the p66 subdomains of HIV-1 RT Q151M superposed well onto those of the closed structures (PDB entries 1dlo and 3ith; Figs. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 73 78 RT 70 72 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. It is evident that the Q151M mutation causes a loss of the capacity to form hydrogen bonds; therefore, the abovementioned hydrogen bonds could not be formed in the structure of the Q151M mutant. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M;Q151M 23;181 28;186 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Of these two regions, the conformation of the beta2-beta3 strands in the HIV-1 RT Q151M structure is different from those in any of the other HIV-1 RT structures in the closed conformation (PDB entries 1dlo, 3ith and 1hmv; Rodgers et al., 1995), which might be caused by the Q151M mutation, as described below. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M;Q151M 82;275 87;280 RT;RT 79;148 81;150 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Structural comparison of the dNTP-binding pocket between NRTI-bound HIV-1 RT and the Q151M mutant . 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 85 90 RT 74 76 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Structural comparison of the dNTP-binding pocket between NRTI-bound HIV-1 RT and the Q151M mutant. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 85 90 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The crystal structure of HIV-1 RT Q151M was determined at 2.6 A resolution. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 34 39 RT 31 33 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The displacement of each residue between p66 of HIV-1 RT Q151M and that of other HIV-1 RTs in the open conformation (PDB entries 1rth, 3htv and 2rf2) showed a large movement of the thumb subdomain (~25 A) and a slight movement of the other subdomains (~5 A). 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 57 62 RT;RT 54;87 56;90 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The dNTP-binding site of HIV-1 RT Q151M was compared with azidothymidine triphosphate (AZT)-bound (PDB entry 3v4i; Das et al., 2012) and tenofovir diphosphate (TNV)-bound (PDB entry 1t05; Tuske et al., 2004) HIV-1 RT structures. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 34 39 RT;RT 31;214 33;216 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The HIV-1 RT Q151M structure reported in this study may serve as the basis for an atomic model for molecular-dynamics and/or docking-simulation studies. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 13 18 RT 10 12 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The p51 subunit of HIV-1 RT Q151M superposed very well onto each of the HIV-1 RT structures. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 28 33 RT;RT 25;78 27;80 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The refined HIV-1 RT Q151M structure is well ordered, and the maps show clear electron density for the rebuilt thumb subdomain. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 21 26 RT 18 20 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. The structural comparison also suggests that hydrophobic interactions between the methyl group of TNV and the thioether group of methionine might compensate for the loss of hydrogen bonds; hence, tenofovir exhibits an inhibitory action towards both HIV-1 RT Q151M and HBV Pol. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 258 263 P;RT 272;255 275;257 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Therefore, it is possible that the hydrogen-bonding network between amino acids and inhibitors cannot be formed in the structure of the Q151M mutant. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 136 141 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. Therefore, we propose that the structure of the dNTP-binding pocket of HIV-1 RT Q151M may provide some clues regarding the dNTP/NRTI-binding pocket of HBV Pol. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 80 85 P;RT 155;77 158;79 26527265 Structure of the HIV-1 reverse transcriptase Q151M mutant: insights into the inhibitor resistance of HIV-1 reverse transcriptase and the structure of the nucleotide-binding pocket of Hepatitis B virus polymerase. These structural comparisons among various types of HIV-1 RTs revealed that HIV-1 RT Q151M forms the closed conformation. 2015 Acta crystallographica. Section F, Structural biology communications Result HBV Q151M 85 90 RT;RT 82;58 84;61 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. After a stepwise regression analysis, the HBV genotype, the 11 independent HCC-related mutations, the HLA SNPs (rs9272105 and rs9275319) and the interaction of rs9272105 with A1752G were entered into the HCC prediction model (Table 2). 2015 Scientific reports Result HBV A1752G 175 181 Hepatocellular carcinoma;Hepatocellular carcinoma 75;204 78;207 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. After Bonferroni correction, HBV mutations C1653T, T1674C/G, A1752G, T1753C, A1762T, G1764A, G1899A, and C1969T were still significant associated with HCC risk. 2015 Scientific reports Result HBV C1653T;T1674C;T1674G;A1752G;T1753C;A1762T;G1764A;G1899A;C1969T 43;51;51;61;69;77;85;93;105 49;59;59;67;75;83;91;99;111 Hepatocellular carcinoma 151 154 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. Of those 19 hotspot mutations, C1653T, T1674C/G, A1703G, G1719T, T1727A/G, T1753C, A1762T, G1764A, G1799C, G1899A, G1915A/C and C1969T were significantly associated with an increased risk of HCC, whereas C1673T, A1726C, C1730G and A1752G were significantly associated with a reduced risk of HCC, when adjusted for age and gender (Supplementary Table S7). 2015 Scientific reports Result HBV T1674G;T1727G;C1653T;T1674C;A1703G;G1719T;T1727A;T1753C;A1762T;G1764A;G1799C;G1899A;G1915A;G1915C;C1969T;C1673T;A1726C;C1730G;A1752G 39;65;31;39;49;57;65;75;83;91;99;107;115;115;128;204;212;220;231 47;73;37;47;55;63;73;81;89;97;105;113;123;123;134;210;218;226;237 Hepatocellular carcinoma;Hepatocellular carcinoma 191;291 194;294 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. rs9272105 multiplicatively interacted with C1673T, G1719T, A1726C, C1730G, A1752G and G1799C. 2015 Scientific reports Result HBV C1673T;G1719T;A1726C;C1730G;A1752G;G1799C 43;51;59;67;75;86 49;57;65;73;81;92 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. The results indicated that the HBV mutation C1730G was correlated with T1727A/G and G1799C (r2 > 0.800). 2015 Scientific reports Result HBV C1730G;T1727A;T1727G;G1799C 44;71;71;84 50;79;79;90 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. We detected significant interactions between rs9272105 and the HBV mutations C1673T, G1719T, A1726C, C1730G, A1752G and G1799C on HCC risk (P < 0.05). 2015 Scientific reports Result HBV C1673T;G1719T;A1726C;C1730G;A1752G;G1799C 77;85;93;101;109;120 83;91;99;107;115;126 Hepatocellular carcinoma 130 133 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. We then used a conditional logistic regression analysis to test the independence of these hotspot mutations and found that the effects of C1653T, C1673T, T1674C/G, C1730G, A1752G, T1753C, A1762T, G1764A, G1899A, G1915A/C and C1969T on HCC development remained in existence after being conditioned on the other mutations (Supplementary Table S7). 2015 Scientific reports Result HBV C1653T;C1673T;T1674C;T1674G;C1730G;A1752G;T1753C;A1762T;G1764A;G1899A;G1915A;G1915C;C1969T 138;146;154;154;164;172;180;188;196;204;212;212;225 144;152;162;162;170;178;186;194;202;210;220;220;231 Hepatocellular carcinoma 235 238 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Important mutations in the MHL of the surface gene that were detectable in acute hepatitis, were T125M (2.5%), T126I (10%), and Y134F (35%). 2015 PloS one Result HBV T125M;T126I;Y134F 97;111;128 102;116;133 S 38 45 Acute Hepatitis B 75 90 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Important substitutions in the X gene included I127T, K130M, and V131I whose frequencies in acute infection were 4%, 8% and 12% respectively and in chronic infection were 24.99%, 45.57%, 45.57% respectively. 2015 PloS one Result HBV I127T;K130M;V131I 47;54;65 52;59;70 X 31 32 Chronic HBV infection 148 165 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Interestingly, the substitution M133I was detectable in 2 isolates (5%) manifesting acute infection but was completely absent in all the chronic isolates. 2015 PloS one Result HBV M133I 32 37 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. It is noteworthy, that the C69stop codon mutation in the surface gene, the C1766T /T1768A mutation in the basal core promoter and the H94Y mutation in the x gene were found only in chronic patients. 2015 PloS one Result HBV T1768A;C69X;C1766T;H94Y 83;27;75;134 89;34;81;138 BCP;S;X 106;57;155 125;64;156 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Major substitutions that were detectable in the BCP/PC region of acute isolates included T1753C (2.7%), A1762T/G1764A (8.1%), A1814C (2.7%), G1896A (10.8%) and G1899A (5.4%). 2015 PloS one Result HBV G1764A;T1753C;A1762T;A1814C;G1896A;G1899A 111;89;104;126;141;160 117;95;110;132;147;166 BCP;Precore 48;52 51;54 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. No such changes were found in the X gene except at positions overlapping with the BCP (amino acid substitutions T127I, M130K and I131V). 2015 PloS one Result HBV T127I;M130K;I131V 112;119;129 117;124;134 BCP;X 82;34 85;35 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Notably, the frequency of pre-core substitutions (A1814C, G1896A, and G1899A) was relatively high in acute infection reaching to almost half of that present in chronic infection. 2015 PloS one Result HBV A1814C;G1896A;G1899A 50;58;70 56;64;76 Precore 26 34 Chronic HBV infection 160 177 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Substitution H94Y was absent in acute infection. 2015 PloS one Result HBV H94Y 13 17 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. The C1766T/T1768A double mutation was however detectable in only chronic infection (2%). 2015 PloS one Result HBV T1768A;C1766T 11;4 17;10 Chronic HBV infection 65 82 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. The C69stop codon mutation was undetectable in acute infection. 2015 PloS one Result HBV C69X 4 11 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. There were no drug resistant mutations (lamivudine-resistant pattern: rtM204V/I, rtL180M, rtV173L, adefovir-resistant pattern: rtA181V/T, tenofovir-resistant pattern: rtA194T and entecavir-resistant pattern: rtL180M, rtS202G, rtM204V) detectable in acute patients belonging to our study population. 2015 PloS one Result HBV M204V;M204I;A181V;A181T;A194T;L180M;V173L;L180M;S202G;M204V 72;72;129;129;169;83;92;210;219;228 79;79;136;136;174;88;97;215;224;233 RT;RT;RT;RT;RT;RT;RT;RT 70;81;90;127;167;208;217;226 72;83;92;129;169;210;219;228 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. We noted significant changes at position 528 (C T) (amino acid substitution T125M) in the S gene and positions 1753 (T C), 1762(A T), 1764(G A), 1933 (T G), and 1938 (T C) in the BCP/PC region. 2015 PloS one Result HBV T125M 76 81 BCP;Precore;S 179;183;90 182;185;91 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. compared with wild-type mouse model, viral replication decreases about 10.06-fold in the rtL180M-rtM204V double mutants, but increases about 7.79-fold in the rtL180M-rtM204V-rtV173L triple mutants. 2014 Acta pharmaceutica Sinica. B Result HBV L180M;M204V;L180M;M204V;V173L 91;99;160;168;176 96;104;165;173;181 RT;RT;RT;RT;RT 89;97;158;166;174 91;99;160;168;176 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. However, in another LAM-resistant model (triple mutants), the level reached the peak on day 9 after injection of pTmcs-HBV1.3-3TCR-V173L and the decrease speed was slower than the wild-type model. 2014 Acta pharmaceutica Sinica. B Result HBV V173L 131 136 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. On day 5 after injection, the percentage of HBsAg-positive with injection of pTmcs-HBV1.3, pTmcs-HBV1.3-3TCR and pTmcs-HBV1.3-3TCR-V173L were 95.24%, 100% and 100%, respectively. 2014 Acta pharmaceutica Sinica. B Result HBV V173L 131 136 S 44 49 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. suggesting that rtM204V and rtL180M double mutations in LAM-resistant HBV mutants resulted in the decline of replication ability, but the third compensatory rtV173L mutation significantly increased the HBV replication ability in vivo. 2014 Acta pharmaceutica Sinica. B Result HBV M204V;L180M;V173L 18;30;159 23;35;164 RT;RT;RT 16;28;157 18;30;159 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Taken together, serum viral level and sustained time were different among the three models, with pTmcs-HBV1.3-3TCR-V173L displaying the superiority. 2014 Acta pharmaceutica Sinica. B Result HBV V173L 115 120 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Taking advantage of the hydrodynamic-based procedure, we established two LAM-resistant HBV replication mouse models by injecting pTmcs-HBV1.3-3TCR and pTmcs-HBV1.3-3TCR-V173L, respectively, into NOD/SCID mice to transfect hepatocytes in vivo. 2014 Acta pharmaceutica Sinica. B Result HBV V173L 169 174 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. The copy numbers are 116.5x106 and 65.0x106 copies/mL on day 9 and 17 after injection of pTmcs-HBV1.3-3TCR-V173L. 2014 Acta pharmaceutica Sinica. B Result HBV V173L 107 112 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Age comparison among HBV patients harboring G1896A revealed that, in all 3 genotypes (B, C and D), middle-aged adults (36 - 55 years old) had prominent distribution of the mutation (41.7%, 12.5% and 4.2%), respectively. 2015 Hepatitis monthly Result HBV G1896A 44 50 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Among the basal core promoter mutations, A1762T-G1764A double mutation was present in 26.9%, C1653T in 8.6%, A1752G in1 0.8% and C1766T in 2.2% of all isolates. 2015 Hepatitis monthly Result HBV A1762T;G1764A;C1653T;A1752G;C1766T 41;48;93;109;129 47;54;99;115;135 BCP 10 29 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Chi-square analysis revealed a significant association between HBV genotype and G1896A mutation, whereby subjects infected with HBV genotype B had G1896A mutation more commonly (P < 0.05). 2015 Hepatitis monthly Result HBV G1896A;G1896A 80;147 86;153 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896 A Mutation in Relation to HBeAg Status. 2015 Hepatitis monthly Result HBV G1896A 0 7 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A Mutation and e-Seroconversion. 2015 Hepatitis monthly Result HBV G1896A 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A Mutation in Relation to Clinical Status of Subjects. 2015 Hepatitis monthly Result HBV G1896A 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Genotype and Association With G1896A Mutation. 2015 Hepatitis monthly Result HBV G1896A 30 36 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. However, there was no statistical association between HCC and G1896A. 2015 Hepatitis monthly Result HBV G1896A 62 68 Hepatocellular carcinoma 54 57 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. In total, there were 24 hepatitis B infected subjects with G1896A mutant, of whom all were HBeAg-negative except three. 2015 Hepatitis monthly Result HBV G1896A 59 65 C 91 96 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. It was observed that the prevalence of HBV infected subjects with G1896A mutation in genotypes B and C was comparable. 2015 Hepatitis monthly Result HBV G1896A 66 72 HBV infections 39 51 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Precore stop codon G1896A was detected in 30.4% (21/69) of HBeAg-negative subjects and 12.5% (3/24) of HBeAg-positive cases. 2015 Hepatitis monthly Result HBV G1896A 19 25 C;C;Precore 59;103;0 64;108;7 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Prevalence of G1896A Mutation in Comparison to Age and Genotypes. 2015 Hepatitis monthly Result HBV G1896A 14 20 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Subjects with G1896A mutations were mainly in asymptomatic chronic HB (58.3%) and liver cirrhosis (41.7%) groups. 2015 Hepatitis monthly Result HBV G1896A 14 20 Liver cirrhosis 82 97 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The most commonly observed mutation in the precore region was C1858T, which comprised 64.5% of all isolates sequenced. 2015 Hepatitis monthly Result HBV C1858T 62 68 Precore 43 50 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. There was a significant association between G1896A occurrence in subjects and liver cirrhosis (P < 0.05). 2015 Hepatitis monthly Result HBV G1896A 44 50 Liver cirrhosis 78 93 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Three of 24 subjects with G1896A were HBeAg-positive. 2015 Hepatitis monthly Result HBV G1896A 26 32 C 38 43 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Two subjects infected with HBV and had G1896A mutation diagnosed with HCC. 2015 Hepatitis monthly Result HBV G1896A 39 45 Hepatocellular carcinoma 70 73 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. Analysis of the pre-core/core regions showed nucleic acid replacement in position G1896A, which results in an unwanted stop codon ( Figure 4). 2015 Jundishapur journal of microbiology Result HBV G1896A 82 88 C;Precore 25;16 29;24 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. In this study, we observed a substitution in the RT region (Y135S) and three amino-acid substitutions in the S region (T127P, P153L, F170S); T127P was an escape mutant that produce different surface antigen (Figure 3). 2015 Jundishapur journal of microbiology Result HBV Y135S;T127P;P153L;F170S;T127P 60;119;126;133;141 65;124;131;138;146 RT;S;S 49;109;191 51;110;198 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. Moreover, sequencing of HBV-DNA of the S region of all four (1.97%) samples showed arginine (R) in position 122 and lysine (K) in position 160, indicating the presence of HBV subtype awy and genotype D. 2015 Jundishapur journal of microbiology Result HBV R122R;K160K 82;115 112;143 S 39 40 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. 1C, Supplementary Table S2), neither rtA181T nor rtM204I was found at a frequency >=1% in any of the subjects at baseline measurement. 2015 Scientific reports Result HBV A181T;M204I 39;51 44;56 RT;RT 37;49 39;51 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. A theoretical analysis based on the above simulation showed that relatively low packaging efficiency (delta <= 0.5) prevents rtA181T mutants from achieving dominance when coexisting with the wild-type quasispecies, in accord with the observed frequencies of rtA181T mutants (1.7 ~ 10.6%) in the viral populations of PVR patients (Supplementary Table S2). 2015 Scientific reports Result HBV A181T;A181T 127;260 132;265 RT;RT 125;258 127;260 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Although the rtM204I mutant was not detected at any of the time points from baseline to VB in patient VB.3, the rtA181T mutant was detected 12 weeks earlier than when its VB occurred. 2015 Scientific reports Result HBV M204I;A181T 15;114 20;119 RT;RT 13;112 15;114 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. At baseline and week 12, the rtM204I mutants were observed to be absent or extremely rare. 2015 Scientific reports Result HBV M204I 31 36 RT 29 31 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Because the rtA181T substitution at the RT region plays an essential role in development of resistance to treatments with LdT, this novel observation regarding its quantitative dynamic variation during the course of drug treatment in the PVR group suggested that rtA181T mutants might be responsible for the patients' partial virological responses to LdT. 2015 Scientific reports Result HBV A181T;A181T 14;265 19;270 RT;RT;RT 12;40;263 14;42;265 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. By contrast, when drug-resistant mutants such as rtM204I, which causes a function-preserving (delta 1) sW196L mutation in the overlapping S protein (Supplementary Table S3), coexist with wild-type viruses in a population, the model predicts that those mutants can dominate the population. 2015 Scientific reports Result HBV M204I;W196L 51;105 56;111 RT;S;S 49;105;140 51;106;141 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Competition between rtM204I mutants and other quasispecies. 2015 Scientific reports Result HBV M204I 22 27 RT 20 22 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Cooperation between the rtA181T mutant and wild-type viruses. 2015 Scientific reports Result HBV A181T 26 31 RT 24 26 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Furthermore, at week 12 and thereafter, the frequencies of rtA181T mutants were higher than 1% in 15 of the 20 PVR and VB subjects but in none of the 10 CVR patients (Supplementary Table S2). 2015 Scientific reports Result HBV A181T 61 66 RT 59 61 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Furthermore, the rtM204I mutant could be detected 12 weeks (patients VB.1, 2) or 16 weeks (patients VB.6, 8-10) earlier than the VB. 2015 Scientific reports Result HBV M204I 19 24 RT 17 19 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Hence, the rtA181T/sW172* mutants need the aid of coexisting wild-type quasispecies to provide a functional S protein for virion packaging. 2015 Scientific reports Result HBV W172X;A181T 19;13 25;18 RT;S;S 11;19;108 13;20;109 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. However, at week 24 and thereafter, the frequency of rtM204I mutants reached 1% or greater in 9 of the 10 VB patients but remained at zero or less than 1% in the PVR patients (p <= 1.19E-4 in Fisher's exact test). 2015 Scientific reports Result HBV M204I 55 60 RT 53 55 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In a simulation with the presence of rtM204I mutants, the mutants will eventually dominate the entire population. 2015 Scientific reports Result HBV M204I 39 44 RT 37 39 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In a viral population without an rtM204I mutant, the frequency of rtA181T mutants increases to approximately 10% and then stabilizes. 2015 Scientific reports Result HBV A181T;M204I 68;35 73;40 RT;RT 33;66 35;68 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In contrast to the abundance of rtM204I mutants, the rtA181T mutants never reach a significant level if present at a proportion similar to or lower than that of the rtM204I mutants at baseline. 2015 Scientific reports Result HBV A181T;M204I;M204I 55;34;167 60;39;172 RT;RT;RT 32;53;165 34;55;167 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Notably, among these 9 patients, the rtA181T mutant was detectable in six of them (patients VB.4-8 and 10) either 24 (patients VB.6, 10) or 40 (patients VB.4, 5, 7) weeks earlier than when rtM204I was detected; however, its frequency dropped below 1% once the frequency of rtM204I increased to 90%. 2015 Scientific reports Result HBV A181T;M204I;M204I 39;191;275 44;196;280 RT;RT;RT 37;189;273 39;191;275 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Supplementary Table S2),, the rtA181T mutant was not detected with a frequency >=1% in any of the subjects at baseline (week 0), but it was continuously found from week 12 to week 36 in 8 (patients PVR. 2015 Scientific reports Result HBV A181T 32 37 RT 30 32 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The frequencies of rtA181T mutants were significantly lower in the CVR patients than in the other two sub-optimal groups at baseline (p <= 0.023 in the permutation test). 2015 Scientific reports Result HBV A181T 21 26 RT 19 21 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The rtA181T mutation also causes a stop-codon mutation in the overlapping surface protein (S protein) gene (Supplementary Table S3), i.e., sW172*, which causes a 55 amino acid-residue truncation in the S protein. 2015 Scientific reports Result HBV A181T;W172X 6;139 11;145 RT;S;S;S;S 4;91;139;202;74 6;92;140;203;81 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The rtM204I mutant was not detected at a frequency >=1% in any of the examined samples from the PVR group. 2015 Scientific reports Result HBV M204I 6 11 RT 4 6 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The simulated dynamic patterns coincided well with the corresponding clinical observations, which indicated that rtM204I mutants have a significant advantage in competitive survival, even in the presence of drug-resistant rtA181T mutants. 2015 Scientific reports Result HBV M204I;A181T 115;224 120;229 RT;RT 113;222 115;224 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Therefore, the proportion of the rtA181T mutant in the patient at the early phase of treatment (including baseline) can distinguish patients who will experience the optimal response (i.e., CVR) from those who will experience sub-optimal responses (i.e., PVR and VB). 2015 Scientific reports Result HBV A181T 35 40 RT 33 35 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Therefore, the proportions of rtA181T and rtM204I mutants at the early stage of treatment were significantly different among the CVR, PVR and VB groups, thus implying a potential association between quasispecies composition and later-phase virological responses. 2015 Scientific reports Result HBV A181T;M204I 32;44 37;49 RT;RT 30;42 32;44 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. This prediction is consistent with the observation that the frequency of drug-resistant rtM204I mutants reached nearly 100% in VB patients (Supplementary Table S2). 2015 Scientific reports Result HBV M204I 90 95 RT 88 90 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. To further inspect the competition between rtM204I and other quasispecies, we simulated the dynamics of the quasispecies during antiviral treatment. 2015 Scientific reports Result HBV M204I 45 50 RT 43 45 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. To understand the mechanism of co-existence between the rtA181T mutant and wild-type viruses in PVR patients, we theoretically modeled their cooperative relationship, highlighting the complementary nature of their RT and S proteins. 2015 Scientific reports Result HBV A181T 58 63 RT;RT;S 56;214;221 58;216;222 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Two critical LdT-resistant mutations, rtA181T and rtM204I, were distributed differently in the three patient groups. 2015 Scientific reports Result HBV A181T;M204I 40;52 45;57 RT;RT 38;50 40;52 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. When the proportion of rtA181T mutants is much greater than that of rtM204I mutants at baseline, the proportion of rtA181T mutants could rise to approximately 10% of the total viral population before decreasing rapidly as the proportion of rtM204I mutants increased. 2015 Scientific reports Result HBV A181T;A181T;M204I;M204I 25;117;70;242 30;122;75;247 RT;RT;RT;RT 23;68;115;240 25;70;117;242 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. When the VB occurred, either at week 36 (in patients VB.1-3) or week 52 (in patients VB.4-10), the rtM204I mutant was detected in 9 (patients VB.1-2 and 4-10) of 10 subjects, and it accounted for a dominant portion of the viral population in these subjects. 2015 Scientific reports Result HBV M204I 101 106 RT 99 101 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. and so did other mutations (rtN/H238T P < 0.001, rtP237H P = 0.002, and rtV214A P = 0.006). 2015 Scientific reports Result HBV H238T;N238T;P237H;V214A 32;30;51;74 37;37;56;79 RT;RT;RT 28;49;72 30;51;74 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. As shown in Table 2, ADV-associated mutation rtA181V/T/S demonstrated a remarkable higher prevalence in genotype C than genotype B (13.5% vs. 2015 Scientific reports Result HBV A181V;A181T;A181S 47;47;47 56;56;56 RT 45 47 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Besides, another ADV-associated resistant mutation rtN236T had a higher prevalence in genotype B than genotype C in ADV-resistant patients (66.7% vs. 2015 Scientific reports Result HBV N236T 53 58 RT 51 53 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. In patients resistant to LMV and LdT, mutation rtM204V and rtM204I showed no difference between genotypes, while mutant rtL180M had a higher frequency in genotype C isolates than genotype B isolates in both subgroups (54.7% vs. 2015 Scientific reports Result HBV M204V;M204I;L180M 49;61;122 54;66;127 RT;RT;RT 47;59;120 49;61;122 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Interestingly, cross-resistant mutation rate of rtA181V/T/S was higher in patients harboring genotype C than genotype B in LMV-resistant patients (29.3% vs. 2015 Scientific reports Result HBV A181V;A181T;A181S 50;50;50 59;59;59 RT 48 50 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Nevertheless, LMV-associated mutation rtM204V/I and rtL180M, LdT-associated mutation rtM204I, and ETV-associated mutations rtT184A/I/S, rtS202G and rtM250L didn't differ significantly between genotype B and C (P > 0.05). 2015 Scientific reports Result HBV M204V;M204I;T184A;T184I;T184S;M250L;L180M;M204I;S202G 40;40;125;125;125;150;54;87;138 47;47;134;134;134;155;59;92;143 RT;RT;RT;RT;RT;RT 38;52;85;123;136;148 40;54;87;125;138;150 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. The frequency of LMV-associated mutation models, like rtL180M+rtM204V and rtL180M+rtM204V+rtV173L, showed no statistical difference, except rtL180M+rtM204I, the frequency of which was higher in genotype C than genotype B (10.7% vs. 2015 Scientific reports Result HBV L180M;M204V;L180M;M204V;V173L;M204I;L180M 56;64;76;84;92;150;142 61;69;81;89;97;155;147 RT;RT;RT;RT;RT;RT;RT 54;62;74;82;90;140;148 56;64;76;84;92;142;150 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. The most common drug resistant mutation model was dual mutation rtL180M+rtM204V, followed by rtL180M+rtM204I. 2015 Scientific reports Result HBV L180M;M204V;M204I;L180M 66;74;103;95 71;79;108;100 RT;RT;RT;RT 64;72;93;101 66;74;95;103 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. The rate of other drug-associated resistant mutation models, such as rtA181T+rtN236T for ADV, rtL180M+rtM204V+rtS202G for ETV, and rtL180M+rtM204V+rtT184L for ETV, did not differ between genotypes as well. 2015 Scientific reports Result HBV A181T;N236T;L180M;M204V;S202G;L180M;M204V;T184L 71;79;96;104;112;133;141;149 76;84;101;109;117;138;146;154 RT;RT;RT;RT;RT;RT;RT;RT 69;77;94;102;110;131;139;147 71;79;96;104;112;133;141;149 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. Amino acid transitions induced by G1719T, A1726C, A1752G/T and BCP A1762T/G1764A mutants had higher prevalence of 39.7% (23/58), 29.3% (17/58), 27.6% (16/58) and 31.0% (18/58), which mainly occurred in genotype C (21/23), genotype B (16/17), genotype B (13/16) and genotype C (16/18) infection patients, respectively. 2015 Scientific reports Result HBV G1764A;A1752T;G1719T;A1726C;A1752G;A1762T 74;50;34;42;50;67 80;58;40;48;58;73 BCP 63 66 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. besides classical A1762T/G1764A and G1896A mutants affecting codons 130/131 of X gene (K130M/V131I) and codon 28 of PC gene (W28stop), another 12 SNPs (nt.1719, nt.1726, nt.1727, nt.1730, nt.1752, nt.1753, nt.1768, nt.1800, nt.1803, nt.1804, nt.1805 and nt.1825) also caused amino acid changes. 2015 Scientific reports Result HBV G1764A;V131I;A1762T;G1896A;K130M;W28X 25;93;18;36;87;125 31;98;24;42;92;132 Precore;X 116;79 118;80 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. Genotype C infection had a higher prevalence of BCP A1762T/G1764A mutants than genotype B infection (70.0% vs 38.9%, P = 0.0413) (Table 2), which is coincident with most previous studies. 2015 Scientific reports Result HBV G1764A;A1762T 59;52 65;58 BCP 48 51 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. HBV BCP A1762T/G1764A and PC G1896A combinational patterns. 2015 Scientific reports Result HBV G1764A;A1762T;G1896A 15;8;29 21;14;35 BCP;Precore 4;26 7;28 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. In addition, among the twelve hotspots, G1719T and T1753V were significantly associated with genotype C (P < 0.05), while A1726C and A1752G/T were genotype B related (P < 0.05) (Table 2). 2015 Scientific reports Result HBV G1719T;T1753V;A1726C;A1752G;A1752T 40;51;122;133;133 46;57;128;141;141 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. No significant difference was observed for PC G1896A mutant (45.0% vs 61.1%, P = 0.3950). 2015 Scientific reports Result HBV G1896A 46 52 Precore 43 45 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. Of all the above mutants in BCP and PC regions, we defined the A1762T/G1764A double mutants as BCP mutants and G1896A as PC mutant. 2015 Scientific reports Result HBV G1764A;A1762T;G1896A 70;63;111 76;69;117 BCP;BCP;Precore;Precore 28;95;36;121 31;98;38;123 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Although all 12 patients experienced viral breakthrough during the treatment with LAM, low rates of drug resistance-associated mutations were observed at week 0 prior to the treatment, with the exception of patient D, who exhibited a rate of 94.03 for M204I, and patient G, who exhibited a rate of 97.59 for A181V. 2016 Molecular medicine reports Result HBV M204I;A181V 252;308 257;313 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Furthermore, the increased mutation rate of rt180 or rt80 was accompanied by the occurrence of the high mutation rate of M204I during the virological breakthrough. 2016 Molecular medicine reports Result HBV M204I 121 126 RT;RT 44;53 46;55 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. In all four patients, the M204V mutation was accompanied by the L180M mutation, and an identical trend was observed in the two mutation sites (Table III). 2016 Molecular medicine reports Result HBV M204V;L180M 26;64 31;69 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Notably, the mutation rate of rtM204I/V was markedly increased at the time of virological breakthrough in eight patients, and this was accompanied by an increased mutation rate of rtL180M and/or rtL80I/V. 2016 Molecular medicine reports Result HBV M204V;L180M;L80I;L80V;M204I 32;182;197;197;32 39;187;203;203;39 RT;RT;RT 30;180;195 32;182;197 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. the characteristics in common of these four patients were that the viral breakthrough was caused by the high rate of M204I mutation during the treatment with LAM, and that the domi nation of the M204I mutation continued following the ADV add-on therapy. 2016 Molecular medicine reports Result HBV M204I;M204I 117;195 122;200 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. the M204V mutation in patients E and F eventually disappeared following the ADV add-on therapy, which also occurred in the other two patients. 2016 Molecular medicine reports Result HBV M204V 4 9 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Virological breakthrough in patients A, B, C and D was dominated by the YIDD motif variant, since their virological breakthrough was caused by a markedly increased mutation rate of M204I during the LAM treatment. 2016 Molecular medicine reports Result HBV M204I 181 186 P 72 76 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. One HBV/A strain (1/8, 12.5%) had BCP mutations whereas three (3/6, 50%) HBV/E strains showed the A1762T and G1764A double mutation (P = .35) (Table 2). 2016 PloS one Result HBV A1762T;G1764A 98;109 104;115 BCP 34 37 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Regarding RAMs, the mutation M204V/I, associated with the compensatory mutation L180M, was significantly more common in genotype HBV/A (9/19, 47.4%) than in genotype HBV/E (0/9, 0%) (Yate's corrected chi2, P = .04) (Fig 6, Table 2). 2016 PloS one Result HBV M204V;M204I;L180M 29;29;80 36;36;85 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. The classical PC G1896A mutation was found in two (2/8, 14%) and four (4/6, 66.7%) HBV/A and HBV/E isolates, respectively (P = .31). 2016 PloS one Result HBV G1896A 17 23 Precore 14 16 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Additionally, 2 patients harbored rtV214A substitutions (1% and 1.1%). 2016 Medicine Result HBV V214A 36 41 RT 34 36 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. At baseline, patient 2 harbored an rtA181T substitution (1.4%), and other resistance mutations were present at low levels (<1%). 2016 Medicine Result HBV A181T 37 42 RT 35 37 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. At baseline, the virus only harbored an rtA181T substitution (1.2%) and had low fluctuations during the follow-up period. 2016 Medicine Result HBV A181T 42 47 RT 40 42 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. At baseline, this patient displayed rtM204I/V (3.5%), rtL180 M (2.1%), and rtS202G (3.4%) substitutions, and the resistance and nonresistance mutations frequencies were significantly different (P = 0.011). 2016 Medicine Result HBV M204I;M204V;L180M;S202G 38;38;56;77 45;45;62;82 RT;RT;RT 36;54;75 38;56;77 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Eight patients harbored rtM204I/V substitutions of at least 1% (ranging from 1% to 3.6%); 2 of these patients also presented rtL180 M substitutions (2.3% and 2.4%) and rtS202G substitutions (3.2% and 3.5%), whereas the other 6 harbored a low frequency of rtS202G substitutions (ranging from 1% to 1.4%), with 1 harboring rtQ215R/H substitutions (6.7%) and another harboring rtV173A/M substitutions (1.7%). 2016 Medicine Result HBV M204I;M204V;Q215R;Q215H;V173A;V173M;L180M;S202G;S202G 26;26;323;323;376;376;127;170;257 33;33;330;330;383;383;133;175;262 RT;RT;RT;RT;RT;RT 24;125;168;255;321;374 26;127;170;257;323;376 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Fourteen patients harbored rtM204I/V substitutions of at least 1% (ranging from 1% to 3.5%), and 5 of these patients also presented rtL180 M substitutions (ranging from 1.8% to 2.6%) and rtS202G substitutions (ranging from 1% to 3.4%), which are both known to confer resistance to ETV. 2016 Medicine Result HBV M204I;M204V;S202G;L180M 29;29;189;134 36;36;194;140 RT;RT;RT 27;132;187 29;134;189 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. However, several other variants fluctuated at relatively high levels (ranging from 3.56% to 7.89%), including rtN248H, rtS223A, rtS256C, and rtI224 V (Figure 2B). 2016 Medicine Result HBV I224V;N248H;S223A;S256C 143;112;121;130 149;117;126;135 RT;RT;RT;RT 110;119;128;141 112;121;130;143 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In addition, 2 variants (rtI187L/rtV191I) rose to a high level during the 4th year (84.43%/83.41%), and 2 other variants, namely rtN248H and rtS256G, were maintained at a high level (>60%) (Figure 3B). 2016 Medicine Result HBV I187L;V191I;N248H;S256G 27;35;131;143 32;40;136;148 RT;RT;RT;RT 25;33;129;141 27;35;131;143 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In the CVR group, all treatment-naive patients harbored rtA181 V/T substitutions (ranging from 1.2% to 4.6%). 2016 Medicine Result HBV A181V;A181T 58;58 66;66 RT 56 58 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In the PVR group, all treatment-naive patients harbored rtA181 V/T substitutions (ranging from 1.1% to 3.8%) and rtN236T substitutions (ranging from 1.5% to 6.1%). 2016 Medicine Result HBV A181V;A181T;N236T 58;58;115 66;66;120 RT;RT 56;113 58;115 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Meanwhile, the rtA181T substitution rose from 2.17% to 64.15% by 2 years, and certain nonresistance mutations (rtN248A, rtI224 V, and rtS223A) had increased significantly. 2016 Medicine Result HBV N248A;A181T;I224V;S223A 113;17;122;136 118;22;128;141 RT;RT;RT;RT 15;111;120;134 17;113;122;136 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Other substitutions (rtI169T/V, rtT184A/I, rtA194 V/T, rtV214A, rtM250 V) were present at low levels (<1%). 2016 Medicine Result HBV I169T;I169V;T184A;T184I;A194V;A194T;V214A;M250V 23;23;34;34;45;45;57;66 30;30;41;41;53;53;62;72 RT;RT;RT;RT;RT 21;32;43;55;64 23;34;45;57;66 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Other substitutions (rtI169T/V, rtV173A/M, rtT184A/I, rtA194 V/T, rtQ215R/H, rtM250 V) were presented at low levels (<1%). 2016 Medicine Result HBV I169T;I169V;V173A;V173M;T184A;T184I;A194V;A194T;Q215R;Q215H;M250V 23;23;34;34;45;45;56;56;68;68;79 30;30;41;41;52;52;64;64;75;75;85 RT;RT;RT;RT;RT;RT 21;32;43;54;66;77 23;34;45;56;68;79 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Resistance mutations displayed low levels of fluctuation (<7%), and other nonresistant variants (rtN248H/rtS223A) rose to 12.88%/13.1% by 2 years, whereas rtS256G substitutions were maintained at a high level (>55%) (Figure 4B). 2016 Medicine Result HBV N248H;S223A;S256G 99;107;157 104;112;162 RT;RT;RT 97;105;155 99;107;157 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Resistant variants (rtM204I/rtV173 M/A) increased to 9.23%/1.87% in 24 weeks and declined to <1% at 1 year. 2016 Medicine Result HBV M204I;V173M;V173A 22;30;30 27;38;38 RT;RT 20;28 22;30 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. The results in Figure 5B demonstrated that from 1 to 2 years, resistant variants (rtL180 M, rtM204 V, rtS202G) began to rise to a high peak (84.60%, 79.56%, 76.88%) and that double amino acid substitutions (rtL180M+rtM204 V) and triple substitutions (rtL180M+rtM204V+rtS202G) also began to rise. 2016 Medicine Result HBV M204V;L180M;M204V;S202G;L180M;S202G;L180M;M204V 217;84;94;104;209;269;253;261 223;90;100;109;214;274;258;266 RT;RT;RT;RT;RT;RT;RT;RT 82;92;102;207;215;251;259;267 84;94;104;209;217;253;261;269 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. The wave of resistant variants detected at 1 year, including several single amino acid substitutions, such as rtM204 V (19.95%), rtL180 M (19.12%), and rtS202G (18.33%), decreased to <1% by 2 years. 2016 Medicine Result HBV M204V;L180M;S202G 112;131;154 118;137;159 RT;RT;RT 110;129;152 112;131;154 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. There was no occurrence of complications, including mortality and morbidity, related to HBV with rtA181T/V mutants during the 48 weeks of rescue therapy. 2016 Saudi journal of gastroenterology Result HBV A181T;A181V 99;99 106;106 RT 97 99 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. A similar trend in A1762T/G1764A dual mutations was found in HCC and ASC patients. 2016 Oncotarget Result HBV G1764A;A1762T 26;19 32;25 Hepatocellular carcinoma 61 64 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. A1762T/G1764A mutations from HBeAg-positive and HBeAg-negative patients. 2016 Oncotarget Result HBV G1764A;A1762T 7;0 13;6 C;C 29;48 34;53 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. A1762T/G1764A mutations in different HBV genotypes. 2016 Oncotarget Result HBV G1764A;A1762T 7;0 13;6 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Additionally, A1762T/G1764A dual mutations contributed to a higher risk of HCC occurrence compared with CHB patients (OR = 2.87, 95% CI = 1.96-4.20, P < 0.00001, Table 3 and Supplementary Figure S5). 2016 Oncotarget Result HBV G1764A;A1762T 21;14 27;20 Hepatocellular carcinoma;Chronic Hepatitis B 75;104 78;107 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Chronic HBV-infected patients with genotype B had a significant lower incidence of A1762T/G1764A dual mutations compared with those with genotype C (OR = 0.30, 95% CI = 0.18-0.52, P < 0.0001, Figure 2.1); no heterogeneity was found when we compared BCP dual mutations between HBV genotypes B and C in HCC patients (P = 0.27, I2 = 24%). 2016 Oncotarget Result HBV G1764A;A1762T 90;83 96;89 BCP 249 252 Hepatocellular carcinoma;HBV infections 301;8 304;20 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Compared to LC patients, HCC patients had a higher risk of A1762T/G1764A dual mutations (OR = 1.55, 95% CI = 1.06-2.26, P = 0.02, Table 3 and Supplementary Figure S2). 2016 Oncotarget Result HBV G1764A;A1762T 66;59 72;65 Hepatocellular carcinoma;Liver cirrhosis 25;12 28;14 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Given the above results, we assumed that BCP A1762T/G1764A dual mutations might promote hepatocarcinogenesis even without progression to cirrhosis. 2016 Oncotarget Result HBV G1764A;A1762T 52;45 58;51 BCP 41 44 Liver cirrhosis 137 146 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. HCC patients had a significantly higher frequency of A1762T/G1764A dual mutations than the ASC patients (OR = 5.59, 95% CI = 3.17-9.83, P < 0.00001, Table 3 and Supplementary Figure S6). 2016 Oncotarget Result HBV G1764A;A1762T 60;53 66;59 Hepatocellular carcinoma 0 3 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Heterogeneity was significant among the included studies when comparing the prevalence of A1762T/G1764A dual mutations between HCC and non-HCC patients (P < 0.00001, I2 = 82%). 2016 Oncotarget Result HBV G1764A;A1762T 97;90 103;96 Hepatocellular carcinoma;Hepatocellular carcinoma 127;139 130;142 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Heterogeneity was significant among the included studies, which described A1762T/G1764A dual mutations from chronic HBV infection in HBV genotypes B and C. 2016 Oncotarget Result HBV G1764A;A1762T 81;74 87;80 Chronic HBV infection 108 129 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Heterogeneity was significant among these studies (P < 0.00001, I2 = 81%), and no significance in BCP A1762T/G1764A mutations was observed in either HBeAg-positive or HBeAg-negative chronic HBV-infected patients (OR = 1.06, 95% CI = 0.63-1.78, P = 0.83, Figure 4.1). 2016 Oncotarget Result HBV G1764A;A1762T 109;102 115;108 BCP;C;C 98;149;167 101;154;172 HBV infections 190 202 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In addition, we performed a subgroup analysis to compare A1762T/G1764A dual mutations between ASC, CHB, LC and HCC patients. 2016 Oncotarget Result HBV G1764A;A1762T 64;57 70;63 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 99;111;104 102;114;106 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In HBV genotype C subjects, BCP A1762T/G1764A dual mutations contributed to significantly higher risk for HCC developing compared with non-mutation ones (OR = 3.47, 95% CI = 2.28-5.27, P < 0.00001, Figure 3.1). 2016 Oncotarget Result HBV G1764A;A1762T 39;32 45;38 BCP 28 31 Hepatocellular carcinoma 106 109 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In HCC, there was no difference of A1762T/G1764A mutations between HBeAg-positive and HBeAg-negative patients (OR = 1.38, 95% CI = 0.84-2.27, P = 0.20, Figure 4.2). 2016 Oncotarget Result HBV G1764A;A1762T 42;35 48;41 C;C 67;86 72;91 Hepatocellular carcinoma 3 6 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In summary, the frequency of A1762T/G1764A dual mutations increased in this manner: from ASC to chronic disease, and then to HCC (Supplementary Table S1). 2016 Oncotarget Result HBV G1764A;A1762T 36;29 42;35 Hepatocellular carcinoma 125 128 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Moreover, a subgroup analysis of four studies with a random-effects model revealed no statistically significant difference between cirrhotic HCC (LC-HCC) and non-cirrhotic HCC (non-LC-HCC) patients in terms of the frequency of A1762T/G1764A dual mutations (OR = 2.06, 95% CI = 0.99-4.28, P = 0.05, Table 3 and Supplementary Figure S3). 2016 Oncotarget Result HBV G1764A;A1762T 234;227 240;233 Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis 131;149;184;162;146;181 144;152;187;171;148;183 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Nine studies reported A1762T/G1764A dual mutations based on HBeAg status in chronic HBV infection. 2016 Oncotarget Result HBV G1764A;A1762T 29;22 35;28 C 60 65 Chronic HBV infection 76 97 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Our data revealed that more HCC patients had A1762T/G1764A dual mutations compared with non-HCC patients (66.5% vs. 2016 Oncotarget Result HBV G1764A;A1762T 52;45 58;51 Hepatocellular carcinoma;Hepatocellular carcinoma 28;92 31;95 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Prevalence of A1762T/G1764A mutations from ASC, CHB, LC and HCC. 2016 Oncotarget Result HBV G1764A;A1762T 21;14 27;20 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 48;60;53 51;63;55 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Similarly, HCC patients with HBV genotype B had lower levels of A1762T/G1764A dual mutations compared with those with genotype C (OR = 0.34, 95% CI = 0.13-0.94, P = 0.04, Figure 2.2). 2016 Oncotarget Result HBV G1764A;A1762T 71;64 77;70 Hepatocellular carcinoma 11 14 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Using a random-effects model, a meta-analysis of four studies showed that the non-LC-HCC patients had a significantly higher frequency of A1762T/G1764A dual mutations compared with the CHB and ASC patients (OR = 2.16, 95% CI = 1.08-4.32, P = 0.03, Table 3 and Supplementary Figure S4). 2016 Oncotarget Result HBV G1764A;A1762T 145;138 151;144 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 85;185;82 88;188;84 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. 2A is summarized as follows: i) No substitution was detected in the baseline sample; ii) the rtN236T substitution was present in ~10% of the viral population, whereas the wild-type virus was predominantly repressed at month 12. 2016 Experimental and therapeutic medicine Result HBV N236T 95 100 RT 93 95 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. 2B may be summarized as follows: i) At baseline, rtL180M, rtM204V and rtM204I were detected in ~30, 10 and 70% of the viral population, respectively; ii) at month 24, rtT184F was present in ~20% of the viral population, within the background of rtL180M and rtM204I/V, which was accompanied by a virological breakthrough; iii) with the outgrowth of rtL180M, rtM204V and rtT184F, rtM204I was gradually outcompeted by other viral mutants and was undetectable in the viral population; iv) following the initiation of ADV treatment at month 31, the quantity of HBV started to decline gradually. 2016 Experimental and therapeutic medicine Result HBV M204I;T184F;M204V;T184F;L180M;M204V;L180M;M204I;L180M;M204V;M204I 72;169;259;371;51;60;247;259;350;359;380 77;174;266;376;56;65;252;266;355;364;385 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 49;58;70;167;245;257;348;357;369;378 51;60;72;169;247;259;350;359;371;380 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. A clonal analysis of the samples at month 24 (a virological breakthrough) and at month 36 (ETV + ADV combination therapy) revealed that rtL180 M and rtM204V were co-localized in the same viral strain. 2016 Experimental and therapeutic medicine Result HBV L180M;M204V 138;151 144;156 RT;RT 136;149 138;151 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. A clonal analysis of the samples at month 30, the point of virological breakthrough, revealed that rtL180M and rtM204 were always co-localized in the same viral strain. 2016 Experimental and therapeutic medicine Result HBV L180M 101 106 RT;RT 99;111 101;113 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. At month 24, the rtL180M + rtM204V, rtM204I and wild-type viral strains co-existed and were present in 17% (5/30), 47% (14/30) and 37% (11/30) of the viral population, respectively. 2016 Experimental and therapeutic medicine Result HBV L180M;M204V;M204I 19;29;38 24;34;43 RT;RT;RT 17;27;36 19;29;38 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. At month 36, rtT184F emerged and was co-localized with L180M + M204V in the same virus-isolate clone. 2016 Experimental and therapeutic medicine Result HBV T184F;L180M;M204V 15;55;63 20;60;68 RT 13 15 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. At this time, the viral strains of rtL180M + rtM204V + rtS202G, rtL180M + rtM204V + rtT184S and rtL180M + rtM204V + rtS202G + rtT184S were co-existent and represented 83% (25/30), 10% (3/30) and 7% (2/30) of the viral population, respectively. 2016 Experimental and therapeutic medicine Result HBV L180M;M204V;S202G;L180M;M204V;T184S;L180M;M204V;S202G;T184S 37;47;57;66;76;86;98;108;118;128 42;52;62;71;81;91;103;113;123;133 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 35;45;55;64;74;84;96;106;116;126 37;47;57;66;76;86;98;108;118;128 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. Prior to the virological breakthrough, the ETV-associated variant, rtS202G, had been detected at month 24 and was present in ~20% of the viral population; v) after ADV therapy was initiated at month 37, the viral load gradually declined; the rtL180M, rtT184S, rtS202G and rtM204V variants were persistently dominant in the viral population during the combination therapy. 2016 Experimental and therapeutic medicine Result HBV S202G;L180M;T184S;S202G;M204V 69;244;253;262;274 74;249;258;267;279 RT;RT;RT;RT;RT 67;242;251;260;272 69;244;253;262;274 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. rtM204I was outcompeted by other mutants, and became undetectable at month 30, whereas rtM204V and other mutant strains became dominant in the viral population; iv) at month 30 the rtM204V, rtL180M, rtS202G and rtT184S variants were present in ~100, 100, 80 and 15% of the viral population, respectively, which was accompanied by a virological breakthrough. 2016 Experimental and therapeutic medicine Result HBV T184S;M204I;M204V;M204V;L180M;S202G 213;2;89;183;192;201 218;7;94;188;197;206 RT;RT;RT;RT;RT;RT 0;87;181;190;199;211 2;89;183;192;201;213 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. rtV173M was detectable in ~50% of the viral population at month 36, while rtL180M, rtM204V and rtT184F were persistently dominant in the viral population. 2016 Experimental and therapeutic medicine Result HBV V173M;L180M;M204V;T184F 2;76;85;97 7;81;90;102 RT;RT;RT;RT 0;74;83;95 2;76;85;97 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. The rtL180M + rtT184F + rtM204V and rtV173M + rtL180M + rtT184F + rtM204V viral strains represented 33% (9/27) and 67% (18/27) of the viral population, respectively. 2016 Experimental and therapeutic medicine Result HBV L180M;T184F;M204V;V173M;L180M;T184F;M204V 6;16;26;38;48;58;68 11;21;31;43;53;63;73 RT;RT;RT;RT;RT;RT;RT 4;14;24;36;46;56;66 6;16;26;38;48;58;68 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. The rtN236T reappeared at month 24 with the viral load fluctuation and was undetectable when outgrowth of the ETV-resistant variants was observed; iii) among the LAM-resistant variants, the rtM204I mutation emerged earlier than rtM204V, at month 18. 2016 Experimental and therapeutic medicine Result HBV M204I;N236T;M204V 192;6;230 197;11;235 RT;RT;RT 4;190;228 6;192;230 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. In the context of "a" determinant, four mutation spots have been described in viral strains in Saudi Arabia including a single previously recorded site (T388C in Riyadh 112/2013 strain) and three unique sites (C381A, C404T and A414G in Riyadh 121/2013, Riyadh 108/2013 and Riyadh 121/2013 in order). 2016 Saudi journal of gastroenterology Result HBV T388C;C381A;C404T;A414G 153;210;217;227 158;215;222;232 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. No record for the well-established "vaccine escape" mutant G145R was observed in any of the sequenced samples. 2016 Saudi journal of gastroenterology Result HBV G145R 59 64 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. The first; T388C, changed the amino acid at position 130 from phenylalanine (F) to leucine (L), which is a common amino acid change recorded previously in many countries such as China and Philippines. 2016 Saudi journal of gastroenterology Result HBV T388C 11 16 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. The second; C404T, induced a unique amino acid change at position 135 from serine (S) to phenylalanine (F). 2016 Saudi journal of gastroenterology Result HBV C404T 12 17 S 83 84 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. These changes include an overall of 11 unique sites that locate in the three different fragments of S proteins; D16E, T40P, F56L, Q75H, L77R, Q107K, and W111Sc in pre-S1, S135F in pre-S2, and F183S, C239Y, and Y369H in S. 2016 Saudi journal of gastroenterology Result HBV D16E;T40P;F56L;Q75H;L77R;Q107K;S135F;F183S;C239Y;Y369H 112;118;124;130;136;142;171;192;199;210 116;122;128;134;140;147;176;197;204;215 PreS1;PreS2;S;S 163;180;100;219 169;186;101;220 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. As shown in Figure 1, rs11489585 multiplicatively interacted with G1799C. 2016 Cancer medicine Result HBV G1799C 66 72 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. Of those 19 hotspot mutations, C1653T, T1674C/G, A1703G, G1719T, T1727A/G, T1753C, A1762T, G1764A, G1799C, G1899A, G1915A/C, and C1969T were significantly associated with an increased risk of HCC, whereas C1673T, A1726C, C1730G, and A1752G were significantly associated with a reduced risk of HCC, when adjusted for age and gender 20. 2016 Cancer medicine Result HBV T1727G;G1915C;C1653T;T1674C;T1674G;A1703G;G1719T;T1727A;T1753C;A1762T;G1764A;G1799C;G1899A;G1915A;C1969T;C1673T;A1726C;C1730G;A1752G 65;115;31;39;39;49;57;65;75;83;91;99;107;115;129;205;213;221;233 73;123;37;47;47;55;63;73;81;89;97;105;113;123;135;211;219;227;239 Hepatocellular carcinoma;Hepatocellular carcinoma 192;293 195;296 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. We detected interaction between rs11489585 and the HBV mutation (P = 0.050 for G1799C). 2016 Cancer medicine Result HBV G1799C 79 85 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Additionally, 1 clone and 15 clones harboring rtA181 T mutations in in patients 3 and 4, respectively, showed sW172* mutations. 2016 Annals of clinical microbiology and antimicrobials Result HBV A181T;W172X 48;110 54;116 RT;S 46;110 48;111 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Additionally, one clone (4.17 %) bore rtM204 V+rtL180 M+rtM250 V+rtA181 V mutations, which resulted in resistance to LAM+ADV+ETV (Additional file 3: Figure S2). 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;M250V;A181V 40;49;58;67 46;55;64;73 RT;RT;RT;RT 38;47;56;65 40;49;58;67 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. All clones harbored rtM204 V+rtL180 M+rtA181 V mutations, consistent with the sequencing results, and no de novo ETV resistance mutations were detected. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;A181V 22;31;40 28;37;46 RT;RT;RT 20;29;38 22;31;40 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. described a patient who received LAM+ADV and then developed de novo ETV resistance with rtM204 V+rtL180 M+rtT184 S mutations. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;T184S 90;99;108 96;105;114 RT;RT;RT;S 88;97;106;113 90;99;108;114 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. In addition, 17.39 % (4/23) and 13.04 % (3/23) of the clones harbored the rtM204 I and rtA181 T mutations, respectively, which were not found by direct sequencing. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204I;A181T 76;89 82;95 RT;RT 74;87 76;89 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. In addition, one clone (5.0 %) bore rtM204 V+rtA181 T mutations. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;A181T 38;47 44;53 RT;RT 36;45 38;47 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. In patient 1, 3 clones harboring the rtA181 T mutation had sW172*(stop codon) mutations in the overlapping S gene. 2016 Annals of clinical microbiology and antimicrobials Result HBV A181T;W172X 39;59 45;65 RT;S;S 37;59;107 39;60;108 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. In this study, all genotype C HBV clones harboring the rtA181 T mutation had sW172* mutations in the overlapping S-gene. 2016 Annals of clinical microbiology and antimicrobials Result HBV A181T;W172X 57;77 63;83 RT;S;S 55;77;113 57;78;114 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. It has been reported that the rtA181 T mutation in HBV may cause sW172* in the overlapping S gene in genotype D HBV infection. 2016 Annals of clinical microbiology and antimicrobials Result HBV A181T;W172X 32;65 38;71 RT;S;S 30;65;91 32;66;92 HBV infections 112 125 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Moreover, one clone (4.35 %) harbored rtM204 I+rtL180 M+rtM250 V+rtA181 V mutations, which resulted in resistance to LAM+ADV+ETV (Additional file 2: Figure S1); however, this patient had never received ETV therapy. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204I;L180M;M250V;A181V 40;49;58;67 46;55;64;73 RT;RT;RT;RT 38;47;56;65 40;49;58;67 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Notably, this study also included two patients with de novo ETV resistance mutations at rtT184 A and rtM250 L after LAM+ADV treatment, but no further clonal analyses were conducted in these patients. 2016 Annals of clinical microbiology and antimicrobials Result HBV M250L;T184A 103;90 109;96 RT;RT 88;101 90;103 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Patient 1 received ADV and LAM sequential therapy, and direct sequencing of the nested PCR product showed rtM204 V+rtL180 M+rtA181 V mutations upon secondary virological breakthrough, whereas rtM204 V+rtL180 M+rtA181 V strains accounted for 78.26 % (18/23) of the clones in the clonal analysis. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;A181V;M204V;L180M;A181V 108;117;126;194;203;212 114;123;132;200;209;218 RT;RT;RT;RT;RT;RT 106;115;124;192;201;210 108;117;126;194;203;212 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Patient 2 received ADV and LAM sequential therapy, and sequencing revealed rtM204 V+rtL180 M+rtA181 V mutations upon secondary virological breakthrough, whereas rtM204 V+rtL180 M+rtA181 V strains comprised 95.83 % (23/24) of the clones in the clonal analysis. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;A181V;M204V;L180M;A181V 77;86;95;163;172;181 83;92;101;169;178;187 RT;RT;RT;RT;RT;RT 75;84;93;161;170;179 77;86;95;163;172;181 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Patient 3 received ADV and LAM sequential therapy, and sequencing showed rtM204 V+rtL180 M+rtA181 V mutations upon secondary virological breakthrough, whereas 85.0 % (17/20) of the clones harbored rtM204 V+rtL180 M+rtA181 V mutations. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;M204V;L180M;A181V;A181V 75;84;199;208;93;217 81;90;205;214;99;223 RT;RT;RT;RT;RT;RT 73;82;91;197;206;215 75;84;93;199;208;217 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Patient 4 received ADV+LAM for rescue therapy upon ADV resistance, and sequencing showed rtM204 I+rtA181 V+rtA181 T mutations upon secondary virological breakthrough. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204I;A181V;A181T 91;100;109 97;106;115 RT;RT;RT 89;98;107 91;100;109 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Sequencing identified rtM204 V+rtL180 M+rtA181 V mutations upon secondary virological breakthrough. 2016 Annals of clinical microbiology and antimicrobials Result HBV M204V;L180M;A181V 24;33;42 30;39;48 RT;RT;RT 22;31;40 24;33;42 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. Strains harboring the rtA181 T/sW172* mutation accounted for 13.04 % (3/23), 4.17 % (1/24), and 50.0 % (15/30) of the total clones in patients 1, 3, and 4, respectively. 2016 Annals of clinical microbiology and antimicrobials Result HBV W172X;A181T 31;24 37;30 RT;S 22;31 24;32 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. The possible overlapping S-gene mutations of all clones harboring the rtA181 T mutation were analyzed (Additional file 6: Table S2). 2016 Annals of clinical microbiology and antimicrobials Result HBV A181T 72 78 RT;S 70;25 72;26 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. The rtN236 T mutation was not found by direct sequencing of PCR products, and no ETV-resistance mutations were detected in this patient. 2016 Annals of clinical microbiology and antimicrobials Result HBV N236T 6 12 RT 4 6 27079793 De novo entecavir+adefovir dipivoxil+lamivudine triple-resistance mutations resulting from sequential therapy with adefovir dipivoxil, and lamivudine. This also confirms that the HBV rtA181 T/sW172*mutation is usually detected in a mixed population with lower replication efficiency. 2016 Annals of clinical microbiology and antimicrobials Result HBV W172X;A181T 41;34 47;40 RT;S 32;41 34;42 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. Additional immunoprophylaxis mutations were observed in patients 224E (sI110L), 080N (sT131N), and 132E (sM133T). 2017 Antiviral therapy Result HBV I110L;T131N;M133T 71;86;105 77;92;111 S;S;S 71;86;105 72;87;106 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. All patients had the N204S mutation, and all but patient 132E had the sI126T mutation. 2017 Antiviral therapy Result HBV I126T;N204S 70;21 76;26 S 70 71 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. Four (6.35%) patients - 006N, 040N, 125E, and 218E - had both sT131N and sS143T mutations. 2017 Antiviral therapy Result HBV T131N;S143T 62;73 68;79 S;S 62;73 63;74 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. Vaccine escape mutations were found in 7 (11.1%) patients including 040N (sG145R), 159N (sQ129H), 007N (sQ129R), 054N (sD144A), 127E (sD144E), 006N (sD144E), and 119E (sD144E). 2017 Antiviral therapy Result HBV G145R;Q129H;Q129R;D144A;D144E;D144E;D144E 74;89;104;119;134;149;168 80;95;110;125;140;155;174 S;S;S;S;S;S;S 74;89;104;119;134;149;168 75;90;105;120;135;150;169 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. By contrast, M3 with the s126-127 "RPCMNCTI" insertion, which also introduced an additional N-glycosylated site, showed reduced binding (by 23.2%) of anti-HBs to target HBsAg; M4 (sG145R) had little influence on this binding (Fig 4B and 4C). 2016 PloS one Result HBV G145R 180 186 S;S;S;S 155;169;25;180 158;174;26;181 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. These mutation were the following: (1) sI/T126V+sG145R (KR014124); (2) preS1 nt 3014-3198 deletion (KR014127); (3) preS1 nt 3046-3177 deletion (KR014128); (4) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion (KR014129); (5) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion+sG145R (KR014130); (6) preS1 nt 3115-3123 deletion+sQ129N (KR014131); (7) preS1 nt 3115-3123 deletion+s126-127 "RPCMNCTI" insertion (KR014132); (8) s115-116 "INGTST" insertion (KR014133); (9) s115-116 "INGTST" insertion+sG145R (KR014134); (10) s126-127 "RPCMNCTI" insertion (KR014135); (11) preS1 nt 2848-2862 deletion+preS2 initiation codon M I (KR014141); (12) s122-123 "KSTGLCK" insertion+sQ129N (KR014142); and (13) preS2 initiation codon M I+s131-133TSM NST (KR014143). 2016 PloS one Result HBV T126V;I126V;Q129N;Q129N;G145R;G145R;G145R 42;39;338;679;48;287;507 47;47;344;685;54;293;513 PreS1;PreS1;PreS1;PreS1;PreS1;PreS1;PreS1;PreS2;PreS2;S;S;S;S;S;S;S;S;S;S;S;S;S;S 71;115;159;231;310;361;578;606;707;39;48;187;259;287;338;389;435;479;507;531;650;679;734 76;120;164;236;315;366;583;611;712;40;49;188;260;288;339;390;436;480;508;532;651;680;735 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Among 13 newborn-infant pairs that were successfully sequenced, only three infants had three unique mutation sites not present in newborns, including ntC1139A (7.70%, 1/13) in the X-S overlapping reading frame as well as ntA273G (7.70%, 1/13) and ntC512T (7.70%, 1/13) in the S region and outside the "a" antigenic determinant cluster. 2016 Hepatitis monthly Result HBV C1139A;A273G;C512T 151;222;248 158;228;254 S;S;X 182;276;180 183;277;181 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Among 45 control group mothers, nine, seven and three mothers shared an identical mutation site of ntC531T, ntC508G and ntA633G, respectively (Table 3). 2016 Hepatitis monthly Result HBV C531T;C508G;A633G 100;109;121 106;115;127 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Among these mutations, one case in vaccine failure group had ntA826G (6.67%, 1/15), 2 cases in control group had ntC531T mutation (4.44%, 2/45), one case in control group had ntT667C mutation (2.22%, 1/45) and ntC512T and ntC546A were detected in one case in case group (6.67%, 1/15) and one case in control group(2.22%, 1/45). 2016 Hepatitis monthly Result HBV A826G;C531T;T667C;C512T;C546A 62;114;176;211;223 68;120;182;217;229 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Five mothers shared the same 5 mutation sites of ntA482C, ntC592T, ntC598T, ntG783A and ntG799A. 2016 Hepatitis monthly Result HBV A482C;C592T;C598T;G783A;G799A 50;59;68;77;89 56;65;74;83;95 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Only five mutations including ntA826G, ntC531T, ntT667C, ntC512T and ntC546A were missense mutations. 2016 Hepatitis monthly Result HBV A826G;C531T;T667C;C512T;C546A 31;40;49;58;70 37;46;55;64;76 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Six mothers shared the same 8 mutation sites; ntT454C, ntT491A, ntA562T, ntA581T, ntT667C, ntA791T, ntG793A and ntT820C. 2016 Hepatitis monthly Result HBV T454C;T491A;A562T;A581T;T667C;A791T;G793A;T820C 47;56;65;74;83;92;101;113 53;62;71;80;89;98;107;119 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. The mutations of ntA273G and ntC512T, not ntC1139A were located within ORF of Pre-S/S gene, ntA273G and ntC512T affected aa41 and aa162 synthesis, respectively. 2016 Hepatitis monthly Result HBV A273G;C512T;C1139A;A273G;C512T 18;30;43;93;105 24;36;50;99;111 PreS;S 78;84 83;85 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. The mutations of ntA826G, ntT667C and ntC512T were located in non-"a" determinant cluster in S gene. 2016 Hepatitis monthly Result HBV A826G;T667C;C512T 18;27;39 24;33;45 S 93 94 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. The mutations of ntC531and ntC546A were located in "a" determinant cluster. 2016 Hepatitis monthly Result HBV C546A 28 34 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. There were five important point mutations that could cause amino acid change in nucleotides of PreS/S region including ntA826G (aa L V), ntC531T (aa T A), ntT667C (aa L M), ntC512T (aa P A) and ntC546A (aa T N). 2016 Hepatitis monthly Result HBV A826G;C531T;T667C;C512T;C546A 120;140;160;180;203 126;146;166;186;209 PreS;S 95;100 99;101 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Two mothers shared the same six mutation sites of ntT870C, ntT941A, ntG942A, ntT975C, ntC1020C and ntC1120T. 2016 Hepatitis monthly Result HBV T870C;T941A;G942A;T975C;C1020C;C1120T 51;60;69;78;87;100 57;66;75;84;94;107 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. The other 22 mutations were outside the "a" determinant (18 involving T118A/V, 4 involving Y206S/C) (Table 1). 2016 PloS one Result HBV T118A;T118V;Y206S;Y206C 70;70;91;91 77;77;98;98 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. The prevalence of amino acid substitutions in HBsAg was 38% (24/63), but only 2 of these 24 mutations were within the "a" determinant of HBsAg (1 M133T mutation, 1 G145S mutation). 2016 PloS one Result HBV M133T;G145S 146;164 151;169 S;S 46;137 51;142 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. ADV-resistant variant rtA181T then decreased and became undetected after 23 months of combination therapy. 2016 Experimental and therapeutic medicine Result HBV A181T 24 29 RT 22 24 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. ADV-resistant variant rtN236T decreased and became undetected following 2 years of combination therapy. 2016 Experimental and therapeutic medicine Result HBV N236T 24 29 RT 22 24 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. ADV-resistant variants rtA181 V/T and rtN236T went from being dominant at initiation of ADV-ETV combination to undetectable, during an average duration of combination therapy of 19.33 months (range, 11-24 months). 2016 Experimental and therapeutic medicine Result HBV A181V;A181T;N236T 25;25;40 33;33;45 RT;RT 23;38 25;40 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. After a mean of 37.33 months (range, 30-41 months) combination treatment, LAM-resistant variants (rtM204I/V with or without rtL180 M) remained dominant in the viral population. 2016 Experimental and therapeutic medicine Result HBV M204I;M204V;L180M 100;100;126 107;107;132 RT;RT 98;124 100;126 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. During sequential monotherapy, the levels of LAM-resistant variants (rtM204I/V with or without rtL180 M) gradually decreased as treatment progressed, whereas ADV-resistant rtA181 V/T and rtN236T gradually increased and became dominant in the viral populations. 2016 Experimental and therapeutic medicine Result HBV M204I;M204V;A181V;A181T;N236T;L180M 71;71;174;174;189;97 78;78;182;182;194;103 RT;RT;RT;RT 69;95;172;187 71;97;174;189 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. ETV was administered after 19 months of monotherapy, and resistant rtA181 V gradually decreased and became undetectable after 11 months of combination therapy. 2016 Experimental and therapeutic medicine Result HBV A181V 69 75 RT 67 69 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. Following passage to an ADV-ETV combination regimen, ADV-resistant rtA181 V/T and rtN236T gradually decreased and became undetected in the viral population, whereas LAM-resistant variant (rtM204I/V with or without rtL180 M) was dominant in the viral population during combination therapy. 2016 Experimental and therapeutic medicine Result HBV A181V;A181T;N236T;M204I;M204V;L180M 69;69;84;190;190;216 77;77;89;197;197;222 RT;RT;RT;RT 67;82;188;214 69;84;190;216 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In contrast to Patient 2, dominant resistant variants rtL180 M and rtM204 V were replaced by dominant variant rtN236T following sequential ADV monotherapy, and were then replaced by dominant variants rtL180 M and rtM204 V during ADV-ETV combination therapy. 2016 Experimental and therapeutic medicine Result HBV L180M;M204V;N236T;L180M;M204V 56;69;112;202;215 62;75;117;208;221 RT;RT;RT;RT;RT 54;67;110;200;213 56;69;112;202;215 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In Patient 1, in addition to rtM204I, the serum sample taken at the initiation of sequential ADV monotherapy harbored ADV-resistant rtA181 V. 2016 Experimental and therapeutic medicine Result HBV A181V;M204I 134;31 140;36 RT;RT 29;132 31;134 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In Patient 2, resistant rtA181T was rapidly selected and accompanied by virological breakthrough following 12 months of ADV monotherapy. 2016 Experimental and therapeutic medicine Result HBV A181T 26 31 RT 24 26 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In Patient 3, the viral load of the virus harboring rtN236T gradually increased for 6 months prior to virological breakthrough. 2016 Experimental and therapeutic medicine Result HBV N236T 54 59 RT 52 54 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The biochemical breakthrough coincided with the shift from dominant rtM204I to dominant rtA181T after 18 months. 2016 Experimental and therapeutic medicine Result HBV M204I;A181T 70;90 75;95 RT;RT 68;88 70;90 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The dynamics of resistant variants was characterized by successive waves, with the rtM204I variant being initially dominant, then being replaced by the rtA181T variant, and finally, by the rtL180 M and rtM204 V variants. 2016 Experimental and therapeutic medicine Result HBV A181T;M204I;L180M;M204V 154;85;191;204 159;90;197;210 RT;RT;RT;RT 83;152;189;202 85;154;191;204 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The emergence of LAM-resistant variants, such as rtM204 V/I and/or rtL180 M, was observed in all patients. 2016 Experimental and therapeutic medicine Result HBV M204V;M204I;L180M 51;51;69 59;59;75 RT;RT 49;67 51;69 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The resistant variant rtN236T became dominant and accompanied by virological breakthrough after 24 months. 2016 Experimental and therapeutic medicine Result HBV N236T 24 29 RT 22 24 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The three patients had LAM-resistant variants (rtM204I/V with or without rtL180 M) at the initiation of sequential ADV monotherapy. 2016 Experimental and therapeutic medicine Result HBV M204I;M204V;L180M 49;49;75 56;56;81 RT;RT 47;73 49;75 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. T1753A/A1762T/G1764A/T1768A mutations were rarely found in these samples (2-4%). 2016 Cancer science Result HBV A1762T;G1764A;T1768A;T1753A 7;14;21;0 13;20;27;6 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. T1753V or T1768A mutation always occurred along with the TA double mutation (8/50, 16%; 1/50, 2%, respectively) (Table 1). 2016 Cancer science Result HBV T1753V;T1768A 0;10 6;16 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. The most frequently occurring mutation in this region was A1762T/G1764A, present in 20/50 (40%) HCC tissues and 19/50 (38%) non-tumorous tissues. 2016 Cancer science Result HBV G1764A;A1762T 65;58 71;64 Hepatocellular carcinoma 96 99 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. To study the biological functions of HBx mutations in hepatoma cells, we first constructed recombinant adenovirus Ad-HBx WT (wild-type), Ad-HBx A1762T (T mutant), Ad-HBx G1764A (A mutant), Ad-HBx A1762T/G1764A (TA mutant), and Ad-HBx T1753A/A1762T/G1764A/T1768A (Combo mutant). 2016 Cancer science Result HBV G1764A;A1762T;G1764A;T1768A;A1762T;G1764A;A1762T;T1753A 203;241;248;255;144;170;196;234 209;247;254;261;150;176;202;240 X;X;X;X;X;X 37;117;140;166;192;230 40;120;143;169;195;233 Hepatocellular carcinoma 54 62 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Finally, 4 patients showed an AA mutation in the pre-S2 region: P41H in 3 patients and P66L in one (Table 3). 2016 Oncotarget Result HBV P41H;P66L 64;87 68;91 PreS2 49 55 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. In patient n 4, apart from the AA substitution Q129H in the S region in both tissues, sequencing in HCC and non-HCC liver tissue showed differences in the AA substitutions and deletions both in the pre-S1 region (T40S and AA deletion in positions 4, 8 and 17 for HCC and S98T, N103D, T114I, T119P and the AA deletion in position 128-131 for non-HCC liver tissue) and in the pre-S2 region (no AA substitution or deletion in HCC tissue and the AA substitutions F75S and Q184H and AA deletion in position 19-22 in the non-HCC liver tissue). 2016 Oncotarget Result HBV Q129H;T40S;S98T;N103D;T114I;T119P;F75S;Q184H 47;213;271;277;284;291;459;468 52;217;275;282;289;296;463;473 PreS1;PreS2;S 198;374;60 204;380;61 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 100;423;112;263;345;519 103;426;115;266;348;522 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. In patient n 6 no mutation was observed in the pre-S1, pre-S2 and S regions in the HCC tissue, whereas in the non-HCC liver tissue the N59T and I110L AA substitutions were observed in the S region, no mutation in the pre-S1 region and the AA substitutions H114T and I165L in the pre-S2 region. 2016 Oncotarget Result HBV N59T;I110L;H114T;I165L 135;144;256;266 139;149;261;271 PreS1;PreS1;PreS2;PreS2;S;S 47;217;55;279;66;188 53;223;61;285;67;189 Hepatocellular carcinoma;Hepatocellular carcinoma 83;114 86;117 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. In this patient, the HCC tissue showed no mutation in the S region, AA substitutions L54P and G76A and AA deletions in positions 4, 8 and 17 in the pre-S1 region and AA substitution P41H in the pre-S2 region, whereas the non-HCC liver tissue showed the G44G/E and I92T AA substitutions in the S region, G91A and I255T AA substitutions in the pre-S1 region and AA substitutions G99E and I147T in the pre-S2 regions. 2016 Oncotarget Result HBV L54P;G76A;P41H;G44G;G44E;I92T;G91A;I255T;G99E;I147T 85;94;182;253;253;264;303;312;377;386 89;98;186;259;259;268;307;317;381;391 PreS1;PreS1;PreS2;PreS2;S;S 148;342;194;399;58;293 154;348;200;405;59;294 Hepatocellular carcinoma;Hepatocellular carcinoma 21;225 24;228 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. More precisely, as regards the S region, 4 patients showed AA substitutions: Q129H in two patients, P24L in one and F19L, S59F and T131I in one (Table 3). 2016 Oncotarget Result HBV Q129H;P24L;F19L;S59F;T131I 77;100;116;122;131 82;104;120;126;136 S 31 32 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Regarding the pre-S1 region, 5 patients showed AA mutations (T40S in two patients, P124K in one, L54P and G76A in one, N222T and I273L in one) and 4 showed deletions(in positions 4, 8 and 17 in 3 patients and positions 8, 17 and 86 in one) (Table 3). 2016 Oncotarget Result HBV T40S;P124K;L54P;G76A;N222T;I273L 61;83;97;106;119;129 65;88;101;110;124;134 PreS1 14 20 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. The following AA substitutions and deletions were observed: a) G44E, I92T, Q129H, N59T, and I110L AA substitutions in the S region; b) AA deletions in position 128-131 and G91A, I255T, S98T, N310D, T114I, and T119P AA substitutions in the pre-S1 region; c) AA deletions in position 19-22 and G99E, I147T, F75S, Q184H, H114T and I165L AA substitutions in the pre-S2 region (Table 3). 2016 Oncotarget Result HBV G44E;I92T;Q129H;N59T;I110L;G91A;I255T;S98T;N310D;T114I;T119P;G99E;I147T;F75S;Q184H;H114T;I165L 63;69;75;82;92;172;178;185;191;198;209;292;298;305;311;318;328 67;73;80;86;97;176;183;189;196;203;214;296;303;309;316;323;333 PreS1;PreS2;S 239;358;122 245;364;123 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Thus, the mutations most frequently observed in these 6 patients were AA substitutions Q129H in the S region (2 of 6 patients), T40S in the pre-S1 (2 of 6 patients) and P41H in the pre-S2 region (4 of 6 patients) and deletions in positions 8 and 17 in the pre-S1 region (4 of 6 patients), associated with a deletion in position 4 in 3 cases and in position 86 in one. 2016 Oncotarget Result HBV Q129H;T40S;P41H 87;128;169 92;132;173 PreS1;PreS1;PreS2;S 140;256;181;100 146;262;187;101 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. Again, N236T, which is related to ADV therapy, was absent in this group (Table 2). 2016 Electronic physician Result HBV N236T 7 12 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. As was expected, M204I/V showed the highest frequency in all of the groups that were studied (the highest and the lowest values were 22.4 and 68.7% in groups IV and III, respectively). 2016 Electronic physician Result HBV M204I;M204V 17;17 24;24 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. D263E was found in groups II (3%) and III (13%). 2016 Electronic physician Result HBV D263E 0 5 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. F221Y/S was highest in groups I and IV, at 25 and 19.2%, respectively. 2016 Electronic physician Result HBV F221Y;F221S 0;0 7;7 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. Group I: In addition to the nine amino acid substitutions that related to LAM resistance, F221Y/S, which is related to ADV resistance, also was found in the patients in this group, who only received LAM (Table 2). 2016 Electronic physician Result HBV F221Y;F221S 90;90 97;97 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. I187L was distributed in groups I (25%), II (< 5%), and III (< 5%). 2016 Electronic physician Result HBV I187L 0 5 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. I191L/V was found in 60% of group I. 2016 Electronic physician Result HBV I191L;I191V 0;0 7;7 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. I266R/M was found in all of the groups with a frequency > 20% (Table 3). 2016 Electronic physician Result HBV I266R;I266M 0;0 7;7 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. I54V (ADV-related variant) was found in group IV with the highest frequency (22%). 2016 Electronic physician Result HBV I54V 0 4 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. Interestingly, residues W153Q, I169T, A200V, and S202G, which are related to LAM resistance, were found only in this group with a frequency between 3.3 and 9.9% (Table 2). 2016 Electronic physician Result HBV W153Q;I169T;A200V;S202G 24;31;38;49 29;36;43;54 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. L180M mutation (common to both LAM and ADV drug resistant variants) was found to range from 9.9% of the patients in group II to 43.75% of the patients in group III. 2016 Electronic physician Result HBV L180M 0 5 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. L72I was found in groups II (5%) and III (10%). 2016 Electronic physician Result HBV L72I 0 4 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. L80I/V was found at the frequencies of 40 and 25% in groups I and III, respectively. 2016 Electronic physician Result HBV L80V;L80I 0;0 6;6 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. N236T and compensatory mutation (A181T/P) were found to be between 3.2 and 6.4%, respectively (Table 2). 2016 Electronic physician Result HBV N236T;A181T;A181P 0;33;33 5;40;40 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. No ADV-related variant N236T was found in this group. 2016 Electronic physician Result HBV N236T 23 28 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. Q215P/S was found in all groups except group II with frequencies of 6.25 to 25%. 2016 Electronic physician Result HBV Q215P;Q215S 0;0 7;7 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. They contained the highest frequency of substitutions for residues L180M (43.7%) and M204I/V (68.7%) among all the groups. 2016 Electronic physician Result HBV L180M;M204I;M204V 67;85;85 72;92;92 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Among these sites, the rtL180 M came along with rtM204I/V as previous reports, but here we noticed it was not along with rtM204I in genotype B and majority of genotype C. 2016 SpringerPlus Result HBV L180M;M204I;M204V;M204I 25;50;50;123 31;57;57;128 RT;RT;RT 23;48;121 25;50;123 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Interestingly, their converted ratios were always lower than that of rtM204I/V itself. 2016 SpringerPlus Result HBV M204I;M204V 71;71 78;78 RT 69 71 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. It demonstrated the previously reported rtL180 M was not the unique compensatory variance. 2016 SpringerPlus Result HBV L180M 42 48 RT 40 42 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Moreover, we noticed that some variances occurred at the historical genotyping sites (labeled by asterisk in Table 2), among which, new amino acid could appear, such as rtR13L in genotype B, but many of them trended to transform into other genotyping amino acid, such as rtL91I in genotype D, etc. 2016 SpringerPlus Result HBV R13L;L91I 171;273 175;277 RT;RT 169;271 171;273 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Taken together, it reflected that the co-variance went through several steps during the evolutionary process, and the multiple-sites combined co-variance trended to an ideal state after rtM204I/V mutation. 2016 SpringerPlus Result HBV M204I;M204V 188;188 195;195 RT 186 188 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. A wave of resistantance-associated variants was detected at 3 year, as the frequency of the rtA181T substitution rose from 1.91% to 54.23%. 2016 Oncotarget Result HBV A181T 94 99 RT 92 94 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. All treatment-naive patients carried rtA181V/T substitutions (ranging from 1.1% to 8.7%) and rtN236T substitutions (ranging from 1.4% to 6.1%). 2016 Oncotarget Result HBV A181V;A181T;N236T 39;39;95 46;46;100 RT;RT 37;93 39;95 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. As shown in Figure 8B, this patient harbored the rtA181T (1.3%) and rtN236T (1.6%) substitutions at baseline, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;N236T 51;70 56;75 RT;RT 49;68 51;70 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, patient 2 harbored the rtA181T (4.7%), rtN236T (5.7%), rtL180M (12.5%), rtS202G (3.2%), and rtM204I/V (7%) substitutions, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;L180M;M204I;M204V;N236T;S202G 38;70;107;107;54;87 43;75;114;114;59;92 RT;RT;RT;RT;RT 36;52;68;85;105 38;54;70;87;107 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, patient 4 harbored the rtA181T (1.2%), rtN236T (1.4%), and rtV214A (1.2%) substitutions, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;N236T;V214A 38;54;74 43;59;79 RT;RT;RT 36;52;72 38;54;74 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient carried with rtL180M (2.4%), rtM204I/V (3.4%), rtS202G (3.3%), rtA181V/T (4.7%), and rtN236T (6%) substitutions. 2016 Oncotarget Result HBV M204I;M204V;A181V;A181T;L180M;S202G;N236T 57;57;91;91;41;75;113 64;64;98;98;46;80;118 RT;RT;RT;RT;RT 39;55;73;89;111 41;57;75;91;113 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient harbored the rtA181T (1.2%), rtN236T (1.5%), and rtV214A (1%) substitutions, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;N236T;V214A 41;57;77 46;62;82 RT;RT;RT 39;55;75 41;57;77 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Figure 3B shows that this patient harbored the rtA181T (1.4%), rtN236T (1.8%), rtS202G (1%), and rtM204I/V (1%) substitutions at baseline, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;N236T;M204I;M204V;S202G 49;65;99;99;81 54;70;106;106;86 RT;RT;RT;RT 47;63;79;97 49;65;81;99 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Figure 6B showed that this patient harbored the rtA181T (8.7%), rtN236T (1.7%), rtL180M(10.5%), rtM204I/V (7.5%), and rtV173A/M (1.6%) substitutions at baseline, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Result HBV A181T;N236T;L180M;M204I;M204V;V173A;V173M 50;66;82;98;98;120;120 55;71;87;105;105;127;127 RT;RT;RT;RT;RT 48;64;80;96;118 50;66;82;98;120 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Five patients harbored rtL180M substitutions (2.1% / 12.5%), and they also presented rtM204I/V substitutions (2.9% / 7.5%) and rtS202G substitutions (2.9% / 3.3%), which are all known to confer resistance to ETV. 2016 Oncotarget Result HBV M204I;M204V;L180M;S202G 87;87;25;129 94;94;30;134 RT;RT;RT 23;85;127 25;87;129 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. However, the frequencies of the rtS223A and rtN248H mutations declined in the first year after combined with LdT but were significantly increased at the two-year mark. 2016 Oncotarget Result HBV S223A;N248H 34;46 39;51 RT;RT 32;44 34;46 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. However, the frequency of the rtS223A mutation increased significantly (ranging from 18.14% to 77.62%) with the addition of LdT (Figure 2B). 2016 Oncotarget Result HBV S223A 32 37 RT 30 32 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In contrast, the rtQ215R substitution increased to 10.89% in the second with multi-drugs. 2016 Oncotarget Result HBV Q215R 19 24 RT 17 19 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In the ADV group, the rtA181V/T substitutions rang from 1.2% to 8.7%, and the rtN236T substitutions rang from 1.4% to 6%. 2016 Oncotarget Result HBV A181V;A181T;N236T 24;24;80 31;31;85 RT;RT 22;78 24;80 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. It is noteworthy that the frequency of the rtN236T mutation began to increase significantly after two years of ADV monotherapy and was present in up to 50% of circulating viruses during follow-up treatment. 2016 Oncotarget Result HBV N236T 45 50 RT 43 45 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Meanwhile some non-resistance-related mutations, such as rtL145M (ranging from 76.77% to 7.30%) and rtF151Y (ranging from 72.61% to 7.15%) had decreased significantly with the addition of LdT. 2016 Oncotarget Result HBV L145M;F151Y 59;102 64;107 RT;RT 57;100 59;102 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Other substitutions (rtI169T/V, rtP177G, rtT184A/I, rtA194V/T, rtV214A, rtQ215R/H, rtF249A, and rtM250V) were present at low levels (<1%). 2016 Oncotarget Result HBV I169T;I169V;T184A;T184I;A194V;A194T;Q215R;Q215H;P177G;V214A;F249A;M250V 23;23;43;43;54;54;74;74;34;65;85;98 30;30;50;50;61;61;81;81;39;70;90;103 RT;RT;RT;RT;RT;RT;RT;RT 21;32;41;52;63;72;83;96 23;34;43;54;65;74;85;98 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Some certain non-resistance mutations of rtD134N (ranging from 91.97% to 0.21%), rtL145M (ranging from 78.58% to 0.27%) and rtF151Y (ranging from 74.89% to 0.27%) had decreased significantly with the addition of LdT. 2016 Oncotarget Result HBV D134N;L145M;F151Y 43;83;126 48;88;131 RT;RT;RT 41;81;124 43;83;126 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Some non-resistance-associated mutations of rtD134N (ranging from 20.33% to 74.63%), rtL145M (ranging from 2.83% to 78.82%), rtF151Y (ranging from 2.92% to 75.51%)and rtS223A (ranging from 5.77% to 18.44%) increased significantly with ADV monotherapy, then declined with the addition of LdT. 2016 Oncotarget Result HBV D134N;L145M;F151Y;S223A 46;87;127;169 51;92;132;174 RT;RT;RT;RT 44;85;125;167 46;87;127;169 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtA181T and rtN236T mutation increased during ADV monotherapy and declined when LdT was added, but the fluctuations were minor. 2016 Oncotarget Result HBV A181T;N236T 25;37 30;42 RT;RT 23;35 25;37 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtA181V and rtN236T mutations in the HBV RT region were significantly elevated (up to 84.35% and 67.67%, respectively) after two years of ADV monotherapy, and did not decrease after the addition of LdT. 2016 Oncotarget Result HBV A181V;N236T 25;37 30;42 RT;RT;RT 23;35;64 25;37;66 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtA181V and rtN236T mutations increased slowly (ranging from 1.22% to 4.78% and 1.51% to 3.57%) after long-term treatment. 2016 Oncotarget Result HBV A181V;N236T 25;37 30;42 RT;RT 23;35 25;37 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtI224V, rtS223A, rtD134E mutations slowly increased after 4 year of treatment. 2016 Oncotarget Result HBV I224V;S223A;D134E 25;34;43 30;39;48 RT;RT;RT 23;32;41 25;34;43 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtL180M and rtM204V mutation fluctuated slightly after the addition of LdT (Figure 4B). 2016 Oncotarget Result HBV L180M;M204V 25;37 30;42 RT;RT 23;35 25;37 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtA181T mutation significantly increased after the second year, with a 50% increase during follow-up treatment. 2016 Oncotarget Result HBV A181T 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtA181T mutation was more than 10% after four years of treatment. 2016 Oncotarget Result HBV A181T 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtA181T substitution increased to 75.41% in the first year with the addition of LdT, then declined to 28.07% in the second year. 2016 Oncotarget Result HBV A181T 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtA181V mutation significantly fluctuated (ranging from 57.34% to 1.14%) after combination with LdT. 2016 Oncotarget Result HBV A181V 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtI224V mutation increased slowly. 2016 Oncotarget Result HBV I224V 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtI224V mutation was always high (70-80%) (Figure 8B). 2016 Oncotarget Result HBV I224V 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtN139K mutation slowly increased after one year of treatment. 2016 Oncotarget Result HBV N139K 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtN248H mutation was high (70%). 2016 Oncotarget Result HBV N248H 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The results in Figure 5B demonstrated that patient 5 harbored the rtA181T (1.2%), rtN236T (1.8%), rtS202G (1.1%), and rtM204I/V (1.1%) substitutions, and other resistance mutations were present at low levels (<1%) at baseline. 2016 Oncotarget Result HBV A181T;N236T;M204I;M204V;S202G 68;84;120;120;100 73;89;127;127;105 RT;RT;RT;RT 66;82;98;118 68;84;100;120 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The rtR153Q mutation was always present at a high frequency (70%). 2016 Oncotarget Result HBV R153Q 6 11 RT 4 6 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. This phenomenon usually appeared in non-resistance mutations of rtS223A (ranging from 79.67% to 4.41%) and rtN248H (ranging from 72.38% to 5.03%) (Figure 5B). 2016 Oncotarget Result HBV S223A;N248H 66;109 71;114 RT;RT 64;107 66;109 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. A calculation of the accessibility surface area (ASA) showed that the surface accessibility of the G145R mutant HBsAg was reduced upon G145R substitution. 2016 Hepatitis monthly Result HBV G145R;G145R 99;135 104;140 S;S;S 112;35;70 117;42;77 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. A decrease in the mutant HBsAg ASA suggests that the G145R mutation converts the HBsAg structure to a compact configuration with buried functional segments, such as epitopes. 2016 Hepatitis monthly Result HBV G145R 53 58 S;S 25;81 30;86 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. A secondary structure analysis of the G145R mutant revealed that this substitution inserted a new beta-strand at the 121 - 124 position (Figure 1). 2016 Hepatitis monthly Result HBV G145R 38 43 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. An analysis of the transmembrane regions revealed that the number of transmembrane helices in the G145R mutant was not altered compared to the wild-type. 2016 Hepatitis monthly Result HBV G145R 98 103 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. An evaluation of the protein antigenicity revealed that the antigenic potential of G145R mutant HBsAg was reduced compared to the wild-type (Figure 7). 2016 Hepatitis monthly Result HBV G145R 83 88 S 96 101 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Figure 5A represents the structural alignment of the G145R mutant and wild-type HBsAg. 2016 Hepatitis monthly Result HBV G145R 53 58 S 80 85 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R Mutation Alters the Secondary Structure and Membrane Orientation of the HBsAg. 2016 Hepatitis monthly Result HBV G145R 0 5 S 78 83 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R Mutation Decreases the Binding Affinity of the HBsAg to the MAb12. 2016 Hepatitis monthly Result HBV G145R 0 5 S 53 58 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R Mutation Reduces the Antigenic Potential of the HBsAg. 2016 Hepatitis monthly Result HBV G145R 0 5 S 54 59 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. However, the differences between the secondary structure of the G145R mutant and the wild-type HBsAg at all other regions of the protein were extensively subtle. 2016 Hepatitis monthly Result HBV G145R 64 69 S 95 100 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. However, the orientation of transmembrane segments between the G145R mutant and wild-type was clearly different, suggesting the possible impact of the G145R mutation on the altered localization of the mutant HBsAg within the ER membrane. 2016 Hepatitis monthly Result HBV G145R;G145R 63;151 68;156 S 208 213 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Interestingly, the flexibility of the mutant HBsAg, especially in the antigenic regions, was considerably reduced, indicating that the G145R mutation resulted in increased protein rigidity (Figure 9), which makes the HBsAg unsuitable for interacting with antibodies. 2016 Hepatitis monthly Result HBV G145R 135 140 S;S 45;217 50;222 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Molecular docking showed that the G145R mutation caused a noticeable decreased binding affinity between the HBsAg and MAb12. 2016 Hepatitis monthly Result HBV G145R 34 39 S 108 113 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The "a" determinant region in the wild-type and G145R mutants is positioned at the ER lumen and in the cytoplasmic area, respectively (Figure 2). 2016 Hepatitis monthly Result HBV G145R 48 53 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The ASA of the side chains in the wild-type and the G145R mutant were 13,219.2 and 13,017.8 A 2, respectively. 2016 Hepatitis monthly Result HBV G145R 52 57 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The Effect of G145R Substitution on the 3D Structure of the HBsAg. 2016 Hepatitis monthly Result HBV G145R 14 19 S 60 65 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The results demonstrated that the G145R mutation likely reduced the number of H-bonds through residue-residue approximation constraints with adjacent amino acids. 2016 Hepatitis monthly Result HBV G145R 34 39 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The RMSD plots of the wild-type and G145R mutant HBsAg revealed that the G145R mutation further stabilized the HBsAg's structure (Figure 8A). 2016 Hepatitis monthly Result HBV G145R;G145R 36;73 41;78 S;S 49;111 54;116 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The very low RMSD value (0.38) and the high TM-score (0.99) that resulted from the structural alignment demonstrate that the G145R mutant and wild-type HBsAg have almost the same folding character. 2016 Hepatitis monthly Result HBV G145R 125 130 S 152 157 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The wild-type and G145R mutant HBsAgs were bound to the MAb12 with weighted scores of -626.7 and -309.1, respectively, implicating the lower binding affinity of G145R mutant to MAb12 compared to wild type. 2016 Hepatitis monthly Result HBV G145R;G145R 18;161 23;166 S 31 37 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. To determine the structural dynamics of the wild-type and G145R mutant, the root mean square fluctuation (RMSF) of the Calpha of the HBsAg protein was compared between the trajectories generated at 300 K to gain an insight into the flexible nature of the G145R mutant compared with the wild-type. 2016 Hepatitis monthly Result HBV G145R;G145R 58;255 63;260 S 133 138 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Based on the ELISA and Western blot results, sE2G, sC69*, sL95W, sl98V and sG145R appeared to express significantly decreased HBsAg levels. 2017 Journal of hepatology Result HBV E2G;C69X;L95W;G145R 45;51;58;75 49;56;63;81 S;S;S;S;S;S 126;45;51;58;65;75 131;46;52;59;66;76 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Due to the overlapping nature of the S and RT gene regions, mutations in the S gene may result in concomitant mutations in RT, such as sC69*/rtS78T, sL98V/rtS106C and sG145R/rtR153Q, potentially affecting RT activity and HBV replication. 2017 Journal of hepatology Result HBV S78T;S106C;R153Q;C69X;L98V;G145R 143;157;176;135;149;167 147;162;181;140;154;173 RT;RT;RT;RT;RT;RT;S;S;S;S;S 43;123;141;155;174;205;37;77;135;149;167 45;125;143;157;176;207;38;78;136;150;168 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. HBV total RNA and pgRNA levels from sC69* and sG145R were significantly lower than WT. 2017 Journal of hepatology Result HBV C69X;G145R 36;46 41;52 S;S 36;46 37;47 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. However, intracellular HBsAg could be detected for all mutants except for sC69*, although the band intensities varied among different mutants. 2017 Journal of hepatology Result HBV C69X 74 79 S;S 23;74 28;75 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. However, some S gene mutations, e.g., sE2G/rtG10G and sL95W/rtV103V, do not result in AA changes in the RT due to the degeneracy of the genetic code. 2017 Journal of hepatology Result HBV G10G;V103V;E2G;L95W 45;62;38;54 49;67;42;59 RT;RT;RT;S;S;S 43;60;104;14;38;54 45;62;106;15;39;55 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. However, the sG24K and sT47A/K mutations did not significantly affect the extracellular and intracellular HBsAg levels compared to WT. 2017 Journal of hepatology Result HBV G24K;T47A;T47K 13;23;23 18;30;30 S;S;S 106;13;23 111;14;24 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. In addition, most mutants showed similar intracellular HBsAg band intensities to WT except for sL21R and sC69*, which were undetectable. 2017 Journal of hepatology Result HBV L21R;C69X 95;105 100;110 S;S;S 55;95;105 60;96;106 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. In this study, sG145R was used as a control for a mutation known to inhibit virion secretion and antibody detection and the YMHD RT mutation, to abolish RT activity and control for input plasmid DNA background. 2017 Journal of hepatology Result HBV G145R 15 21 RT;RT;S 129;153;15 131;155;16 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Interestingly, co-transfection of sE2G, sC69* and sG145R with pLMS showed higher extracellular HBV DNA levels as well. 2017 Journal of hepatology Result HBV E2G;C69X;G145R 34;40;50 38;45;56 S;S;S 34;40;50 35;41;51 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Most of the mutants showed lower extracellular HBsAg than WT except for sT47K/A. 2017 Journal of hepatology Result HBV T47K;T47A 72;72 79;79 S;S 47;72 52;73 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Our results showed that there was significantly less extracellular HBV DNA for sE2G, sC69*, sL98V and sG145R compared to WT (p < 0.05). 2017 Journal of hepatology Result HBV E2G;C69X;L98V;G145R 79;85;92;102 83;90;97;108 S;S;S;S 79;85;92;102 80;86;93;103 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. revealed previously identified immune escape mutations within the 'a' determinant region (sS117T, sK122R, sI126N/S/T, and sG145R), carboxyl terminal truncation mutations (sC69* and sW182*) and additional rarely described mutations (sE2G, sL21S, sR24K, sT47K/A, sL95W and sL98V). 2017 Journal of hepatology Result HBV S117T;K122R;I126N;I126S;I126T;G145R;C69X;W182X;E2G;L21S;R24K;T47K;T47A;L95W;L98V 90;98;106;106;106;122;171;181;232;238;245;252;252;261;271 96;104;116;116;116;128;176;187;236;243;250;259;259;266;276 S;S;S;S;S;S;S;S;S;S;S;S;S 67;90;98;106;122;171;181;232;238;245;252;261;271 81;91;99;107;123;172;182;233;239;246;253;262;272 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Specifically, mutations sE2G, sC69*, sL95W, sL98V and sG145R resulted in lower extracellular HBsAg levels compared to WT. 2017 Journal of hepatology Result HBV E2G;C69X;L95W;L98V;G145R 24;30;37;44;54 28;35;42;49;60 S;S;S;S;S;S 93;24;30;37;44;54 98;25;31;38;45;55 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Specifically, sL95W, sL98V and sG145R showed much lower intracellular HBsAg than WT. 2017 Journal of hepatology Result HBV L95W;L98V;G145R 14;21;31 19;26;37 S;S;S;S 70;14;21;31 75;15;22;32 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Taken together, these results show that the mutations decrease HBsAg levels by influencing either detection (Fig. 3C, sL21R) or secretion (sE2G, sC69*, sL95W, sl98V and sG145R) (Fig. 4B). 2017 Journal of hepatology Result HBV L21R;E2G;C69X;L95W;G145R 118;139;145;152;169 123;143;150;157;175 S;S;S;S;S;S;S 63;118;139;145;152;159;169 68;119;140;146;153;160;170 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. The intracellular HBV DNA from the mutants sC69* and sG145R but not sE2G, sL95W and sL98V was significantly lower than WT, respectively. 2017 Journal of hepatology Result HBV C69X;G145R;E2G;L95W;L98V 43;53;68;74;84 48;59;72;79;89 S;S;S;S;S 43;53;68;74;84 44;54;69;75;85 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. The potential factors might include the altered RT activities of rtS78T/sC69* and rtR153Q/sG145R, the altered stabilities of mutant mRNAs, the replenishment efficacies of cccDNA pool and so on. 2017 Journal of hepatology Result HBV C69X;G145R;S78T;R153Q 72;90;67;84 77;96;71;89 RT;RT;RT;S;S 48;65;82;72;90 50;67;84;73;91 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. the reduced amounts of HBV mRNAs from sC69* and sG145R might reflect the net effects of many factors. 2017 Journal of hepatology Result HBV C69X;G145R 38;48 43;54 S;S 38;48 39;49 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. To note, 75.00% (9/12) of their sequences harbor one or two of our newly identified SHBs mutations (sL21R, sT47K, sL95W, sK122R, sI126T, sG145R and sW182*) (Supplementary Table 2). 2017 Journal of hepatology Result HBV L21R;T47K;L95W;K122R;I126T;G145R;W182X 100;107;114;121;129;137;148 105;112;119;127;135;143;154 S;S;S;S;S;S;S;S 100;107;114;121;129;137;148;84 101;108;115;122;130;138;149;88 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. To study whether the S mutants influence HBsAg levels, we introduced individual mutations (sE2G, sL21R, sG24K, sT47A, sT47K, sC69*, sL95W, sL98V, and sG145R) in the background of HBV plasmid pBB4.5 1.2/PC. 2017 Journal of hepatology Result HBV E2G;L21R;G24K;T47A;T47K;C69X;L95W;L98V;G145R 91;97;104;111;118;125;132;139;150 95;102;109;116;123;130;137;144;156 S;S;S;S;S;S;S;S;S;S;S 41;21;91;97;104;111;118;125;132;139;150 46;22;92;98;105;112;119;126;133;140;151 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. we conclude that mutants sE2G, sL95W and sL98V might negatively influence HBV virion secretion and mutants sC69* and sG145R may influence HBV replication. 2017 Journal of hepatology Result HBV E2G;L95W;L98V;C69X;G145R 25;31;41;107;117 29;36;46;112;123 S;S;S;S;S 25;31;41;107;117 26;32;42;108;118 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. In addition, some other mutations were observed in the S promoter region and CCAAT box including V80I in 7 (8.5 %) cases and S90T in 6 (7.3 %) strains. 2016 Infectious agents and cancer Result HBV V80I;S90T 97;125 101;129 S promoter 55 65 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The distribution of substitutions in pres1 region, shown 8.5 % (7/82) of mutations observed were located in B-cell and T-cell region and in hepatocyte binding site including R38K (17.1 %), H44L (13.4 %) and N29K (9.8 %). 2016 Infectious agents and cancer Result HBV R38K;H44L;N29K 174;189;207 178;193;211 PreS1 37 42 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The most prevalent variant were R38K found in 14 (17.1 %) sequences, following by H44L in 11 (13.4 %), K13E in 8 (9.8 %), N29K in 8 (9.8 %), A35E in 8 (9.8 %), V80I in 7 (8.5 %) and in 6 (7.3 %) sequences for S90T (Table 2). 2016 Infectious agents and cancer Result HBV R38K;H44L;K13E;N29K;A35E;V80I;S90T 32;82;103;122;141;160;209 36;86;107;126;145;164;213 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The sequences with A35E and H44L amino acid substitutions were significantly more frequent in cases with LCC and HCC infection than in other patients groups (P < 0.05). 2016 Infectious agents and cancer Result HBV A35E;H44L 19;28 23;32 Liver cirrhosis 105 108 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. There was no significant difference between substitutions V80I and S90T found in S promoter region with clinical status. 2016 Infectious agents and cancer Result HBV V80I;S90T 58;67 62;71 S promoter 81 91 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. These mutations were observed among different clinical groups; In the 11 sequences with R38K (17.1 %, 14/82) substitutions, high rate were observed in patients with LC (35.7 %, 5/14) and HCC (28.6 %, 4/14). 2016 Infectious agents and cancer Result HBV R38K 88 92 Hepatocellular carcinoma;Liver cirrhosis 187;165 190;167 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. On the other hand, there were several amino acid mutations like K122R (amino acid Lysine at 122 position of S protein instead of Arginine), T131S and I208T in genotype C. 2016 SpringerPlus Result HBV K122R;T131S;I208T 64;140;150 69;145;155 S 108 109 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Several mutations were observed in 'a' determinant region of S gene such as, T118V, T125M, T126I, P127T, A128V and T/S143L/M according to different genotypes of HBV (Table 1). 2016 SpringerPlus Result HBV T143L;T143M;S143L;S143M;T118V;T125M;T126I;P127T;A128V 115;115;115;115;77;84;91;98;105 124;124;124;124;82;89;96;103;110 S;S 36;61 50;62 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Among 99 HCC cases with success sequence data, 11 HCC cases with adequate sequential serum samples were selected for this longitudinal investigation of specific mutation patterns (A2159G, A2189Y, G2203W, and C2288R mutations). 2016 International journal of molecular sciences Result HBV A2159G;A2189Y;G2203W;C2288R 180;188;196;208 186;194;202;214 Hepatocellular carcinoma;Hepatocellular carcinoma 9;50 12;53 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Among these, 10 were point mutations, two (pre-S2 start codon mutation and pre-S deletion) were located in the pre-S gene, four (G1613A, C1653T, A1762T, and G1764A mutations) were located in the X gene, and four (A2159G, A2189Y, G2203W, and C2288R mutations) were in the C gene. 2016 International journal of molecular sciences Result HBV G1613A;C1653T;A1762T;G1764A;A2159G;A2189Y;G2203W;C2288R 129;137;145;157;213;221;229;241 135;143;151;163;219;227;235;247 C;PreS;PreS;PreS2;X 271;75;111;43;195 272;80;116;49;196 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. However, G1613A (OR, 1.769; 95% CI, 0.932-3.358) and pre-S2 start codon (OR, 2.233; 95% CI, 0.795-6.274) mutations were not related to a higher risk of developing HCC. 2016 International journal of molecular sciences Result HBV G1613A 9 15 PreS2 53 59 Hepatocellular carcinoma 163 166 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. In the current study, the risk of combined mutations in the C gene on HCC was explored, including the A2159G, A2189Y, G2203W, and C2288R mutations. 2016 International journal of molecular sciences Result HBV A2159G;A2189Y;G2203W;C2288R 102;110;118;130 108;116;124;136 C 60 61 Hepatocellular carcinoma 70 73 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Meanwhile, the frequencies of hot-spot mutations in the C gene increased in the HCC group, from 6.1% (deletion), 15.2% (T1938C), 11.1% (C2002T), 13.1% (T2045A), 35.4% (A2159G), 40.4% (A2189Y), 10.1% (G2203W), and 22.2% (C2288R) in HCC cases to 2.0%, 7.1%, 7.1%, 14.3%, 20.4%, 22.4%, 2.0%, and 11.2% in controls, respectively. 2016 International journal of molecular sciences Result HBV T1938C;C2002T;T2045A;A2159G;A2189Y;G2203W;C2288R 120;136;152;168;184;200;220 126;142;158;174;190;206;226 C 56 57 Hepatocellular carcinoma;Hepatocellular carcinoma 80;231 83;234 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Similar to the results from initial full genome analysis, HCC patients had significantly higher frequencies of A2159G, A2189Y, G2203W, and C2288R mutations than controls (p = 0.020, p = 0.006, p = 0.037, and p = 0.030, respectively). 2016 International journal of molecular sciences Result HBV A2159G;A2189Y;G2203W;C2288R 111;119;127;139 117;125;133;145 Hepatocellular carcinoma 58 61 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Therefore, using stepwise logistic regression analysis, the following were found to be independent risk factors of HCC: A2159G (OR, 2.037; 95% CI, 1.033-4.015), A2189Y (OR, 2.833; 95% CI, 1.453-5.526), pre-S deletion (OR, 2.272; 95% CI, 1.037-4.979), and A1762T/G1764A double mutations (OR, 2.333; 95% CI, 1.240-4.390) (Table 4). 2016 International journal of molecular sciences Result HBV G1764A;A2159G;A2189Y;A1762T 262;120;161;255 268;126;167;261 PreS 202 207 Hepatocellular carcinoma 115 118 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. These include some well-studied mutations, such as pre-S2 start codon mutation, pre-S deletion, C1653T, T1753V, A1762T/G1764A, and G1896A mutations. 2016 International journal of molecular sciences Result HBV G1764A;C1653T;T1753V;A1762T;G1896A 119;96;104;112;131 125;102;110;118;137 PreS;PreS2 80;51 85;57 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. When we examined HBV DNA sequences in the pre-S and Enh II/BCP regions, pre-S deletion, C1653T, and A1762T/G1764A, double mutations were significantly associated with HCC, showing adjusted ORs from 1.929 to 2.385 (Table 3). 2016 International journal of molecular sciences Result HBV G1764A;C1653T;A1762T 107;88;100 113;94;106 BCP;Enh II;PreS;PreS 59;52;42;72 62;58;47;77 Hepatocellular carcinoma 167 170 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. Mutations rtV173L, rtL180M, rtM204V conferring resistance to lamivudine and other L-nucleoside analogues were identified in six patients while one patient had the rtL180M + rtM204V + rtT184S mutations associated with resistance to both L-nucleoside analogues and entecavir. 2016 Virology journal Result HBV V173L;L180M;M204V;L180M;M204V;T184S 12;21;30;165;175;185 17;26;35;170;180;190 RT;RT;RT;RT;RT;RT 10;19;28;163;173;183 12;21;30;165;175;185 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. The most prevalent mutations observed were found either in the 'a' region (L127P, S140T and S143T) or the B cell epitope and its surrounding region (G159A, F161Y and A168V). 2016 Virology journal Result HBV L127P;S140T;S143T;G159A;F161Y;A168V 75;82;92;149;156;166 80;87;97;154;161;171 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Age, gender, HBV DNA level, HBeAg, HBV genotype (genotype C), and transmission route (MTCT) were evaluated for association with the detection of G145R. 2016 PloS one Result HBV G145R 145 150 C 28 33 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. All of the 13 patients had the G145R mutant as a minor population. 2016 PloS one Result HBV G145R 31 36 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. All of the 4 pregnant women with the G145R mutant were positive for HBeAg, infected with genotype C and showed a high viral load (7.8 log copies/mL or more) before delivery. 2016 PloS one Result HBV G145R 37 42 C 68 73 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Although HBeAg-positive status showed a close association with the G145R mutant, univariate analysis revealed that there was no significant association between HBeA-positive status and detection of the G145R mutant (p = 0.07). 2016 PloS one Result HBV G145R;G145R 67;202 72;207 C 9 14 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Although immunoprophylaxis failure was related to the detection of the G145R mutant, there was no significant difference in the positive rate from real-time PCR between the two cohorts (OR value = 2.74, 95% CI: 0.93-8.10, P = 0.06). 2016 PloS one Result HBV G145R 71 76 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. As shown in Table 4, thirty-two patients, who were evaluated by deep sequencing, were classified into 4 groups: (A) breakthrough with LNA negative; n = 18, (B) breakthrough with LNA positive; n = 4, (C) control with LNA positive; n = 7, and (D) breakthrough with G145R major or G145K major; n = 3. 2016 PloS one Result HBV G145R;G145K 263;278 268;283 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Because the remaining patient had the G145K (GGA AAA) mutant as a major strain, which was confirmed by direct sequencing, the frequency of the G to A change at nt.587 was 98.6%. 2016 PloS one Result HBV G587A;G145K 143;38 166;43 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Deep sequencing showed that the proximal mutations (amino acid position;143 and 144) of G145R were more detectable in G145R LNA-positive patients than in G145R LNA-negative patients. 2016 PloS one Result HBV G145R;G145R;G145R 88;118;154 93;123;159 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Deep sequencing was performed in all of the 25 patients who belonged to the breakthrough cohort and the 7 patients belonging to the control cohort who were positive for the LNA-based probe real-time PCR, but in whom the G145R mutant was not confirmed by cloning of a PCR product. 2016 PloS one Result HBV G145R 220 225 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, multivariate analysis showed that the positivity of HBeAg was not significantly associated with detection of the G145R mutant (p = 0.12). 2016 PloS one Result HBV G145R 122 127 C 61 66 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, the remaining 3 patients were negative for the G145R mutant based on the cloning and sequencing of PCR products in our previous study. 2016 PloS one Result HBV G145R 56 61 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, the T/I126S mutant was undetectable in the breakthrough cohort with the G145R/K mutant as a major population. 2016 PloS one Result HBV I126S;T126S;G145R;G145K 13;13;81;81 20;20;88;88 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In contrast to the LNA-based probe real-time PCR-positive patients, the frequency of the G145R mutation ranged from 0% to 0.0007% in 18 of 19 patients who were negative for the real-time PCR. 2016 PloS one Result HBV G145R 89 94 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In contrast, the T/I126S mutant was detected in 4 (22%) of 18 patients who were negative for the LNA-based probe real-time PCR in the breakthrough cohort. 2016 PloS one Result HBV I126S;T126S 17;17 24;24 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In one patient, who was positive for the LNA-based probe real-time PCR, the frequency of the G145R mutation was 0.25%, which was not considered to be valid. 2016 PloS one Result HBV G145R 93 98 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In our previous study, the presence of the G145R mutant was evaluated by cloning the PCR product. 2016 PloS one Result HBV G145R 43 48 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In the breakthrough cohort, the T/I126S mutant showed the second highest frequency. 2016 PloS one Result HBV I126S;T126S 32;32 39;39 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Moreover, deep sequencing could not detect the G145K mutant in the mother whose child was infected with the G145K as a major population. 2016 PloS one Result HBV G145K;G145K 47;108 52;113 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Moreover, we confirmed that the LNA-based probe real-time PCR could detect 1,000 copies/mL or more in both wild-type and G145R mutant-type plasmid DNA. 2016 PloS one Result HBV G145R 121 126 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. None of patients belonging to the control cohort showed evidence of the G145R mutant. 2016 PloS one Result HBV G145R 72 77 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the 25 patients belonging to the breakthrough cohort, however, 2 (8%) had the G145R mutant (GGA AGA) and one (4%) had the G145K mutant (GGA AAA). 2016 PloS one Result HBV G145R;G145K 81;125 86;130 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the 25 patients in the breakthrough cohort, 6 showed that the frequency of the G145R mutation (nucleotide position at 587: G A) was 0.4% or more (Table 3); all of these patients showed positive results for the LNA-based probe real-time PCR. 2016 PloS one Result HBV G145R 82 87 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the 31 pregnant women, 4 (12.9%) showed positive results for the LNA-based probe real-time PCR, and all of them had the G145R mutant as a minor population. 2016 PloS one Result HBV G145R 123 128 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the 7 patients belonging to the control cohort, the frequency of the G145R mutation was 0.4% or more in all but one. 2016 PloS one Result HBV G145R 72 77 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the remaining 3 pregnant women, one had a 3 year-old child who was infected with G145R as a major form despite immunoprophylaxis (No. 2016 PloS one Result HBV G145R 84 89 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the two patients who had the G145G mutant as a predominant strain (patient Nos. 2016 PloS one Result HBV G145G 32 37 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of these 10 patients, 7 (breakthrough cohort;1, control cohort; 6) were already confirmed to have the G145R mutant as a minor form in the previous study. 2016 PloS one Result HBV G145R 102 107 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of these 6 patients, 2 had the G145R mutant as a major strain, which was consistent with the results of direct sequencing. 2016 PloS one Result HBV G145R 31 36 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. One was the confirmation of the existence of the G145R mutant as a minor strain. 2016 PloS one Result HBV G145R 49 54 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Similarly, when the G145R mutant-type plasmid DNA (5x1010 copies/mL) was applied in real-time PCR, the wild-type was also undetectable. 2016 PloS one Result HBV G145R 20 25 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Table 1 shows the predictive factors for the detection of the G145R mutant. 2016 PloS one Result HBV G145R 62 67 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The emergence of the G145R mutant showed a positive association with the amino acid mutations in the "a" determinant region. 2016 PloS one Result HBV G145R 21 26 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The frequency of G145R ranged from 0.42% to 4.10%. 2016 PloS one Result HBV G145R 17 22 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The frequency of the G145R mutation ranged from 0.54% to 6.58% in 4 patients belonging to the breakthrough cohort with the G145R mutant as a minor strain. 2016 PloS one Result HBV G145R;G145R 21;123 26;128 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The G145R mutant was also undetectable in the remaining 3 mothers by deep sequencing. 2016 PloS one Result HBV G145R 4 9 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The G145R mutant/wild HBV DNA ratio ranged from 1.5% to 60%, and the frequency of the G145R mutation evaluated by deep sequencing ranged from 1.5% to 23.8%. 2016 PloS one Result HBV G145R;G145R 4;86 9;91 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The highest frequency of amino acid changes was observed in children with the G145R/K mutant as a major population. 2016 PloS one Result HBV G145R;G145K 78;78 85;85 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The outcome of infants born to HBV carriers with G145R is shown in Table 6. 2016 PloS one Result HBV G145R 49 54 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The predictive factors of G145R in the pregnant women are shown in Table 5. 2016 PloS one Result HBV G145R 26 31 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The quantifications of wild-type DNA and G145R mutant DNA were performed in the 19 patients who showed positive results for the LNA-based probe real-time PCR. 2016 PloS one Result HBV G145R 41 46 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The ratio of G145R mutant DNA to wild-type DNA (mutant/wild ratio) is shown in Table 3. 2016 PloS one Result HBV G145R 13 18 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The remaining 17 patients had the G145R mutant as a minor population and the mutant/wild ratio ranged from 2% to 50%. 2016 PloS one Result HBV G145R 34 39 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The remaining 4 patients had the G145R mutant as a minor strain. 2016 PloS one Result HBV G145R 33 38 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The wild-type and G145R mutant plasmids were mixed in the 25-muL PCR mixture as follows: (A) wild:mutant = 2:1, the wild-type [2x108 copies/mL] and the mutant-type [1x108copies/mL] were mixed, (B) wild:mutant = 20:1, the wild-type [2x108 copies/mL] and the mutant-type [1x107copies/mL] were mixed, (C) wild:mutant = 200:1, the wild-type [2x108 copies/mL] and the mutant-type [1x106 copies/mL] were mixed, and (D) wild:mutant = 2,000:1, the wild-type [2x108 copies/mL] and the mutant-type [1x105 copies/mL] were mixed. 2016 PloS one Result HBV G145R 18 23 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Then, we evaluated the discrimination ability of the LNA-base probe between wild-type and G145R plasmid DNA in the mixture of wild-type and G145R mutant DNA. 2016 PloS one Result HBV G145R;G145R 90;140 95;145 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings indicated that LNA-based probe real-time PCR could accurately detect the G145R mutant as a minor population. 2016 PloS one Result HBV G145R 88 93 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings suggest that pre-existence of the G145R mutant as a minor strain in pregnant mothers did not always cause breakthrough infection in children. 2016 PloS one Result HBV G145R 49 54 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings suggested that G145R mutation tended to be accompanied with proximal mutations induced by the host immunological pressure. 2016 PloS one Result HBV G145R 30 35 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings suggested that strong immunological pressure influencing the entire "a" determinant region was needed to produce the G145R/K mutant as a major population. 2016 PloS one Result HBV G145R;G145K 132;132 139;139 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings suggested that the LNA-based probe real-time PCR was superior to the cloning technique in the detection of the G145R mutant and could distinguish the G145R mutant existing as a low percentage of the excessive wild-type viral population. 2016 PloS one Result HBV G145R;G145R 126;165 131;170 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. To evaluate the specificity of the LNA based probe, wild-type and G145R mutant type (nucleotide position at 587: G A) recombinant plasmid DNA were used for the LNA-based probe real-time PCR. 2016 PloS one Result HBV G145R 66 71 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Univariate analysis showed that the positivity of HBeAg had a close association with the detection of the G145R mutant (p = 0.05). 2016 PloS one Result HBV G145R 106 111 C 50 55 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Univariate analysis showed that there was no predictive factor for the detection of G145R in the breakthrough cohort (Table 2). 2016 PloS one Result HBV G145R 84 89 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. We retrospectively evaluated 4 of 6 HBV carrier mothers whose children were positive for the LNA-based probe real-time PCR in the breakthrough cohort (G145R major strain; No. 2016 PloS one Result HBV G145R 151 156 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. When wild-type plasmid DNA (2x1011 copies/mL) was applied to real-time PCR, the G145R mutant was undetectable. 2016 PloS one Result HBV G145R 80 85 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. However, we found that the medium/low MBL2 group has higher mutation rate in T1653, T1674, T1753, A1726T and G1764A when being compared with high MBL2 group, and significance was observed (Table 3 and Figure 2). 2016 Aging Result HBV A1726T;G1764A 98;109 104;115 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. Importantly, 3 mutations (S101L, L165F, S96S/A) located in known T-/B-cell epitopes in Pre-S region. 2016 PloS one Result HBV S101L;L165F;S96S;S96A 26;33;40;40 31;38;46;46 PreS 87 92 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. The most common immune escape mutation, G145R, was found in none. 2016 PloS one Result HBV G145R 40 45 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. The exclusive detection of subgenotype A2 sequences with the abovementioned substitutions in the PBL clearly suggest the selective advantage of the pgRNA with 358C and 587A, and in turn the importance of G145R immune escape mutation in the PBL compartment. 2016 World journal of virology Result HBV G145R 204 209 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. Q62R, N76D, S78T, L91I, R110G, V112A, A113V/S, L115V, S119P, Q125R, M129L, N131D/S, S135Y, L145M, G152R, V173A/L, S180P. 2016 Hepatitis monthly Result HBV Q62R;N76D;S78T;L91I;R110G;V112A;A113V;A113S;L115V;S119P;Q125R;M129L;N131D;N131S;S135Y;L145M;G152R;V173A;V173L;S180P 0;6;12;18;24;31;38;38;47;54;61;68;75;75;84;91;98;105;105;114 4;10;16;22;29;36;45;45;52;59;66;73;82;82;89;96;103;112;112;119 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The Q149K was the most frequently identified amino acid substitution observed in these isolates (9.83%), followed by L122F (8.19%), N118D/T (6.55%), L157M (4.91%), and H124Y (3.27%). 2016 Hepatitis monthly Result HBV Q149K;L122F;N118D;N118T;L157M;H124Y 4;117;132;132;149;168 9;122;139;139;154;173 27882070 Serological Patterns and Molecular Characterization of Occult Hepatitis B Virus Infection among Blood Donors. The well-known G145A/R variant was not observed. 2016 Hepatitis monthly Result HBV G145A;G145R 15;15 22;22 27882070 Serological Patterns and Molecular Characterization of Occult Hepatitis B Virus Infection among Blood Donors. Variants were found in 30.4% (21/69) of cases with OBI and included S114T, G119R, P120S, T125M, C139Y, T140I, C147W, T148A, A159V/G, E164D, V168A and R169C. 2016 Hepatitis monthly Result HBV S114T;G119R;P120S;T125M;C139Y;T140I;C147W;T148A;A159V;A159G;E164D;V168A;R169C 68;75;82;89;96;103;110;117;124;124;133;140;150 73;80;87;94;101;108;115;122;131;131;138;145;155 Occult Hepatitis B 51 54 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Activation of miR-873 to target CSMD3 by pre-S/S-sW172* expression in hepatoma cell lines. 2016 Oncogenesis Result HBV W172X 49 55 PreS;S;S 41;47;49 46;48;50 Hepatocellular carcinoma 70 78 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Consistently, a higher percentage of positive cells was found for all three Tg mice compared with that of the null mice and a higher percentage was observed for TgsW172*-H mice compared with that of TgWT-H mice. 2016 Oncogenesis Result HBV W172X 163 169 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Despite a significantly increased number of apoptotic cells in TgSW172*-H mice compared with that of TgWT-H mice (Figure 2a), both lines shared similar profiles of ER stress response, increased apoptosis and increased hepatocyte proliferation. 2016 Oncogenesis Result HBV W172X 65 71 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Development of HCC in TgSW172* mice. 2016 Oncogenesis Result HBV W172X 24 30 Hepatocellular carcinoma 15 18 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. In total, 27, 27, 24 and 26 transgenic mice (TgWT-L, TgWT-H, TgSW172*-L and TgSW172*-H, respectively) were examined. 2016 Oncogenesis Result HBV W172X;W172X 63;78 69;84 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. It was found that no HCC developed in TgWT-H and L mice, whereas 2 (8.3%) and 6 (23.1%) of TgSW172*-L and TgSW172*-H mice, respectively, developed HCC (TgWT versus TgSW172*, P=0.0021) (Table 1). 2016 Oncogenesis Result HBV W172X;W172X;W172X 93;108;166 99;114;172 Hepatocellular carcinoma;Hepatocellular carcinoma 21;147 24;150 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Low level of serum HBsAg (10.2+-19.1 IU/ml) was detected in TgSW172*-H mice, whereas serum HBsAg was undetectable in TgSW172*-L mice. 2016 Oncogenesis Result HBV W172X;W172X 62;119 68;125 S;S 19;91 24;96 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Small amounts of truncated S proteins (St), gp18 and gp22, were detected (Figure 1d, left panel) in TgSW172*-L and H mice. 2016 Oncogenesis Result HBV W172X 102 108 S 27 28 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. TgSW172*-L and TgSW172*-H carried HBV pre-S/S gene containing the sW172* mutation and expressed low and high levels of intrahepatic HBsAg respectively, determined by western blot and immunohistochemistry (IHC) analysis (Figures 1c-e). 2016 Oncogenesis Result HBV W172X;W172X;W172X 2;17;66 8;23;72 S;PreS;S;S 132;38;44;66 137;43;45;67 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. These results indicated that pre-S/S-sW172* could upregulate miR-873 expression in at least two hepatoma cell lines (Hepa1-6 and HepY2). 2016 Oncogenesis Result HBV W172X 37 43 PreS;S;S 29;35;37 34;36;38 Hepatocellular carcinoma 96 104 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. To further clarify the regulation cascade, pTg-sW172* was transfected into BNL, Hepa1-6, HepY2, Huh7, J7, and Mahlavu cells and miR-873 was assayed 3 days after transfection. 2016 Oncogenesis Result HBV W172X 47 53 S 47 48 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. To understand whether the increased ER stress in transgenic mice was caused by pre-S/S-sW172* alone or also by miR-873 upregulation, the GRP78 levels were also compared between hepatoma cells with or without miR-873 overexpression. 2016 Oncogenesis Result HBV W172X 87 93 PreS;S;S 79;85;87 84;86;88 Hepatocellular carcinoma 177 185 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. TUNEL assay to estimate the numbers of apoptotic cells in liver showed a significantly higher percentage of apoptotic cells in TgsW172*-H mice compared with that in TgWT-H mice (Figures 2a and b). 2016 Oncogenesis Result HBV W172X 129 135 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Western blot analysis confirmed CSMD3 downregulation in TgSW172*-H and L mice, but not in TgWT-H mice (Figure 3c). 2016 Oncogenesis Result HBV W172X 58 64 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Western blot analysis using monoclonal antibody against HBsAg detected small surface (S) proteins, gp24 and gp27, only in TgWT-L and H mice but not in TgSW172*-L and H mice (Figure 1c, left panel). 2016 Oncogenesis Result HBV W172X 153 159 S;S;S 56;86;71 61;87;84 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As compared to negative control pcDNA3.1 transfected cells, the relative luciferase activity of CpLUC increased 40% in pcDNA-HBs(sW172*) transfected cells; but no obvious change was observed in either pcDNA-HBs(wt) or pcDNA-HBs (sW172L) transfected cells. 2016 Scientific reports Result HBV W172X;W172L 129;229 135;235 S;S;S;S;S 125;207;224;129;229 128;210;227;130;230 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As compared to wild-type pHBV4.1 transfected cells, both the supernatant HBsAg and HBV DNA levels decreased significantly in pHBV-rtA181T/sW172* transfected cells, but not that obvious in pHBV-rtA181T/sW172L transfected cells(Fig. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 138;201;132;195 144;207;137;200 S;RT;RT;S;S 73;130;193;138;201 78;132;195;139;202 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. But in respect to supernatant HBeAg titre, there was no significant difference among wild-type pHBV4.1, pHBV-rtA181T/sW172* or pHBV-rtA181T/sW172L transfected cells(Fig. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 117;140;111;134 123;146;116;139 C;RT;RT;S;S 30;109;132;117;140 35;111;134;118;141 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. For the cellular HBV DNA replication intermediates, there was a small decline in both pHBV-rtA181T/sW172* and pHBV-rtA181T/sW172L transfected cells as compared to wild-type pHBV4.1 transfected cells(Fig. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 99;123;93;117 105;129;98;122 RT;RT;S;S 91;115;99;123 93;117;100;124 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, the levels of HBsAg were extremely lower in pHBV-rtA181T/sW172* injected mice, and no peak was observed. 2016 Scientific reports Result HBV W172X;A181T 66;60 72;65 S;RT;S 23;58;66 28;60;67 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, the levels of HBV DNA replication intermediates in pHBV-rtA181T/sW172* injected mice maintained high for 15 days, which is significantly different from that in either wild-type pHBV4.1 or pHBV-rtA181T/sW172L injected mice. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 73;210;67;204 79;216;72;209 RT;RT;S;S 65;202;73;210 67;204;74;211 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, the serum levels of HBV DNA in pHBV-rtA181T/sW172* injected mice were significantly lower than that of either wild-type pHBV4.1 or pHBV-rtA181T/sW172L injected mice. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 53;153;47;147 59;159;52;152 RT;RT;S;S 45;145;53;153 47;147;54;154 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In contrast, the number of HBsAg staining cells in pHBV-rtA181T/sW172* injected mice was significantly increased, and the signal strength of HBsAg staining was also significantly high from day 3 to day 15. 2016 Scientific reports Result HBV W172X;A181T 64;58 70;63 S;S;RT;S 27;141;56;64 32;146;58;65 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In liver tissue of wild-type pHBV4.1 or pHBV-rtA181T/sW172L injected mice, the number of HBsAg staining cells reached its peak on day 3, reduced since day 5 and became scarce from day 10 to day 15. 2016 Scientific reports Result HBV W172L;A181T 53;47 59;52 S;RT;S 89;45;53 94;47;54 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Interesting, at the day 5 to day 15, serum HBeAg levels in pHBV-rtA181T/sW172* injected mice were significant higher than that in either wild-type pHBV4.1 or pHBV-rtA181T/sW172L injected mice(Fig. 2016 Scientific reports Result HBV W172X;W172L;A181T;A181T 72;171;66;165 78;177;71;170 C;RT;RT;S;S 43;64;163;72;171 48;66;165;73;172 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. It is worth to mention that there was no statistical difference of the relative luciferase activity of either PS1pLUC, SpLUC or XpLUC among pcDNA-HBs(wt), pcDNA-HBs (sW172L) and pcDNA-HBs (sW172L) tranfected cells. 2016 Scientific reports Result HBV W172L;W172L 166;189 172;195 S;S;S;S;S 146;161;184;166;189 149;164;187;167;190 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Similar dynamic change trend was also observed in pHBV-rtA181T/sW172L injected mice, though the levels of HBsAg were relatively lower than that in wild-type pHBV4.1 injected mice. 2016 Scientific reports Result HBV W172L;A181T 63;57 69;62 S;RT;S 106;55;63 111;57;64 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Similar findings were also observed in pHBV-rtA181T/sW172L injected mice, though there seems to be weakened expression as compared to wild-type pHBV4.1. 2016 Scientific reports Result HBV W172L;A181T 52;46 58;51 RT;S 44;52 46;53 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The serum HBV DNA test results of the wild-type pHBV4.1 were 4.27 +- 0.16, 6.85 +- 0.15, 6.24 +- 0.35, 4.71 +- 0.44, 3.89 +- 0.05, 4.02 +- 0.08 log10 copies/mL on day 1, 3, 5, 7, 10, 15 respectively; the serum HBV DNA test results of the rtA181T/sW172* mutant strain were 4.11 +- 0.26, 4.17 +- 0.42, 3.46 +- 0.52, 3.47 +- 0.07, 3.30 +- 0.05, 2.90 +- 0.24 log10 copies/mL on day 1, 3, 5, 7, 10, 15 respectively; the serum HBV DNA test results of the rtA181T/sW172L mutant strain were 4.03 +- 0.27, 6.91 +- 0.19, 6.25 +- 0.40, 5.13 +- 0.04, 3.88 +- 0.12, 3.76 +- 0.21 log10 copies/ mL on day 1, 3, 5, 7, 10, 15 respectively There were no obvious differences in HBV DNA levels between wild-type pHBV4.1 and pHBV-rtA181T/sW172L injected mice. 2016 Scientific reports Result HBV W172X;W172L;W172L;A181T;A181T;A181T 246;457;717;240;451;711 252;463;723;245;456;716 RT;RT;RT;S;S;S 238;449;709;246;457;717 240;451;711;247;458;718 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Among the mutants tested in this analysis, the supernatants of W1S Q129R/G145R showed remarkably reduced reactivity both in the HBsAg ELISA and against the anti-tag Ab, probably due to the secretion defect as reported previously. 2017 PloS one Result HBV G145R;W1S;Q129R 73;63;67 78;66;72 S 128 133 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. And they clearly detected adr4 (wt; X01587) and W1S (wt) but unable to detect W3S (wt) like as mock infection. 2017 PloS one Result HBV W1S;W3S 48;78 51;81 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Based on the ELISA reactivity, the W1S and adr4 HBsAgs were clearly detected in both cell lysates and culture supernatants, whereas the W3S was undetectable using the same kit (Fig 3A). 2017 PloS one Result HBV W1S;W3S 35;136 38;139 S 48 54 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Five amino acid mutations were found at different positions within the MHR (amino acid residues 99 to 169) of W3S, compared to W1S (Fig 1B). 2017 PloS one Result HBV W3S;W1S 110;127 113;130 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. For this purpose, we constructed a series of synthetic mutants of W3S to observe their potential recovery of antigenicity; the mutants were based on the W1S amino acid sequence, because it was easily determined with ELISA kits (Fig 3A). 2017 PloS one Result HBV W3S;W1S 66;153 69;156 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. From the results shown above, lysine (K120) and aspartate (D123) would be expected to be very important for HBsAg antigenicity, since there was a huge reduction in W1S reactivity when the P120 and T123 were changed to K and D, respectively. 2017 PloS one Result HBV W1S 164 167 S 108 113 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. However, three other single amino acid-substituted mutants; C100Y, V134F and E185G did not show any effect on HBsAg antigenicity (Fig 5A). 2017 PloS one Result HBV C100Y;V134F;E185G 60;67;77 65;72;82 S 110 115 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Immunofluorescence and Western blot results demonstrated that all the above mutants of W3S were well-expressed and secreted into the culture medium (Fig 4A and 4B). 2017 PloS one Result HBV W3S 87 90 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Interestingly, the predicted antigenic index analysis of amino acid mutation at position 145 (G145R) altered the Ai of seventeen amino acids with a lesser degree of changes (-0.2 to +1.4). 2017 PloS one Result HBV G145R 94 99 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Interestingly, the W1S-aW3S mutant showed a higher glycosylation isoform as W3S HBsAg and vice versa and W3S-aW1S had an opposite phenotype (Fig 4A). 2017 PloS one Result HBV W1S;W3S;W3S 19;76;105 22;79;108 S 80 85 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Moreover, among the single mutants of W3S described above, only the W3S K120P and W3S D123T showed slight increases in the reactivity of HBsAg (Fig 5A). 2017 PloS one Result HBV W3S;W3S;W3S;K120P;D123T 38;68;82;72;86 41;71;85;77;91 S 137 142 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Next, we prepared different multiple mutants of W3S along with the single one to check the combined effects of multiple amino acid substitutions on the HBsAg antigenicity. 2017 PloS one Result HBV W3S 48 51 S 152 157 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. On the other hand, all the wt-HBsAgs (W1S, W3S and adr4) were clearly detected on a histidine binding assay plate (HIS-Select High Capacitty (HC) Nickel coated plates; Sigma-Aldrich) with the anti-Xpress mAb (Fig 3B) in addition to the reactivity against an anti-tag Ab in the Western blot (Fig 2A). 2017 PloS one Result HBV W1S;W3S 38;43 41;46 S 30 36 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. On the other hand, the mutation at position 134 with valine (F134V) affected only six surrounding amino acids with very minor changes of Ai (-0.4 to +0.3). 2017 PloS one Result HBV F134V 61 66 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. On the other hand, W1S P120K/T123D exhibited a complete loss of the reactivity (Fig 5B). 2017 PloS one Result HBV T123D;W1S;P120K 29;19;23 34;22;28 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Only one amino acid was affected (-0.05 to +0.15) due to the mutation at 146 in which asparagine was replaced with glycine (W1S N146G). 2017 PloS one Result HBV W1S;N146G 124;128 127;133 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Our results showed that the glycosylated isoform of W3S HBsAg from both the supernatants and the cell lysates was more predominant in the case of W3S, compared with the cases of W1S and adr4. 2017 PloS one Result HBV W3S;W3S;W1S 52;146;178 55;149;181 S 56 61 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Our Western blot analysis revealed that the level of the glycosylated isoform of the wt-W3S HBsAg was much greater than that of W1S. 2017 PloS one Result HBV W3S;W1S 88;128 91;131 S 92 97 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Since multiple amino acid residues within the MHR might be crucial for HBsAg antigenicity, we focused on identifying a specific amino acid residue(s) that played an important role in the complete loss of antigenicity of W3S HBsAg. 2017 PloS one Result HBV W3S 220 223 S;S 71;224 76;229 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Substitution of glutamine at position 129 with arginine (Q129R) altered the Ai of nine amino acids around this position with -0.4 to +1.85 magnitude, which might have led to a secretion defect of the HBs. 2017 PloS one Result HBV Q129R;Q129R 57;16 62;55 S 200 203 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The multiple amino acid substitutions were located both within the MHR of W3S and outside of it, resulting in the mutants W3S VDCR98-101LDYQ (V98L/C100Y/R101Q), K27T (K27T/VDCR98-101LDYQ), G204S (K27T/VDCR98-101LDYQ/G204S), and F213L (K27T/VDCR98-101LDYQ/G204S/F213L) (Fig 1B). 2017 PloS one Result HBV C100Y;R101Q;G204S;G204S;F213L;W3S;W3S;V98L;K27T;K27T;G204S;K27T;F213L;K27T 147;153;216;255;261;74;122;142;161;167;189;196;228;235 152;158;221;260;266;77;125;146;165;171;194;200;233;239 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The mutant W1S F134V showed no change in HBsAg antigenicity. 2017 PloS one Result HBV W1S;F134V 11;15 14;20 S 41 46 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The results showed that the W1S-aW3S mutant completely lost its reactivity, while the P120K and the T123D mutants exhibited a significant reduction in reactivity in the immunoassay (Fig 5A). 2017 PloS one Result HBV W1S;P120K;T123D 28;86;100 31;91;105 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The single amino acid-substituted mutations within the first antigenic loop, W1S P120K and W1S T123D, were predicted to affect ten of their surrounding amino acids (aa 114 to 124 for P120K and aa 116 to 126 for T123D) with Ai changes at a magnitude of -0.4 to +1.18 and -0.27 to +1.43, respectively. 2017 PloS one Result HBV W1S;W1S;P120K;T123D;P120K;T123D 77;91;81;95;183;211 80;94;86;100;188;216 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. These findings indicated that the three original HBsAgs (W1S, W3S and adr4) were well-expressed and secreted into the culture medium. 2017 PloS one Result HBV W1S;W3S 57;62 60;65 S 49 55 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Though we had thought that the higher glycosylation of W3S might affect the HBsAg antigenicity, the W3S N146G could not recover its antigenicity while the mutant W1S N146G showed only modestly reduced reactivity (Fig 5B). 2017 PloS one Result HBV W3S;W3S;W1S;N146G;N146G 55;100;162;104;166 58;103;165;109;171 S 76 81 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Three HBsAg cDNAs, namely W1S, W3S (subtype adr) and adr4 (subtype adr, genotype C), were cloned into a mammalian expression vector (pEBV His) and expressed by transient transfection in HEK293-T cells. 2017 PloS one Result HBV W1S;W3S 26;31 29;34 S 6 11 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Thus, we speculated that the impaired reactivity (antigenicity) of the W3S HBsAg might have been due to natural mutations in its amino acid sequence that occurred at different positions compared to those in the adr4 and W1S HBsAgs (Fig 1A). 2017 PloS one Result HBV W3S;W1S 71;220 74;223 S;S 75;224 80;230 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. To confirm the effect of amino acid mutations within the MHR, we replaced the amino acids of the MHR of the W1S HBsAg with those of the MHR of the W3S HBsAg, resulting in the mutant W1S-aW3S, and also tested the antigenicity of three single reverse mutants of W1S, i.e., P120K, T123D and F134V, to determine their effects on these specific positions. 2017 PloS one Result HBV W1S;W3S;W1S;W1S;P120K;T123D;F134V 108;147;182;260;271;278;288 111;150;185;263;276;283;293 S;S 112;151 117;156 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. We also generated different single amino acid-substituted mutants of W3S within the MHR at C100Y, K120P, D123T and V134F to investigate whether their specific and individual amino acid sequences had an effect on HBsAg antigenicity (Fig 1B), and another single amino acid-substituted mutant of W3S (E185G) outside the MHR of HBsAg to check its effect on antigenicity (Fig 1B). 2017 PloS one Result HBV W3S;W3S;C100Y;K120P;D123T;V134F;E185G 69;293;91;98;105;115;298 72;296;96;103;110;120;303 S;S 212;324 217;329 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. We first replaced the amino acid residues of MHR of W3S with W1S (W3S-aW1S). 2017 PloS one Result HBV W3S;W1S;W3S 52;61;66 55;64;69 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. We found natural mutations in the HBsAg-coding region of the W1S, W3S and adr4 by comparing them with other published sequences (Fig 1A), and the antigenicity of all three HBsAgs either from the transfected cell lysates or the culture supernatants was tested with commercially available ELISA kits. 2017 PloS one Result HBV W1S;W3S 61;66 64;69 S;S 34;172 39;178 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. We found that the antigenicity of the mutant W3S K120P/D123T was restored to a level nearly comparable to the antigenicity of W1S HBsAg (Fig 5B). 2017 PloS one Result HBV D123T;W3S;W1S;K120P 55;45;126;49 60;48;129;54 S 130 135 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. We therefore generated two double amino acid-substituted mutants, W3S K120P/D123T and W1S P120K/T123D, to test the simultaneous effect of amino acids at positions 120 and 123. 2017 PloS one Result HBV D123T;T123D;W3S;W1S;K120P;P120K 76;96;66;86;70;90 81;101;69;89;75;95 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. When a commercial immunoassay was used to measure the antigenic reactivity, only the (W3S-aW1S) mutant exhibited an almost complete recovery of antigenicity, whereas the antigenicities of the K120P and the D123T mutants were recovered to a much smaller degree (Fig 5A). 2017 PloS one Result HBV W3S;K120P;D123T 86;192;206 89;197;211 28103819 Telbivudine versus entecavir in patients with undetectable hepatitis B virus DNA: a randomized trial. Of these patients, genotypic resistance mutations to Telbivudine (M204I +/- L180M) were detected in seven during the virologic breakthrough. 2017 BMC gastroenterology Result HBV M204I;L180M 66;76 71;81 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. Mutation in the YMDD, M204V (methionine to valine) in 39.3 per cent and along with L180M (leucine to methionine) in 10.7 per cent was detected in the conserved regions C and B of reverse transcriptase (rt) domain of HBV polymerase, respectively, after 24 months of LAM therapy. 2016 The Indian journal of medical research Result HBV M204V;L180M 22;83 27;88 C;P;RT;RT;P 168;220;179;202;16 169;230;200;204;20 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. VBT on ADV monotherapy was noted in eight patients (33.3%), rtA181T and rtN236T mutants were detected alone in 8.1 and 8.3 per cent in the conserved regions B and D of rt region of HBV polymerase gene, respectively. 2016 The Indian journal of medical research Result HBV A181T;N236T 62;74 67;79 P;RT;RT;RT 185;60;72;168 195;62;74;170 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. All three mutants carrying sP203Q, sS210R, and sP203Q+sS210R determined a reduction of HBsAg secretion factor compared to wild-type at each time-point analyzed (P <0.05) (Figure 3A). 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 27;35;47;54 33;41;53;60 S;S;S;S;S 87;27;35;47;54 92;28;36;48;55 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. By analysing the overlapping between the HBsAg and RT genes, sP203Q did not result in any amino acid substitution in RT, while sS210R corresponded to rtS219A. 2017 Oncotarget Result HBV S219A;P203Q;S210R 152;61;127 157;67;133 S;RT;RT;RT;S;S 41;51;117;150;61;127 46;53;119;152;62;128 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Conversely, sS210R significantly correlated with an increased percentage of cells in the G2/M phase of cellular cycle (26+-8% for wild type versus 33+-6% for sS210R, P <0.001), thus supporting an induction of cell cycle progression and cell division (data not shown). 2017 Oncotarget Result HBV S210R;S210R 12;158 18;164 S;S 12;158 13;159 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Furthermore, multifocal HCC was found to occur more frequently in patients with either P203Q or S210R (4/8 [50%]) than in patients without these mutations (3/15 [20%]). 2017 Oncotarget Result HBV P203Q;S210R 87;96 92;101 Hepatocellular carcinoma 24 27 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Impact of sP203Q, sS210R and sP203Q+sS210R mutations on cell proliferation. 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 10;18;29;36 16;24;35;42 S;S;S;S 10;18;29;36 11;19;30;37 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Impact of sP203Q, sS210R and sP203Q+sS210R mutations on the extracellular on intracellular HBsAg ratio. 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 10;18;29;36 16;24;35;42 S;S;S;S;S 91;10;18;29;36 96;11;19;30;37 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In HCC patients, sP203Q and/or sS210R occurred with a median (IQR) intrapatient prevalence of 70.6% (12.7%-100%). 2017 Oncotarget Result HBV P203Q;S210R 17;31 23;37 S;S 17;31 18;32 Hepatocellular carcinoma 3 6 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In line with this datum, the level of alpha-fetoprotein (AFP) at HCC diagnosis was higher in patients with either P203Q or S210R than in patients without these mutations (median [IQR] AFP: 6500 [212-18250] ng/mL vs 58 (7-2139) ng/mL). 2017 Oncotarget Result HBV P203Q;S210R 114;123 119;128 Hepatocellular carcinoma 65 68 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In particular, at day 4 of culture (characterized by the peak in HBsAg production), HBsAg secretion factor decreased from 4.42+-0.3 for wild-type to 2.22+-0.2 for P203Q (P <0.001), to 3.52+-0.2 for S210R (P <0.05), and to 2.33+-0.2 for P203Q+S210R (P <0.01) (Figure 3A). 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 163;198;236;242 168;203;241;247 S;S 65;84 70;89 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In particular, the double mutant sP203Q+sS210R was detected exclusively in HCC-patients (17.4% [4/23] versus 0% [0/105], P=0.001) (Figure 1). 2017 Oncotarget Result HBV P203Q;S210R 33;40 39;46 S;S 33;40 34;41 Hepatocellular carcinoma 75 78 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In particular, the percentage of cells in the S phase at 7 days post transfection increased from 18%+-9 for wild-type up to 26+-13% for P203Q and 29+-14% for P203Q+S210R (P <0.001 for both) (Figure 3B). 2017 Oncotarget Result HBV P203Q;P203Q;S210R 136;158;164 141;163;169 S 46 47 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In this analysis, sP203Q and sP203Q+sS210R significantly correlated with an increased percentage of cells in the S phase of cellular cycle, thus supporting an induction of cell cycle progression (Figure 3B). 2017 Oncotarget Result HBV P203Q;P203Q;S210R 18;29;36 24;35;42 S;S;S 18;29;36 19;30;37 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Multivariate analysis confirmed that the presence of either sP203Q or sS210R was independently associated with a higher probability of developing HCC (adjusted Odd-Ratio [95% C.I.]: 12.0 [1.6-78.8], P=0.02), after correction for patients' age, gender, HBV genotype, serum HBV-DNA, ALT and AST (Table 2). 2017 Oncotarget Result HBV P203Q;S210R 60;70 66;76 S;S 60;70 61;71 Hepatocellular carcinoma 146 149 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. No deletions were found with sP203Q or sS210R in both HCC and control group. 2017 Oncotarget Result HBV P203Q;S210R 29;39 35;45 S;S 29;39 30;40 Hepatocellular carcinoma 54 57 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. No differences in intracellular cyclin levels were observed in hepatoma cells transfected with plasmid carrying P203Q and P203Q+S210R HBsAg mutations compared to wt (fold compared to mock = 1.8+-0.2 and 1.8+-0.1 versus 1.7+-0.04 for wt, respectively). 2017 Oncotarget Result HBV P203Q;P203Q;S210R 112;122;128 117;127;133 S 134 139 Hepatocellular carcinoma 63 71 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Notably, cells transfected with HBsAg plasmid carrying the mutation sS210R showed increased intracellular levels of cyclin A, compared to those transfected with wild type HBsAg (fold compared to mock = 2.1+-0.08 versus 1.7+-0.04 for wt). 2017 Oncotarget Result HBV S210R 68 74 S;S;S 32;171;68 37;176;69 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Similarly, sS210R was found in 34.8% (8/23) of HCC-patients and in 3.8% (4/105) of patients without HCC (P <0.001) (Figure 1). 2017 Oncotarget Result HBV S210R 11 17 S 11 12 Hepatocellular carcinoma;Hepatocellular carcinoma 47;100 50;103 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. sP203Q never occurred as single mutation but only in association with sS210R, with an intrapatient ranging from 86.7% to 100% (Figure 2A). 2017 Oncotarget Result HBV P203Q;S210R 0;70 6;76 S;S 0;70 1;71 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. sP203Q occurred as a mixture in 2/4 HCC patients while sS210R occurred as a mixture only in 1 patient. 2017 Oncotarget Result HBV P203Q;S210R 0;55 6;61 S;S 0;55 1;56 Hepatocellular carcinoma 36 39 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. sP203Q occurred in 17.4% (4/23) of HCC-patients versus 1.0% (1/105) of patients without HCC (P=0.004) (Figure 1). 2017 Oncotarget Result HBV P203Q 0 6 S 0 1 Hepatocellular carcinoma;Hepatocellular carcinoma 35;88 38;91 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The impact of sP203Q, sS210R and sP203Q+sS210R on cell proliferation was then evaluated by flow cytometry (DNA propidium iodide-staining) on transfected GFP+ cells at day 7 post transfection (Figure 3B). 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 14;22;33;40 20;28;39;46 S;S;S;S 14;22;33;40 15;23;34;41 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The next step of this study was to investigate the impact of sP203Q, sS210R and sP203Q+sS210R on HBsAg release. 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 61;69;80;87 67;75;86;93 S;S;S;S;S 97;61;69;80;87 102;62;70;81;88 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The percentage of patients with sS210R/rtS219A was comparable between drug naive HCC-patients (33.3%, 3/9) and drug-treated HCC-patients (35.7%, 5/14), thus excluding the impact of antiviral therapy on the selection of this mutation. 2017 Oncotarget Result HBV S219A;S210R 41;32 46;38 RT;S 39;32 41;33 Hepatocellular carcinoma;Hepatocellular carcinoma 81;124 84;127 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Therefore, the sS210R mutants within C-terminal HBsAg might contribute to cell cycle progression by modulating the expression of cyclin A. 2017 Oncotarget Result HBV S210R 15 21 S;S 48;15 53;16 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. These results reflects the ability of sP203Q, sS210R and sP203Q+sS210R to negatively affect HBsAg release. 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 38;46;57;64 44;52;63;70 S;S;S;S;S 92;38;46;57;64 97;39;47;58;65 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. This suggests that sP203Q/sS210R in HBsAg C-terminus and deletions in pre-S1 and pre-S2 lie on divergent evolutionary pathways contributing to HCC development. 2017 Oncotarget Result HBV S210R;P203Q 26;19 32;25 S;PreS1;PreS2;S;S 36;70;81;19;26 41;76;87;20;27 Hepatocellular carcinoma 143 146 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Thus, the presence of pre-S1 and pre-S2 deletions was investigated, as well as their co-occurrence with sP203Q or sS210R. 2017 Oncotarget Result HBV P203Q;S210R 104;114 110;120 PreS1;PreS2;S;S 22;33;104;114 28;39;105;115 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Two specific mutations (sP203Q and sS210R) were significantly correlated with the presence of HCC (Figure 1). 2017 Oncotarget Result HBV P203Q;S210R 24;35 30;41 S;S 24;35 25;36 Hepatocellular carcinoma 94 97 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. UDPS analysis was performed in 13 HCC patients (6/13 carrying sP203Q or sS210R by population-based sequencing) and 27 reference patients (2/27 carrying sP203Q or SS210R by population-based sequencing) (Figure 2). 2017 Oncotarget Result HBV P203Q;S210R;P203Q;S210R 62;72;152;162 68;78;158;168 S;S;S 62;72;152 63;73;153 Hepatocellular carcinoma 34 37 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. A bulky substitution of V124F is likely causing steric clash with the 5th positioned methoxycarbonyl group of HAP, but not with SBA. 2017 Scientific reports Result HBV V124F 24 29 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Because SBA does not possess the thiazole group, it may tolerate the conformation changes induced by P25A or P25S mutation. 2017 Scientific reports Result HBV P25A;P25S 101;109 105;113 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Because Y132A is an assembly-deficient mutant representing a subset of WT dimer conformation, yet HAP_R01 and SBA_01 have drastically different effects on WT dimer assembly. 2017 Scientific reports Result HBV Y132A 8 13 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Comparing the ligand binding sites of HAP_R01 and SBA_R01 on Y132A hexamer. 2017 Scientific reports Result HBV Y132A 61 66 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Cp149_Y132A crystallizes in three forms: (A) open triangle, formed by trimer of dimers, (B) closed triangle, mimicking the three CD dimers around the threefold axes of HBV capsid. 2017 Scientific reports Result HBV Y132A 6 11 Capsid 172 178 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Crystal structures of HBV core protein Y132A hexamer in complex with HAP_R01 and SBA_R01. 2017 Scientific reports Result HBV Y132A 39 44 C 26 30 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Finally, the V124I virus has increased susceptibility to all tested compounds. 2017 Scientific reports Result HBV V124I 13 18 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Furthermore, it remains to be evaluated whether the HAP-bound Y132A structure is consistent with the interactions between HAP and misassembled capsid in solution. 2017 Scientific reports Result HBV Y132A 62 67 Capsid 143 149 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. HAP_R01 and SBA_R01 bind to the same dimer-dimer interface in the Y132A structures. 2017 Scientific reports Result HBV Y132A 66 71 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. However, a new space group was discovered during our crystallization screening of Y132A mutant. 2017 Scientific reports Result HBV Y132A 82 87 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Interestingly, P25A or P25S mutation leads to a significant decrease of HAP sensitivity in the range of 8- to 29-fold, whereas only a 2-fold reduction in sensitivity is observed when treated with SBA_R01. 2017 Scientific reports Result HBV P25A;P25S 15;23 19;27 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Interestingly, we find low-abundance quasispecies (frequency bellow 2.5%) containing substitutions P25S in one patient and V124F in four patients (Table 2). 2017 Scientific reports Result HBV P25S;V124F 99;123 103;128 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. It appears that a small increase of the sidechain volume (V124I) favours the interaction with both HAP_R01 and SBA_R01. 2017 Scientific reports Result HBV V124I 58 63 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. On the basis of the similar rationale, P25G mutant decreases the sensitivity to both SBA and HAP to different levels (12 to more than 67 fold EC50 increase). 2017 Scientific reports Result HBV P25G 39 43 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Placing a bulky function group like thiazole, HAP_R01 can induce local rearrangements at F23 and Y118 of the concave and the proline-rich loop 6 (P130, A131, Y132A) of the cap. 2017 Scientific reports Result HBV Y132A 158 163 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The cap is composed of V124, W125, R127 from helix5 and T128, P129, Y132A, R133, P134 from loop 6 of chain C. 2017 Scientific reports Result HBV Y132A 68 73 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The carbonyl oxygen is solvent accessible, whereas the thiazole occupies a largely hydrophobic subpocket composed of F23, P25, W102, Y118, F122 from the concave, and T128, P129, Y132A from the cap. 2017 Scientific reports Result HBV Y132A 178 183 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. the corresponding RMSD values for Y132A-SBA_R01 have the same trend (3.74 A and 3.94 A, respectively). 2017 Scientific reports Result HBV Y132A 34 39 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The data again confirm our prediction: T33N and T33Q mutants show an over 13-fold change in EC50 by SBA_R01; in contrast, T33S mutant only shows a 2-fold increase. 2017 Scientific reports Result HBV T33N;T33Q;T33S 39;48;122 43;52;126 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The evidence from cell-based assay confirms our prediction on mutants with altered HAP/SBA potency, thus indicating that the compound binding pocket at the dimer-dimer interface observed in the Cp149_Y132A structure resembles the HAP interacting site in capsid. 2017 Scientific reports Result HBV Y132A 200 205 Capsid 254 260 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The interactions between the compounds and the Y132A mutant derived from the high resolution crystal structures have successfully guided lead optimization for HBV capsid inhibitors (see further evaluation in photoaffinity results and discussion). 2017 Scientific reports Result HBV Y132A 47 52 Capsid 163 169 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The labeling sites Y118, Y38 and R127 are clustered at the dimer-dimer interface in capsid, consistent with the Y132A crystal structures. 2017 Scientific reports Result HBV Y132A 112 117 Capsid 84 90 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The results show T33N and T33S found in 0.075% and 0.05% of the cases respectively (Table 2). 2017 Scientific reports Result HBV T33N;T33S 17;26 21;30 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. To identify the specific interaction modes between core protein and HAP_R01 or SBA_R01, we crystallized the Cp149 mutant Y132A, which remains as dimer in high salt solution and destabilizes Cp149 capsid. 2017 Scientific reports Result HBV Y132A 121 126 Capsid;C;C;C 196;51;108;190 202;55;110;192 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. When superimposing Y132A-HAP_R01 hexamer onto the hexamer around the icosahedral three-fold axis (chains CDCDCD from 1QGT), the root-mean-square deviation (RMSD) for alpha carbon is 3.42 A, which is slightly larger when superimposing to the hexamer (chain ABCDBA) around the quasi three-fold axis (3.67 A). 2017 Scientific reports Result HBV Y132A 19 24 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. When superposing Calpha of pocket residues with apo Y132A structure (4BMG), HAP_R01 pocket and SBA_R01 pocket give RMSDs of 0.81 A and 0.59 A, respectively. 2017 Scientific reports Result HBV Y132A 52 57 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Y132A mutation generates two binding sites per dimer for HAP molecules in the crystal structure reported here, while there is only one HAP1 site for two dimers from the low resolution capsid crystal structure. 2017 Scientific reports Result HBV Y132A 0 5 Capsid 184 190 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Y132A or F23A mutation is known to disrupt capsid formation. 2017 Scientific reports Result HBV Y132A;F23A 0;9 5;13 Capsid 43 49 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. alphalM0 was derived from alphal, a naturally occurring HBeAg-negative mutant, by introducing the A1896G and A1899G back mutations. 2017 Virology Result HBV A1896G;A1899G 98;109 104;115 C 56 61 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Although the C1817T nonsense mutation should permit the packaging of pcRNA, encapsidated pcRNA should generate double stranded linear DNA rather than RC DNA due to the inability of the RNA primer generated by RNase H digestion to translocate to DR2. 2017 Virology Result HBV C1817T 13 19 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. As for the alphalM0 +36 series, the replication impact of the G1896A mutation was mild. 2017 Virology Result HBV G1896A 62 68 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Comparison of alphalM0, F (alphalM0 with mutated precore ATG), and alphal in the same blot indicates that G1896A/G1899A were more effective than mutated precore ATG in augmenting core protein expression, although ol+36 did not show higher core protein level than F+36. 2017 Virology Result HBV G1899A;G1896A 113;106 119;112 C;C;Precore;Precore 179;239;49;153 183;243;56;160 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Considering that genotype G harbors two nonsense mutations in the precore region (C1817T and G1896A), we introduced C1817T mutation to alphal and alphal+36, respectively to generate construct G and G+36. 2017 Virology Result HBV C1817T;G1896A;C1817T 82;93;116 88;99;122 Precore 66 73 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Core protein expression from alphalM0 was slightly diminished by both T1846A and G1888A mutations. 2017 Virology Result HBV T1846A;G1888A 70;81 76;87 C 0 4 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. G1896A markedly increased core protein expression, which was largely blocked by concurrent C1817T mutation. 2017 Virology Result HBV G1896A;C1817T 0;91 6;97 C 26 30 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. In the reverse experiment, we introduced the T1817C back mutation to clone g1 of genotype G. 2017 Virology Result HBV T1817C 45 51 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. In this regard, G1896A converts precore codon 28 into a stop codon. 2017 Virology Result HBV G1896A 16 22 Precore 32 39 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Introduction of the additional C1817T mutation reverted genome replication to a low level. 2017 Virology Result HBV C1817T 31 37 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. The T1817C back mutation did not alter DNA replication for clone g1 of genotype G, but specifically reduced relaxed circular (RC) DNA form. 2017 Virology Result HBV T1817C 4 10 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Therefore, by shifting the site of translational termination from codon 28 to codon 2, the extra C1817T mutation abolished or diminished the enhancing effect of G1896A mutation on core protein expression. 2017 Virology Result HBV C1817T;G1896A 97;161 103;167 C 180 184 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Thus, reduced RC DNA production by the T1817C mutant was most likely attributable to the single nucleotide change in pgRNA. 2017 Virology Result HBV T1817C 39 45 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. We introduced this frameshift mutation as well as an A1814C mutation converting precore ATG to CTG, to alphalM0 and alphalM0+36. 2017 Virology Result HBV A1814C 53 59 Precore 80 87 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. When introduced to alphalM0+36, both T1846A and G1888A also slightly reduced core protein expression. 2017 Virology Result HBV T1846A;G1888A 37;48 43;54 C 77 81 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. After implementing Benjamini-Hochberg correction, 3 (rtM204I, rtL80I, rtY54H) out these 7 RT substitutions and 6 (sS45A, sP46T, sI68T/A, sT118V, sW196L and sR210N) out of 8 S-substitutions remained significantly less frequent in the responders (Table 4). 2017 Scientific reports Result HBV L80I;Y54H;M204I;S45A;P46T;I68T;I68A;T118V;W196L;R210N 64;72;55;114;121;128;128;137;145;156 68;76;60;119;126;135;135;143;151;162 RT;RT;RT;RT;S;S;S;S;S;S;S 53;62;70;90;114;121;128;137;145;156;173 55;64;72;92;115;122;129;138;146;157;174 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Among these, only one RT-variant, rtH124N and 6 S-variants sS45A, sA/S113T, sT118V, sT125M, sA128V and sR210N remained significant following Benjamini Hochberg adjustment (Table 3), implying that the presence of these variants were associated with non-response to TDF. 2017 Scientific reports Result HBV S113T;H124N;S45A;A113T;T118V;T125M;A128V;R210N 67;36;59;66;76;84;92;103 74;41;64;74;82;90;98;109 RT;RT;S;S;S;S;S;S;S 22;34;48;59;66;76;84;92;103 24;36;49;60;67;77;85;93;104 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Among these, sT114S, sA194V and sW196L corresponded to rtF/H122L, rtS202G and rtM204V respectively. 2017 Scientific reports Result HBV H122L;F122L;S202G;M204V;T114S;A194V;W196L 57;57;68;80;13;21;32 64;64;73;85;19;27;38 RT;RT;RT;S;S;S 55;66;78;13;21;32 57;68;80;14;22;33 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. At 48 week of TDF therapy, the frequencies of rtM204I, rtL80I, sS45A, sT118V, sW196L and sA128V continued to be significantly reduced from baseline in responders, although an increase in frequency of the substitution rtV278I was noted in the HBV clones of the responders during this observational period (Table 5). 2017 Scientific reports Result HBV L80I;M204I;V278I;S45A;T118V;W196L;A128V 57;48;219;63;70;78;89 61;53;224;68;76;84;95 RT;RT;RT;S;S;S;S 46;55;217;63;70;78;89 48;57;219;64;71;79;90 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Direct sequencing of the PCR amplified RT domain of HBV/D from 16 LMV-failed patients demonstrated the presence of well-known LMV resistance mutations, rtM204V/I, rtL180M, rtS202G, rtL80I and rtA181T, either singly or in combinations. 2017 Scientific reports Result HBV M204V;M204I;S202G;L80I;A181T;L180M 154;154;174;183;194;165 161;161;179;187;199;170 RT;RT;RT;RT;RT;RT 39;152;163;172;181;192 41;154;165;174;183;194 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Except for A/S113T, all the other 5 S-substitutions were localized in B- or T-cell epitope regions. 2017 Scientific reports Result HBV S113T;A113T 11;11 18;18 S 36 37 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. For those LMV- failed patients whose HBV carried either rtM204V + rtL180M or rtM204I + rtL80I substitutions, these viral variants were found to comprise 20-100% or 50-100% respectively of said viral quasispecies pool. 2017 Scientific reports Result HBV L80I;M204V;L180M;M204I 89;58;68;79 93;63;73;84 RT;RT;RT;RT 56;66;77;87 58;68;79;89 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. For WT, 6.7 +- 0.4 muM tenofovir reduced the replicative level to 50% while the presence of rtH124N increased the IC50 to 44.0 +- 3.2 muM, that corresponded to a 6.5 fold decreased susceptibility to tenofovir. 2017 Scientific reports Result HBV H124N 94 99 RT 92 94 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. However, at the end of 24-week of TDF therapy, decline in the frequencies of rtM204I, rtL80I, rtN53D, rtY54H, rtH124N, rtN131D and rtH248N together with sS45A, sP46T, sI68T/A, sA/S113T, sT118V, sT125M, sW196L and sR210N from basal values were noted exclusively in the TDF-responder group at the nominal 0.05 significance level (Table 4). 2017 Scientific reports Result HBV S113T;L80I;N53D;Y54H;H124N;N131D;H248N;M204I;S45A;P46T;I68T;I68A;A113T;T118V;T125M;W196L;R210N 177;88;96;104;112;121;133;79;153;160;167;167;176;186;194;202;213 184;92;100;108;117;126;138;84;158;165;174;174;184;192;200;208;219 RT;RT;RT;RT;RT;RT;RT;S;S;S;S;S;S;S;S 77;86;94;102;110;119;131;153;160;167;176;186;194;202;213 79;88;96;104;112;121;133;154;161;168;177;187;195;203;214 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. However, out of these 20 S-substitutions, 10 (sT114S, sT126I, sP127T, sN131T, sN143S, sY/S161F, sA194V, sI195M, sW196L and sR210N) remained significant after application of Benjamini-Hochberg correction (Table 2). 2017 Scientific reports Result HBV S161F;T114S;T126I;P127T;N131T;N143S;Y161F;A194V;I195M;W196L;R210N 87;46;54;62;70;78;86;96;104;112;123 94;52;60;68;76;84;94;102;110;118;129 S;S;S;S;S;S;S;S;S;S;S 25;46;54;62;70;78;86;96;104;112;123 26;47;55;63;71;79;87;97;105;113;124 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. In contrast, there were no significant change in percentages of RT and S variants from the baseline values in the non-responders after 24 and 48-week TDF therapy following Bejamini-Hochberg adjustment, although the frequencies of rtM204I and rtL80I were found to be nominally significantly lower than baseline frequency post 24 week and 48 week therapy (Tables 4 and 5). 2017 Scientific reports Result HBV L80I;M204I 244;232 248;237 RT;RT;RT;S 64;230;242;71 66;232;244;72 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. In the remaining 4 (25%) patients, the multi-drug resistant mutation rtA181T was identified. 2017 Scientific reports Result HBV A181T 71 76 RT 69 71 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Interestingly, there was no statistically significant difference with respect to baseline in the proportions of LMV-associated mutations, rtM204V, rtL180M and rtS202G in both TDF responders and non-responders even after 48 week-therapy. 2017 Scientific reports Result HBV M204V;L180M;S202G 140;149;161 145;154;166 RT;RT;RT 138;147;159 140;149;161 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Notably, 9 out of the 10 substitutions resided in the known B- and T-cell epitopes of HBsAg that included 4 substitutions (sT126I, sP127T, sN131T and sN143S) within the "a"-determinant region (aa s124-147), the primary target for neutralizing antibody produced by B cells during natural infection or following active or passive immunization. 2017 Scientific reports Result HBV T126I;P127T;N131T;N143S 123;131;139;150 129;137;145;156 S;S;S;S;S;S 86;123;131;139;150;196 91;124;132;140;151;197 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Notably, rtM204V/I were found in 12 out of 16 (75%) LMV-failed patients, of which 9 (75%) had rtM204V in association with rtL180M while the other 3 (25%) patients had rtM204I together with rtL80I mutation. 2017 Scientific reports Result HBV M204V;M204I;M204V;L180M;M204I;L80I 11;11;96;124;169;191 18;18;101;129;174;195 RT;RT;RT;RT;RT 9;94;122;167;189 11;96;124;169;191 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Out of the 17 aa substitutions where significant differences were observed in frequencies between HBV clones, 10 substitutions (rtN53D, rtI121L, rtF/H122L, rtH124N, rtQ130P, rtN131D, rtL180M, rtM204V, rtM204I and rtV278I) exhibited significant differences in the proportion of individuals having HBV clones carrying the corresponding mutation. 2017 Scientific reports Result HBV H122L;N53D;F122L;N131D;I121L;H124N;Q130P;L180M;M204V;M204I;V278I 147;130;147;176;138;158;167;185;194;203;215 154;134;154;181;143;163;172;190;199;208;220 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 128;136;145;156;165;174;183;192;201;213 130;138;147;158;167;176;185;194;203;215 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Out of the 9 patients whose HBV harbored rtM204V mutation, four patients also had rtS202G in their HBV DNA. 2017 Scientific reports Result HBV M204V;S202G 43;84 48;89 RT;RT 41;82 43;84 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Remarkably, HBV clones having the mutational combination of rtM204V + rtL180M always carried the novel substitution rtH/L267Q while those with rtM204I + rtL80I co-existed with rtR266I. 2017 Scientific reports Result HBV L267Q;H267Q;L80I;M204V;L180M;M204I;R266I 118;118;155;62;72;145;178 125;125;159;67;77;150;183 RT;RT;RT;RT;RT;RT 60;70;116;143;153;176 62;72;118;145;155;178 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Six (rtL80I, rtL91I, rtL180M, rtS202G, rtM204V/I, rtH248N) (35.3%) out of 17 substitutions were located within different RT domains while 11 substitutions (64.7%) were mapped in inter-domains. 2017 Scientific reports Result HBV L80I;L91I;M204V;M204I;H248N;L180M;S202G 7;15;41;41;52;23;32 11;19;48;48;57;28;37 RT;RT;RT;RT;RT;RT;RT 5;13;21;30;39;50;121 7;15;23;32;41;52;123 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Susceptibility of rtH124N mutant and wild-type HBV to Tenofovir in vitro. 2017 Scientific reports Result HBV H124N 20 25 RT 18 20 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. The clonal analysis showed that there was no significant difference at baseline in the frequencies of classical LMV-resistant mutations, rtL80I, rtL180M, rtS202G and rtM204V/I in both groups of patients. 2017 Scientific reports Result HBV M204V;M204I;L80I;L180M;S202G 168;168;139;147;156 175;175;143;152;161 RT;RT;RT;RT 137;145;154;166 139;147;156;168 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. The rtA181T variant was detected in 10-40% of the HBV clones from four LMV-failed patients while the clonal prevalence of rtS202G ranged from 20-100%. 2017 Scientific reports Result HBV S202G;A181T 124;6 129;11 RT;RT 4;122 6;124 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. These include five classical LMV-resistant mutations, rtM204V, rtM204I, rtL180M, rtS202G and rtL80I and 14 novel substitutions namely, rtN53D, rtY54H, rtL91I, rtI121L, rtF/H122L, rtH124N, rtQ130P, rtN131D, rtA219S, rtH248N, rtS256C, rtR266I, rtH/L267Q and rtV278I. 2017 Scientific reports Result HBV H122L;L267Q;L80I;N53D;Y54H;L91I;F122L;N131D;R266I;H267Q;V278I;M204V;M204I;L180M;S202G;I121L;H124N;Q130P;A219S;H248N;S256C 170;244;95;137;145;153;170;199;235;244;258;56;65;74;83;161;181;190;208;217;226 177;251;99;141;149;157;177;204;240;251;263;61;70;79;88;166;186;195;213;222;231 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 54;63;72;81;93;135;143;151;159;168;179;188;197;206;215;224;233;242;256 56;65;74;83;95;137;145;153;161;170;181;190;199;208;217;226;235;244;258 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. To determine whether rtH124N mutation impact the viral susceptibility to tenofovir, we engineered rtH124N into wild-type (WT) laboratory strain of HBV belonging to genotype D and tested the abilities of WT and rtH124N mutant HBV to replicate in Huh7 human hepatoma cells in the presence of increasing concentrations of tenofovir by quantifying intracellular HBV DNA levels by real time PCR. 2017 Scientific reports Result HBV H124N;H124N;H124N 23;100;212 28;105;217 RT;RT;RT 21;98;210 23;100;212 Hepatocellular carcinoma 256 264 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. with the exception of sP127T, where no difference was noted. 2017 Scientific reports Result HBV P127T 22 28 S 22 23 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. A direct DNA sequence analysis was performed, and HBV genotype C with a G145R mutation was confirmed at the time of admission (Figure 2A). 2017 Emerging microbes & infections Result HBV G145R 72 77 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Accordingly, the patient was diagnosed with hepatitis B caused by a G145R immune escape mutant. 2017 Emerging microbes & infections Result HBV G145R 68 73 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. As shown in Supplementary Figure S1, the frequencies of mutations (L173P, Q181R and A184V) in cytotoxic T lymphocyte (CTL) epitopes were increased before entecavir treatment, whereas mutations in the CTL domain aa 44-59 unexpectedly increased after entecavir treatment. 2017 Emerging microbes & infections Result HBV L173P;Q181R;A184V 67;74;84 72;79;89 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Dynamic changes in clinical characteristics during infection by G145R mutant HBV. 2017 Emerging microbes & infections Result HBV G145R 64 69 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Evolution of the viral quasispecies during G145R mutant HBV infection. 2017 Emerging microbes & infections Result HBV G145R 43 48 HBV infections 56 69 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In addition to G145R, new dominant and minor mutations were detected. 2017 Emerging microbes & infections Result HBV G145R 15 20 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. The frequencies of four mutations in the S region (G145R, K160R, L173P and Q181R), four mutations in the RT region (R153Q, S256G, C332S and L336M) and five mutations in the X region (S54P, L55F, R56P, L58P and C69P) decreased in the 8th week, whereas the frequencies of many mutations in the S, P and X regions clearly increased. 2017 Emerging microbes & infections Result HBV G145R;K160R;L173P;Q181R;R153Q;S256G;C332S;L336M;S54P;L55F;R56P;L58P;C69P 51;58;65;75;116;123;130;140;183;189;195;201;210 56;63;70;80;121;128;135;145;187;193;199;205;214 P;RT;S;S;X;X 295;105;41;292;173;301 296;107;42;293;174;302 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Unlike mutations in the CTL domain, Y221C in the T-helper cell domain exhibited a high frequency both before and after entecavir treatment. 2017 Emerging microbes & infections Result HBV Y221C 36 41 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. We also screened several mutations relevant to antiviral resistance, such as I169L, L180M, A181V, T184I, S202C, M204V/I, N236T and M250I in the RT region. 2017 Emerging microbes & infections Result HBV I169L;L180M;A181V;T184I;S202C;M204V;M204I;N236T;M250I 77;84;91;98;105;112;112;121;131 82;89;96;103;110;119;119;126;136 RT 144 146 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. With regard to the 'hot-spot' mutations in the HBV genome, G1896A in the preC region and A1762T/G1764A in the basic core promoter region were studied. 2017 Emerging microbes & infections Result HBV G1764A;G1896A;A1762T 96;59;89 102;65;95 BCP;Precore 110;73 129;77 28332360 Entecavir to Telbivudine Switch Therapy in Entecavir-Treated Patients with Undetectable Hepatitis B Viral DNA. All five patients with virological rebound had evidence of drug-resistant mutations, with three patients with the rtM204I mutation and two with the rtM204V mutation. 2017 Yonsei medical journal Result HBV M204I;M204V 116;150 121;155 RT;RT 114;148 116;150 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. A11T, D14N, R16K, G19D, F22L, G30E, N33H, I42T, and P54Q/T were found; these mutations were not reported previously. 2017 Yonsei medical journal Result HBV A11T;D14N;R16K;G19D;F22L;G30E;N33H;I42T;P54Q;P54T 0;6;12;18;24;30;36;42;52;52 4;10;16;22;28;34;40;46;58;58 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Among them, S114T (patients #2 and 10), P127S/T (patients #2, 12, and 21), and M133T (patients #2, 10, and 14) were commonly found. 2017 Yonsei medical journal Result HBV P127T;S114T;P127S;M133T 40;12;40;79 47;17;47;84 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Among these, F22L (patients #9 and 23) and P54T (patient #22) were detected in the control group (C1, C8, C9, and C10). 2017 Yonsei medical journal Result HBV F22L;P54T 13;43 17;47 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Besides I84T found in C1, no mutations of occult HBV infection were detected. 2017 Yonsei medical journal Result HBV I84T 8 12 HBV infections 49 62 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Five mutations from the control group were found at the same location (aa58-aa100), including A60V in nine patients (C2, C3, C12, C13, and C16-C20), L74I in C2, I84T in C1, L85V in C2, and A95V in C3. 2017 Yonsei medical journal Result HBV A60V;L74I;I84T;L85V;A95V 94;149;161;173;189 98;153;165;177;193 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. G83S was detected in five patients (patients #14 and 18-21) who all simultaneously showed mutation on D114E. 2017 Yonsei medical journal Result HBV G83S;D114E 0;102 4;107 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Only I126T was found in five subjects of the control group (C4, C8, C15, C16, and C20), although this mutation was not found in the occult HBV infection group. 2017 Yonsei medical journal Result HBV I126T 5 10 HBV infections 139 152 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Patient #10 showed 11 mutations of Q101K, S114T, P120T, T123A, I126N, P127T, T113N, M133T, G145A, S154P, and P160K. 2017 Yonsei medical journal Result HBV Q101K;S114T;P120T;T123A;I126N;P127T;T113N;M133T;G145A;S154P;P160K 35;42;49;56;63;70;77;84;91;98;109 40;47;54;61;68;75;82;89;96;103;114 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Patient #2 showed eight mutations of Q101R, L104S, P105N, S114T, I126M, P127S, M133T, and D144E. 2017 Yonsei medical journal Result HBV Q101R;L104S;P105N;S114T;I126M;P127S;M133T;D144E 37;44;51;58;65;72;79;90 42;49;56;63;70;77;84;95 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Patients #12 and 21 showed the same mutations of Y100S, M103I, P105R, G112K, T113A, S117G, and P127T. 2017 Yonsei medical journal Result HBV Y100S;M103I;P105R;G112K;T113A;S117G;P127T 49;56;63;70;77;84;95 54;61;68;75;82;89;100 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Patients #7 and 14 showed single mutations of S132F and M133T in a determinant, respectively. 2017 Yonsei medical journal Result HBV S132F;M133T 46;56 51;61 S 65 78 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. T49I was seen in three controls (C4, C6, and C7), but was not observed in the occult HBV infection group. 2017 Yonsei medical journal Result HBV T49I 0 4 HBV infections 85 98 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. All the high replicating clones harbored A1762T/ G1764A mutations, and all but the three non-HCC clones harbored G1896A precore mutation. 2017 Virus research Result HBV A1762T;G1764A;G1896A 41;49;113 47;55;119 Precore 120 127 Hepatocellular carcinoma 93 96 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Among samples with extremely low HBeAg titers, G1896A was present in all the clones from patient #1, #11, #13, #17, and most clones from #18. 2017 Virus research Result HBV G1896A 47 53 C 33 38 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Among these clones, 13 (9 from HCC patients) harbored additional T1753C mutation (Fig. 1), 2 had additional C1766T mutation. 2017 Virus research Result HBV C1766T;T1753C 108;65 114;71 Hepatocellular carcinoma 31 34 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Consistent with the high prevalence of core promoter mutations in genotype C, especially at the advanced stages of liver diseases, 34 of the 36 clones (including all the 20 HCC-derived clones) harbored the A1762T/G1764A double mutation. 2017 Virus research Result HBV G1764A;A1762T 213;206 219;212 Core promoter 39 52 Liver disease;Hepatocellular carcinoma 115;173 129;176 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Conversely, the Q182* nonsense mutation, which shortened core protein by just two residues without impairing its function in supporting genome replication, was present in 8 HCC clones but only 1 non-HCC clone. 2017 Virus research Result HBV Q182X 16 21 C 57 61 Hepatocellular carcinoma;Hepatocellular carcinoma 173;199 176;202 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Finally, the only two clones lacking A1762T/G1764A mutations (12.1 and 12.3 from a non-HCC patient) had nt 1727 and 1768-1775 deleted (Supplementary Table 1). 2017 Virus research Result HBV G1764A;A1762T 44;37 50;43 Hepatocellular carcinoma 87 90 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. For #5, one clone harbored G1896A, while the other clone had deletion of codons 84-121. 2017 Virus research Result HBV G1896A 27 33 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. HBeAg was undetectable from culture supernatant of Huh7 cells transfected with the 18 clones harboring the G1896A mutation, even without sample dilution. 2017 Virus research Result HBV G1896A 107 113 C 0 5 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. HCC clones showed high prevalence of G1896A mutation in association with low serum HBeAg titers. 2017 Virus research Result HBV G1896A 37 43 C 83 88 Hepatocellular carcinoma 0 3 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. In addition, the E180G, S181P, and Q182K missense mutations were identified in 12 clones derived from 5 HCC patients but only 3 clones from 2 non-HCC patients (Table 2). 2017 Virus research Result HBV E180G;S181P;Q182K 17;24;35 22;29;40 Hepatocellular carcinoma;Hepatocellular carcinoma 104;146 107;149 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. In particular, clone 14.3 harbored a D99G missense mutation but no preS deletion or nonsense mutation in the envelope gene. 2017 Virus research Result HBV D99G 37 41 S;PreS 109;67 117;71 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. In this regard 7 of the 12 highest replicating clones harbored either T1753C or C1766T. 2017 Virus research Result HBV T1753C;C1766T 70;80 76;86 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. On the other hand, introducing the S155P mutation (found in clones 12.1 and 12.3) failed to impair HBeAg expression. 2017 Virus research Result HBV S155P 35 40 C 99 104 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Our previous studies found that T1753C and C1766T could enhance the replication promoting effect of A1762T/G1764A hot spot mutations in genotype A. 2017 Virus research Result HBV G1764A;T1753C;C1766T;A1762T 107;32;43;100 113;38;49;106 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Remarkably, the D99G mutation completely abolished HBsAg for both cell lysate and culture supernatant. 2017 Virus research Result HBV D99G 16 20 S 51 56 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Sequencing using the P1 primer also allowed us to read DNA sequence at the 3' precore region, where the G1896A hot spot mutation to abolish HBeAg expression is located. 2017 Virus research Result HBV G1896A 104 110 C;Precore 140;78 145;85 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Similar results were obtained for clone 19.3, which had T1753C/ A1762T/G1764A triple core promoter mutations. 2017 Virus research Result HBV G1764A;T1753C;A1762T 71;56;64 77;62;70 Core promoter 85 98 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The G145R immune escape mutation caused low S protein level by Western blot. 2017 Virus research Result HBV G145R 4 9 S 44 45 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The most common (hot spot) core promoter mutations are A1762T in conjunction with G1764A. 2017 Virus research Result HBV A1762T;G1764A 55;82 61;88 Core promoter 27 40 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The P120T, I126S, and R160G mutations did not affect intracellular HBsAg level, although R160G slightly reduced extracellular HBsAg. 2017 Virus research Result HBV P120T;I126S;R160G;R160G 4;11;22;89 9;16;27;94 S;S 67;126 72;131 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The T1762A/A1764G back mutations markedly reduced genome replication for clone 4.2, whereas the A1896G back mutation had limited effect. 2017 Virus research Result HBV A1764G;T1762A;A1896G 11;4;96 17;10;102 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Therefore, the low HBeAg titers in most serum samples correlated with the high prevalence of G1896A mutation to abolish HBeAg expression. 2017 Virus research Result HBV G1896A 93 99 C;C 19;120 24;125 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. These two clones happened to be HBeAg negative despite the lack of a G1896A nonsense mutation, although a causative role of core promoter deletions on negative HBeAg phenotype was not determined. 2017 Virus research Result HBV G1896A 69 75 Core promoter;C;C 124;32;160 137;37;165 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Fifteen (43%) had the double A1762T/G1764A mutation ("TA mutation") in the BCP region; an additional patient had only G1764A. 2017 Tropical medicine & international health Result HBV G1764A;A1762T;G1764A 36;29;118 42;35;124 BCP 75 78 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Notably, all three HBeAg (+) patients with the double TA mutation, including one patient also with G1896A, experienced HBeAg seroconversion over the study period. 2017 Tropical medicine & international health Result HBV G1896A 99 105 C;C 19;119 24;124 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. One patient had a preS2 glycine insertion after the third amino acid and one patient had the F22S mutation. 2017 Tropical medicine & international health Result HBV F22S 93 97 PreS2 18 23 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. One well described vaccine-escape mutation, sG145R, occurred in two patients. 2017 Tropical medicine & international health Result HBV G145R 44 50 S 44 45 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Outside of the 'a' determinant, common mutations occurred at residues 164 (sE164G in 5/46 and sE164A in 1/46), 110 (sI110L in 5/46) and 184 (sA184V in 2/46). 2017 Tropical medicine & international health Result HBV E164G;E164A;I110L;A184V 75;94;116;141 81;100;122;147 S;S;S;S;S 16;75;94;116;141 30;76;95;117;142 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Six patients had C1766G and four patients had T1753C. 2017 Tropical medicine & international health Result HBV C1766G;T1753C 17;46 23;52 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. The majority of the BCP/PC mutations were found in HBeAg-negative patients [BCP "TA": 12/30 eAg (-), 3/5 eAg (+); PC G1896A: 19/30 eAg (-), 1/5 eAg (+)], although analysis is limited by very low number of eAg+ sequences (n=5) and this was not statistically significant. 2017 Tropical medicine & international health Result HBV G1896A 117 123 BCP;BCP;C;Precore;Precore 20;76;51;24;114 23;79;56;26;116 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. The most frequent mutations in this region were sT131P (4/45) and sS140L (3/45). 2017 Tropical medicine & international health Result HBV T131P;S140L 48;66 54;72 S;S 48;66 49;67 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Twenty patients (57%) had PC G1896A mutations and 12 (34%) had PC G1899A mutations. 2017 Tropical medicine & international health Result HBV G1896A;G1899A 29;66 35;72 Precore;Precore 26;63 28;65 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. We saw a higher frequency of the 1762/1764 "TA mutation" and a lower frequency of the G1896A mutation in patients with HBV DNA >= 20,000 IU/ml, but these differences were not statistically significant (data not shown). 2017 Tropical medicine & international health Result HBV G1896A 86 92 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. After emergence of mutant, the serum HBV DNA, HBsAg and ALT levels did not differ significantly between the rtA181T/sW172* mutation group and other missense mutations group (4.16 versus 3.61 log10 IU/mL; P = 0.298, 3.52 versus 3.46 log10 IU/mL; P = 0.795, 142.5 versus 59.0 U/L; P = 0.524, respectively). 2017 Virology journal Result HBV W172X;A181T 116;110 122;115 S;RT;S 46;108;116 51;110;117 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. After emergence of rtA181T/V mutant, mean serum HBV DNA increased over 4 log10 IU/mL. 2017 Virology journal Result HBV A181T;A181V 21;21 28;28 RT 19 21 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. However, the mean reduction of serum HBV DNA at 6th month did not differ significantly between the rtA181T/V group (3.18 +- 1.92 log10 IU/ml) and the rtA181 + rtN236 group (3.52 +- 2.04 log10 IU/ml) (P = 0.520). 2017 Virology journal Result HBV A181T;A181V 101;101 108;108 RT;RT;RT 99;150;159 101;152;161 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In 56 CHB patients appeared rtA181T/V mutation, 51 (91.1%) were male and 5 (8.9%) were female, and the mean age was 42.1 +- 8.6 years. 2017 Virology journal Result HBV A181T;A181V 30;30 37;37 RT 28 30 Chronic Hepatitis B 6 9 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Responses between different rtA181T/sW172 mutations. 2017 Virology journal Result HBV A181T 30 35 RT;S 28;36 30;37 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. The rtA181T substitution was mainly associated with an sW172* substitution, only 15.4% (4/26) had other missense mutations (three with sW172L, one with sW172S). 2017 Virology journal Result HBV A181T;W172X;W172L;W172S 6;55;135;152 11;61;141;158 RT;S;S;S 4;55;135;152 6;56;136;153 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. 93.05% of the viral population were detected with rtS78T and 93.22% with sC69* (* represents the stop codon) at first analysis, and at the second sampling (6 months later), the entire isolates were carrying rtS78T/sC69* mutations. 2017 Journal of hepatology Result HBV C69X;S78T;S78T;C69X 214;52;209;73 219;56;213;78 RT;RT;S;S 50;207;73;214 52;209;74;215 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. As anticipated from the sC69* stop mutation, no HBsAg was detectable using anti-HBs antibodies. 2017 Journal of hepatology Result HBV C69X 24 29 S;S;S 80;48;24 83;53;25 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Based on the emergence of rtS78T/sC69* and preS1/preS2deldeletion during dual ETV/TDF therapy in patients, we next assessed the susceptibility of the mutants to ETV or TDF in vitro by measuring the intracellular HBV-DNA and HBV-progeny DNA levels (indicating active replication) and also the extracellular HBV-DNA that was extracted from PEG precipitated particles. 2017 Journal of hepatology Result HBV C69X;S78T 33;28 38;32 PreS1;RT;S 43;26;33 48;28;34 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. By linkage analysis, the stop codon in the S-open reading frame (S-ORF) was always linked to sI68T, which is a silent mutation in polymerase-ORF (Table 1). 2017 Journal of hepatology Result HBV I68T 93 98 P;S;S;S 130;43;65;93 140;44;66;94 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. ETV (1 muM) or TDF (20 muM) exposure was associated with a >50% reduction in intracellular HBV DNA formation in wild type virus, while M1 and M3 (both containing the rtS78T mutation) retained a higher replication level. 2017 Journal of hepatology Result HBV S78T 168 172 RT 166 168 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Functional consequences of rtS78T/sC69* and preS1/preS2del on viral replication and secretion. 2017 Journal of hepatology Result HBV C69X;S78T 34;29 39;33 PreS;PreS1;RT;S 50;44;27;34 54;49;29;35 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. However, the core protein expression was increased due to the rts78T/sC69* mutation in M1, compared to the wild type HBV. 2017 Journal of hepatology Result HBV C69X 69 74 C;RT;S 13;62;69 17;64;70 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. More detailed analysis on the resistance level of the mutants revealed 1.57- and 1.63-fold changes in the half maximal effective concentration (EC50) to ETV and TDF treatment (compared to the wild type HBV) related to rtS78T/sC69* in M1 and M3 mutants. 2017 Journal of hepatology Result HBV C69X;S78T 225;220 230;224 RT;S 218;225 220;226 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Other mutations, especially those related to LAM or ETV resistance (rtL180M and rtM204V/I) and classical immune escape (sG145R and/or P120T) variants were noted at no or very low frequencies (Table 1), despite ETV treatment. 2017 Journal of hepatology Result HBV M204V;M204I;L180M;G145R;P120T 82;82;70;120;134 89;89;75;126;139 RT;RT;S 68;80;120 70;82;121 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Our UDPS analysis revealed over-representation of the rtS78T mutation in the reverse transcriptase (rt) gene of the HBV genome that creates a premature stop codon in the overlapping surface (s) protein at sC69, thereby deleting almost the entire small HBV surface protein. 2017 Journal of hepatology Result HBV S78T 56 60 RT;RT;RT;S;S;S;S 77;54;100;191;205;182;256 98;56;102;192;206;189;263 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Patient B showed 13.96% frequency for rtS78T and 14.21% for sC69* at first sampling, which increased to 38.16% for rtS78T and 37.78% for sC69* 8 months later. 2017 Journal of hepatology Result HBV S78T;S78T;C69X;C69X 40;117;60;137 44;121;65;142 RT;RT;S;S 38;115;60;137 40;117;61;138 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Selection of the rtS78T and sC69* mutations during dual antiviral treatment. 2017 Journal of hepatology Result HBV S78T;C69X 19;28 23;33 RT;S 17;28 19;29 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The relative position of the observed mutations in the two patients to the coding regions in the HBV genome, including preS1/S2 deletion and rtS78T/sC69*, is shown in. 2017 Journal of hepatology Result HBV C69X;S78T 148;143 153;147 PreS1;PreS2;RT;S 119;119;141;148 124;125;143;149 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The relevant position of sC69* and preS1/preS2 mutations in multispanning transmembrane surface proteins of HBV is schematically shown in. 2017 Journal of hepatology Result HBV C69X 25 30 PreS1;PreS2;S;S 35;41;25;88 40;46;26;95 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The rtS78T/sC69* caused the same increase in GFP expression and interestingly could also restore the neutral effect of preS1/preS2del (M2) on GFP expression, presumably through an increase in viral replication and hence the expression of X protein. 2017 Journal of hepatology Result HBV C69X;S78T 11;6 16;10 PreS;PreS1;RT;S;X 125;119;4;11;238 129;124;6;12;239 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. To further investigate the potential impact of rtS78T/sC69* and preS1/preS2del mutations on virion release, when S protein is defective or absent, we performed HBV-DNA analysis on the isolated exosomes from supernatants as well as immunoprecipitated viral particles by using mouse monoclonal preS1 and core antibodies. 2017 Journal of hepatology Result HBV C69X;S78T 54;49 59;53 C;PreS;PreS1;PreS1;RT;S;S 302;70;64;292;47;54;113 306;74;69;297;49;55;114 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. To investigate if the presence of rtS78T/sC69* has a general impact on cellular transcription level ("transactivator function"), we performed a co-transfection of wild type and mutant HBV constructs with pCDNA3.1(-)-eGFP. 2017 Journal of hepatology Result HBV C69X;S78T 41;36 46;40 RT;S 34;41 36;42 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. To investigate the effects of rtS78T/sC69* and preS1/preS2del mutations on replication of HBV, three replication-competent HBV constructs containing the rtS78T/sC69* mutation (M1), the preS1/S2 deletion (preS1/preS2del, M2) as well as the combination of the two, rtS78T/sC69* + preS1/S2del (M3), were generated and studied using transient transfection of Huh7 human hepatoma cells. 2017 Journal of hepatology Result HBV C69X;C69X;C69X;S78T;S78T;S78T 37;160;270;32;155;265 42;165;275;36;159;269 PreS;PreS;PreS1;PreS1;PreS1;PreS1;PreS2;RT;RT;RT;S;S;S 53;210;47;204;278;185;185;30;153;263;37;160;270 57;214;52;209;283;190;191;32;155;265;38;161;271 Hepatocellular carcinoma 366 374 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. While sC69* is invariably linked to sI68T, rtS78T seems to occur preferentially alone, and only in very low percentages with other variants. 2017 Journal of hepatology Result HBV S78T;C69X;I68T 45;6;36 49;11;41 RT;S;S 43;6;36 45;7;37 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. As shown in Figure 2A, a lower concentration of HBsAg was detected in the supernatant of Huh7 cells transfected with the P120T variant compared with wild type or S143L variant transfected cells. 2017 World journal of hepatology Result HBV P120T;S143L 121;162 126;167 S 48 53 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Collectively, these results suggest that the P120T mutation reduces the antigenicity of HBsAg in vitro. 2017 World journal of hepatology Result HBV P120T 45 50 S 88 93 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Further analysis was applied to the major hydrophilic region (MHR) of the HBV genome, revealing the presence of two prevalent amino acid substitutions; P120T in patients Egl4, A79, D1, and D79 and S143L in U31 and Egl4 (Table 2). 2017 World journal of hepatology Result HBV P120T;S143L 152;197 157;202 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. In vitro analysis of P120T and S143L mutations. 2017 World journal of hepatology Result HBV P120T;S143L 21;31 26;36 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Of the 12 samples, escape mutation Q129R was present in 7, while P120T was detected in 4 and S143L was present in 1, suggesting that the clones with 129R mutation were from a minor population with relatively low HBV-DNA levels. 2017 World journal of hepatology Result HBV Q129R;P120T;S143L 35;65;93 40;70;98 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. P120T mutation reduces in vitro antigenicity of HBsAg. 2017 World journal of hepatology Result HBV P120T 0 5 S 48 53 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Taken together, these results indicate that P120T strongly reduces HBsAg levels as detected by CLEIA without affecting the HBV DNA replicative capacity. 2017 World journal of hepatology Result HBV P120T 44 49 S 67 72 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. The above data suggest that the P120T mutation either prevents the secretion of HBsAg or reduces the antigenicity of HBsAg. 2017 World journal of hepatology Result HBV P120T 32 37 S;S 80;117 85;122 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. The result suggests that the reduced HBsAg level detected by CLEIA in the supernatant of P120T mutant transfected cells was caused by reduced antigenicity in vitro rather than intracellular retention of the mutant HBsAg. 2017 World journal of hepatology Result HBV P120T 89 94 S;S 37;214 42;219 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. To distinguish between these alternatives, we examined the extracellular and intracellular expression levels of denatured HBsAg by Western blot after transfecting Huh7 cell with the wild type genotype D clone, and both the P120T, and S143L mutants. 2017 World journal of hepatology Result HBV P120T;S143L 223;234 228;239 S 122 127 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. To elucidate the virological characteristics of P120T and S143L mutations obtained from the complete sequences in this study, these mutations were individually inserted by site mutagenesis into a 1.24-fold replication competent HBV clone based on genotype D. 2017 World journal of hepatology Result HBV P120T;S143L 48;58 53;63 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Wild type genotype D clone, and two variants containing P120T and S143L mutations were transfected to Huh7 cells, and supernatants (extracellular) and cell lysates (intracellular) were collected to compare HBsAg and HBcAg levels. 2017 World journal of hepatology Result HBV P120T;S143L 56;66 61;71 C;S 216;206 221;211 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. As seen in Figure 3, the primer can amplify the HBV DNA product containing the M204I mutation, indicating that the probe and the primer design were correct. 2017 Sensors (Basel, Switzerland) Result HBV M204I 79 84 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Based on this method, we established quantum dot-labeled DNA fluorescent probes to detect HBV M204I mutations, which showed a superior sensitive performance. 2017 Sensors (Basel, Switzerland) Result HBV M204I 94 99 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Figure 3 shows the representative fluorescence signals for HBV M204I mutation detection on the glass-slide with a green light under fluorescence microscopy. 2017 Sensors (Basel, Switzerland) Result HBV M204I 63 68 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Furthermore, for the negative control where HBV DNA was 106 IU/mL containing the M204I mutation, but without streptavidin-QDs, the result was black as there was no fluorescence to be observed under the fluorescence microscope. 2017 Sensors (Basel, Switzerland) Result HBV M204I 81 86 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. In order to further verify the accuracy of the new method, we employed PCR to detect these two samples, and the results confirmed that the two samples did contain the HBV M204V mutation, suggesting that the accuracy of the serum HBV DNA extraction combined with QDs-mediated fluorescent method was higher than that of the direct sequencing method. 2017 Sensors (Basel, Switzerland) Result HBV M204V 171 176 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. In real serum samples analysis, 11 samples were detected to be M204I mutation-positive samples, and 17 samples were detected to be samples by the direct sequencing method. 2017 Sensors (Basel, Switzerland) Result HBV M204I 63 68 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. It is worth noting that QDs possess excellent fluorescence and photostability, and provide a simple, rapid and accurate method for the visualization detection of the HBV DNA M204I mutation. 2017 Sensors (Basel, Switzerland) Result HBV M204I 174 179 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. It was confirmed that the primers used for amplification in this study did contain the M204I mutation, which indicated that the primer sequence was correct. 2017 Sensors (Basel, Switzerland) Result HBV M204I 87 92 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. Next, the amino-fixed probe could detect the target DNA (including the M204I mutation), which had been recognized by the biotin-labeled DNA (Figure 1b). 2017 Sensors (Basel, Switzerland) Result HBV M204I 71 76 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. The HBV M204I mutation was detected by the new method in 28 patients with chronic hepatitis B and a poor response to the nucleoside(s) treatment. 2017 Sensors (Basel, Switzerland) Result HBV M204I 8 13 Chronic Hepatitis B 74 93 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. The target HBV DNA were extracted and amplified from the serum of a lamivudine-resistant patient, and was detected from this system and confirmed to contain M204I mutation through direct sequencing. 2017 Sensors (Basel, Switzerland) Result HBV M204I 157 162 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. We also used the new method to detect the above serum samples and found that the abovementioned 11 samples were again detected to be M204I mutations-positive samples, while two serum samples of the 17 mutation-negative samples were in fact detected to be M204V mutations-positive samples, which were thus inconsistent with the results of direct sequencing. 2017 Sensors (Basel, Switzerland) Result HBV M204I;M204V 133;255 138;260 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. A1762T increases the risk of HCC (summary OR = 3.96, 95% CI = 1.98-7.92), see. 2017 Medicine Result HBV A1762T 0 6 Hepatocellular carcinoma 29 32 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Even with statistical heterogeneity eliminated, significant correlations were still found, and the above mutations were again shown to increase the risk of HCC (ORadjusted G1896A = 2.10, 95% CI = 1.71-2.59, I2 = 12.9%, Pheterogeneity = .312; ORadjusted A1762T = 3.16, 95% CI = 2.28-4.37, I2 = 45.0%, Pheterogeneity = .106; ORadjusted G1764A = 2.60, 95% CI = 1.90-3.57, I2 = 19.9%, Pheterogeneity = .278; ORadjusted A1762T/G1764A = 3.22, 95% CI = 2.68-3.86, I2 = 23.6%, Pheterogeneity = .186). 2017 Medicine Result HBV G1764A;G1896A;A1762T;G1764A;A1762T 422;172;253;334;415 428;178;259;340;421 Hepatocellular carcinoma 156 159 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For genotype D, only the double mutation, A1762T/G1764A, increases the risk of HCC, see Table 3. 2017 Medicine Result HBV G1764A;A1762T 49;42 55;48 Hepatocellular carcinoma 79 82 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For patients with genotype B or C HBV infection, the risk of HCC was associated with A1762T, G1764A, and A1762T/G1764A. 2017 Medicine Result HBV G1764A;A1762T;G1764A;A1762T 112;85;93;105 118;91;99;111 HBV infections;Hepatocellular carcinoma 34;61 47;64 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For the double mutation A1762T/G1764A, 22 studies were included in the meta-analysis. 2017 Medicine Result HBV G1764A;A1762T 31;24 37;30 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For the mutation A1762T, 10 studies were included in this meta-analysis. 2017 Medicine Result HBV A1762T 17 23 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For the mutation G1764A, 10 studies were included in the meta-analysis. 2017 Medicine Result HBV G1764A 17 23 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For the mutation G1896A, 18 studies were included in this meta-analysis. 2017 Medicine Result HBV G1896A 17 23 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. G1764A increases the risk of HCC (summary OR = 3.48, 95% CI = 1.99-6.09), see. 2017 Medicine Result HBV G1764A 0 6 Hepatocellular carcinoma 29 32 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. G1896A increases the risk of HCC (summary OR = 2.04, 95% CI = 1.41-2.95), see. 2017 Medicine Result HBV G1896A 0 6 Hepatocellular carcinoma 29 32 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. In the subgroup analysis by genotype, a single study indicated that in patients with genotype A HBV infection, there was no statistically significant correlation between the risk of HCC and A1762T/G1764A. 2017 Medicine Result HBV G1764A;A1762T 197;190 203;196 HBV infections;Hepatocellular carcinoma 96;182 109;185 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Significant correlation was found between A1762T, an A to T mutation at nucleotide 1762, and the occurrence of HCC. 2017 Medicine Result HBV A1762T;A1762T 42;53 48;87 Hepatocellular carcinoma 111 114 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Significant correlation was found between A1762T/G1764A and the occurrence of HCC, the double mutation increases the risk of HCC (summary OR = 3.96, 95% CI = 2.77-5.65), see. 2017 Medicine Result HBV G1764A;A1762T 49;42 55;48 Hepatocellular carcinoma;Hepatocellular carcinoma 78;125 81;128 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Significant correlation was found between G1764A, a G to A mutation at nucleotide 1764, and the occurrence of HCC. 2017 Medicine Result HBV G1764A;G1764A 42;52 48;86 Hepatocellular carcinoma 110 113 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Significant correlation was found between the mutation G1896A, a G to A substitution at nucleotide 1896, and the occurrence of HCC. 2017 Medicine Result HBV G1896A;G1896A 55;65 61;103 Hepatocellular carcinoma 127 130 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. We found no existent bias via application of Egger test (tG1896A = 0.14, P = .889; tA1762T = 1.34, P = .217; tG1764A = 0.86, P = .413; tA1762T/G1764A = 1.64, P = .101). 2017 Medicine Result HBV G1764A 143 149 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. A total of 22 strains had mutations only within E2; S143L (n = 11), S143SL (n = 3), D144A (n = 1), D144E (n = 2), D144DG (n = 1), G145A (n = 2), and G145GR (n = 2). 2017 PloS one Result HBV S143L;D144A;D144E;G145A 52;84;99;130 57;89;104;135 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. E1 mutants included P120S (n = 3), P120PS (n = 1), P120PT plus T123TI (n = 1) and T123S (n = 1). 2017 PloS one Result HBV P120S;T123S 20;82 25;87 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. Finally 15 strains had mutations outside of E1 and E2; Y100C plus Q129R (n = 1), L109LR (n = 1), T126S (n = 1), T126TS (n = 1), A128V (n = 1), Q129H (n = 1), Q129QH (n = 1), G130R (n = 1), G130R, T131N and M133T (n = 1), T131N (n = 1), T131TN (n = 1), T131I (n = 1), T133TLMS (n = 1), Y134S (n = 1), and Y134YN (n = 1). 2017 PloS one Result HBV Y100C;Q129R;T126S;A128V;Q129H;G130R;G130R;T131N;M133T;T131N;T131I;Y134S 55;66;97;128;143;174;189;196;206;221;252;285 60;71;102;133;148;179;194;201;211;226;257;290 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. H166 S/N value is low relative to H53 and H57 but is not nonreactive. 2017 PloS one Result HBV H166S;H166N 0;0 8;8 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. Six strains had mutations exclusively in E1 including changes at P120, which were included with the E1 mutations because the 3 P120S mutants were all classified as E1 mutants in the HBsAg mutant assay. 2017 PloS one Result HBV P120S 127 132 S 182 187 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. The nomenclature to specify mutants used here is the one letter code for the wild type amino acid, the amino acid position within HBsAg and the one letter code for the mutant amino acid; for example, P120S designates proline at position 120 changed to serine. 2017 PloS one Result HBV P120S;P120S 200;217 205;258 S 130 135 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. There were 2 strains that had mutations in both E1 and E2; T123TS plus S143L and T123TI plus S143SL. 2017 PloS one Result HBV S143L 71 76 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. Those omitted included R122K which is the determinant for subtyping HBsAg as ad versus ay, T126I for genotype C, A128V for genotype D2, and T131N for genotype A1. 2017 PloS one Result HBV R122K;T126I;A128V;T131N 23;91;113;140 28;96;118;145 S 68 73 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. Three strains had mutations within E2 plus additional mutations outside of E1 and E2; S143SL, T131TN, and M133MT (n = 1), D144A, G145A, and M133I (n = 1), and G145R, T126TI, and Y134YN (n = 1). 2017 PloS one Result HBV D144A;G145A;M133I;G145R 122;129;140;159 127;134;145;164 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. 10 of 11 (91%) of the occult D1 sequences harbored this sQ129R mutation (Fig 5). 2017 PloS one Result HBV Q129R 56 62 S 56 57 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Despite the patient population being ART-naive, one OBI sample (O-EICIS.9; belonging to HBV/A1) of 17 (5.9%) harbored the rtL180M+rtM204V lamivudine resistant mutations. 2017 PloS one Result HBV L180M;M204V 124;132 129;137 RT;RT 122;130 124;132 Occult Hepatitis B 52 55 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. In addition, on analyzing the complete genome of 5 occult HBV/D1 strains, it was found to be associated with mutations such as psA39T in preS, xP42T in X, and cT80I in the core gene. 2017 PloS one Result HBV P39T;S39T;P42T;T80I;A39T 127;127;143;159;127 133;133;148;164;133 C;C;PreS;X;X 159;172;137;143;152 160;176;141;144;153 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Other diagnostic escape mutations found in the surface ORF were sR122K (5.9%), sG145A (5.9%), and sW172* (5.9%). 2017 PloS one Result HBV R122K;G145A;W172X 64;79;98 70;85;104 S;S;S;S 64;79;98;47 65;80;99;54 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The major mutation detected among occult D1 sequences was Q129R (58.8%) in the S gene and N33D (58.8%) in the RT region of the P gene. 2017 PloS one Result HBV Q129R;N33D 58;90 63;94 P;RT;S 127;110;79 128;112;80 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. Precore (G1896A) mutation was found in 34.1% (62 samples) of the study population, which produced two fragments of 261 and 34 bp in length, which were observable by electrophoresis (Figures 1, 2). 2017 Electronic physician Result HBV G1896A 9 15 Precore 0 7 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. In the pre S/S region, there were sI195M and sQ129H. 2017 Infection and drug resistance Result HBV I195M;Q129H 34;45 40;51 PreS;S;S 7;34;45 12;35;46 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. However, the relationship between other atypical AA substitutions with susceptibility to NUCs has not been characterized in vitro, such as rtI169L (not typical rtI169T) and rtM204L (not typical rtM204I/V). 2017 Viruses Result HBV M204I;M204V;I169L;I169T;M204L 196;196;141;162;175 203;203;146;167;180 RT;RT;RT;RT 139;160;173;194 141;162;175;196 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Interestingly, only rtL80V (n = 7), rtV173L (n = 2) and rtT184A/S (n = 2) were typical NUCr substitutions, whose ability to confer resistance to NUCs have been well elucidated in vitro. 2017 Viruses Result HBV L80V;T184A;T184S;V173L 22;58;58;38 26;65;65;43 RT;RT;RT 20;36;56 22;38;58 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Among 9 mutated isolates sharing 6 types of aa substitutions with HBV genotype B, three types of VEMs (T126A, Q129H and D144A) were also detected (Table 4). 2017 Scientific reports Result HBV T126A;Q129H;D144A 103;110;120 108;115;125 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Eight types of these mutations (I126S, I126N, Q129H, S143L, D144A, D144E, G145A, and G145R) had demonstrated low ability to bind antibodies and were identified as VEMs previously. 2017 Scientific reports Result HBV I126S;I126N;Q129H;S143L;D144A;D144E;G145A;G145R 32;39;46;53;60;67;74;85 37;44;51;58;65;72;79;90 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. In addition, the other six mutations types (P127T, A128V, G130E, T131P, M133I and D144N) were not yet identified as VEMs, and D144N was a newly identified mutation (Table 3). 2017 Scientific reports Result HBV P127T;A128V;G130E;T131P;M133I;D144N;D144N 44;51;58;65;72;82;126 49;56;63;70;77;87;131 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Notably, two T131N/M133T (a novel N-linked glycosylation site) double mutations associated with I126S were observed in our study. 2017 Scientific reports Result HBV M133T;T131N;I126S 19;13;96 24;18;101 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. The most prevalent mutation position was aa 126 [I126S (n = 24), I126N (n = 6), T126A (n = 2), 29.63%], and aa145 [G145R (n = 5), G145A (n = 23), 25.93%], all of which were recognized as VEMs. 2017 Scientific reports Result HBV I126S;I126N;T126A;G145R;G145A 49;65;80;115;130 54;70;85;120;135 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. Six out of the 44 isolates of HBV genotype B4 (13.6%) had a promoter mutation in G1613A (Fig 6). 2017 PloS one Result HBV G1613A 81 87 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. There were no C1653T mutations, two (4.5%) T1753V mutations, five (11.4%) double mutations of A1762T/G1764A, and three (6.8%) double mutations of C1766T/T1768A. 2017 PloS one Result HBV G1764A;T1768A;C1653T;T1753V;A1762T;C1766T 101;153;14;43;94;146 107;159;20;49;100;152 28859616 Molecular characterization of hepatitis B virus in Vietnam. A double mutation (A1762T and G1764A) was identified in 67.5% (25/37) of the C1 subgenotype isolates compared to 8.2% (8/98) of the genotype B isolates (p < 0.001). 2017 BMC infectious diseases Result HBV A1762T;G1764A 19;30 25;36 28859616 Molecular characterization of hepatitis B virus in Vietnam. A G1896A mutation in PC gene was present in 22.2% (30/135) of the isolates, including 30.6% (30/98) of the genotype B isolates compared to 0% of the C1 isolates (p < 0.000). 2017 BMC infectious diseases Result HBV G1896A 2 8 Precore 21 23 28859616 Molecular characterization of hepatitis B virus in Vietnam. A2962G and C2964A mutations were identified in 99% (97/98) and 98% (96/98) of the genotype B isolates (Table 2). 2017 BMC infectious diseases Result HBV A2962G;C2964A 0;11 6;17 28859616 Molecular characterization of hepatitis B virus in Vietnam. Among the isolates, 8.1% (11/135) had a mutation in the "a" determinant region including 2.2% (3/135) P120S/T, 2.2% (3/135) I/T126S/A, 3% (4/135) M133 L/T and 0.7% (1/135) G145R. 2017 BMC infectious diseases Result HBV I126S;I126A;T126S;T126A;P120T;P120S;M133L;M133T;G145R 124;124;124;124;102;102;146;146;172 133;133;133;133;109;109;154;154;177 28859616 Molecular characterization of hepatitis B virus in Vietnam. BCP/preC/core gene mutation: BCP mutations at T1753C, G1757A, A1762T, G1764 T and C1766G were analyzed and 30.4% (41/135) of all isolates including 78.4% (29/37) of the C1 isolates had at least one mutation. 2017 BMC infectious diseases Result HBV T1753C;G1757A;A1762T;G1764T;C1766G 46;54;62;70;82 52;60;68;77;88 BCP;BCP;C;Precore 0;29;9;4 3;32;13;8 28859616 Molecular characterization of hepatitis B virus in Vietnam. N3S mutation was significantly higher in genotype C isolates (p < 0.001) isolates (Table 2). 2017 BMC infectious diseases Result HBV N3S 0 3 28859616 Molecular characterization of hepatitis B virus in Vietnam. T1753C, G1757A, A1762T, G1764A and C1766G mutations were identified in 11.1% (5/135), 7.4% (10/137), 25.9%% (35/135), 24.4% (33.135) and 2.2% (3/135) of the isolates and A1762T and G1764 T mutations were significantly more frequent in the genotype C1 isolates (p < 0.001) (Table 3). 2017 BMC infectious diseases Result HBV T1753C;G1757A;A1762T;G1764A;C1766G;A1762T;G1764T 0;8;16;24;35;170;181 6;14;22;30;41;176;188 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Activation of Wnt/beta-catenin signaling pathways in livers of C1458T-HBxTg mice. 2017 Scientific reports Result HBV C1458T 63 69 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Although no significant difference was observed in the incidence of liver tumors in male mice among the two C1485T-HBx Tg mouse lines and two WT-HBx Tg mouse lines, there was a significant difference in the number of liver tumors per body between these two lines; the tumor emergence was significantly higher in C1485T-HBxTg mice than in WT-HBxTg mice (p = 0.060) as well as control non-Tg mice (p = 0.002. 2017 Scientific reports Result HBV C1485T;C1485T 108;312 114;318 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Among these five HBx mutations, C1485T and C1653T mutations were more frequently detected in HCC than in non-HCC cases (Table 1). 2017 Scientific reports Result HBV C1485T;C1653T 32;43 38;49 X 17 20 Hepatocellular carcinoma;Hepatocellular carcinoma 93;109 96;112 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Collectively, these results strongly suggest that hepatocytes overexpressing C1485T-HBx show higher sensitivity to DEN-induced carcinogenesis than those overexpressing intact HBx. 2017 Scientific reports Result HBV C1485T 77 83 X;X 84;175 87;178 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Collectively, these results suggest that C1485T and C1653T mutations in HBx contribute more significantly to HBV-related hepatocarcinogenesis in patients without LC than in those with LC where direct role of HBx should be less critical. 2017 Scientific reports Result HBV C1485T;C1653T 41;52 47;58 X;X 72;208 75;211 Liver cirrhosis;Liver cirrhosis 162;184 164;186 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Collectively, these results suggest that the promotion of hepatocarcinogenesis induced by the overexpression of HBx-C1485T is accompanied by the enhanced activation of JNK signaling pathways and subsequent production of ROS. 2017 Scientific reports Result HBV C1485T 116 122 X 112 115 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with the results obtained for p-GSK3beta, beta-catenin levels in the liver were higher in C1485T-HBxTg mice than in WT-HBxTg mice. 2017 Scientific reports Result HBV C1485T 101 107 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with the results of BrdU and cyclin D1 staining, the expression of the oncogenic protein, c-myc, was significantly enhanced in the hepatocytes of mice overexpressing C1485T-HBx than in those overexpressing WT-HBx and those not expressing HBx. 2017 Scientific reports Result HBV C1485T 177 183 X;X;X 184;220;249 187;223;252 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with this finding, oxidized protein levels were significantly higher in C1485T-HBxTg mice than in WT-HBxTg mice, as assessed by OxyBlot. 2017 Scientific reports Result HBV C1485T 83 89 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Expression vectors containing WT- or C1485T-HBx were transfected into HepG2 cells in order to compare their effects on the activation of several oncogenic pathways (Wnt, extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK), p53, nuclear factor-kappa B (NF-kappaB), hypoxia induced factor (HIF), Notch, transforming growth factor-beta (TGF-beta), retinoblastoma protein (pRb)-E2F, and Myc. 2017 Scientific reports Result HBV E2F;C1485T 395;37 398;43 X 44 47 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Following confirmation of the effects of C1485T-HBx on hepatocyte proliferation, as assessed by BrdU and cyclin D1 staining, we attempted to identify the signaling pathways responsible for enhanced hepatocyte proliferation. 2017 Scientific reports Result HBV C1485T 41 47 X 48 51 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Following the identification of the susceptible viral mutations (the C1485T HBx or C1653T HBx mutation) and host factor (the presence of LC) for HBV-related hepatocarcinogenesis in the multivariate analysis, we compared the frequencies of HBx mutations between HCC and non-HCC cases in the context of background liver conditions. 2017 Scientific reports Result HBV C1485T;C1653T 69;83 75;89 X;X;X 76;90;239 79;93;242 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 261;273;137 264;276;139 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In contrast, HepG2 cells overexpressing C1485T-HBx showed weaker NF-kappaB transcriptional activity than those overexpressing control and WT-HBx (p = 0.028 vs. 2017 Scientific reports Result HBV C1485T 40 46 X;X 47;141 50;144 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In contrast, the expression of IkappaB -alpha in the liver was markedly reduced in WT-HBxTg mice than in C1485T-HBxTg mice. 2017 Scientific reports Result HBV C1485T 105 111 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In order to confirm the effects of WT- and C1485T-HBx on hepatocyte proliferation, we compared the degree of DNA synthesis in livers after the DEN injection using BrdU staining. 2017 Scientific reports Result HBV C1485T 43 49 X 50 53 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Increased cell proliferation in livers of C1458T-HBxTg mice. 2017 Scientific reports Result HBV C1458T 42 48 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. It might be possible that difference in sensitivity to DEN-induced hepatocarcinogenesis between WT-HBxTg mice and C1485T-HBxTg mice may be caused by different expression levels of HBx between these two lines. 2017 Scientific reports Result HBV C1485T 114 120 X 180 183 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Moreover, a cell-cycle analysis using cyclin D1 staining also revealed higher numbers of cyclin D1-positive hepatocytes in mice overexpressing C1485T-HBx than in those overexpressing WT-HBx. 2017 Scientific reports Result HBV C1485T 143 149 X;X 150;186 153;189 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. No specific gene loci were identified as integration sites of transgenes in any of WT-HBxTg and C1485T-HBxTg mice (Supplementary Table 1), suggesting that the integration event should result in structural alterations of known cancer-related genes that could enhance oncogenic pathways. 2017 Scientific reports Result HBV C1485T 96 102 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. p-GSK3beta expression levels in the liver were higher in C1485T-HBx mice than in control non-Tg and WT-HBxTg mice. 2017 Scientific reports Result HBV C1485T 57 63 X 64 67 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Since the presence of the C1485T mutation showed a higher odds ratio for the development of HCC than the C1653T mutation (Table 2), we focused on the role of C1485T mutation on carcinogenesis and then attempted to directly confirm the oncogenic potential of C1485T-HBx in an in vivo experimental model. 2017 Scientific reports Result HBV C1485T;C1653T;C1485T;C1485T 26;105;158;258 32;111;164;264 X 265 268 Hepatocellular carcinoma 92 95 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Subsequently, we tried to evaluate the development of liver tumor in WT-HBxTg and C1485T-HBx Tg mice. 2017 Scientific reports Result HBV C1485T 82 88 X 89 92 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Suppression of NF-kappaB in livers of C1458T-HBxTg mice. 2017 Scientific reports Result HBV C1458T 38 44 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The analysis of patients with non-LC revealed that C1485T and C1653T mutations were more frequent in HCC than in non-HCC cases (p = 0.003 and p = 0.004 for the C1485T and C1653T mutations, respectively. 2017 Scientific reports Result HBV C1485T;C1653T;C1485T;C1653T 51;62;160;171 57;68;166;177 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. the expression of p-IkappaB -alpha in the liver was significantly reduced in C1485T-HBxTg mice than in control non-Tg and WT-HBxTg mice. 2017 Scientific reports Result HBV C1485T 77 83 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The expression of phosphorylated c-Jun in the liver was stronger in C1485T-HBxTg than in WT-HBxTg mice as assessed by immunoblotting. 2017 Scientific reports Result HBV C1485T 68 74 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. the greater incorporation of BrdU was observed in the nuclei of hepatocytes in mice overexpressing C1485T-HBx than in those overexpressing WT-HBx and those not expressing HBx. 2017 Scientific reports Result HBV C1485T 99 105 X;X;X 106;142;171 109;145;174 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. the number of male mice that developed liver tumor was significantly higher in the C1485T-HBxTg mouse lines than in control non-Tg mice eight months after the injection of DEN (p = 0.014. 2017 Scientific reports Result HBV C1485T 83 89 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The presence of the C1485T or C1653T mutation in HBx in combination with LC was identified as an independent factor for the development of HCC (Table 2). 2017 Scientific reports Result HBV C1485T;C1653T 20;30 26;36 X 49 52 Hepatocellular carcinoma;Liver cirrhosis 139;73 142;75 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The results of the Cignal Finder reporter assay suggested that the presence of C1485T-HBx in hepatocytes inhibited the activation of NF-kappaB. 2017 Scientific reports Result HBV C1485T 79 85 X 86 89 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The transfection of the WT- or C1485T-HBx gene into HepG2 cells did not alter reporter gene activity regulated by the ERK, JNK, p53, HIF, Notch, TGF-beta, pRb-E2F, or Myc signaling pathways, probably because these signaling pathways are constitutively activated in HepG2 cells, as previously described. 2017 Scientific reports Result HBV E2F;C1485T 159;31 162;37 X 38 41 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Therefore, we performed a quantitative PCR analysis, and found that the HBx mRNA level was not higher, or rather lower, in mice overexpressing C1485T-HBx, which was more susceptible for hepatocarcinogenesis, than in those carrying WT-HBx overexpression. 2017 Scientific reports Result HBV C1485T 143 149 X;X;X 72;150;234 75;153;237 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. This increase in transcriptional activity was significantly greater in HepG2 cells overexpressing C1485T-HBx than in those overexpressing WT-HBx (p = 0.007. 2017 Scientific reports Result HBV C1485T 98 104 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. This result prompted us to investigate the effects of C1485T-HBx on the NF-kappaB pathway in vivo. 2017 Scientific reports Result HBV C1485T 54 60 X 61 64 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, it is conceivable that the presence of C1485T-HBx interferes with NF-kappaB signaling, the effects of which were accompanied by the activation of c-Jun with the potent ability to accelerate cell proliferation, as reported previously. 2017 Scientific reports Result HBV C1485T 45 51 X 52 55 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the higher incidence of tumor emergence in C1485T-HBxTg mice could be caused by C1485T mutation rather than the expression levels of HBx. 2017 Scientific reports Result HBV C1485T;C1485T 49;86 55;92 X 139 142 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the promotion of DEN-induced hepatocarcinogenesis observed in C1485T- HBxTg mice was characterized by the enhanced activation of the Wnt signaling pathway combined with attenuated activation of NF-kappaB signaling pathways. 2017 Scientific reports Result HBV C1485T 68 74 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the results of immunoblotting and tissue staining strongly suggest the suppression of NF-kappaB activation in the livers of C1458T-HBxTg mice. 2017 Scientific reports Result HBV C1458T 130 136 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Transfection with WT- and C1485T-HBx enhanced the transcriptional activity of the Wnt signaling cascade more than the control empty vector. 2017 Scientific reports Result HBV C1485T 26 32 X 33 36 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We analyzed the transcriptional activity of WT- and C1485T-HBx genes using the Cignal Finder Reporter Array, as previously reported. 2017 Scientific reports Result HBV C1485T 52 58 X 59 62 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We compared the frequencies of C1485T and C1653T mutations in LC and non-LC cases. 2017 Scientific reports Result HBV C1485T;C1653T 31;42 37;48 Liver cirrhosis;Liver cirrhosis 62;73 64;75 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We created Tg mice overexpressing the HBx C1485T mutation (referred to as C1485T-HBxTg) and WT-HBx (WT-HBxTg). 2017 Scientific reports Result HBV C1485T;C1485T 42;74 48;80 X;X 38;95 41;98 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We established two Tg lines overexpressing WT-HBxTg and two Tg lines overexpressing C1485T-HBx. 2017 Scientific reports Result HBV C1485T 84 90 X 91 94 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We examined the activation status of Wnt signaling pathways because the reporter gene assay showed an increase in activation of the Wnt signaling pathway in WT- and C1485T-HBx-overexpressing cells, particularly in those overexpressing HBx-C1485T. 2017 Scientific reports Result HBV C1485T;C1485T 165;239 171;245 X;X 172;235 175;238 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We found that the presence of a double core promoter mutation (A1762T and G1764A) correlated with the development of HCC, as reported previously (data not shown). 2017 Scientific reports Result HBV A1762T;G1764A 63;74 69;80 Core promoter 39 52 Hepatocellular carcinoma 117 120 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We initially analyzed the level of IkappaB -alpha phosphorylation (p-IkappaB -alpha) in the livers of male control non-Tg and Tg mice carrying WT-HBx and C1485T-HBx four hours after the administration of DEN. 2017 Scientific reports Result HBV C1485T 154 160 X;X 146;161 149;164 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We then attempted to identify HBx mutations associated with HBV-related hepatocarcinogenesis and found five different HBx mutations (C1653T, C1485T, C1470A, C1479A, and C1575G) in CHB patients. 2017 Scientific reports Result HBV C1653T;C1485T;C1470A;C1479A;C1575G 133;141;149;157;169 139;147;155;163;175 X;X 30;118 33;121 Chronic Hepatitis B 180 183 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Among patients with HBV genotype D, the PC mutation G1896A was detected in 84.1% of the cases (53/63), while the G1862T mutation was detected in 92.3% of the subjects infected with HBV genotype A (36/39) (p < 0.01). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A;G1862T 52;113 58;119 Precore 40 42 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Among the 58 sequences classified as genotype A in this study, only one exhibited the G1896A mutation. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A 86 92 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. An association between infection with the HBV A1762T/G1764A BCP mutant and the presence of moderate and severe fibrosis, clinically detected hepatic cirrhosis, and the presence of HCC was verified in this study. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 53;46 59;52 BCP 60 63 Liver cirrhosis;Hepatocellular carcinoma 141;180 158;183 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. BCP and PC mutations and forms of chronic HBV infection - Among the 129 patients in whom the HBV PC region was analysed, a high frequency of HBV strains with G1896A mutation (53/129, 41%) was detected, alone or in G1896A/G1899A double mutation, particularly in the subgroup with HBeAg-negative chronic hepatitis (39/85, 45.9%) (p = 0.03). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1899A;G1896A;G1896A 221;158;214 227;164;220 BCP;C;Precore;Precore 0;279;8;97 3;284;10;99 HBV infections;Chronic Hepatitis B 34;279 55;311 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. HBV strains with BCP mutations, the most frequent being the A1762T/G1764A double mutation, were detected in 59.3% (70/118) of the patients studied. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 67;60 73;66 BCP 17 20 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. HBV with G1862T and G1896A mutations, alone or in double mutation patterns, were the most frequent (31% and 44.2%, respectively). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1862T;G1896A 9;20 15;26 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. HCC and cirrhosis were found to be associated with the presence of the A1762T/G1764A mutant (OR = 5.42, 95% CI 1.41-20.87; and OR = 5.37, 95% CI 1.07-27.08, respectively). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 78;71 84;77 Hepatocellular carcinoma;Liver cirrhosis 0;8 3;17 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. In a large population-based prospective study conducted in 10 urban centres in Taiwan, in which there was a greater prevalence of infection with HBV genotypes B and C, detected the highest rates of progression to HCC among individuals infected by HBV carrying the A1762T/G1764A double mutation. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 271;264 277;270 Hepatocellular carcinoma 213 216 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. In this viral sequence, as expected, the presence of the C1858T mutation was noted. 2017 Memorias do Instituto Oswaldo Cruz Result HBV C1858T 57 63 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Infection with the HBV BCP A1762T/G1764A mutant was associated with advanced fibrosis [odds ratio (OR) = 7.76, 95% confidence interval (95%CI) 1.57-38.39]. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 34;27 40;33 BCP 23 26 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. It was also observed that patients with HCC were more frequently infected with the BCP A1762T/G1764A mutant than those without HCC (77.8% versus 39.4%; p = 0.03) (Table IV). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 94;87 100;93 BCP 83 86 Hepatocellular carcinoma;Hepatocellular carcinoma 40;127 43;130 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. No association was detected between the presence of the A1762T/G1764A mutation and the different HBV genotypes. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 63;56 69;62 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Regarding comparisons between genotypes A and D in an Indian study, the progression of chronic hepatitis B to HCC seemed to be more frequent in patients infected by HBV genotype D and was associated with the A1762T/G1764A mutant. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 215;208 221;214 Chronic Hepatitis B;Hepatocellular carcinoma 87;110 106;113 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Some studies have associated the presence of the A1762T/G1764A mutation with a lower expression of viral antigens, in vitro or in vivo. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 56;49 62;55 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. Switching base G to A at position 1896 of the genome, base T is included at position 1858. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A 15 38 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The A1762T/G1764A double mutation was less frequent among inactive carriers (5/23, 21.7%) (p = 0.03) and the wild-type for the BCP region (without mutations) was more frequent among inactive carriers (18/23, 66.7%) (p < 0.01) (Table II). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 11;4 17;10 BCP 127 130 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The A1762T/G1764A variant was identified in 36.7% of patients with grade 1 and 2 liver fibrosis (29/79) and in 81.8% with grade 3 and 4 (9/11) (p < 0.01); and in 76.9% of patients with cirrhosis (10/13) and in 38.1% of patients without cirrhosis (40/105) (p = 0.01). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 11;4 17;10 Liver fibrosis;Liver cirrhosis;Liver cirrhosis 81;185;236 95;194;245 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The frequency of the A1762T/G1764A BCP double mutation was similar among the different HBV genotypes (44.2% in HBV genotype A, 40.6% in HBV genotype D, and 50% in HBV genotype F). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 28;21 34;27 BCP 35 38 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The G1862T mutation was previously described in association with HBV genotype A, particularly with sub-genotype A1. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1862T 4 10 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The G1896A HBV mutation is related to HBeAg negative forms of infection . 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A 4 10 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The presence of T in position 1858 is common among HBV genotype D and uncommon among HBV genotype A, so finding this type of mutation in HBV genotype A sequences is not expected unless the virus has the C1858T mutation . 2017 Memorias do Instituto Oswaldo Cruz Result HBV C1858T 203 209 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The presence of the HBV A1762T/G1764A BCP double mutant was independently associated with the presence of advanced forms of chronic liver disease, such as severe fibrosis, liver cirrhosis, and HCC, in Brazilian infected patients. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 31;24 37;30 BCP 38 41 Liver cirrhosis;Hepatocellular carcinoma 172;193 187;196 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The rate of infection with the HBV BCP A1762T/G1764A mutant was also higher in patients with cirrhosis than in patients without cirrhosis (76.9% versus 38.1%; p = 0.01). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 46;39 52;45 BCP 35 38 Liver cirrhosis;Liver cirrhosis 93;128 102;137 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. The reason why there are high proportions of G1896A HBV mutations in the present study is possibly related to the high prevalence of genotype D. 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A 45 51 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. There was an association between the presence of the G1896A mutation and genotype D in the subjects studied here (p < 0.01). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1896A 53 59 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. With regard to the presence of BCP or PC mutations, the A1762T/G1764A variant was identified in 36.7% of patients with grade 1 and 2 liver fibrosis (29/79) and in 81.8% of patients with grade 3 and 4 liver fibrosis (9/11) (p < 0.01); in 76.9% of patients with cirrhosis (10/13) and in 38.1% of patients without cirrhosis (40/105) (p = 0.01). 2017 Memorias do Instituto Oswaldo Cruz Result HBV G1764A;A1762T 63;56 69;62 BCP;Precore 31;38 34;40 Liver fibrosis;Liver fibrosis;Liver cirrhosis;Liver cirrhosis 133;200;260;311 147;214;269;320 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The first escape mutant had change from guanine to adenine in nucleotide 587, resulting in the amino acid change from glycine to arginine in residue 145 (G145R) of the HBsAg; this mutation was present in sample obtained from a mother (127_Boyahuazu_AM Accession number MF400839). 2017 PloS one Result HBV G145R;G145R 154;118 159;152 S 168 173 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The second escape mutant identified had a change from guanine to adenine in nucleotide 621, which generated a stop codon in position 156 (W156*); this mutation was identified in sample 189_Tarapaca_AM (Accession number MF400842) obtained from a child with Occult HBV infection (OBI) (Table 2). 2017 PloS one Result HBV W156X 138 143 Occult Hepatitis B 278 281 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. Higher incidence of A1762T/G1764A and G1896A mutations in HBV BCP/PC region in HBeAg negative hepatitis B patients. 2017 Virology journal Result HBV G1764A;A1762T;G1896A 27;20;38 33;26;44 BCP;C;Precore 62;79;66 65;84;68 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. In addition, the A1762T/G1764A mutations were more frequently seen in immune active CHB group than in both ACLF-CHB groups (*****p < 0.0001. 2017 Virology journal Result HBV G1764A;A1762T 24;17 30;23 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. Similarly, the incidence of classic G1896A mutation in HBV precore region was significantly higher in HBeAg negative hepatitis group (80%) than that in both ACLF-CHB groups (0%, ****p < 0.0001) and immune active group (0%, ****p < 0.0001. 2017 Virology journal Result HBV G1896A 36 42 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The median frequency of A1762T/G1764A dual mutations in BCP region was significantly higher in HBeAg negative hepatitis CHB (67%, **** p < 0.0001) as well as the immune active CHB group (6%, *p < 0.05) compared to the ACLF-CHB cohort (both 0% in both HBeAg positive and HBeAg negative). 2017 Virology journal Result HBV G1764A;A1762T 31;24 37;30 BCP;C;C;C 56;95;251;270 59;100;256;275 Chronic Hepatitis B;Chronic Hepatitis B 176;223 179;226 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. However, the classical vaccine escape mutation G145R was not detected. 2017 PloS one Result HBV G145R 47 52 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. rtV173L, rtL180M, and/or rtM204V) in 7/13 HBV/HIV co-infected patients tested. 2017 PloS one Result HBV L180M;M204V;V173L 11;27;2 16;32;7 RT;RT;RT 0;9;25 2;11;27 HBV-HIV coinfections 46 61 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. The most frequent HBV DRM found was rtL180M (53.8%), followed by rtV173L (46.2%), and rtM204V (46.2%). 2017 PloS one Result HBV L180M;V173L;M204V 38;67;88 43;72;93 RT;RT;RT 36;65;86 38;67;88 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A combinational mutation with substitutions of K to M at position 130 and V to I at position 131 was present in 16.33% of IC, 24% of AC, 26.93% of LC, and 46.42% of HCC patients. 2017 Oncotarget Result HBV K130M;V131I 47;74 69;96 Hepatocellular carcinoma;Liver cirrhosis 165;147 168;149 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A triple mutation with substitution of I to T at position 127, K to M at position 130, and V to Isoleucine (I) at position 131 of HBx was observed in 9.38% of IC, 8.8% of AC, 11.54% of LC, and 46.42% of HCC patients. 2017 Oncotarget Result HBV I127T;K130M;I131I 39;63;95 61;85;127 X 130 133 Hepatocellular carcinoma;Liver cirrhosis 203;185 206;187 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Another triple mutation with substitution of K to M, V to I, and F to Y at positions 130, 131, and 132, respectively, was present in 32.14% of HCC patients, while its frequency was very low in the IC group (0.41%). 2017 Oncotarget Result HBV F130Y 65 88 Hepatocellular carcinoma 143 146 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Both AC and LC groups did not have this combinational mutation (K130M+V131I+F132Y). 2017 Oncotarget Result HBV K130M;V131I;F132Y 64;70;76 69;75;81 Liver cirrhosis 12 14 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. F132Y/I/R was present in 39.3% of HCC patients, while it showed low prevalence in LC (3.85%), AC (4%), and IC groups (4.49%). 2017 Oncotarget Result HBV F132Y;F132I;F132R 0;0;0 9;9;9 Hepatocellular carcinoma;Liver cirrhosis 34;82 37;84 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Furthermore, multivariate regression analysis revealed that HBV viral load (p < 0.0001), mutation from H to Y at aa94 with (p = 0.011), and mutation from F to Y at aa132 (p = 0.035) were independently associated with LC+HCC (Table 5). 2017 Oncotarget Result HBV H94Y;F132Y 103;154 117;169 Hepatocellular carcinoma;Liver cirrhosis 220;217 223;219 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Histidine (H) at position 94 was substituted to tyrosine (Y) in 25% of HCC samples, while this mutation was present at low frequency in the other clinical groups (Table 2). 2017 Oncotarget Result HBV H94H -2 29 Hepatocellular carcinoma 71 74 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. I127T+K130M+V131I combinational mutation showed a significant difference in occurrence when the AC group was compared with the LC+HCC group (p < 0.0001) as well as when the HCC group was compared with the IC+AC+LC group (p < 0.0001). 2017 Oncotarget Result HBV I127T;K130M;V131I 0;6;12 5;11;17 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 130;173;127;211 133;176;129;213 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. In addition, multivariate analysis showed a significant association with HBV viral load (p < 0.0001), ALT (p = 0.002) and the mutation from F to Y at aa132 (p = 0.007) (Table 4). 2017 Oncotarget Result HBV F132Y 140 155 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. K130M+V131I+F132Y combinational mutation was significantly associated with the risk of HCC development (p < 0.0001). 2017 Oncotarget Result HBV K130M;V131I;F132Y 0;6;12 5;11;17 Hepatocellular carcinoma 87 90 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. The combinational mutation of K130M+V131I was significantly associated with the risk of HCC development (p = 0.001). 2017 Oncotarget Result HBV K130M;V131I 30;36 35;41 Hepatocellular carcinoma 88 91 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. The prevalence of I127T mutation was 50% in HCC, 19.23% in LC, 13.6% in AC, and 11.84% in IC groups. 2017 Oncotarget Result HBV I127T 18 23 Hepatocellular carcinoma;Liver cirrhosis 44;59 47;61 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. These included mutations of isoleucine (I) to threonine (T) at position 127 (p < 0.0001), valine (V) to I at position 131 (p = 0.025), and phenylalanine (F) at position 132 to either tyrosine (Y), isoleucine (I), or arginine (R) (p < 0.0001). 2017 Oncotarget Result HBV F132F 138 173 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. This combinational mutation (I127T+K130M+V131I) was significantly associated with the risk of HCC development (p < 0.0001). 2017 Oncotarget Result HBV I127T;K130M;V131I 29;35;41 34;40;46 Hepatocellular carcinoma 94 97 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Univariate analysis showed that age (p < 0.0001), HBV viral load (p < 0.0001), mutation from A to S at aa47 (p = 0.047), mutation from H to Y at aa94 (p = 0.002), mutation from I to T at aa127 (p = 0.001), mutation from F to Y at aa132 (p = 0.001) and mutation from A to V at aa146 (p = 0.025) showed a significant correlation with HBV-related LC+HCC (Table 5). 2017 Oncotarget Result HBV A47S;H94Y;I127T;F132Y;A146V 93;135;177;220;266 107;149;192;235;281 Hepatocellular carcinoma;Liver cirrhosis 347;344 350;346 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Univariate analysis showed that gender (p < 0.0001), HBV viral load (p < 0.0001), ALT (p = < 0.0001), mutation from K to M at amino acid (aa) 130 (p = 0.002) and V to I at aa131 (p = 0.042) had a significant positive correlation when the IC group was compared with AC+LC+HCC (Table 4). 2017 Oncotarget Result HBV V131I 162 177 Hepatocellular carcinoma;Liver cirrhosis 271;268 274;270 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. V131I mutation was more prevalent in HCC (53.57%) than in LC (34.62%), AC (34.4%), and IC (26.94%). 2017 Oncotarget Result HBV V131I 0 5 Hepatocellular carcinoma;Liver cirrhosis 37;58 40;60 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. As shown in Table 4, after adjusting for clinical characteristics, the following three mutation sites were identified as independent predictors of a shorter survival period in HCC at statistically significant levels: mutation at nucleotide 31 (RR, 8.929; 95% CI, 3.433-23.22; P = 0.000) inducing the 314 Ser to Pro amino acid substitution in the spacer domain; at nucleotide 529 (RR, 5.656; 95% CI, 1.599-19.999; P = 0.007) inducing the 480 Asp to Asn amino acid substitution; and at nucleotide 1078 (RR, 3.442; 95% CI, 1.070-11.068; P = 0.038) inducing the 663 Ser to Ala amino acid substitution in the RT domain of HBV polymerase (Table 3). 2017 PloS one Result HBV S314P;D480N;S663A 300;437;558 314;451;572 P;RT 621;604 631;606 Hepatocellular carcinoma 176 179 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. Of these 86 sites, the following 19 were associated with postoperative survival at statistically significant levels (P<0.05) in HCC tissue based on the log-rank test with the Kaplan-Meier method (Table 3): nucleotides 2525 (Asp73Glu), 2733 (Lys143Gln), 2738, 2768, 2946 (Val210Ile), 3063, 3066 (Pro249Ser), 3109 (Thr268Ser), 31 (Ser314Pro), 529 (Asp480Asn), 735, 939, 1078 (Ser663Ala), 1137, 1383, 1461, 1485, 1544 (Val818Asp or Val818Ala); and 1613 (Arg841Lys). 2017 PloS one Result HBV D73E;K143Q;V210I;P249S;T268S;S314P;D480N;S663A;V818D;V818A;R841K 224;241;271;295;313;329;346;374;416;429;451 232;250;280;304;322;338;355;383;425;438;460 Hepatocellular carcinoma 128 131 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. All patients with RAM M204V/I received 3TC-based therapy. 2018 PloS one Result HBV M204V;M204I 22;22 29;29 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. However, 60% of our strains had the S143T polymorphic mutation followed by G145K and K141R (for 2 patients) and M133I and D144N (for one patient) (Fig 4, Table 4). 2018 PloS one Result HBV S143T;G145K;K141R;M133I;D144N 36;75;85;112;122 41;80;90;117;127 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. Looking for VEMs, MRT showed only one patient highlighted the VEM G130N. 2018 PloS one Result HBV G130N 66 71 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. The analysis of HBV strains for the S/Pol gene by the MRT online software showed that of the major RAMs, M204V/I was the most frequent (4/10, 40%), followed by its compensatory RAMs; L180M (3/10, 30%) and V173L (2/10, 20%). 2018 PloS one Result HBV M204V;M204I;L180M;V173L 105;105;183;205 112;112;188;210 P;S 38;36 41;37 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. The MRT revealed I169L mutation in one patient (Fig 4, Table 4). 2018 PloS one Result HBV I169L 17 22 29326804 Occult Hepatitis B Virus Infection and Associated Genotypes among HBsAg-negative Subjects in Burkina Faso. A single strain of "false OBI "carried the G145R mutation (Table 3). 2018 Mediterranean journal of hematology and infectious diseases Result HBV G145R 43 48 Occult Hepatitis B 26 29 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Among 48 HIV co-infected subjects analyzed, 31.3% (15) of them developed 3TC/ETV resistance at YMDD RT motif due to rtM204V/I+rtL180M and/or rtV173L HBV gene mutations (Table 4). 2018 PloS one Result HBV M204V;M204I;L180M;V173L 118;118;128;143 125;125;133;148 RT;RT;RT;RT;P 100;116;126;141;95 102;118;128;143;99 HBV-HIV coinfections 9 24 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. However, only three HIV co-infected patients (ETH1480, ETH2120 and ETH4480) with the ADV resistance associated gene mutations developed G1862T and the other two patients (ETH1649 and ETH2520) showed mutant variant G1896A (Table 3). 2018 PloS one Result HBV G1862T;G1896A 136;214 142;220 HBV-HIV coinfections 20 35 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. In respect to PC mutations, co-distribution of the overall PC mutations and ADV resistance gene variants (rtQ215H and rtI233V) were common during HIV co-infection. 2018 PloS one Result HBV Q215H;I233V 108;120 113;125 Precore;Precore;RT;RT 14;59;106;118 16;61;108;120 HBV-HIV coinfections 146 162 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Many of the BCP mutations showed no significant difference among the study groups except for the A1762T, G1764A and T1768A mutant variants (Table 2). 2018 PloS one Result HBV A1762T;G1764A;T1768A 97;105;116 103;111;122 BCP 12 15 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Moreover, HBV mono-infected blood donors and CLD patients who had no any drug resistance gene variants developed comparable G1862T (60.6% (20/33) vs. 2018 PloS one Result HBV G1862T 124 130 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Only mutant variants A1814C/C1816T (23.5 vs. 5.6%) and G1896/C1858T (31.5 vs. 5.6%) were significantly higher in HBeAg negative cases than positives (Fig 2B). 2018 PloS one Result HBV C1858T;C1816T;A1814C 61;28;21 67;34;27 C 113 118 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Other than the YMDD RT motif associated HBV drug resistance, none of the HIV co-infected patients who developed 16.7% (8/48) of ADV associated gene mutations (rtQ215H and rtI233V) revealed BCP double mutations (Table 3). 2018 PloS one Result HBV I233V;Q215H 173;161 178;166 BCP;RT;RT;RT;P 189;20;159;171;15 192;22;161;173;19 HBV-HIV coinfections 73 88 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Similarly, the co-prevalence of YMDD RT motif 3TC/ETV resistance and the PC initiation mutant variants such as the A1814C/C1816T, G1862T and G1896A/C1858T showed 8.3% (4/48), 18.8% (9/48) and 4.2% (2/48), respectively. 2018 PloS one Result HBV C1816T;C1858T;A1814C;G1862T;G1896A 122;148;115;130;141 128;154;121;136;147 Precore;RT;P 73;37;32 75;39;36 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Similarly, the majority of the BCP mutations showed no significant difference among HBeAg status with the exception of A1676T (32.9%), C1678T/A (32.9%), G1719T (40.6%) and T1773C (18.9%) (Table 2) and the Kozak sequence mutant variants, which were higher in subjects with HBeAg negative status (Fig 2B). 2018 PloS one Result HBV A1676T;C1678T;C1678A;G1719T;T1773C 119;135;135;153;172 125;143;143;159;178 BCP;C;C 31;84;272 34;89;277 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. The classical PC mutant variants such as A1814C/C1816T (15.4%), G1862T (40.4%) and G1896/C1858T (23.1%) (Fig 2A) and many of other common PC mutants (Table 2) were detected with an overall frequency of 84.6% (121). 2018 PloS one Result HBV C1816T;C1858T;A1814C;G1862T 48;89;41;64 54;95;47;70 Precore;Precore 14;138 16;140 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. The double BCP mutations (A1762T/G1764A) accounted to 25.9% and showed no statistical difference between blood donors (32.6%) and CLD patients (36.5%), but were least detected in HIV co-infected patients (8.3%) (Fig 2A). 2018 PloS one Result HBV G1764A;A1762T 33;26 39;32 BCP 11 14 HBV-HIV coinfections 179 194 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. The frequency of the major BCP mutants; A1762T and G1764A was 28.7% and 35.0%, respectively (Table 2). 2018 PloS one Result HBV A1762T;G1764A 40;51 46;57 BCP 27 30 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. The Kozak sequence mutants (nt 1809-1812) with a prevalence of 51.7% (74) includes T1809G (32.9%), C1810A/T (2.8%), A1811C (9.8%) and T1812C (38.5%) (Table 2). 2018 PloS one Result HBV C1810T;T1809G;C1810A;A1811C;T1812C 99;83;99;116;134 107;89;107;122;140 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Unlike the major double BCP mutants (A1762T and G1764A), which were significantly higher among subjects with genotype A, many of the BCP mutant variants were either significantly higher in subjects with genotype D or showed no difference among genotypes (Table 2). 2018 PloS one Result HBV A1762T;G1764A 37;48 43;54 BCP;BCP 24;133 27;136 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Among them, the W4R, L30S and Q118R/Stop mutations were more prevalent in OBI-related HCC (Table 3). 2018 Infectious agents and cancer Result HBV W4R;Q118X;L30S;Q118R 16;30;21;30 19;40;25;40 Hepatocellular carcinoma;Occult Hepatitis B 86;74 89;77 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Differences in the major populations were attributed to the I126S/T, Y200F/S, and Y206C/H/S mutations, while those in the minor populations were attributed to the L21F/S, L42F/S, W182Stop, and L213F/I/T mutations. 2018 Infectious agents and cancer Result HBV Y206C;Y206H;Y206S;L213F;L213I;L213T;L21S;L42S;I126S;I126T;Y200F;Y200S;L21F;L42F;W182X 82;82;82;193;193;193;163;171;60;60;69;69;163;171;179 91;91;91;202;202;202;169;177;67;67;76;76;169;177;187 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. I126S/T, known as an escape mutation in the alpha determinant region, was found only in HBsAg-positive HCC (Table 3). 2018 Infectious agents and cancer Result HBV I126S;I126T 0;0 7;7 S;S 44;88 61;93 Hepatocellular carcinoma 103 106 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. The different mutations detected were W4R, S5A/P/T, L30S, G35R, H51P/R, E54K, A60V, W77R/Stop, I84T, N98 K/T, G102R, Q118R/Stop, N123D and S124F/P. 2018 Infectious agents and cancer Result HBV W4R;S5P;S5T;W77X;Q118X;L30S;G35R;H51P;H51R;E54K;A60V;W77R;I84T;N98K;N98T;G102R;Q118R;N123D;S124F;S124P 38;43;43;84;117;52;58;64;64;72;78;84;95;101;101;110;117;129;139;139 41;50;50;93;127;56;62;70;70;76;82;93;99;108;108;115;127;134;146;146 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Comparison of WT and W4P mutant LHB region sequences is shown in Supplementary Figure 1. 2018 World journal of gastroenterology Result HBV W4P 21 24 S 32 35 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Construction of TG mice harboring full HBV genome with the W4P mutation in preS1. 2018 World journal of gastroenterology Result HBV W4P 59 62 PreS1 75 80 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Examination of histological samples stained with hematoxylin and eosin revealed that the incidence of mice generating lipid granules was higher in W4P male mice compared to that in W4P TG female mice and nonTG littermates (Figure 3). 2018 World journal of gastroenterology Result HBV W4P;W4P 147;181 150;184 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Higher serum levels of HBsAg and increased amounts of LHBs in the livers of male W4P TG mice. 2018 World journal of gastroenterology Result HBV W4P 81 84 S;S 23;54 28;58 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Immunohistochemical staining of the liver samples using an anti-preS1 antibody also showed increased LHB production in W4P TG male mice (Figure 4). 2018 World journal of gastroenterology Result HBV W4P 119 122 S;PreS1 101;64 104;69 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Increased hepatomegaly and lipid granule content in male W4P TG mice. 2018 World journal of gastroenterology Result HBV W4P 57 60 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Increased serum levels of ALT and IL-6 in male W4P TG mice. 2018 World journal of gastroenterology Result HBV W4P 47 50 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. It has been reported previously that the presence of the W4P mutation in the preS1 region sex-dependently affected IL-6 production in the xenograft nude mouse model system, which could be one of the reasons for increased male susceptibility to HCC. 2018 World journal of gastroenterology Result HBV W4P 57 60 PreS1 77 82 Hepatocellular carcinoma 244 247 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Next, to check whether there was sex disparity in HBV production, we determined HBsAg levels in the serum and LHB levels in the livers of W4P TG mice (24 males, 18 females) and their nonTG littermates (17 males, 15 females) at 10 mo of age. 2018 World journal of gastroenterology Result HBV W4P 138 141 S;S 80;110 85;113 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. TG mice generated on B6D2F1/J background expressed the full-length HBV genome with the W4P mutation in preS1 under the control of the cytomegalovirus (CMV) promoter. 2018 World journal of gastroenterology Result HBV W4P 87 90 PreS1 103 108 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Thus, to check whether there was sex disparity in the induction of IL-6-mediated inflammation, we next examined serum IL-6 levels in W4P TG mice (24 males, 18 females) and their nonTG littermates (17 males, 15 females) at 10 mo of age. 2018 World journal of gastroenterology Result HBV W4P 133 136 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. To check whether there was sex disparity in hepatomegaly, we examined the ratio of the liver weight to total body weight between W4P TG mice (24 males, 18 females) and their nonTG littermates (17 males, 15 females) at 10 mo of age. 2018 World journal of gastroenterology Result HBV W4P 129 132 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. W4P TG male mice showed a significantly higher level of HBsAg in the serum compared to that in mice from the other three groups. 2018 World journal of gastroenterology Result HBV W4P 0 3 S 56 61 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. W4P TG male mice showed a significantly higher liver to total body weight ratio compared to that in mice of the three other groups, including W4P TG female mice and nonTG littermates (male and female mice) (Figure 2). 2018 World journal of gastroenterology Result HBV W4P;W4P 0;142 3;145 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. W4P TG male mice showed significantly higher serum IL-6 levels than did mice of the other three groups (Figure 5). 2018 World journal of gastroenterology Result HBV W4P 0 3 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. We found that W4P TG male mice had significantly higher serum levels of ALT than mice from the other three groups. 2018 World journal of gastroenterology Result HBV W4P 14 17 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. A similar situation was observed also for patients 2 and 3, and it was characterized by specific mutational profiles (L49R+S193L and G102A/G+S193S/L+S210S/R+L216 stop) observed only in plasma and not in liver tissue (Fig 3). 2018 PloS one Result HBV L216X;L49R;S193L;G102A;G102G;S193S;S193L;S210S;S210R 157;118;123;133;133;141;141;149;149 166;122;128;140;140;148;148;156;156 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. Additional immune escape mutations were detected in 3 patients: T116N, Y100C, and P142L+S143L (Fig 1). 2018 PloS one Result HBV T116N;Y100C;P142L;S143L 64;71;82;88 69;76;87;93 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. In patient 4 of Fig 3, the HBsAg mutation S204N was detected only in plasma and not in the liver. 2018 PloS one Result HBV S204N 42 47 S 27 32 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. Notably, T116N introduces an additional N-linked glycosylation site in HBsAg (Fig 1). 2018 PloS one Result HBV T116N 9 14 S 71 76 29596494 High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. The analysis of the HBsAg sequence in 1 patient with atypical positivity for both HBsAg (31,202 IU/ml) and anti-HBs (101 mIU/ml) revealed the presence of a G112R substitution, which is known to introduce a positively charged amino acid in the first loop of HBsAg, thus potentially hampering binding between HBsAg and anti-HBs (Fig 1). 2018 PloS one Result HBV G112R 156 161 S;S;S;S;S;S 112;322;20;82;257;307 115;325;25;87;262;312 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Besides M133T, immune escape mutations can be accompanied by other mutations creating novel N-linked glycosylation sites elsewhere. 2018 Virology Result HBV M133T 8 13 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Both G145R and N146Q mutations impaired virion secretion through the S protein rather than L/M proteins. 2018 Virology Result HBV G145R;N146Q 5;15 10;20 S 69 70 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. By simultaneous detection of HBsAg in cell lysate and culture supernatant using this ELISA kit, we found that HBsAg secretion (as defined by ratio of cextracellular HBsAg/intracellular HBsAg) was severely impaired by the C138Y, R169L, R169P, and C149R mutations. 2018 Virology Result HBV C138Y;R169L;R169P;C149R 221;228;235;246 226;233;240;251 S;S;S;S 29;110;165;185 34;115;170;190 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Consistent with our previous report, virion secretion was impaired by the T114R, T115A, K141E, and D144G immune escape mutations introduced into the 0.7mer construct. 2018 Virology Result HBV T114R;T115A;K141E;D144G 74;81;88;99 79;86;93;104 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Furthermore, we compared ability of the five novel glycosylation mutations to rescue virion secretion of the G145R or N146Q mutant in cis. 2018 Virology Result HBV G145R;N146Q 109;118 114;123 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. However, ELISA using a commercial kit (KHB, Shanghai, China) revealed less dramatic reduction of HBsAg titer in culture supernatant for these mutants, especially the D144G mutant. 2018 Virology Result HBV D144G 166 171 S 97 102 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In another approach, the L+/M+/S+ 0.7mer construct of the G145R or N146Q mutant was co-transfected with the L+/M+/S+, L+/M+/S-, or L-/M-/S+ 0.7mer construct of WT HBV or the M133T mutant. 2018 Virology Result HBV G145R;N146Q;M133T 58;67;174 63;72;179 S;S;S;S 31;114;124;137 32;115;125;138 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In contrast, presence of the M133T mutation in the L/M expressing construct alone failed to rescue virion secretion (lane 5). 2018 Virology Result HBV M133T 29 34 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. It turned out that the L/M proteins of the G145R or N146Q mutant supported efficient virion secretion if co-expressed with WT S protein. 2018 Virology Result HBV G145R;N146Q 43;52 48;57 S 126 127 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. L+/M+/S- and L-/M-/S+ 0.7mer constructs were generated to establish whether the G145R and N146Q mutations impair virion secretion through L, M, or S protein. 2018 Virology Result HBV G145R;N146Q 80;90 85;95 S;S;S 6;19;147 7;20;148 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Mutations that abolish N-linked glycosylation (N146Q and N146S) or create an extra glycosylation site (M133T) did not markedly affect HBsAg secretion. 2018 Virology Result HBV N146Q;N146S;M133T 47;57;103 52;62;108 S 134 139 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. N-linked glycosylation sites other than N131 could rescue virion secretion of the G145R and N146Q mutants. 2018 Virology Result HBV G145R;N146Q 82;92 87;97 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Presence of the M133T mutation in only the S expressing construct of the G145R mutant restored virion secretion as efficiently as its presence in both the S expressing and L/M expressing constructs. 2018 Virology Result HBV M133T;G145R 16;73 21;78 S;S 43;155 44;156 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Similar effect was observed for mutants creating extra glycosylation sites, especially M133T. 2018 Virology Result HBV M133T 87 92 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Similar findings were made for the N146Q mutant. 2018 Virology Result HBV N146Q 35 40 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Similarly, the L-/M-/S+ rather than L+/M+/S- 0.7mer construct of the WT HBV and especially the M133T mutant rescued virion secretion of the N146Q mutant. 2018 Virology Result HBV M133T;N146Q 95;140 100;145 S;S 21;42 22;43 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Such impairment could be partially rescued by the additional M133T mutation. 2018 Virology Result HBV M133T 61 66 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The amount of secreted HBsAg according to Abbott Architect i2000 quantitative assay was rather reduced, especially for the M133T and 114NT115 mutants. 2018 Virology Result HBV M133T 123 128 S 23 28 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The K141E, D144G, and G145R mutants showed little or mild reduction in HBsAg secretion despite near loss of virion secretion. 2018 Virology Result HBV K141E;D144G;G145R 4;11;22 9;16;27 S 71 76 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation could improve virion secretion of T114R, T115A, K141E, and D144G mutants. 2018 Virology Result HBV M133T;T114R;T115A;K141E;D144G 4;53;60;67;78 9;58;65;72;83 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation creates a novel N-linked glycosylation site at N131. 2018 Virology Result HBV M133T 4 9 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation rescued virion secretion of the G145R or N146Q mutant in cis through the S protein. 2018 Virology Result HBV M133T;G145R;N146Q 4;51;60 9;56;65 S 92 93 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation was most efficient at rescuing virion secretion of the G145R mutant, followed by G115N and G130N. 2018 Virology Result HBV M133T;G145R;G115N;G130N 4;74;100;110 9;79;105;115 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The novel glycosylation sites could also rescue virion secretion of the N146Q mutant, with the efficiency being highest for the 114NT115 and M133T mutations. 2018 Virology Result HBV N146Q;M133T 72;141 77;146 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. This allowed us to establish whether WT virus or the M133T mutant could rescue virion secretion in trans, and if so whether through L/M proteins or the S protein. 2018 Virology Result HBV M133T 53 58 S 152 153 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Thus, the K141E and D144G mutants were associated with extremely low HBsAg titer in culture supernatant according to Abbott Architect i2000 assay. 2018 Virology Result HBV K141E;D144G 10;20 15;25 S 69 74 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Thus, while the WT HBV and immune escape mutants such as T114R and T115A produced p24 (nonglycosylated S protein) and gp27 (singly glycosylated S protein), the T114R/M133T and T115A/M133T double mutants produced gp30 (doubly glycosylated S protein) as well. 2018 Virology Result HBV M133T;M133T;T114R;T115A;T114R;T115A 166;182;57;67;160;176 171;187;62;72;165;181 S;S;S 103;144;238 104;145;239 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. To characterize their biological properties, we generated 0.7mer expression construct containing T115N, G130N, 112NG113 (insertion of the NG dipeptide between residues 112 and 113. 2018 Virology Result HBV T115N;G130N 97;104 102;109 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. To establish whether M133T rescues virion secretion of the G145R and N146Q mutants through L/M proteins or the S protein, it was introduced to the L+/M+/S- construct or the L-/M-/S+ construct of the G145R (or N146Q) mutant. 2018 Virology Result HBV M133T;G145R;N146Q;G145R;N146Q 21;59;69;199;209 26;64;74;204;214 S;S;S 111;153;179 112;154;180 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Virion secretion of both G145R and N146Q mutants could be rescued in trans by S protein of WT HBV and especially the M133T mutant. 2018 Virology Result HBV G145R;N146Q;M133T 25;35;117 30;40;122 S 78 79 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. virion secretion of the G145R mutant could be rescued by L+/M+/S+ 0.7mer construct of the WT HBV, but more efficiently by the M133T mutant (lanes 3 & 4). 2018 Virology Result HBV G145R;M133T 24;126 29;131 S 63 64 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. When co-transfected with the 1.5mer replication construct into Huh7 cells, the glycosylation mutants, especially M133T, supported more efficient virion secretion than the WT envelope proteins. 2018 Virology Result HBV M133T 113 118 S 174 182 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. with the 0.7mer construct harboring both G145R and T115N mutations, for example). 2018 Virology Result HBV G145R;T115N 41;51 46;56 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Additionally, the tumor volume was significantly larger in nude mice with pcDNA3.1-HBs(sW172*) as compared to other three groups. 2018 Virology journal Result HBV W172X 87 93 S;S 83;87 86;88 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. After a cultural period of 21 days in soft agar, L02-pHBV4.1-HBs(sW172*) cell clones were well formed with a ratio of 60%; while the ratio of cell clones were less than 30% in L02-pHBV4.1-HBs(sW172L) and L02- pHBV4.1-HBs(wt). 2018 Virology journal Result HBV W172X;W172L 65;192 71;198 S;S;S;S;S 61;188;217;65;192 64;191;220;66;193 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Among nude mice injected with HBV replication L02 cell lines stably expressing HBsAg, the tumorgenesis rates of pHBV4.1-HBs(wt), pHBV4.1-HBs(sW172L) and pHBV4.1-HBs(sW172*) group were all 100% (4/4). 2018 Virology journal Result HBV W172X;W172L 165;141 171;147 S;S;S;S;S;S 120;137;161;79;141;165 123;140;164;84;142;166 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Among nude mice injected with L02 cell lines stably expressing HBsAg(without HBV replication), the tumorgenesis rate of pcDNA3.1(blank control), pcDNA3.1-HBs(wt), pcDNA3.1-HBs(sW172L) and pcDNA3.1-HBs(sW172*) group were 0 (0/4), 50%(2/4), 50%(2/4) and 100% (4/4), respectively. 2018 Virology journal Result HBV W172X;W172L 201;176 207;182 S;S;S;S;S;S 154;172;197;63;176;201 157;175;200;68;177;202 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. As compared to pHBV4.1-HBs(wt) and pHBV4.1-HBs(sW172L) transfected cells, the mRNA levels of TGFBI significantly decreased and CyclinD1 significantly increased in pHBV4.1-HBs(sW172*) transfected cells. 2018 Virology journal Result HBV W172X;W172L 175;47 181;53 S;S;S;S;S 23;43;171;47;175 26;46;174;48;176 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. As compared to pHBV4.1-HBs(wt) and pHBV4.1-HBs(sW172L) transfected cells, the protein levels of Smad3/2, CREB and CyclinD1 were significantly higher and TGFBI level was significantly lower in pHBV4.1-HBs(sW172*) transfected cells. 2018 Virology journal Result HBV W172X;W172L 204;47 210;53 S;S;S;S;S 23;43;200;47;204 26;46;203;48;205 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. However, as compared to nude mice with pHBV4.1-HBs(wt) and pHBV4.1-HBs(sW172L), the tumor volume was significantly higher in nude mice with pHBV4.1-HBs(sW172*). 2018 Virology journal Result HBV W172X;W172L 152;71 158;77 S;S;S;S;S 47;67;148;71;152 50;70;151;72;153 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Importantly, the tumor size of nude mice transplanted with stably transfected pHBV4.1-HBs(sW172*) L02 cells were significantly smaller in TGF-beta1 treatment group than in the PBS group (2.33+-0.79 cm3 vs.4.45+-1.03 cm3, P = 0.017). 2018 Virology journal Result HBV W172X 90 96 S;S 86;90 89;91 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In L02 cells with stably transfected pHBV-HBs(sW172*), the levels of Smad3/2, CREB and CyclinD1 decreased significantly after the administration of TGF-beta1. 2018 Virology journal Result HBV W172X 46 52 S;S 42;46 45;47 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In this study, the mRNA levels of molecules involved in LEF/Wnt (C-Myc and C-fos), c-Raf-1/Erk2 (AP-1 and NF-kappaB) and TGF-beta/Smad (TGFBI and CyclinD1) pathways were measured in pHBV4.1-HBs(wt), pHBV4.1-HBs(sW172L) and pHBV4.1-HBs(sW172*) stably transfected L02 cells, respectively. 2018 Virology journal Result HBV W172X;W172L 235;211 241;217 S;S;S;S;S 190;207;231;211;235 193;210;234;212;236 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Increasing TGFBI expression inhibits the growth of tumor induced by pHBV4.1-HBs(sW172*) in nude mouse. 2018 Virology journal Result HBV W172X 80 86 S;S 76;80 79;81 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Though the ratio of cell clones were less than 20% in either L02-pcDNA3.1, L02-pcDNA3.1-HBs(wt), L02-pcDNA3.1-HBs(sW172L) or L02-pcDNA3.1-HBs(sW172*), the ratio of cell clones was more in L02-pcDNA3.1-HBs(sW172*) than other three groups. 2018 Virology journal Result HBV W172X;W172X;W172L 142;205;114 148;211;120 S;S;S;S;S;S;S 88;110;138;201;114;142;205 91;113;141;204;115;143;206 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. A1762T/G1764A mutation and Pre S deletion predict survival. 2018 Cancer management and research Result HBV G1764A;A1762T 7;0 13;6 PreS 27 32 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. A1762T/G1764A mutation and Pre S deletion related to early recurrence. 2018 Cancer management and research Result HBV G1764A;A1762T 7;0 13;6 PreS 27 32 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. According to different mutation regions, A1752T/G, T1753C, G1757A, A1762T/G1764A, C1766T, T1768A, A1775G, C1799G, A1846T, T1858C, G1896A, G1898A, G1899A, and Pre S deletion mutations were recognized in 9.8% (39/131), 31.3% (41/131), 42.7% (56/131), 74.0% (97/131), 7.6% (10/131), 5.3% (7/131), 43.5% (57/131), 38.9% (51/131), 35.1% (46/131), 47.3% (62/131), 33.6% (44/131), 17.6% (23/131), 12.2% (16/131), and 16.8% (22/131) cases, respectively (Table 2). 2018 Cancer management and research Result HBV G1764A;A1752T;A1752G;T1753C;G1757A;A1762T;C1766T;T1768A;A1775G;C1799G;A1846T;T1858C;G1896A;G1898A;G1899A 74;41;41;51;59;67;82;90;98;106;114;122;130;138;146 80;49;49;57;65;73;88;96;104;112;120;128;136;144;152 PreS 158 163 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. All variables with p<0.10 in univariate analysis, as well as A1762T/G1764A, G1899A and Pre S deletion mutations, were further included in multivariate analysis with Cox proportional hazards model. 2018 Cancer management and research Result HBV G1764A;A1762T;G1899A 68;61;76 74;67;82 PreS 87 92 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. As shown in Table 2, most of the HBV genomic mutations (including A1752T/G, T1753C, G1757A, C1766T, T1768A, A1775G, C1799G, A1846T, T1858C, G1896A, and G1898A) did not make a significant statistical difference in OS and DFS. 2018 Cancer management and research Result HBV A1752T;A1752G;T1753C;G1757A;C1766T;T1768A;A1775G;C1799G;A1846T;T1858C;G1896A;G1898A 66;66;76;84;92;100;108;116;124;132;140;152 74;74;82;90;98;106;114;122;130;138;146;158 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. As shown in Table 3, macrovascular invasion (HR=4.994, 95% CI 2.060-12.107, p<0.001), TBil level (HR=18.188, 95% CI 4.153-79.644, p<0.001), A1762T/G1764A mutation (HR=3.701, 95% CI 1.390-9.855, p=0.009), and Pre S deletion (HR=4.816, 95% CI 2.311-10.032, p<0.001) were independent prognostic factors for OS. 2018 Cancer management and research Result HBV G1764A;A1762T 147;140 153;146 PreS 208 213 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. As shown in Table 4, patients with A1762T/G1764A mutation or Pre S deletion were more likely to have early recurrence (p=0.042 and p=0.019, respectively). 2018 Cancer management and research Result HBV G1764A;A1762T 42;35 48;41 PreS 61 66 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. As shown in Tables S1, S2, and S3, the A1762T/G1764A mutation is correlated with tumor size (r=0.204, p=0.019), G1899A mutation with vascular invasion (r=0.332, p<0.001), and Pre S deletion with AFP (r=0.254, p=0.003), positively. 2018 Cancer management and research Result HBV G1764A;A1762T;G1899A 46;39;112 52;45;118 PreS 175 180 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Especially for patients with A1762T/G1764A and Pre S deletion dual mutation, the early recurrence rate (62.5%, 10/16) was much higher than for those with single mutation (44.8%, 39/87) or no mutation (17.9%, 5/28, p=0.008). 2018 Cancer management and research Result HBV G1764A;A1762T 36;29 42;35 PreS 47 52 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. However, A1762T/G1764A mutation related to worse OS and DFS (p=0.040 and p=0.006, respectively), G1899A mutation related to worse OS (p=0.030), and Pre S deletion mutation related to worse OS and DFS (p<0.001 and p<0.001, respectively, Table 2, Figure 1). 2018 Cancer management and research Result HBV G1764A;A1762T;G1899A 16;9;97 22;15;103 PreS 148 153 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Macrovascular invasion (HR=2.656, 95% CI 1.052-6.253, p=0.038), tumor number (HR=2.033, 95% CI 1.147-3.606, p=0.015), TBil level (HR=4.902, 95% CI 1.084-22.162, p=0.039), A1762T/G1764A mutation (HR=3.245, 95% CI 1.400-7.521, p=0.006), and Pre S deletion (HR=2.437 95% CI 1.311-4.530, p<0.001) were independent prognostic factors for DFS. 2018 Cancer management and research Result HBV G1764A;A1762T 178;171 184;177 PreS 239 244 Hepatocellular carcinoma 333 336 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. No relationships can be identified between A1762T/G1764A mutation and/or Pre S deletion with late recurrence (data not shown). 2018 Cancer management and research Result HBV G1764A;A1762T 50;43 56;49 PreS 73 78 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Since both A1762T/G1764A mutation and Pre S deletion were independent prognostic factors for OS and DFS, the 131 patients were divided into three groups according to A1762T/G1764A mutation and Pre S deletion status: no mutation (26 cases), single mutation (77 cases), and dual mutations (16 cases). 2018 Cancer management and research Result HBV G1764A;G1764A;A1762T;A1762T 18;173;11;166 24;179;17;172 PreS;PreS 38;193 43;198 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The relationships between A1762T/G1764A, G1899A, and Pre S deletion mutations and clinical parameters were analyzed respectively. 2018 Cancer management and research Result HBV G1764A;A1762T;G1899A 33;26;41 39;32;47 PreS 53 58 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Conversely, rtA181T and rtA181V (conferring full-resistance to ADV and associated with TDF suboptimal response) were detected in 2.3% (19/828) and 3.6% (30/828) of patients, respectively. 2018 BMC infectious diseases Result HBV A181T;A181V 14;26 19;31 RT;RT 12;24 14;26 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Conversely, the immune-associated escape mutation G130 N occurred more frequently in genotype-A than D (2%[5/255] vs 0.2%[1/573], P = 0.012). 2018 BMC infectious diseases Result HBV G130N 50 56 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. In particular, sP120T significantly correlated with rtM204V/I (P = 0.001): 16/20 patients with sP120T had also rtM204V/I. 2018 BMC infectious diseases Result HBV M204V;M204I;M204V;M204I;P120T;P120T 54;54;113;113;15;95 61;61;120;120;21;101 RT;RT;S;S 52;111;15;95 54;113;16;96 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. In particular, the primary mutation rtM204V (conferring full-resistance to LAM, LdT, and partially to ETV) was observed in 25.8% (214/828) of patients, while rtM204I (conferring full-resistance to LAM and LdT) in 20% (166/828). 2018 BMC infectious diseases Result HBV M204V;M204I 38;160 43;165 RT;RT 36;158 38;160 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. In particular, the vaccine-escape mutational pattern sI195M + sE164D (resulting from rtM204V + rtV173L) was present in 7.1% (18/255) of HBV genotype-A infected patients and in 3.7% (21/573) of HBV genotype-D infected patients (P = 0.03). 2018 BMC infectious diseases Result HBV M204V;V173L;I195M;E164D 87;97;53;62 92;102;59;68 RT;RT;S;S 85;95;53;62 87;97;54;63 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Moreover, patients with rtM204V/I + sP120T had higher serum HBV-DNA than patients with rtM204V/I alone (5.5[3.2-7.2]logIU/ml vs 4.3[3.2-6.3]logIU/ml). 2018 BMC infectious diseases Result HBV M204V;M204I;M204V;M204I;P120T 26;26;89;89;36 33;33;96;96;42 RT;RT;S 24;87;36 26;89;37 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. The only primary drug-resistance mutations detected were rtM204I (0.4%, 1/245) and rtN236T (0.4%, 1/245), while the only secondary mutations detected were rtL180M and rtV173L, each present in 0.4% of patients. 2018 BMC infectious diseases Result HBV M204I;N236T;L180M;V173L 59;85;157;169 64;90;162;174 RT;RT;RT;RT 57;83;155;167 59;85;157;169 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. The prevalence of such mutations (sI195M, sI196S, and sE164D resulting from drug-resistance mutation rtM204 V, rtM204I, and rtV173L) was thus investigated. 2018 BMC infectious diseases Result HBV M204V;M204I;V173L;I195M;I196S;E164D 103;113;126;34;42;54 109;118;131;40;48;60 RT;RT;RT;S;S;S 101;111;124;34;42;54 103;113;126;35;43;55 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. These results were confirmed also when the analysis was focused on LAM-treated patients, thus limiting the impact of anti-HBV drugs on the selection of these mutations (sA128V: 4.4%[16/362] vs 0.5%[2/209], P = 0.008; sP120S: 5.5%[20/362] vs 1%[2/209], P = 0.006; sG130N: 0.3%[1/362] vs 1.9%[4/209], P = 0.063). 2018 BMC infectious diseases Result HBV A128V;P120S;G130N 169;217;263 175;223;269 S;S;S 169;217;263 170;218;264 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. They occurred at 20 HBsAg-positions, including 172 (corresponding to drug-resistance mutation rtA181T) and 182, both known to increase HBV oncogenic potential (Lee et al.,). 2018 BMC infectious diseases Result HBV A181T 96 101 S;RT 20;94 25;96 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. This is the case of sA128V and sP120S selected with higher prevalence in genotype-D than A (sA128V: 3.3%[19/573] vs 0.8%[2/255], P = 0.032; sP120S: 5.1%[29/573] vs 0.8[2/255], P = 0.003). 2018 BMC infectious diseases Result HBV A128V;P120S;A128V;P120S 20;31;92;140 26;37;98;146 S;S;S;S 20;31;92;140 21;32;93;141 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. A study in South Africa that recruited 3TC-naive HBV infected adults with or without HIV, reported rtM204I in 13/35 (37%) individuals. 2018 PLoS neglected tropical diseases Result HBV M204I 101 106 RT 99 101 HBV infections 49 61 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. All these mutations are associated with 3TC resistance; rtA181V has also been associated with reduced susceptibility to TDF. 2018 PLoS neglected tropical diseases Result HBV A181V 58 63 RT 56 58 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Although TDF has a high genetic barrier to resistance, and is associated with reliable suppression of HBV viraemia, mutations rtN236T and rtA194T, which have been linked with resistance to both TDF and ADV, have been identified in Southern Africa in both treatment naive and treatment experienced patients. 2018 PLoS neglected tropical diseases Result HBV N236T;A194T 128;140 133;145 RT;RT 126;138 128;140 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Another significant VEM, sG145K/R, was identified in six studies and sM133L/T, associated with VEM, immunoglobulin and diagnostic escape mutation, was identified in seven studies (Fig 2). 2018 PLoS neglected tropical diseases Result HBV G145K;G145R;M133L;M133T 25;25;69;69 33;33;77;77 S;S 25;69 26;70 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. In addition to South Africa, rtM204I/V was also frequent in Malawi among treatment experienced patients (n = 24/154, 16%) (Fig 3), and in genotype non-A infection: in this setting, the mutation was detected in genotype C infection (n = 2/17, 12%) (S2 Fig). 2018 PLoS neglected tropical diseases Result HBV M204I;M204V 31;31 38;38 RT 29 31 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Overall, the most prevalent RAM was rtM204V/I in both treatment experienced and treatment naive individuals, and occurring either alone or in combination with other polymorphisms rtL80I/V, rtV173L, rtL180M, rtA181S, rtT184S, rtA200V and/or rtS202S (Fig 3); mutations among individuals with and without exposure to HBV therapy are listed in S4 Table and S5 Table, respectively). 2018 PLoS neglected tropical diseases Result HBV M204V;M204I;L80I;L80V;A181S;A200V;S202S;V173L;L180M;T184S 38;38;181;181;209;227;242;191;200;218 45;45;187;187;214;232;247;196;205;223 RT;RT;RT;RT;RT;RT;RT;RT 36;179;189;198;207;216;225;240 38;181;191;200;209;218;227;242 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. rt180M + rtA181V in genotype E (1/69 (1.5%). 2018 PLoS neglected tropical diseases Result HBV A181V 11 16 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. rtM204V + rtL180M in genotype E (1/69, 1.5%). 2018 PLoS neglected tropical diseases Result HBV M204V;L180M 2;12 7;17 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. rtM204V in genotype A (2/69, 2.9% of sequences), this occurred in combination with rtL180M. 2018 PLoS neglected tropical diseases Result HBV M204V;L180M 2;85 7;90 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. rtQ215S identified in genotype D (4/69, 5.8%). 2018 PLoS neglected tropical diseases Result HBV Q215S 2 7 RT 0 2 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. sD144A/E/G occurring in genotype A (6/69, 8.7%), D (10/69, 14.5%) and E (7/69, 10.1%) associated with VEM. 2018 PLoS neglected tropical diseases Result HBV D144A;D144E;D144G 0;0;0 10;10;10 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. sI110L occurring in genotype A (3/69, 4.3%), D (4/69, 5.8%) and E (11/69, 15.9%) associated with immunoglobulin resistance. 2018 PLoS neglected tropical diseases Result HBV I110L 0 6 S 0 1 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. The most common VEM was the triple mutation rtV173L + rtL180M + rtM204I/V, found in the Pol gene. 2018 PLoS neglected tropical diseases Result HBV M204I;M204V;V173L;L180M 66;66;46;56 73;73;51;61 P;RT;RT;RT 88;44;54;64 91;46;56;66 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. The rtM204I/V mutation by itself confers resistance to 3TC; in combination with A194T it may also be associated with reduced efficacy to TDF, and in combination with L180M and V173L with vaccine escape, through corresponding substitutions in the surface antigen sites targeted by neutralising antibodies. 2018 PLoS neglected tropical diseases Result HBV M204I;M204V;A194T;L180M;V173L 6;6;80;166;176 13;13;85;171;181 RT;S 4;246 6;253 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. All 5 patients with the rtA181C substitution were LVD experienced; all except 1 had virologic breakthrough during ETV treatment with rtA181C detected with previously reported ETVr substitutions. 2018 Hepatology communications Result HBV A181C;A181C 26;135 31;140 RT;RT 24;133 26;135 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. As described above, the rtL247F substitution (observed in patient Pt1) was not detected by clonal analysis and was not phenotyped. 2018 Hepatology communications Result HBV L247F 26 31 RT 24 26 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. By contrast, the other patient experienced a virologic breakthrough harboring the novel substitutions rtF88F/Y, rtT184A/S, rtA186A/T, and rtF201F/Y, with LVDr substitutions L180M+M204V that persisted on ETV treatment. 2018 Hepatology communications Result HBV F88F;F88Y;T184A;T184S;A186A;A186T;F201F;F201Y;L180M;M204V 104;104;114;114;125;125;140;140;173;179 110;110;121;121;132;132;147;147;178;184 RT;RT;RT;RT 102;112;123;138 104;114;125;140 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Clonal analysis of the isolate with the rtA181C substitution from Pt23 identified the ETVr S202G substitution in the HBV RT population not observed by direct sequencing of the PCR amplicon (Supporting Table S5). 2018 Hepatology communications Result HBV A181C;S202G 42;91 47;96 RT;RT 40;121 42;123 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Comparison of ETV susceptibilities to rt181C and rt181A in Pt25 confirmed that the novel emergent rtH35N substitution did not influence ETVr. 2018 Hepatology communications Result HBV H35N 100 104 RT;RT;RT 38;49;98 40;51;100 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Due to the presence of ETVr substitutions rtT184A/S in this patient, ETV susceptibility was not assessed. 2018 Hepatology communications Result HBV T184A;T184S 44;44 51;51 RT 42 44 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. ETV ANTI-HBV ACTIVITY AGAINST HBV rtA181C AND OTHER rtA181 SUBSTITUTIONS. 2018 Hepatology communications Result HBV A181C 36 41 RT;RT 34;52 36;54 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. ETV treatment in nucleoside-naive patients can infrequently select for LVDr HBV.( 11 ) Two patients (Pt2 and Pt3) had emergent LVDr substitutions at virologic breakthrough in addition to the novel emergent substitutions rtA27V+rtA200V or rtL229F/V (Table 3). 2018 Hepatology communications Result HBV A27V;A200V;L229F;L229V 222;229;240;240 226;234;247;247 RT;RT;RT 220;227;238 222;229;240 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. ETVr substitutions at rtT184 (rtT184C/G/I/S) have been shown to exhibit low-level ETVr and have only been observed in combination with other ETVr substitutions in patients with virologic breakthrough.( 12 ) The novel emergent rtV191I substitution was phenotyped in an ETVr HBV RT background of rtL180M, rtT184S, and rtM204V and displayed reduced ETV susceptibility (15-fold greater than WT; Table 2) within the range observed for LVDr HBV. 2018 Hepatology communications Result HBV T184C;T184G;T184I;T184S;V191I;L180M;T184S;M204V 32;32;32;32;228;296;305;318 43;43;43;43;233;301;310;323 RT;RT;RT;RT;RT;RT;RT 22;30;226;277;294;303;316 24;32;228;279;296;305;318 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. ETVr substitutions rtT184, rtS202, and rtM250 were detected by direct sequencing of PCR amplicons from patient isolates with the rtA181C substitution in HBV RT populations from 4 of the 5 patients (Pt2, Pt24, Pt25, and Pt26; Supporting Table S5). 2018 Hepatology communications Result HBV A181C 131 136 RT;RT;RT;RT;RT 19;27;39;129;157 21;29;41;131;159 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Five patients (Pt6, Pt7, Pt8, Pt9, and Pt10) had emergent novel HBV RT substitutions rtH13L+rtQ271V+rtF273L, rtQ125K, rtR153Q, rtV214I, or rtQ267N, respectively, at virologic breakthrough to ETV treatment. 2018 Hepatology communications Result HBV H13L;Q267N;Q271V;F273L;Q125K;R153Q;V214I 87;141;94;102;111;120;129 91;146;99;107;116;125;134 RT;RT;RT;RT;RT;RT;RT;RT 68;85;92;100;109;118;127;139 70;87;94;102;111;120;129;141 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. For patients with two of these substitutions, clonal analysis of patient-derived isolates revealed that the rtV214P and rtA329S substitutions were not linked with ETVr substitutions. 2018 Hepatology communications Result HBV A329S;V214P 122;110 127;115 RT;RT 108;120 110;122 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Four LVD-naive patients each harbored the rtS117Y substitution at baseline and all achieved undetectable HBV DNA while on ETV treatment. 2018 Hepatology communications Result HBV S117Y 44 49 RT 42 44 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Furthermore, recombinant clones for 2 additional patients (Pt24 and Pt25) harboring rtA181C with LVDr substitutions were constructed. 2018 Hepatology communications Result HBV A181C 86 91 RT 84 86 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV rtA181C emerged in 4 LVD-experienced patients each with preexisting LVDr substitutions before ETV treatment. 2018 Hepatology communications Result HBV A181C 6 11 RT 4 6 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV rtA181V/T and rtA181V/T+rtN236T substitutions, in addition to conferring reduced susceptibility to ADV and TDF,( 24, 25 ) have also been reported to confer reduced susceptibility to LVD and LdT.( 26, 27 ) One patient (Pt23) harbored the novel emergent substitution rtA181C in combination with LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Result HBV A181V;A181T;A181V;A181T;A181C;N236T;L180M;M204V 20;20;6;6;271;30;318;326 27;27;13;13;276;35;323;331 RT;RT;RT;RT;RT;RT 4;18;28;269;316;324 6;20;30;271;318;326 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV substitutions at rtT184, rtS202, or rtM250 confer resistance to ETV when associated with LVDr substitutions rtM204V/I+-rtL180M and display varying levels of ETV susceptibility depending on the specific resistance substitutions.( 12 ) Fifteen novel emergent substitutions at 12 HBV RT amino acid positions were identified in an ETVr HBV RT background for phenotypic analysis. 2018 Hepatology communications Result HBV M204V;M204I;L180M 114;114;125 121;121;130 RT;RT;RT;RT;RT;RT;RT 21;29;40;112;123;285;340 23;31;42;114;125;287;342 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In addition, recombinant clones were also constructed from patient isolates harboring other rtA181 substitutions, including rtA181G (Pt24), rtA181V (Pt24), rtA181N (Pt27), rtA181S (Pt28), and rtA181T (Pt29). 2018 Hepatology communications Result HBV A181G;A181V;A181N;A181S;A181T 126;142;158;174;194 131;147;163;179;199 RT;RT;RT;RT;RT;RT 92;124;140;156;172;192 94;126;142;158;174;194 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In addition, rtS117Y emerged in 1 LVD-naive patient on ETV treatment at a time point with HBV DNA <50 IU/mL. 2018 Hepatology communications Result HBV S117Y 15 20 RT 13 15 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In addition, they did not confer cross-resistance to ADV or TDV with the exception of the rtA181S substitution that has been reported to confer cross-resistance to ADV.( 28 ) . 2018 Hepatology communications Result HBV A181S 92 97 RT 90 92 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In both these patients, rtV27A was not maintained at subsequent time points on ETV treatment, and 1 patient (Pt12) achieved undetectable HBV DNA subsequent to virologic breakthrough. 2018 Hepatology communications Result HBV V27A 26 30 RT 24 26 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In Pt25, linkage with an additional novel HBV RT substitution (rtH35N) was also observed. 2018 Hepatology communications Result HBV H35N 65 69 RT;RT 46;63 48;65 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Nevertheless, ETV susceptibility analyses were performed on a patient-derived sequence harboring a substitution (rtS117Y) conferring 17-fold reduction in susceptibility greater than WT HBV. 2018 Hepatology communications Result HBV S117Y 115 120 RT 113 115 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One LVD-experienced patient with rtA181C had no available baseline sample for analysis; this substitution was encoded by TGT. 2018 Hepatology communications Result HBV A181C 35 40 RT 33 35 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One patient (Pt11) harbored novel emergent substitutions (rtH13S, rtS78T, and rtQ267R/M) without LVDr substitutions. 2018 Hepatology communications Result HBV H13S;S78T;Q267R;Q267M 60;68;80;80 64;72;87;87 RT;RT;RT 58;66;78 60;68;80 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One patient (Pt14) harboring rtL80I+rtM204I achieved undetectable HBV DNA subsequent to virologic breakthrough. 2018 Hepatology communications Result HBV L80I;M204I 31;38 35;43 RT;RT 29;36 31;38 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One patient (Pt21) harbored the novel substitution rtC188L with the LVDr-associated compensatory substitution rtV173L. 2018 Hepatology communications Result HBV C188L;V173L 53;112 58;117 RT;RT 51;110 53;112 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One patient infected with HBV genotype B experienced virologic breakthrough with detection of a novel substitution rtS202V in combination with rtT184G and LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Result HBV S202V;T184G;L180M;M204V 117;145;176;184 122;150;181;189 RT;RT;RT;RT 115;143;174;182 117;145;176;184 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One patient responded to ETV treatment, and phenotypic analysis of a recombinant clone harboring substitutions rtI163V+rtL180M+rtA186T+rtM204V from this patient showed susceptibility to ETV (4.8-fold greater than WT) similar to LVDr HBV. 2018 Hepatology communications Result HBV L180M;M204V;I163V;A186T 121;137;113;129 126;142;118;134 RT;RT;RT;RT 111;119;127;135 113;121;129;137 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One substitution, rtV214L, was not detected by clonal analysis and was therefore not phenotyped in the LVDr HBV RT background. 2018 Hepatology communications Result HBV V214L 20 25 RT;RT 18;112 20;114 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Patient 17 also harbored the novel emergent substitution rtT128N, and Pt18 harbored rt186T+rtL180M+rtM204V and achieved undetectable HBV subsequent to virologic breakthrough on ETV treatment. 2018 Hepatology communications Result HBV T128N;L180M;M204V 59;93;101 64;98;106 RT;RT;RT;RT 57;84;91;99 59;86;93;101 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Patient 19 harbored the LVDr substitutions rtL180M+rtM204V with either rtV173L or rtV207I while Pt20 harbored the LVDr substitutions rtL180M+rtM204V with either rtL229V or rtL229W, as determined by clonal analysis. 2018 Hepatology communications Result HBV V207I;L229V;L180M;M204V;V173L;L180M;M204V;L229W 84;163;45;53;73;135;143;174 89;168;50;58;78;140;148;179 RT;RT;RT;RT;RT;RT;RT;RT 43;51;71;82;133;141;161;172 45;53;73;84;135;143;163;174 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analyses of rtH35N and rtC188L were each assessed in the context of other substitutions detected at virologic breakthrough (see patient [Pt]21 and Pt25, described below). 2018 Hepatology communications Result HBV H35N;C188L 25;36 29;41 RT;RT 23;34 25;36 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of a laboratory recombinant clone only harboring the rtA181C substitution showed that it remained susceptible to ADV (0.9-fold greater than WT) and TDF (1.0-fold greater than WT), although reduced susceptibilities to LVD (18-fold greater than WT) and LdT (>7.7-fold greater than WT) were observed (Table 6). 2018 Hepatology communications Result HBV A181C 75 80 RT 73 75 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of a recombinant clone from this patient showed susceptibility to ETV (9.7-fold greater than WT; Table 4) similar to LVDr HBV, suggesting that the rtV173L and rtC188L substitutions did not impact resistance development. 2018 Hepatology communications Result HBV C188L;V173L 181;169 186;174 RT;RT 167;179 169;181 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of a recombinant clone harboring HBV substitutions rtL180M+rtA181C+rtM204V revealed a notable reduction in susceptibility to ETV (122-fold greater than WT; Table 4). 2018 Hepatology communications Result HBV A181C;L180M;M204V 81;73;89 86;78;94 RT;RT;RT 71;79;87 73;81;89 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of a recombinant clone harboring rtA181S with LVDr substitutions rtL180M+rtM204V showed reduced susceptibility to ADV (>2.9-fold greater than WT) but remained susceptible to inhibition by TDF (2-fold greater than WT). 2018 Hepatology communications Result HBV A181S;L180M;M204V 55;87;95 60;92;100 RT;RT;RT 53;85;93 55;87;95 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of four patient-derived recombinant clones harboring the HBV rtA181C substitution with LVDr substitutions showed reduced ETV susceptibility ranging from 16-fold to 122-fold greater than WT (Table 5). 2018 Hepatology communications Result HBV A181C 83 88 RT 81 83 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant clones from Pt19 and Pt23 and a laboratory clone harboring the rtA181C substitution with LVDr HBV showed susceptibility to ADV (<=1-fold compared with WT) and TDF (<=1.6-fold compared with WT) similar to the WT clone. 2018 Hepatology communications Result HBV A181C 100 105 RT 98 100 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant clones from these 2 patients showed reduced ETV susceptibility similar to LVDr HBV (5.5-fold to 9.4-fold greater than WT; Table 3), suggesting that the novel HBV substitutions rtA27V+rtA200V, rtL229F, and rtL229V did not contribute to the reduced ETV susceptibility. 2018 Hepatology communications Result HBV A27V;L229V;A200V;L229F 213;242;220;229 217;247;225;234 RT;RT;RT;RT 211;218;227;240 213;220;229;242 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant clones from these patients showed reduced susceptibility to ETV (3.8-fold to 6.3-fold greater than WT; Table 4) similar to LVDr HBV, suggesting that the LVDr-associated compensatory substitutions rtV173L, rtV207I, and rtL229L/W did not impact ETVr. 2018 Hepatology communications Result HBV L229L;L229W;V173L;V207I 255;255;233;242 262;262;238;247 RT;RT;RT 231;240;253 233;242;255 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant clones from this patient harboring either rtS78T+rtQ267R or rtH13S+rtQ267M did not show reduced susceptibility to ETV (<=1.0-fold WT; Table 4), suggesting no impact on ETVr. 2018 Hepatology communications Result HBV S78T;H13S;Q267R;Q267M 79;97;86;104 83;101;91;109 RT;RT;RT;RT 77;84;95;102 79;86;97;104 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant clones harboring rtA181 substitutions G, N, S, T, or V in combination with LVDr substitutions rtL180M+rtM204V showed susceptibility to ETV (0.8-fold to 11-fold greater than WT; Table 5) similar to LVDr HBV, suggesting that these rtA181 substitutions G, N, S, T, or V did not confer resistance to ETV. 2018 Hepatology communications Result HBV L180M;M204V 131;139 136;144 RT;RT;RT;RT 52;129;137;264 54;131;139;266 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of recombinant patient clones harboring these novel emergent substitutions resulted in ETV susceptibilities (<1-fold greater than WT; Table 3) similar to that observed for the WT HBV clone, suggesting that rtH13L+rtQ271V+rtF273L, rtQ125K, rtR153Q, rtV214I, and rtQ267N did not impact ETVr development. 2018 Hepatology communications Result HBV H13L;Q267N;Q271V;F273L;Q125K;R153Q;V214I 228;283;235;243;252;261;270 232;288;240;248;257;266;275 RT;RT;RT;RT;RT;RT;RT 226;233;241;250;259;268;281 228;235;243;252;261;270;283 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of the remaining 12 of 15 identified novel emergent substitutions indicated a reduced susceptibility to ETV (>758-fold greater than WT; Table 2) due to the presence of high-level ETVr HBV RT substitutions rtT184L, rtT184A, rtS202G, or rtM250V (Table 2). 2018 Hepatology communications Result HBV T184L;T184A;S202G;M250V 227;236;245;257 232;241;250;262 RT;RT;RT;RT;RT 208;225;234;243;255 210;227;236;245;257 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of the rt117S clone indicated an ETV susceptibility (10-fold greater than WT) similar to the parental rtS117Y clone. 2018 Hepatology communications Result HBV S117Y 124 129 RT;RT 27;122 29;124 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of these clones resulted in ETV susceptibilities of 43-fold and 1.7-fold greater than WT for clones harboring rtV173L+rtL180M+rtA181C+rtM204V and rtA181C, respectively (Table 5). 2018 Hepatology communications Result HBV A181C;V173L;L180M;M204V;A181C 148;132;140;156;168 153;137;145;161;173 RT;RT;RT;RT;RT 130;138;146;154;166 132;140;148;156;168 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis of this clone showed susceptibility to ETV (8.2-fold greater than WT; Table 5) similar to LVDr HBV, confirming that the presence of rtA181C in addition to the LVDr substitutions rtL180M+rtM204V further reduced ETV susceptibility. 2018 Hepatology communications Result HBV A181C;L180M;M204V 154;200;208 159;205;213 RT;RT;RT 152;198;206 154;200;208 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Phenotypic analysis revealed that recombinant clones harboring rtA181 substitutions G, N, T, or V in combination with LVDr substitutions rtL180M+rtM204V remained susceptible to ADV (<1-fold compared with WT) and TDF (<=1.5-fold compared with WT), as shown in Table 6. 2018 Hepatology communications Result HBV L180M;M204V 139;147 144;152 RT;RT;RT 63;137;145 65;139;147 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous analyses have shown that the primary LVDr substitutions (rtL180M+-rtM204V/I) reduce ETV susceptibility by approximately 8-fold and that patients harboring LVDr substitutions display varying levels of ETV susceptibility (3.1-fold to 20-fold greater than WT).( 18 ) Nine novel emergent substitutions at eight HBV RT amino acid positions were identified in an LVDr HBV RT background for phenotypic analysis. 2018 Hepatology communications Result HBV M204V;M204I;L180M 77;77;68 84;84;73 RT;RT;RT;RT 66;75;320;375 68;77;322;377 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous resistance surveillance analyses of six phase 2 and 3 studies in adult patients established the resistance profile for ETV in adults through 5 years of treatment.( 11 ) These analyses indicated that ETVr results from HBV RT substitutions at positions rtT184, rtS202, or rtM250 in combination with LVDr substitutions rtM204I/V+-rtL180M. 2018 Hepatology communications Result HBV M204I;M204V;L180M 327;327;338 334;334;343 RT;RT;RT;RT;RT;RT 230;260;268;279;325;336 232;262;270;281;327;338 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous studies have shown that rtA181S conferred reduced sensitivity to ADV but remained susceptible to LVD, TDF, and ETV,( 28 ) whereas rtA181S+M204I conferred reduced sensitivity to both ADV and LVD.( 29 ) Taken together, our results from this phenotypic analysis suggest that rtA181 substitutions G, N, S, T, or V in combination with LVDr substitutions rtL180M+rtM204V were not associated with ETVr. 2018 Hepatology communications Result HBV A181S;A181S;L180M;M204V;M204I 35;141;360;368;147 40;146;365;373;152 RT;RT;RT;RT;RT 33;139;281;358;366 35;141;283;360;368 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Sequence linkage of the rtA181C substitution with ETVr and LVDr substitutions was detected in 2 patients (Pt23 and Pt25); however, the ETVr combination was not the major HBV RT species. 2018 Hepatology communications Result HBV A181C 26 31 RT;RT 24;174 26;176 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Substitutions at rtI169 have been considered as secondary changes not specific for ETV that may contribute to the growth efficiency of ETVr HBV.( 14 ) In our analysis, 7 LVD-experienced patients were infected with HBV genotype C with the novel substitution rtI169V; 6 of these patients had virologic breakthrough. 2018 Hepatology communications Result HBV I169V 259 264 RT;RT 17;257 19;259 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Taken together, our phenotypic and virologic outcomes data for patients harboring the rtA186T substitution suggested that rtA186T did not contribute to ETVr. 2018 Hepatology communications Result HBV A186T;A186T 88;124 93;129 RT;RT 86;122 88;124 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Taken together, the results from the patient-derived and laboratory-derived clones harboring the rtA181C substitution exhibited reduced susceptibility to ETV but only in combination with LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Result HBV A181C;L180M;M204V 99;208;216 104;213;221 RT;RT;RT 97;206;214 99;208;216 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Taken together, these data suggest that the rtS117Y substitution does not contribute to reduced ETV susceptibility. 2018 Hepatology communications Result HBV S117Y 46 51 RT 44 46 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Ten of the 12 HBV RT substitutions preexisted in other patients, suggestive of natural genetic drift and not related to ETVr, while two substitutions (rtH35N and rtC188L) did not preexist. 2018 Hepatology communications Result HBV H35N;C188L 153;164 157;169 RT;RT;RT 18;151;162 20;153;164 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The 1 LVD-experienced patient without virologic breakthrough showed a decline in HBV DNA that remained detectable (>=3 log10 IU/mL) on ETV therapy, with the emergence of rtA181C/G and ETVr substitutions at the last available visit. 2018 Hepatology communications Result HBV A181G;A181C 172;172 179;179 RT 170 172 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The combination of rtA181C with LVDr substitutions was the major HBV RT species in Pt26. 2018 Hepatology communications Result HBV A181C 21 26 RT;RT 19;69 21;71 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The cross-resistance profile of the HBV rtA181C substitution in the absence of LVDr substitutions to other approved anti-HBV drugs was also evaluated. 2018 Hepatology communications Result HBV A181C 42 47 RT 40 42 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The ETV susceptibility for a clone from Pt22 harboring HBV substitutions rtI169V+rtV173L+rtL180M+rtT184L+rtM204V resulted in high-level HBV ETVr (EC50 >15,000 nM) due to the presence of the ETVr substitution rtT184L. 2018 Hepatology communications Result HBV I169V;T184L;V173L;L180M;M204V;T184L 75;99;83;91;107;210 80;104;88;96;112;215 RT;RT;RT;RT;RT;RT 73;81;89;97;105;208 75;83;91;99;107;210 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The HBV rtA181C substitution was detected in 0.5% (5/982) of evaluable HBV RT sequences. 2018 Hepatology communications Result HBV A181C 10 15 RT;RT 8;75 10;77 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The HBV rtA181C substitution was introduced into laboratory clone p180B3, with and without LVDr substitutions. 2018 Hepatology communications Result HBV A181C 10 15 RT 8 10 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The infrequent occurrence (0.5%) of the rtA181C substitution was most likely due to the requirement for a two-nucleotide change. 2018 Hepatology communications Result HBV A181C 42 47 RT 40 42 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The phenotypic and virologic outcomes data for these patients with rtV27A suggested that this substitution did not impact ETVr development. 2018 Hepatology communications Result HBV V27A 69 73 RT 67 69 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The phenotypic and virologic outcomes data suggested that rtL80I+-rtN131G+rtQ316H did not impact ETVr development. 2018 Hepatology communications Result HBV L80I;N131G;Q316H 60;68;76 64;73;81 RT;RT;RT 58;66;74 60;68;76 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The phenotypic data suggest that the rtV214P and rtA329S substitutions are the result of natural genetic drift and unrelated to ETVr. 2018 Hepatology communications Result HBV V214P;A329S 39;51 44;56 RT;RT 37;49 39;51 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtA181C substitution required a two-nucleotide change. 2018 Hepatology communications Result HBV A181C 6 11 RT 4 6 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtA186T substitution has been reported to be associated with ETVr.( 20 ) Two additional LVDr patients also harbored emergent rtA186T. 2018 Hepatology communications Result HBV A186T;A186T 6;131 11;136 RT;RT 4;129 6;131 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtA329S substitution was only identified in a WT HBV RT background with ETV susceptibility similar to WT HBV (0.4-fold greater than WT; Table 2). 2018 Hepatology communications Result HBV A329S 6 11 RT;RT 4;57 6;59 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtL80I substitution has been reported to be a compensatory substitution selected by LVD treatment to enhance the replication efficiency of the LVDr substitution rtM204I without affecting LVDr.( 19 ) Two patients (Pt14 and Pt15) harbored rtL80I with LVDr substitutions rtM204I+-rtL180M, while 1 patient (Pt16) harbored rtL80I with the novel emergent substitutions rtN131G+rtQ316H and rtM204I. 2018 Hepatology communications Result HBV L80I;M204I;L80I;L180M;L80I;N131G;M204I;Q316H;M204I 6;167;243;283;324;369;274;377;389 10;172;247;288;328;374;279;382;394 RT;RT;RT;RT;RT;RT;RT;RT;RT 4;165;241;272;281;322;367;375;387 6;167;243;274;283;324;369;377;389 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtV191I substitution in a WT, LVDr, or ETVr HBV RT background did not reduce ETV susceptibility. 2018 Hepatology communications Result HBV V191I 6 11 RT;RT 4;52 6;54 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtV214P substitution linked with LVDr substitutions rtL180M+rtM204I (described above). 2018 Hepatology communications Result HBV V214P;L180M;M204I 6;58;66 11;63;71 RT;RT;RT 4;56;64 6;58;66 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The rtV214P substitution was observed in the ETVr background in 1 patient by population-based sequencing; however, clonal analysis revealed that this substitution was linked to LVDr substitutions rather than signature ETVr substitutions. 2018 Hepatology communications Result HBV V214P 6 11 RT 4 6 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Therefore, rtI169V may have a compensatory role in ETVr HBV as has been described for the rtI169T substitution.( 14 ) 2018 Hepatology communications Result HBV I169V;I169T 13;92 18;97 RT;RT 11;90 13;92 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Therefore, rtI169V may have a compensatory role in ETVr HBV as has been described for the rtI169T substitution.( 14 ) . 2018 Hepatology communications Result HBV I169V;I169T 13;92 18;97 RT;RT 11;90 13;92 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Therefore, the contribution of rtI169V could not be determined in this patient due to the existing reduced susceptibility to ETV; however, rtI169V did not appear to impact susceptibility to ETV in a baseline treatment isolate from Pt24 also harboring the LVDr substitutions rtL180M+rtM204V (Table 5; see below). 2018 Hepatology communications Result HBV I169V;I169V;L180M;M204V 33;141;276;284 38;146;281;289 RT;RT;RT;RT 31;139;274;282 33;141;276;284 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Three of the substitutions, rtR242S, rtL247F, and rtR289S, were not detected by clonal analysis and were therefore not phenotyped whereas the remaining six substitutions were phenotyped (Table 1). 2018 Hepatology communications Result HBV R242S;L247F;R289S 30;39;52 35;44;57 RT;RT;RT 28;37;50 30;39;52 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Three patients had rtA181C encoded by a GCT to TGT change, while rtV181C was encoded by a GTT to TGT change in 1 patient. 2018 Hepatology communications Result HBV A181C;V181C 21;67 26;72 RT;RT 19;65 21;67 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. To investigate the role of the HBV rtA181C substitution in reduced ETV susceptibility, this substitution was introduced into a WT laboratory clone, an LVDr laboratory clone harboring LVDr substitutions rtL173V+rtL180M+rtM204V, and a recombinant clone from a patient (Pt19 harboring LVDr substitutions rtL173V+rtL180M+rtM204V. 2018 Hepatology communications Result HBV A181C;L173V;L180M;M204V;L173V;L180M;M204V 37;204;212;220;303;311;319 42;209;217;225;308;316;324 RT;RT;RT;RT;RT;RT;RT 35;202;210;218;301;309;317 37;204;212;220;303;311;319 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Two patients (Pt12 and Pt13) harbored the novel emergent substitution rtV27A with the LVDr substitution rtM204I. 2018 Hepatology communications Result HBV V27A;M204I 72;106 76;111 RT;RT 70;104 72;106 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Two patients (Pt17 and Pt18) harbored the novel emergent substitution rtA186T with LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Result HBV A186T;L180M;M204V 72;104;112 77;109;117 RT;RT;RT 70;102;110 72;104;112 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Two patients (Pt4 and Pt5) who experienced virologic breakthrough on ETV treatment harbored the novel HBV RT substitutions rtL164F+rtA329S or rtS135F+rtR280G and achieved HBV DNA levels <50 IU/mL subsequent to virologic breakthrough. 2018 Hepatology communications Result HBV A329S;L164F;S135F;R280G 133;125;144;152 138;130;149;157 RT;RT;RT;RT;RT 106;123;131;142;150 108;125;133;144;152 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. We evaluated the cross-resistance profile of the HBV rtA181C substitution in combination with LVDr substitutions to other approved anti-HBV drugs. 2018 Hepatology communications Result HBV A181C 55 60 RT 53 55 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. The expression of flag-tagged HBx could be probed in HBx-wt, HBx-S31A or HBx-S31D (phospho-mimic mutant) plasmid-transfected Huh7 cells, but not in empty vector-transfected cells. 2018 Cancer medicine Result HBV S31A;S31D 65;77 69;81 X;X;X;X 30;53;61;73 33;56;64;76 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. Thus, Huh7 cells (a HBV-free cell line) transfected with HBx-wt or HBx-S31A (serine31 was mutated into alanine31) plasmid were subjected to co-IP and Western blotting assays. 2018 Cancer medicine Result HBV S31A 71 75 X;X 57;67 60;70 30377627 Hepatitis B Virus (HBV) Infection and Re-activation During Nucleos(t)ide Reverse Transcriptase Inhibitor-Sparing Antiretroviral Therapy in a High-HBV Endemicity Setting. In this patient, sequence data from week 48 showed genotype A3 with no resistance mutations in polymerase; the major hydrophobic region (MHR) of surface showed Y100C and Y161FY; in addition, arginine (R) was present at position 122 instead of lysine (K), as per the consensus sequence of genotype A3. 2018 Open forum infectious diseases Result HBV Y100C 160 165 P;S 95;145 105;152 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. Three of 5 (60%) escape mutations isolated from sequences from blood donors resided within the 'a' determinant's first loop (aa 124-137), 1 (20%) within the second loop (aa 138-147), and P120L was present in the mini loop outside the range (aa 124 -147). 2019 Virus genes Result HBV P120L 187 192 S 96 110 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. Twelve mutations including diagnostic escape mutations (sY100C, sR122K, sT123A, sC124R, sM133T), vaccine escape mutations (sT126N, sQ129R, sM133L, sF134V) and immunoglobulin therapy failure (sG119R, sG130N, sT140S) were exclusive to isolates obtained from HBV/HIV patients versus n = 4 including sP120L, sG130R, sY134H, and sD144A) (Fig 4) obtained from some isolates from blood donors. 2019 Virus genes Result HBV Y100C;R122K;T123A;C124R;M133T;T126N;Q129R;M133L;F134V;G119R;G130N;T140S;P120L;G130R;Y134H;D144A 56;64;72;80;88;123;131;139;147;191;199;207;296;304;312;324 62;70;78;86;94;129;137;145;153;197;205;213;302;310;318;330 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 56;64;72;80;88;123;131;139;147;191;199;207;296;304;312;324 57;65;73;81;89;124;132;140;148;192;200;208;297;305;313;325 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A80V mutation also showed significant association in this analysis with a p-value of 0.05 (Table 4). 2018 Frontiers in cellular and infection microbiology Result HBV A80V 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Considering the core mutation E77D/Q, D is absent in AC group but detectable at low frequency in the LC+HCC group. 2018 Frontiers in cellular and infection microbiology Result HBV E77D;E77Q 30;30 36;36 C 16 20 Hepatocellular carcinoma;Liver cirrhosis 104;101 107;103 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Conversely, however, two core mutations were significantly more prevalent in the AC group than in the LC group; mutation A80I (48.30 and 28.89% prevalence in the AC and LC groups, respectively; p = 0.022), and mutation L116I (79.59 and 64.44% prevalence in the AC and LC groups, respectively; p = 0.037). 2018 Frontiers in cellular and infection microbiology Result HBV A80I;L116I 121;219 125;224 C 25 29 Liver cirrhosis;Liver cirrhosis;Liver cirrhosis 102;169;268 104;171;270 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Conversely, two point mutations in the core region were present at significantly higher frequency in the AC group than in the LC+HCC group; mutation A80I (48.30 and 25.37% prevalence in the AC and LC+HCC groups, respectively; p = 0.002), and mutation L116I (79.59 vs. 2018 Frontiers in cellular and infection microbiology Result HBV A80I;L116I 149;251 153;256 C 39 43 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 129;200;126;197 132;203;128;199 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Furthermore, multivariate regression analysis revealed that age (p < 0.0001), gender (p = 0.020), HBV viral load (p = 0.014), and core mutation L116I (p = 0.026) were independently associated with cirrhosis HCC in HBV-infected patients (Table 6). 2018 Frontiers in cellular and infection microbiology Result HBV L116I 144 149 C 130 134 Liver cirrhosis;Hepatocellular carcinoma;HBV infections 197;207;214 206;210;226 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Furthermore, mutation V91T, substituting valine for threonine at the same core position as V91S, was present in large percentage of patients in the AC+LC+HCC group; this prevalence (91.12%) was significantly higher than was seen in the IC group (9.44%; p < 0.0001). 2018 Frontiers in cellular and infection microbiology Result HBV V91T;V91S 22;91 26;95 C 74 78 Hepatocellular carcinoma;Liver cirrhosis 154;151 157;153 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In total, four mutations were significantly more prevalent in the LC group than in the AC group; mutation G29D in the precore region (31.11 and 12.93% prevalence in the LC and AC groups, respectively; p = 0.005), mutation F24Y in the core region (6.67 and 0.68% prevalence in the LC and AC groups, respectively; p = 0.041), mutation A80V in the core region (22.22 and 9.52% prevalence in the LC and AC groups, respectively; p = 0.024), and mutation E180A (11.11 and 2.04% prevalence in the LC and AC groups, respectively; p = 0.018). 2018 Frontiers in cellular and infection microbiology Result HBV G29D;F24Y;A80V;E180A 106;222;333;449 110;226;337;454 C;C;Precore 234;345;118 238;349;125 Liver cirrhosis;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis 66;169;280;392;490 68;171;282;394;492 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Multivariate analysis between the AC and LC groups indicated that age (p = 0.001), gender (p = 0.018), HBV viral load (p = 0.012) and core mutation L116I (p = 0.021) were significantly correlated with HBV-related cirrhosis. 2018 Frontiers in cellular and infection microbiology Result HBV L116I 148 153 C 134 138 Liver cirrhosis;Liver cirrhosis 201;41 222;43 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Mutation E77Q within the core region was significantly more prevalent in the AC+LC+HCC group than in the IC group (7.01 vs. 2018 Frontiers in cellular and infection microbiology Result HBV E77Q 9 13 C 25 29 Hepatocellular carcinoma;Liver cirrhosis 83;80 86;82 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Similarly, mutation V91S was more prevalent in the combined group than in the IC group (3.27 vs. 2018 Frontiers in cellular and infection microbiology Result HBV V91S 20 24 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. The amino acids at the four positions in the core protein that were significantly associated with disease progression (E64D, E77D/Q, A80I/T/V, and L116I) were found to be more variable in the LC+HCC group than in the AC group. 2018 Frontiers in cellular and infection microbiology Result HBV A80I;A80T;A80V;E64D;E77D;E77Q;L116I 133;133;133;119;125;125;147 141;141;141;123;131;131;152 C 45 49 Hepatocellular carcinoma;Liver cirrhosis 195;192 198;194 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. There were eight point mutations whose prevalence differed significantly between the AC and LC+HCC groups, including the precore mutation W28* (tryptophan to stop) which has been reported previously, and is known to be involved in liver disease progression (64.18 and 44.90% prevalence in the LC+HCC and AC groups, respectively; p = 0.009). 2018 Frontiers in cellular and infection microbiology Result HBV W28X 138 142 Precore 121 128 Hepatocellular carcinoma;Liver disease;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 95;231;296;92;293 98;244;299;94;295 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. These analyses revealed significant associations between HBV-related cirrhosis and age (p < 0.0001), viral load (p = 0.001), precore mutation G29D (p = 0.006), core mutation F24Y (p = 0.045), core mutation A80I (p = 0.024), core mutation L116I (p = 0.04), and core mutation E180A (p = 0.017; Table 5). 2018 Frontiers in cellular and infection microbiology Result HBV G29D;F24Y;A80I;L116I;E180A 142;174;206;238;274 146;178;210;243;279 C;C;C;C;Precore 160;192;224;260;125 164;196;228;264;132 Liver cirrhosis 57 78 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. These included the precore mutation G29D (37.31 and 12.93% prevalence in the LC+HCC and AC groups, respectively; p < 0.0001), the core mutation E64D (41.79 and 25.17% prevalence in the LC+HCC and AC groups, respectively; p = 0.014), the core mutation E77Q (13.43 and 4.08% prevalence in the LC+HCC and AC groups, respectively; p = 0.02), the core mutation A80T (47.76 and 29.93% prevalence in the LC+HCC and AC groups, respectively; p = 0.011) and the core mutation A80V (19.40 and 9.52% prevalence in the LC+HCC and AC groups, respectively; p = 0.044). 2018 Frontiers in cellular and infection microbiology Result HBV G29D;E64D;E77Q;A80T;A80V 36;144;251;356;466 40;148;255;360;470 C;C;C;C;Precore 130;237;342;452;19 134;241;346;456;26 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis;Liver cirrhosis 80;188;294;400;509;77;185;291;397;506 83;191;297;403;512;79;187;293;399;508 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Univariate analyses revealed that gender (p = 0.008), HBV viral load (p < 0.0001), and core mutation E77Q (p = 0.047) all displayed a significant positive correlation with disease progression when the IC group was compared with the AC+LC+HCC combined group (Table 4). 2018 Frontiers in cellular and infection microbiology Result HBV E77Q 101 105 C 87 91 Hepatocellular carcinoma;Liver cirrhosis 238;235 241;237 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Univariate analysis showed that age (p < 0.0001), gender (p = 0.022), BMI (p = 0.023), HBV viral load (p < 0.0001), precore mutation W28* (p = 0.01), precore mutation G29D (p < 0.0001), core mutation E64D (p = 0.015), core mutation E77Q (p = 0.019), core mutation A80I (p = 0.002), core mutation A80T (p = 0.012), and core mutation L116I (with a border line p-value of 0.051) were all significantly correlated with HBV-related LC+HCC (Table 6). 2018 Frontiers in cellular and infection microbiology Result HBV W28X;G29D;E64D;E77Q;A80I;A80T;L116I 133;167;200;232;264;296;332 137;171;204;236;268;300;337 C;C;C;C;C;Precore;Precore 186;218;250;282;318;116;150 190;222;254;286;322;123;157 Hepatocellular carcinoma;Liver cirrhosis 430;427 433;429 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. With the core mutation A80I/T/V, I is the most frequent amino acid in the AC group, followed by T and then V, whereas in the LC+HCC group T is the most frequent, followed by I and then V. 2018 Frontiers in cellular and infection microbiology Result HBV A80I;A80T;A80V 23;23;23 31;31;31 C 9 13 Hepatocellular carcinoma;Liver cirrhosis 128;125 131;127 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. G1896A mutation detected by LCR was also confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 0 6 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Significant difference (p < 0.005) was observed in ALT level of HBeAg negative WT (67.6 +- 32.7 IU/L) and precore G1896A (109.82 +- 38.27 IU/L) mutant chronic hepatitis B cases. 2018 Saudi journal of biological sciences Result HBV G1896A 114 120 C;Precore 64;106 69;113 Chronic Hepatitis B 151 170 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The ALT level of precore G1896A mutant (103.23 +- 98.71 IU/L) cases was slightly higher than HBeAg negative WT (89.87 +- 92.43 IU/L) but statistically non significant in liver cirrhosis cases. 2018 Saudi journal of biological sciences Result HBV G1896A 25 31 C;Precore 93;17 98;24 Liver cirrhosis 170 185 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The ALT level was comparable and statistically non significant between HBeAg negative WT (272.52 +- 487.128 IU/L) and precore G1896A (289.57 +- 585.43 IU/L) mutants in AVH cases. 2018 Saudi journal of biological sciences Result HBV G1896A 126 132 C;Precore 71;118 76;125 Acute Hepatitis B 168 171 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The ALT level was comparable between HBeAg negative WT (92 IU/L) and precore G1896A (89.23 +- 78.71 IU/L) mutants in HCC cases. 2018 Saudi journal of biological sciences Result HBV G1896A 77 83 C;Precore 37;69 42;76 Hepatocellular carcinoma 117 120 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The ALT level was significantly raised in all the FH cases than the normal limit but was comparable and statistically non significant between HBeAg negative WT (1749.66 +- 648.27 IU/L) and precore G1896A mutant (1272.52 +- 887.128 IU/L) cases. 2018 Saudi journal of biological sciences Result HBV G1896A 197 203 C;Precore 142;189 147;196 Fulminant Hepatitis B 50 52 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The HBV DNA level (log copies/mL) was also found comparable and statistically non significant between HBeAg negative WT (3.4 +- 1.6) and precore G1896A (3.7 +- 1.4) mutants in AVH cases. 2018 Saudi journal of biological sciences Result HBV G1896A 145 151 C;Precore 102;137 107;144 Acute Hepatitis B 176 179 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The HBV DNA level (log copies/mL) was also found comparable and statistically non significant between HBeAg negative WT (3.76 +- 0.4) and precore G1896A mutants (3.9 +- 1.1). 2018 Saudi journal of biological sciences Result HBV G1896A 146 152 C;Precore 102;138 107;145 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The HBV DNA level (log copies/mL) was also found comparable and statistically non significant between HBeAg negative WT (5.15 +- 1.36) and precore G1896A mutants (5.36 +- 1.47). 2018 Saudi journal of biological sciences Result HBV G1896A 147 153 C;Precore 102;139 107;146 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The HBV DNA level (log copies/mL) was also found comparable between HBeAg negative WT (5.1) and precore G1896A (5.36 +- 1.47). 2018 Saudi journal of biological sciences Result HBV G1896A 104 110 C;Precore 68;96 73;103 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The HBV DNA level (log copies/mL) was found comparable and statistically non significant between HBeAg negative WT (4.36 +- 1.4) and precore G1896A mutants (4.9 +- 1.27). 2018 Saudi journal of biological sciences Result HBV G1896A 141 147 C;Precore 97;133 102;140 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation was confirmed by PCR coupled with LCR in 12 out of 20 (60%) serologically suspicious precore mutant cases (Table 1) which was further confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 12 18 Precore;Precore 4;113 11;120 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation was confirmed by PCR coupled with LCR in 17 out of 18 (94.4%) serologically suspicious precore mutant cases (Table 1) which was further confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 12 18 Precore;Precore 4;115 11;122 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation was confirmed by PCR coupled with LCR in 18 out of 21 (85.7%) serologically suspicious precore mutant cases (Table 1) which was further confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 12 18 Precore;Precore 4;115 11;122 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation was confirmed by PCR coupled with LCR in 20 out of 72 (27.7%) serologically suspicious precore mutant cases (Table 1) which was further confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 12 18 Precore;Precore 4;115 11;122 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The precore G1896A mutation was confirmed by PCR coupled with LCR in 38 out of 79 (48.1%) serologically suspicious precore mutant cases (Table 1) which was further confirmed by direct sequencing. 2018 Saudi journal of biological sciences Result HBV G1896A 12 18 Precore;Precore 4;115 11;122 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The study suggests that the LCR is 100% sensitive for the detection of HBV precore G1896A mutation. 2018 Saudi journal of biological sciences Result HBV G1896A 83 89 Precore 75 82 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Some commonly identified RAMs to NRTIs include M184 V (12.5%) and K70R (10%), and to NNRTIs were K103 N (12.5%) and Y181C (10%), and to PIs M46 L (2.5%) and L90 M (2.5%) (Table 5). 2018 BMC pregnancy and childbirth Result HBV M184V;K70R;K103N;Y181C;M46L;L90M 47;66;97;116;140;157 53;70;103;121;145;162 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Amino acid substitutions associated with immune escape, such as sT118K (n = 3), sG145A (n = 3), and sG145R (n = 1) variants, were abundant, especially in non-HSCT patients at HBV reactivation. 2018 Scientific reports Result HBV T118K;G145A;G145R 64;80;100 70;86;106 S;S;S 64;80;100 65;81;101 Hematopoietic stem cell transplantation 158 162 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Amino acid substitutions of sE2G (n = 3), sL77R (n = 1), and sL98V (n = 1) in the small S protein that were associated with impaired virion secretion were also the predominant clone in patients in the non-HSCT group. 2018 Scientific reports Result HBV E2G;L77R;L98V 28;42;61 32;47;66 S;S;S;S 28;42;61;82 29;43;62;89 Hematopoietic stem cell transplantation 205 209 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Finally, more than 99% of all the circulating HBV isolates became sG145A variants, followed by a subsequent decrease in the viral load mediated by administration of the nucleoside analogue entecavir. 2018 Scientific reports Result HBV G145A 66 72 S 66 67 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. In addition, several variants in the immunodominant loop of surface protein, including sT118K, sQ129H, and sG145R substitutions in the small S protein are reported to induce impaired virion secretion from infected liver cells. 2018 Scientific reports Result HBV T118K;Q129H;G145R 87;95;107 93;101;113 S;S;S;S;S 87;95;107;135;60 88;96;108;142;67 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Indeed, ultra-deep sequencing analysis showed that almost all the reactivated viral clones in four cases in the non-HSCT group were variants with the M1I/V substitution at the PreS2 start codon (frequency of 99.7% to 99.9% for total viral population), suggesting that these viral clones also impaired virion secretion caused by a deficiency of middle S protein production (Figs 3C and 4). 2018 Scientific reports Result HBV M1I;M1V 150;150 155;155 S;PreS2 344;176 352;181 Hematopoietic stem cell transplantation 116 120 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Interestingly, M1I/V variants at the start codon of the PreS2 gene, resulting in defective expression of the middle S protein, were also detected in the reactivated viruses of patients in the non-HSCT group. 2018 Scientific reports Result HBV M1I;M1V 15;15 20;20 S;PreS2 109;56 117;61 Hematopoietic stem cell transplantation 196 200 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Interestingly, sT118K (n = 3) and sQ129H (n = 2) variants were predominant in patients in the non-HSCT group, and sG145R was detected in one patient in the HSCT group. 2018 Scientific reports Result HBV T118K;Q129H;G145R 15;34;114 21;40;120 S;S;S 15;34;114 16;35;115 Hematopoietic stem cell transplantation;Hematopoietic stem cell transplantation 98;156 102;160 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Moreover, three patients in the non-HSCT group had predominant variants with sT116N, sT123N, and sG130N changes, which resulted in the addition of NLG sites by substitutions of threonine or glycine with asparagine. 2018 Scientific reports Result HBV T116N;T123N;G130N 77;85;97 83;91;103 S;S;S 77;85;97 78;86;98 Hematopoietic stem cell transplantation 36 40 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Next, we also identified amino acid substitutions sL21S (n = 3) and sF220C (n = 4) in the MHC class II-restricted T-cell epitope region, which are reported to cause a complete loss of T-cell reactivity and anti-HBs production among individuals vaccinated against HBV in an ex vivo study. 2018 Scientific reports Result HBV L21S;F220C 50;68 55;74 S;S;S 211;50;68 214;51;69 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Of note, the frequency of sG145A variants, representing immune escape variants, increased from 0% to 86.1% for the total viral population in accordance with an increase in HBV DNA levels from 2.4 log IU/ml to 8.2 log IU/ml. 2018 Scientific reports Result HBV G145A 26 32 S 26 27 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. These three altered nucleotides included non-synonymous mutations in the S gene coding region; sG145A, sE164D, and s*223 W (conversion of a stop codon into a tryptophan codon) alterations. 2018 Scientific reports Result HBV G145A;E164D 95;103 101;109 S;S;S;S 73;95;103;115 74;96;104;116 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Variants with the sE164D substitution also increased from 0% to 99.5% for the total population, and variants with the s*223 W substitution expanded from 8.3% to 99.4% of the circulating viral isolates, while the virologic significance of these two substitutions remained unknown. 2018 Scientific reports Result HBV E164D 18 24 S;S 18;118 19;119 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. A peak of the mutations occurred at the 3' end of the C region and that was a T134C mutation. 2019 Viruses Result HBV T134C 78 83 C 54 55 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Accordingly, 12 potential mutations were selected, i.e., C18T, C44T, A75T, G82A, A115C, T118C, G120A, G129A, T134C, A138G, C189A, G228A. 2019 Viruses Result HBV C18T;C44T;A75T;G82A;A115C;T118C;G120A;G129A;T134C;A138G;C189A;G228A 57;63;69;75;81;88;95;102;109;116;123;130 61;67;73;79;86;93;100;107;114;121;128;135 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. As shown in Figure 3 and Figure S2, the distribution of the hottest mutation sites in two groups seemed not to be co-incident, such as C18T, G82A, G120A, and A138G. 2019 Viruses Result HBV C18T;G82A;G120A;A138G 135;141;147;158 139;145;152;163 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. As shown in Figure 6A and B, G82A, A115C and G120A showed higher extracellular and intracellular HBsAg levels compared to WT (p < 0.05). 2019 Viruses Result HBV G82A;A115C;G120A 29;35;45 33;40;50 S 97 102 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. For up-regulation, the top five mutants (G82A, A115C, G120A, A138G and C189A) were selected and for down-regulation, mutant C18T was selected. 2019 Viruses Result HBV G82A;A115C;G120A;A138G;C189A;C18T 41;47;54;61;71;124 45;52;59;66;76;128 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Furthermore, the frequency of G120A mutation was 18.2% in the HS group (8/44), significantly higher than that in the LS group 2.3% (1/43) (p = 0.0298). 2019 Viruses Result HBV G120A 30 35 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. However, A138G and C189A mutants had similar activities as the WT. 2019 Viruses Result HBV A138G;C189A 9;19 14;24 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. In addition, C18T exhibited the down-regulating effect of HBsAg (p < 0.05). 2019 Viruses Result HBV C18T 13 17 S 58 63 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. In comparison with WT, most of the mutants showed enhanced transcription activity, only C18T could inhibit the activity of SPII. 2019 Viruses Result HBV C18T 88 92 S promoter II 123 127 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Similarly, HBV DNA levels were higher in the G120A group than that in the G120 WT group ((8.5 +- 0.7) log IU/mL and (8.1 +- 0.6) log IU/mL, p = 0.0237), shown in Figure 5B. 2019 Viruses Result HBV G120A 45 50 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Specifically, mutations G82A, A115C and G120A also resulted in higher extracellular and intracellular HBsAg levels compared to WT (p < 0.05) (Figure 6C,D). 2019 Viruses Result HBV G82A;A115C;G120A 24;30;40 28;35;45 S 102 107 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. The extracellular and intracellular HBsAg levels from mutant C18T were lower than those from WT (p < 0.05) (Figure 6C,D), consistent with the results of the luciferase assay. 2019 Viruses Result HBV C18T 61 65 S 36 41 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. The HBsAg levels were higher in G120A group than that in G120 WT group ((4.7 +- 0.4) log IU/mL vs. 2019 Viruses Result HBV G120A 32 37 S 4 9 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. The results showed that HBV total RNA levels from G82A, A115C and G120A were significantly higher than that of WT (p < 0.05) (Figure 7B), while C18T down-regulated that (p < 0.05) (Figure 7B). 2019 Viruses Result HBV G82A;A115C;G120A;C18T 50;56;66;144 54;61;71;148 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. The SPII activity of G120A mutant was 15-fold higher than WT. 2019 Viruses Result HBV G120A 21 26 S promoter II 4 8 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Then, we categorized 87 cases into two groups based on G120A detected or not. 2019 Viruses Result HBV G120A 55 60 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. To further study the effect of SPII mutations on HBV transcription and replication, the above mutations (C18T, G82A, A115C, G120A, A138G and C189A) were also constructed into the p1.2/PC plasmid containing 1.2-fold HBV genome. 2019 Viruses Result HBV C18T;G82A;A115C;G120A;A138G;C189A 105;111;117;124;131;141 109;115;122;129;136;146 S promoter II 31 35 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. To study whether mutations of SPII affected HBsAg level, we constructed the recombinant plasmid pLMS with mutations including C18T, G82A, A115C, G120A, A138G and C189A, respectively. 2019 Viruses Result HBV C18T;G82A;A115C;G120A;A138G;C189A 126;132;138;145;152;162 130;136;143;150;157;167 S;S promoter II 44;30 49;34 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. We also analyzed the effect of the six mutants on extracellular and intracellular HBV DNA and found that G120A up-regulated both the extracellular and intracellular DNA levels (Figure 7C,D). 2019 Viruses Result HBV G120A 105 110 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Additional introduction of rtS202G or rtM250V into rtL180M+A181C+M204V mutation pattern resulted in one N-H:O bond reduction with further increased binding energy (Table 4). 2019 Emerging microbes & infections Result HBV M250V;S202G;L180M;M204V;A181C 40;29;53;65;59 45;34;58;70;64 RT;RT;RT 27;38;51 29;40;53 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Afterwards, therapy was switched to an ADV+ETV Clonal sequencing of serum samples E3 and E4 during the combination therapy showed that the rtL180M+A181V+M204V mutant predominantly emerged (64% in E3, 77% in E4) in concomitance with rtL180M+A181C+M204V mutants (20% in E3, 23% in E4), rtA181V mutants (8% in E3), rtL180M+A181C+M204V+M250V mutants (4% in E3), and rtL180M+A181C+S202G+M204V mutants (4% in E3) (Figure 1(E)). 2019 Emerging microbes & infections Result HBV L180M;L180M;A181V;L180M;L180M;A181V;M204V;M204V;A181C;M204V;A181C;M250V;A181C;M204V;S202G 141;234;286;314;364;147;153;246;240;326;320;332;370;382;376 146;239;291;319;369;152;158;251;245;331;325;337;375;387;381 RT;RT;RT;RT;RT 139;232;284;312;362 141;234;286;314;364 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. All rtA181C-positive patients experienced various sequential/combined NAs therapies including ETV and had a history of LAM exposure prior to ETV treatment. 2019 Emerging microbes & infections Result HBV A181C 6 11 RT 4 6 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Clinical course of five representative cases with rtA181C substitution and HBV mutant evolution during antiviral treatment. 2019 Emerging microbes & infections Result HBV A181C 52 57 RT 50 52 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Clonal sequencing of serum sample A2 at virological breakthrough showed that rtL180M+A181C+M204V and rtL180M+A181C+M204V+M250V mutants accounted for 90% and 10% of the tested viral clones, respectively. 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;A181C;M204V;M250V 79;103;85;91;109;115;121 84;108;90;96;114;120;126 RT;RT 77;101 79;103 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Clonal sequencing of serum sample E2 at virological breakthrough during ETV treatment showed that rtL180M+A181C+M204V and rtL180M+A181V+M204V mutants and wild-type strains accounted for 60%, 25%, and 15% of the tested viral clones, respectively. 2019 Emerging microbes & infections Result HBV L180M;L180M;A181V;A181C;M204V;M204V 100;124;130;106;112;136 105;129;135;111;117;141 RT;RT 98;122 100;124 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Clonal sequencing verified that rtL180M+A181C+M204V mutations truly coexisted in the same viral genomes for all 18 samples. 2019 Emerging microbes & infections Result HBV L180M;A181C;M204V 34;40;46 39;45;51 RT 32 34 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Coexistence of rtL180M+M204V mutations was detected in all rtA181C-positive patients. 2019 Emerging microbes & infections Result HBV A181C;L180M;M204V 61;17;23 66;22;28 RT;RT 15;59 17;61 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Compared to the wild-type strain, rtL180M+A181C+M204V and rtL180M+A181V+M204V mutants had a modest decrease in viral replication capacity (45.7% and 43.1% of the wild-type, respectively). 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;M204V;A181V 36;60;42;48;72;66 41;65;47;53;77;71 RT;RT 34;58 36;60 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Consistently, Southern blotting analysis verified that the rtL180M+A181C+M204V mutant had a 70.5-fold increased EC50 of ETV (representing a 70.5-fold ETV resistance) compared to the wild-type (Supplementary Figure 1). 2019 Emerging microbes & infections Result HBV L180M;M204V;A181C 61;73;67 66;78;72 RT 59 61 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Elimination of rtA181C from the rtL180M+A181C+M204V mutant led to a restoration of the ETV-resistance level from 85.6-fold to 17.9-fold, a level similar to that of the rtL180M+A181V+M204V mutant (15.0 folds). 2019 Emerging microbes & infections Result HBV A181C;L180M;L180M;M204V;A181C;M204V;A181V 17;34;170;46;40;182;176 22;39;175;51;45;187;181 RT;RT;RT 15;32;168 17;34;170 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. For patient 2, clonal sequencing of serum sample B3 at virological breakthrough during ETV treatment showed that rtL180M+A181C+M204V, rtL180M+A181C+M204V+M250V, and rtL180M+A181V+M204V mutants accounted for 40%, 35%, and 25% of tested viral clones, respectively (Figure 1(B)). 2019 Emerging microbes & infections Result HBV L180M;L180M;L180M;A181C;M204V;M250V;A181C;M204V;M204V;A181V 115;136;167;121;127;154;142;148;179;173 120;141;172;126;132;159;147;153;184;178 RT;RT;RT 113;134;165 115;136;167 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. For patient 3, clonal sequencing of serum sample C2 at virological breakthrough during ETV treatment showed that rtL180M+A181C+M204V mutants were 86% concomitant with 14% of the rtL180M+A181V+M204V mutants (Figure 1(C)). 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;M204V;A181V 115;180;121;127;192;186 120;185;126;132;197;191 RT;RT 113;178 115;180 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. For patient 4, clonal sequencing of serum sample D2 at virological breakthrough during ETV treatment showed that rtL180M+A181C+M204V and rtL180M+A181V+M204V mutants and wild-type strains accounting for 50%, 45%, and 5% of the tested viral clones, respectively (Figure 1(D)). 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;M204V;A181V 115;139;121;127;151;145 120;144;126;132;156;150 RT;RT 113;137 115;139 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition, a laboratory strain rtL180M+M204V(lab) which was generated by eliminating rt181C mutation of the rtL180M+A181C+M204V was taken into the phenotypic analysis of drug resistance. 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;M204V 35;112;118;41;124 40;117;123;46;129 RT;RT;RT 33;87;110 35;89;112 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition, the colocalization of rtL180M+A181C+M204V mutations and rtT184A or rtM250V mutation on the same viral genome was verified in the samples of three patients (P1, P2, P10). 2019 Emerging microbes & infections Result HBV T184A;L180M;M250V;M204V;A181C 71;37;82;49;43 76;42;87;54;48 RT;RT;RT 35;69;80 37;71;82 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition, the root mean square fluctuation (RMSF) graph showed that the flexibility of the mutant RT was obviously reduced, indicating that rtL180M+A181C+M204V mutation led to greater protein rigidity and therefore made the HBV RT relatively unsuitable for interacting with ETV-TP (Supplementary Figure 3). 2019 Emerging microbes & infections Result HBV L180M;A181C;M204V 145;151;157 150;156;162 RT;RT;RT 101;143;231 103;145;233 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In contrast, replication capacity decreased to a greater extent in rtL180M+A181C+M204V+M250V and rtL180M+A181C+S202G+M204V mutants (25.9% and 25.0% of the wild-type, respectively) (Figure 3). 2019 Emerging microbes & infections Result HBV L180M;L180M;M250V;M204V;A181C;M204V;S202G;A181C 69;99;87;81;75;117;111;105 74;104;92;86;80;122;116;110 RT;RT 67;97 69;99 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Phylogenetic tree analysis was performed for the 22 cloned HBV RT gene sequences that harboured rtA181C mutation, as well as for the nine cloned RT gene sequences from serial serum samples of patient 5. 2019 Emerging microbes & infections Result HBV A181C 98 103 RT;RT;RT 63;96;145 65;98;147 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Replication capacity and drug susceptibility of rtA181C mutants. 2019 Emerging microbes & infections Result HBV A181C 50 55 RT 48 50 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. rtA181C mutation profile and clinical data. 2019 Emerging microbes & infections Result HBV A181C 2 7 RT 0 2 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Serial serum samples were obtained from five rtA181C-positive patients (patient 1 through patient 5 in Table 2) whose clinical information, and dynamic changes of their mutant viruses, were longitudinally analysed. 2019 Emerging microbes & infections Result HBV A181C 47 52 RT 45 47 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Specifically, the rtL180M+A181C+M204V mutant had higher binding energy compared to the rtL180M+M204V mutant (-4.56 kcal/mol vs. 2019 Emerging microbes & infections Result HBV L180M;L180M;M204V;A181C;M204V 20;89;32;26;95 25;94;37;31;100 RT;RT 18;87 20;89 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The HBV genotype distribution showed no significant difference when compared with that of the rtA181C-negative patients across the studied population (HBV/B 14.0%, HBV/C 85.2%, HBV/D 0.8%). 2019 Emerging microbes & infections Result HBV A181C 96 101 RT 94 96 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The median duration for ETV therapy was 39 (7-96) months before rtA181C was detected. 2019 Emerging microbes & infections Result HBV A181C 66 71 RT 64 66 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The modelling structures of the wild-type HBV RT sequence and the HBV RT mutant sequences containing rtA181C plus LAMr, each of which binds to ETV-TP, are shown in Figure 4. 2019 Emerging microbes & infections Result HBV A181C 103 108 RT;RT;RT 46;70;101 48;72;103 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The nucleotide change for rtA181C and rtA181V mutations is summarized in Supplementary Table 1. 2019 Emerging microbes & infections Result HBV A181C;A181V 28;40 33;45 RT;RT 26;38 28;40 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The patterns of LAMr, in the composition of ETV-resistance mutations, included rtM204V+L180M (82.91%), rtM204I +-L180M (15.25%), and rtM204V /I+L180M (1.84%) (Table 1). 2019 Emerging microbes & infections Result HBV M204V;M204I;M204V;L180M;L180M;L180M 81;105;135;87;113;144 86;110;140;92;118;149 RT;RT;RT 79;103;133 81;105;135 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The representative cloned rtL180M+A181C+M204V sequences from each patient, together with other rtA181C-containing sequences, have been deposited in GenBank (accession number: MF682469-MF682490). 2019 Emerging microbes & infections Result HBV L180M;A181C;M204V;A181C 28;97;40;34 33;102;45;39 RT;RT 26;95 28;97 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The results of molecular dynamics simulation suggested that all the mutant proteins showed a lower root mean square deviation than the wild-type form, which may reduce the overall flexibility of the mutant proteins and prevent the ETV-TP from interacting with them Specifically, rtL180M+A181C+M204V mutant protein had lower values than that of wild-type and rtL180M+M204V mutant proteins (Supplementary Figure 2). 2019 Emerging microbes & infections Result HBV L180M;L180M;A181C;M204V;M204V 281;360;287;293;366 286;365;292;298;371 RT;RT 279;358 281;360 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rt180M+M204V-containing mutants changed binding site and bond of RT domain to ETV-TP, and clearly increased the binding energy. 2019 Emerging microbes & infections Result HBV M204V 11 16 RT;RT 4;69 6;71 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtA181C mutation was detected in 18 patients by direct sequence analysis, encompassing 0.08% (18/22,009) of the study population and 0.29% (18/6170) of ETV-experienced patients. 2019 Emerging microbes & infections Result HBV A181C 6 11 RT 4 6 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtA181C-containing mutants had a 2.7 - 3.2-fold decrease in TDF susceptibility which was lower than that of the rtL180M+A181V+M204V mutant but similar with that of the two classical ETV-resistance mutants. 2019 Emerging microbes & infections Result HBV A181C;L180M;M204V;A181V 6;118;130;124 11;123;135;129 RT;RT 4;116 6;118 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtL180M+A181C+M204V, rtL180M+A181C+M204V+M250V, rtL180M+A181C+M204V+S202G, and rtL180M+A181V+M204V exhibited 85.6-, 356.1-, 307.1-, and 15.0-fold decreased susceptibility to ETV, respectively. 2019 Emerging microbes & infections Result HBV L180M;L180M;L180M;L180M;M204V;A181C;M250V;M204V;A181C;S202G;M204V;A181C;M204V;A181V 6;27;54;85;18;12;45;39;33;72;66;60;97;91 11;32;59;90;23;17;50;44;38;77;71;65;102;96 RT;RT;RT;RT 4;25;52;83 6;27;54;85 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Finally, a single patient had Q129R mutation that is a vaccine-escape mutant and affects HBV detection besides the R122K mutation. 2019 PeerJ Result HBV Q129R;R122K 30;115 35;120 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The first patient was a male with history of treatment with lamivudine who had mutations at established drug resistance positions: L180M, T184A, M204V which confer resistance to lamivudine, entecavir and telbivudine. 2019 PeerJ Result HBV L180M;T184A;M204V 131;138;145 136;143;150 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The L109R mutation that is a vaccine-escape mutant was found in a single patient. 2019 PeerJ Result HBV L109R 4 9 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The M133L and D144E mutations that are vaccine-escape mutants, affecting HBV detection and immunoglobulin therapy were found each in a single patient. 2019 PeerJ Result HBV M133L;D144E 4;14 9;19 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The R122K mutation which affects HBV detection was found in three patients. 2019 PeerJ Result HBV R122K 4 9 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The S143L mutation which is both a vaccine-escape mutant and affects HBV detection was found in a single patient. 2019 PeerJ Result HBV S143L 4 9 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The second patient was a female with unknown history of treatment who had mutations at established drug resistance positions: L180M, M204V which confer resistance to lamivudine, telbivudine and partial resistance to entecavir. 2019 PeerJ Result HBV L180M;M204V 126;133 131;138 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The third patient was a male with history of treatment with lamivudine who had mutations at established drug resistance positions: V173L, L180M, M204V which confer resistance to lamivudine, telbivudine and partial resistance to entecavir. 2019 PeerJ Result HBV V173L;L180M;M204V 131;138;145 136;143;150 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. and we have recently reported that a nonsense mutant of LHBs, sW182* (Fig 1A), has an oncogenic potential, as nude mice xenografted with mouse embryonic fibroblasts (NIH3T3) transfected by the mutant showed strong tumorigenicity. 2019 PloS one Result HBV W182X 62 68 S;S 56;62 60;63 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. As anticipated, the levels of p53 and Smad4 that had been downregulated by the sW182* mutant were restored in the Jab1-depleted cells (Fig 4E and 4F). 2019 PloS one Result HBV W182X 79 85 S 79 80 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Based on the result of Fig 3, we examined the effect of the sW182* truncation mutant on the levels of Jab1 target tumor suppressors, p53 and Smad4. 2019 PloS one Result HBV W182X 60 66 S 60 61 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Each of these promoter activities was inhibited by the sW182* mutant (Fig 5A). 2019 PloS one Result HBV W182X 55 61 S 55 56 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Expression of the LHBs sW182* truncation mutant in Huh-7 cells. 2019 PloS one Result HBV W182X 23 29 S;S 18;23 22;24 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Fig 1B shows expression of the wild-type LHBs and the sW182* truncation mutant in the transiently transfected liver cell lines (HepG2 and Huh-7) using different transfection reagents. 2019 PloS one Result HBV W182X 54 60 S;S 41;54 45;55 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. For this purpose we attempted to stably express the sW182* protein in liver cell lines. 2019 PloS one Result HBV W182X 52 58 S 52 53 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In contrast, the immunohistochemistry (IHC) analysis showed a relatively high expression of the sW182* mutant in the liver cells, whereas the wild-type protein was hardly detected (Fig 2). 2019 PloS one Result HBV W182X 96 102 S 96 97 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In contrast, the sW182* mutant had no effect on a non-Jab1 target Smad3 (Fig 4A and 4B). 2019 PloS one Result HBV W182X 17 23 S 17 18 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In the GST-pulldown assay GST-Jab1 precipitated the LHBs sW182*, but not wild-type protein, from the HEK293T cell lysate (We noted that the viral proteins can be well expressed in this cell line) (Fig 3). 2019 PloS one Result HBV W182X 57 63 S;S 52;57 56;58 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In this condition, we failed to express the proteins in HepG2 cells, but both wild-type and the truncation mutant sW182* were expressed in Huh-7 cells. 2019 PloS one Result HBV W182X 114 120 S 114 115 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. On the other hand, the sW182* mutant was not detected in the blood throughout the experiment. 2019 PloS one Result HBV W182X 23 29 S 23 24 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Prolonged expression and retention of the LHBs sW182* truncation mutant in the mouse hepatocytes in vivo. 2019 PloS one Result HBV W182X 47 53 S;S 42;47 46;48 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Prompted by this study, we tested whether the LHBs sW182* truncation mutant could physically interact with Jab1. 2019 PloS one Result HBV W182X 51 57 S;S 46;51 50;52 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Reciprocally, Jab1 was co-immunoprecipitated with the LHBs w182*, but not with wild-type protein, from the cell lysate (Fig 3). 2019 PloS one Result HBV W182X 59 64 S 54 58 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The LHBs sW182* truncation mutant downregulates multiple tumor suppressor proteins. 2019 PloS one Result HBV W182X 9 15 S;S 4;9 8;10 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The LHBs sW182* truncation mutant inhibits downstream genes of p53 and Smad4. 2019 PloS one Result HBV W182X 9 15 S;S 4;9 8;10 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The physical interaction strongly suggested a possible influence of the sW182* mutant on Jab1 function. 2019 PloS one Result HBV W182X 72 78 S 72 73 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The sW182* mutant, but not wild-type LHBs physically interacts with Jab1. 2019 PloS one Result HBV W182X 4 10 S;S 37;4 41;5 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The unstable nature of the LHBs sW182* mutant in the cultured liver cells raised an argument about its potential role in liver carcinogenesis. 2019 PloS one Result HBV W182X 32 38 S;S 27;32 31;33 Liver disease 121 141 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. These results indicated that the Jab1-dependent downregulation of the tumor suppressors by the LHBs sW182* mutant can influence their downstream target genes. 2019 PloS one Result HBV W182X 100 106 S;S 95;100 99;101 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. This result demonstrated that the LHBs sW182* truncation mutant can be expressed and retained in the hepatocytes in the living liver for a prolonged period of time, supporting the relevance of the further functional investigation of the mutant using the cultured liver cells, regardless of its apparent instability in the system. 2019 PloS one Result HBV W182X 39 45 S;S 34;39 38;40 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. To examine if the downstream target genes of the tumor suppressors p53 and Smad4 are affected by the sW182* mutant, we performed luciferase reporter assays. 2019 PloS one Result HBV W182X 101 107 S 101 102 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. To test the involvement of Jab1 in the downregulation of the tumor suppressors by the LHBs sW182* mutant, we depleted the Jab1 from the liver cells by siRNA (Fig 4E and 4F). 2019 PloS one Result HBV W182X 91 97 S;S 86;91 90;92 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. To test whether the truncation mutant can be expressed in the liver in vivo, we hydrodynamically injected mice with the expression construct for the wild-type LHBs or sW182* mutant under a hepatocyte-specific PreS1 promoter. 2019 PloS one Result HBV W182X 167 173 S;PreS1;S 159;209;167 163;214;168 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Treatment of the sW182*-transfected cells with a proteasome inhibitor MG132 restored the levels of p53 and Smad4, indicating that the downregulation of these proteins are through the proteasome-based protein degradation (Fig 4C and 4D). 2019 PloS one Result HBV W182X 17 23 S 17 18 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. We found that the sW182* mutant downregulates these two tumor suppressors in Huh-7 cells (Fig 4A and 4B). 2019 PloS one Result HBV W182X 18 24 S 18 19 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. We noted later that the sW182* protein cannot be expressed very well, even transiently, in the cultured liver cells. 2019 PloS one Result HBV W182X 24 30 S 24 25 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. After L97I reversion in the GYF isolate, the levels of pgRNA encapsidation, core DNA replication, and virion secretion, remained unchanged. 2019 Antiviral research Result HBV L97I 6 10 C 76 80 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Among those, I97L has been reported to be associated with the increased HBV DNA replication in Huh7 cells, we thus first examined the potential role of I97L in the replication fitness of GYF isolate. 2019 Antiviral research Result HBV I97L;I97L 13;152 17;156 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Considering that the P5T mutant did not completely bring up the WT replication to the level of GYF, it is plausible that the multiple core mutations and/or pol mutations of GYF synergistically contribute to the enhanced pgRNA encapsidation and DNA replication of the GYF strain. 2019 Antiviral research Result HBV P5T 21 24 C;P 134;156 138;159 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. further suggesting that one or more core mutations other than I97L are responsible for the high replication fitness of GYF isolate. 2019 Antiviral research Result HBV I97L 62 66 C 36 40 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Furthermore, introducing I97L mutation into WT did not enhance viral DNA replication, but changing WT core to other six mutations together (P5T, S35T, P79Q, E83D, S87G, and Q177K) significantly elevated the replication level of WT. 2019 Antiviral research Result HBV P5T;I97L;S35T;P79Q;E83D;S87G;Q177K 140;25;145;151;157;163;173 143;29;149;155;161;167;178 C 102 106 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Furthermore, the G87S reverse mutation eliminated the presence of naked capsid in cell supernatant (lane 7), inferring a potential role of G87 in the secretion of nonenveloped capsid. 2019 Antiviral research Result HBV G87S 17 21 Capsid;Capsid 72;176 78;182 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Furthermore, the P5T single mutation reduced the level of mature rcDNA and resulted in an altered virion electrophoresis pattern (panel D and E, lane 3), which is consistent with the above result. 2019 Antiviral research Result HBV P5T 17 20 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. I97L mutation is dispensable for the enhanced viral replication of GYF strain. 2019 Antiviral research Result HBV I97L 0 4 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. indicating that I97L is dispensable for the high replication fitness of GYF isolate. 2019 Antiviral research Result HBV I97L 16 20 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Interestingly, the T5P reverse mutation produced slightly more intracellular rcDNA than GYF and restored the wildtype particle gel pattern (lane 3), suggesting that P5 of core may regulate HBV rcDNA synthesis and virion morphogenesis. 2019 Antiviral research Result HBV T5P 19 22 C 171 175 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Moreover, consistent with the phenotype of G87S reverse mutation shown in. 2019 Antiviral research Result HBV G87S 43 47 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Other core mutations (S35T, S87G, Q177K) did not obviously affect the replication of WT HBV (lanes 4-6). 2019 Antiviral research Result HBV S35T;S87G;Q177K 22;28;34 26;32;39 C 6 10 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. P5T promotes HBV replication. 2019 Antiviral research Result HBV P5T 0 3 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. S87G mutation of WT core resulted in an elevated secretion of naked capsid. 2019 Antiviral research Result HBV S87G 0 4 Capsid;C 68;20 74;24 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The capsid gel assay demonstrated that P5T mutation exhibited a significant higher EIA signal of capsid (panel B, lane 3), although it remains unknown whether such phenomena results from enhanced capsid formation or a better epitope accessibility of the core antibodies. 2019 Antiviral research Result HBV P5T 39 42 Capsid;Capsid;Capsid;C 4;97;196;254 10;103;202;258 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The GYF-T5P construct still replicated better than WT (lane 3 vs 1), indicating that other core mutation(s) may also be able to coordinately enhance viral replication (lanes 4-8). 2019 Antiviral research Result HBV T5P 8 11 C 91 95 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The mutations within the core protein of GYF mutant include P5T, S35T, P79Q, E83D, S87G, I97L and Q177K. 2019 Antiviral research Result HBV P5T;S35T;P79Q;E83D;S87G;I97L;Q177K 60;65;71;77;83;89;98 63;69;75;81;87;93;103 C 25 29 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The screening demonstrated that only the T5P restoration in GYF isolate significantly decreased pgRNA encapsidation and core DNA replication. 2019 Antiviral research Result HBV T5P 41 44 C 120 124 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Vice versa, the P5T core mutation of WT HBV markedly upregulated pgRNA encapsidation and ssDNA replication. 2019 Antiviral research Result HBV P5T 16 19 C 20 24 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Common and frequent mutations identified in the cohort of the present study included rtL80V/I, rtV84M, rtL91I, rtN118H/D/T, rtT128A, rtL180M, rtT184L/S/A, rtV191I, rtS202G, rtV207I/M, rtS213T, rtQ215P/S/H, rtL229V/M/W/F, rtS256G/C, and rtN337H/T, as presented in Table II. 2019 Experimental and therapeutic medicine Result HBV L80V;L80I;V84M;L91I;N118H;N118D;N118T;V207I;V207M;Q215P;Q215S;Q215H;L229V;L229M;L229W;L229F;S256G;S256C;N337H;N337T;T128A;L180M;T184L;T184S;T184A;V191I;S202G;S213T 87;87;97;105;113;113;113;175;175;195;195;195;208;208;208;208;223;223;238;238;126;135;144;144;144;157;166;186 93;93;101;109;122;122;122;182;182;204;204;204;219;219;219;219;230;230;245;245;131;140;153;153;153;162;171;191 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 85;95;103;111;124;133;142;155;164;173;184;193;206;221;236 87;97;105;113;126;135;144;157;166;175;186;195;208;223;238 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Furthermore, three out of five stop codons in the S region (sS34*, sW74*, sW172*, sW182*, sW196*) were identified in the RT region; the stop codons have been associated with NAs resistance, also affected the HBsAg reading frame (rtA181T/sW172*, rtV191I/sW182* and rtM204I/sW196*). 2019 Experimental and therapeutic medicine Result HBV W172X;W182X;W196X;A181T;V191I;M204I;S34X;W74X;W172X;W182X;W196X 237;253;272;231;247;266;60;67;74;82;90 243;259;278;236;252;271;65;72;80;88;96 S;RT;RT;RT;RT;S;S;S;S;S;S;S;S;S 208;121;229;245;264;50;60;67;74;82;90;237;253;272 213;123;231;247;266;51;61;68;75;83;91;238;254;273 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. In the present study, the most prevalent mutations were those in the S region (sP120Q, sQ129R, sT131I, sM133I, sG145R, sY161F/H, sI195M/T, sW196S/L, sW199C/L and sM213I/T; Table III). 2019 Experimental and therapeutic medicine Result HBV P120Q;Q129R;T131I;M133I;G145R;Y161F;Y161H;I195M;I195T;W196S;W196L;W199C;W199L;M213I;M213T 79;87;95;103;111;119;119;129;129;139;139;149;149;162;162 85;93;101;109;117;127;127;137;137;147;147;157;157;170;170 S;S;S;S;S;S;S;S;S;S;S 69;79;87;95;103;111;119;129;139;149;162 70;80;88;96;104;112;120;130;140;150;163 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Prior to combination treatment, the rtA181V mutation was identified in one patient in the RS group (two in 24 clones), and no ADV resistance mutation (rtN236T) was detected. 2019 Experimental and therapeutic medicine Result HBV A181V;N236T 38;153 43;158 RT;RT 36;151 38;153 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Sequence analysis revealed that almost all clones had rtM204V/I resistance mutations prior to LAM/ADV combination rescue treatment, and the frequency of this mutation was not significantly different between the RS and NRS [167/173 (96.5%) vs. 2019 Experimental and therapeutic medicine Result HBV M204V;M204I 56;56 63;63 RT 54 56 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. However, the rtV207L substitution is associated with antiviral drug resistance. 2019 Virology journal Result HBV V207L 15 20 RT 13 15 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. PreS1 (aa 1-119) substitutions were: A54Q, L67F, I74V, T86A, S89P, T90A, I91V. 2019 Virology journal Result HBV A54Q;L67F;I74V;T86A;S89P;T90A;I91V 37;43;49;55;61;67;73 41;47;53;59;65;71;77 PreS1 0 5 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. PreS2 (aa 1-55) substitutions were: V32 L, N33S, A35V, N37 T, A47S, T49I, V53A, T54P. 2019 Virology journal Result HBV V32L;N33S;A35V;N37T;A47S;T49I;V53A;T54P 36;43;49;55;62;68;74;80 41;47;53;60;66;72;78;84 PreS2 0 5 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. S (aa 1-226) substitutions were: D144DN, M198I, S207 N, V209 L. 2019 Virology journal Result HBV M198I;S207N;V209L 41;48;56 46;54;62 S 0 1 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. Substitutions in the overlapping RT region (aa 1-230) were: D7A, Y126H, M129 L, G152GE, V163I, I187L, V207 L, R217L. 2019 Virology journal Result HBV D7A;Y126H;M129L;V163I;I187L;V207L;R217L 60;65;72;88;95;102;110 63;70;78;93;100;108;115 RT 33 35 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. The corresponding reverse transcriptase substitution (rtG152E) is not within the active domain of the enzyme. 2019 Virology journal Result HBV G152E 56 61 RT;RT 18;54 39;56 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. The D144N substitution within the immunodominant 'a' determinant occurred as a mixture with wild-type. 2019 Virology journal Result HBV D144N 4 9 S 50 64 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. As shown in Table 3, the ratios of the Sp1 G2765A substitution for each sample were mostly comparable between the cloning and NGS data, which verified that our cloning sequence data were reliable. 2019 Virology journal Result HBV G2765A 43 49 S1 promoter 39 42 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Both m5 (G2765A) and m9 (whole nucleotide mutation) vectors showed significantly impaired luciferase activity (70.7 and 47.9%, respectively) when compared to the WT vector (p < 0.01. 2019 Virology journal Result HBV G2765A 9 15 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. In addition, the G2765A substitution ratio and the HBV viral load showed a negative correlation (r = - 0.473, p < 0.01), and the G2765A substitution ratio and the HBsAg level showed a weak negative correlation (r = - 0.356, p < 0.05. 2019 Virology journal Result HBV G2765A;G2765A 17;129 23;135 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. On the other hand, patients who had the G2765A substitution showed a significantly lower HBV viral load and aspartate transaminase (AST) level when compared to those with the wild-type (WT) sequence (p < 0.05). 2019 Virology journal Result HBV G2765A 40 46 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Substitutions in the Sp1 region were found at the 2765th base (G to A; G2765A), 2768th base (T to G or A), and 2771st base (C to T). 2019 Virology journal Result HBV G2765A 71 77 S1 promoter 21 24 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. The most frequent substitution was the G2765A substitution, which was found in one patient in the high group and eight patients in the low group. 2019 Virology journal Result HBV G2765A 39 45 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. The Sp1 G2765A substitution reduced the level of pre-S1 antigen. 2019 Virology journal Result HBV G2765A 8 14 PreS1;S1 promoter 49;4 55;7 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Therefore, we focused on the G2765A substitution and analyzed its biological function. 2019 Virology journal Result HBV G2765A 29 35 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. To further investigate the effect of the G2765A substitution on HBV production, we constructed a 1.3-fold HBV genome vector that enabled the production of HBV particles when transfected into HepG2 cells. 2019 Virology journal Result HBV G2765A 41 47 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Transfection of the m5 (G2765A) or WT vector into HepG2 cells resulted in no change in virus production (5.6 log IU/ml, 5.7 log IU/ml, respectively). 2019 Virology journal Result HBV G2765A 24 30 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Because theses mutations could be caused by the single treatment of LAM, ADV and ETV respectively; E218D was identified in LAM switched to ADV therapy; R242D was found in ADV switched to ETV therapy. 2019 Scientific reports Result HBV E218D;R242D 99;152 104;157 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Figure 1A showed the association of classical mutation sites to M204I or V in genotypes B and C, respectively. 2019 Scientific reports Result HBV M204I 64 69 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. However, in genotype B, single mutation of M204I was much more frequent in genotype B than in genotype C (37/56, 66.1% vs. 2019 Scientific reports Result HBV M204I 43 48 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In case one, mutation patterns changed from wild-type to M204I and back to wild-type again during 85 months of antiviral therapy. 2019 Scientific reports Result HBV M204I 57 62 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In case three, multiple mutation patterns were observed from L180M + M204V + I224V + N238H to L180M + M204V + T184S + I224V + N238H under LAM and ADV combined therapy, which developed resistance to ETV. 2019 Scientific reports Result HBV L180M;M204V;I224V;N238H;L180M;M204V;T184S;I224V;N238H 61;69;77;85;94;102;110;118;126 66;74;82;90;99;107;115;123;131 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In contrast, the prevalence of mutation pattern of L180 associated to M204I in genotype C was significantly higher than in genotype B (15/47, 31.9% vs. 2019 Scientific reports Result HBV M204I 70 75 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In this study, non-classical mutations were observed in 29 patients who suffering from virological breakthrough and without classical mutations (Table 4) at 9 sites (V191I, V207I/M, S213T, E218D, F221Y, I224V, L229V, N/H238 and R242D). 2019 Scientific reports Result HBV V191I;V207I;V207M;S213T;E218D;F221Y;I224V;L229V;R242D 166;173;173;182;189;196;203;210;228 171;180;180;187;194;201;208;215;233 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Interestingly, mutation pattern of A181T associated to F221Y was detected after 22 months of TDF monotherapy with virological and biochemical breakthrough in case two. 2019 Scientific reports Result HBV A181T;F221Y 35;55 40;60 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. No single mutation of M204V was detected in both genotypes. 2019 Scientific reports Result HBV M204V 22 27 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Notably, 11 mutations at position 169, 202, 250, 173, 180, 200, 207, 214, 237, 242 and 245 coexisted with M204I or V (data not shown). 2019 Scientific reports Result HBV M204I 106 111 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Out of 24 mutations of L229 (Table 3), 18 were associated to M204I or V; 2 coexisted with F221Y (Table 4); 2 were associated to A181T; 2 were associated to V207M (Table 4) and N236V, respectively. 2019 Scientific reports Result HBV M204I;F221Y;A181T;V207M;N236V 61;90;128;156;176 66;95;133;161;181 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Samples included mutations of M204I in genotypes B and C were 56 and 47, respectively. 2019 Scientific reports Result HBV M204I 30 35 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Similarly, samples including mutations of M204V in genotype B and C were 26 and 31, respectively. 2019 Scientific reports Result HBV M204V 42 47 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. These sites could be classified into the following groups: V191I and V207I/M were detected in cases experienced ADV treated; F221Y were found in cases experienced LAM treated; S213T, I224V and H/N238 seemed to be the sharing mutation sites of LAM, ADV and ETV. 2019 Scientific reports Result HBV V191I;V207I;V207M;F221Y;S213T;I224V 59;69;69;125;176;183 64;76;76;130;181;188 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Also, rtS213T, rtV214A, rtL229G/V/W/F, N/H238D/T, and S/C256G were detected in 13 patients by both Sanger sequencing and NGS, including 3 patients with rtS213T (98.44%, 46.88%, and 80.97% by NGS), 2 with rtV214A (49.18% and 99.24%), 1 with rtL229V (50.84%), 1 with rtN238T (98.85%), 5 with S/C256G (97.28%, 97.93%, 92.26%, 97.79%, and 98.31%), and 1 with rtL229V plus rtS/C256G (82.36% for rtL229V and 74.81% for rtS/C256G). 2019 Journal of clinical microbiology Result HBV N238D;N238T;H238D;H238T;C256G;C256G;C256G;C256G;L229G;L229V;L229W;L229F;L229V;N238T;L229V;S256G;L229V;S256G;S213T;V214A;S213T;V214A;S256G;S256G 39;39;39;39;54;290;370;415;26;26;26;26;242;267;357;370;392;415;8;17;154;206;54;290 48;48;48;48;61;297;377;422;37;37;37;37;247;272;362;377;397;422;13;22;159;211;61;297 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 6;15;24;152;204;240;265;355;368;390;413 8;17;26;154;206;242;267;357;370;392;415 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Considering that the low sensitivity of Sanger sequencing limited the detection of NAr mutations with a low rate (<20%), 4 classical drug resistance mutations (S202C/G/I, M204I/V/S, N236T, and M250I/L/V) and 12 putative NAr mutations (V207I, S213T, V214A, Q215P/S, L217R, E218D, L229G/V/W/F, I233V, P237H, N/H238D/S/T, Y245H, and S/C256G) tested by NGS and Sanger sequencing were compared (Table 5). 2019 Journal of clinical microbiology Result HBV N238D;N238S;N238T;H238D;H238S;H238T;C256G;S202C;S202G;S202I;M204I;M204V;M204S;M250I;M250L;M250V;S213T;V214A;L229G;L229V;L229W;L229F;S256G;N236T;V207I;Q215P;Q215S;L217R;E218D;I233V;P237H;Y245H 306;306;306;306;306;306;330;160;160;160;171;171;171;193;193;193;242;249;279;279;279;279;330;182;235;256;256;265;272;292;299;319 317;317;317;317;317;317;337;169;169;169;180;180;180;202;202;202;247;254;290;290;290;290;337;187;240;263;263;270;277;297;304;324 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. In addition, except for only 1 patient with a mutation at rt181 (A181T) in the ALD group, there was not any primary resistance mutation (i.e., I169T, T184A/C/F/G/I/L/M/S, A194T, S202C/G/I, M204I/V/S, N236T, or M250I/L/V) and secondary resistance mutation (i.e., V173L or L180M) found in treatment-naive patients, while 9 putative resistance mutations and 51 pretreatment mutations were detected in these patients. 2019 Journal of clinical microbiology Result HBV T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M204I;M204V;M204S;M250I;M250L;M250V;A181T;I169T;A194T;N236T;V173L;L180M 150;150;150;150;150;150;150;150;178;178;178;189;189;189;210;210;210;65;143;171;200;262;271 169;169;169;169;169;169;169;169;187;187;187;198;198;198;219;219;219;70;148;176;205;267;276 RT 58 60 Liver disease 79 82 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Notably, 3 putative NAr mutations (rtL229V, H238Q, and S/C256G) with rates between 20% and 25% tested by NGS in patients 3, 20, and 497, respectively, were not detected by Sanger sequecing, implying the limitation of Sanger sequencing further. 2019 Journal of clinical microbiology Result HBV C256G;L229V;S256G;H238Q 55;37;55;44 62;42;62;49 RT 35 37 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. The classical drug resistance mutations were not found by Sanger sequencing, while S202C/G/I (0.92% to ~3.45%), M204I/V/S (0.90% to ~8.32%), N236T (1.16% to ~3.63%), and M250I/L/V (0.90% to ~1.83%) were found at a low rate by NGS. 2019 Journal of clinical microbiology Result HBV S202C;S202G;S202I;M204I;M204V;M204S;M250I;M250L;M250V;N236T 83;83;83;112;112;112;170;170;170;141 92;92;92;121;121;121;179;179;179;146 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. Although the frequency of amino acid substitutions were not significantly different, a total of 16 amino acid substitutions in the polymerase domain occurred only in tenofovir-experienced isolates compared to tenofovir-naive isolates, including S117Y, S117C, I121N, T128I, M129L, R138K, R138E, L140P, V142A, I163V, L217R, N238H, R242K, K270R, V278I, and R280S. 2019 Viruses Result HBV S117Y;S117C;I121N;T128I;M129L;R138K;R138E;L140P;V142A;I163V;L217R;N238H;R242K;K270R;V278I;R280S 245;252;259;266;273;280;287;294;301;308;315;322;329;336;343;354 250;257;264;271;278;285;292;299;306;313;320;327;334;341;348;359 P 131 141 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. No mutations known to cause tenofovir resistance (L180M, A181I/V, A194T, M204V/I, V214A, Q215S, N236T) or lamuvudine (3TC) resistance (L80V/I, I169T, V173L, L180M, A181T, T184S, M204V/I/S, Q215S) were observed. 2019 Viruses Result HBV M204V;M204I;M204S;L180M;A181I;A181V;A194T;M204V;M204I;V214A;Q215S;N236T;L80V;L80I;I169T;V173L;L180M;A181T;T184S;Q215S 178;178;178;50;57;57;66;73;73;82;89;96;135;135;143;150;157;164;171;189 187;187;187;55;64;64;71;80;80;87;94;101;141;141;148;155;162;169;176;194 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. Positions R110G, Y126H, T128S, W153R, L220I, T225I, P237H, T259S and H271C were highly polymorphic in tenofovir-naive compared to tenofovir-experienced isolates. 2019 Viruses Result HBV R110G;Y126H;T128S;W153R;L220I;T225I;P237H;T259S;H271C 10;17;24;31;38;45;52;59;69 15;22;29;36;43;50;57;64;74 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Among 435 CHB patients, we identified 19 samples carrying HBV sC69* mutant by analyzing entire SHBs AA sequences. 2019 Frontiers in microbiology Result HBV C69X 62 67 S;S 62;95 63;99 Chronic Hepatitis B 10 13 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. As shown before, the sC69* mutant could inhibit viral replication ability. 2019 Frontiers in microbiology Result HBV C69X 21 26 S 21 22 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. As shown in Figure 2B, HBV pgRNA from WT and sC69* + pLMS increased over time. 2019 Frontiers in microbiology Result HBV C69X 45 50 S 45 46 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. As shown in Supplementary Figure S4B, the expression of HBV pgRNA were almost the same between WT-YMHD and sC69*-YMHD. 2019 Frontiers in microbiology Result HBV C69X 107 112 S 107 108 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Consistent to Figure 2, ISGs expression in the sC69* + pLMS infected cells was significantly lower compared to WT and poly (I:C) treated only cells (mock) (Figure 3C), suggesting that sCS69* could attenuate poly (I:C) stimulated ISGs expression. 2019 Frontiers in microbiology Result HBV C69X;S69X 47;185 52;190 S 47 48 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Consistent to previous study, expression of pgRNA and HBV total RNA in IFNbeta untreated group were significantly higher than those with IFNbeta treatment both in WT and sC69* + pLMS (Figure 4B). 2019 Frontiers in microbiology Result HBV C69X 170 175 S 170 171 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Firstly, we transfected the WT and sC69* + pLMS into HepG2 cells seeded in the insert of the transwell. 2019 Frontiers in microbiology Result HBV C69X 35 40 S 35 36 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Given the very low induction of ISGs expression by sC69* + pLMS in HepG2-NTCP cells, we explored if sC69* mutant could attenuate poly (I:C) mediated immune response by monitoring the activation of ISGs expression. 2019 Frontiers in microbiology Result HBV C69X;C69X 51;100 56;105 S;S 51;100 52;101 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. HepG2-NTCP cell line has been established (Supplementary Figure S2), which highly supported HBV infection and could be used to study sC69* in vitro in this study. 2019 Frontiers in microbiology Result HBV C69X 133 138 S 133 134 HBV infections 92 105 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, HepG2-NTCP cells infected by the virions produced by co-transfecting WT HBs expression plasmid pLMS and full viral genome encoding the sC69* mutant showed high percentage of hepatitis B core antigen (HBcAg) staining positive cells similar to that of the WT infection, indicating that WT HBs can package the sC69* mutant genome and help it infect new cells (Figure 1B). 2019 Frontiers in microbiology Result HBV C69X;C69X 144;316 149;321 C;C;S;S;S;S 195;209;81;296;144;316 199;214;84;299;145;317 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, some of the ISGs were still significantly higher 3 days post-transfection in WT-YMHD than those in sC69*-YMHD, such as IL29, ISG15, RIG-I and viperin (p < 0.05). 2019 Frontiers in microbiology Result HBV C69X 108 113 S 108 109 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, the pgRNA levels from WT are higher than sC69* + pLMS at day 3 of viral infection. 2019 Frontiers in microbiology Result HBV C69X 50 55 S 50 51 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, there were no difference of ISGs expression between WT and sC69* + pLMS (Figure 4C), indicating that sC69* attenuates of ISGs expression at early stage of innate immune response. 2019 Frontiers in microbiology Result HBV C69X;C69X 68;110 73;115 S;S 68;110 69;111 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, when HepG2-NTCP cells were infected with sC69* + pLMS, most of ISGs and cytokines mRNAs were lower compared to WT at day 3 (IL29 and ISG15) and day 5 (RIG-I) (p < 0.05). 2019 Frontiers in microbiology Result HBV C69X 50 55 S 50 51 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, their expression was not largely improved in sC69* + pLMS-derived virus infection, indicating that sC69* could inhibit innate immune responses to escape innate immune surveillance. 2019 Frontiers in microbiology Result HBV C69X;C69X 58;112 63;117 S;S 58;112 59;113 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, we found that the sC69* mutant usually coexisted with WT sC69 shown by double peaks at the third nucleotide of the sC69 codon (TGT and TGA) in PCR direct sequencing electropherograms (Supplementary Figure S1A). 2019 Frontiers in microbiology Result HBV C69X 31 36 S;S;S 31;70;128 32;71;129 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In order to know the distribution of sC69* mutant in different patient groups, we stratified patients by HBeAg status and LMV exposure and analyzed the SHBs sequences. 2019 Frontiers in microbiology Result HBV C69X 37 42 C;S;S 105;37;152 110;38;156 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In order to study if WT and sC69* induce effective IFNs expression, we transferred the supernatant from WT and sC69* + pLMS infected HepG2-NTCP cells to new cells without infection and harvested the cellls 6, 12, 24, and 48 h post-transferring (Supplementary Figure S5A). 2019 Frontiers in microbiology Result HBV C69X;C69X 28;111 33;116 S;S 28;111 29;112 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Interestingly, consistent with HBV infection in HepG2-NTCP system, the sC69* + pLMS showed significantly lower innate immune responses than WT regarding the expression of IL29, ISG15, and RIG-I mRNA levels 4 days post-infection and TNFalpha 7 days post infection (p < 0.05), while the other ISGs expression seemed to show overall lower trend in sC69* + pLMS than that of WT but without statistical difference (Figure 5B), indicating that sC69* could attenuate the expression of some ISGs. 2019 Frontiers in microbiology Result HBV C69X;C69X;C69X 71;345;438 76;350;443 S;S;S 71;345;438 72;346;439 HBV infections 31 44 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Interestingly, WT HBV infection resulted in high positive infected cells, while the sC69* mutant showed no sign of infected cells. 2019 Frontiers in microbiology Result HBV C69X 84 89 S 84 85 HBV infections 18 31 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Maybe the sC69* mutant itself antagonizes the innate immune response. 2019 Frontiers in microbiology Result HBV C69X 10 15 S 10 11 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Of note, the sC69* significantly existed at a higher frequency in HBeAg-negative untreated CHB patients in comparison to that in HBeAg-positive ones (p < 0.05). 2019 Frontiers in microbiology Result HBV C69X 13 18 C;C;S 66;129;13 71;134;14 Chronic Hepatitis B 91 94 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Table 2 showed that 78.95% (15/19) of the sC69* mutations were identified as sC69C/* quasispecies, indicating that sC69* usually coexisted with the WT. 2019 Frontiers in microbiology Result HBV C69X;C69C;C69X 42;77;115 47;84;120 S;S;S 42;77;115 43;78;116 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Taken together, the results suggested that the sC69* mutant could negatively impact viral infection and spread, while WT HBs could rescue sC69* mutant infectivity and spread. 2019 Frontiers in microbiology Result HBV C69X;C69X 47;138 52;143 S;S;S 121;47;138 124;48;139 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The data (Supplementary Figure S5B) showed that WT had higher pgRNA and total RNA expression than sC69* + pLMS, which meant that HepG2-NTCP cells supported well WT and lower sC69* mutant infection. 2019 Frontiers in microbiology Result HBV C69X;C69X 98;174 103;179 S;S 98;174 99;175 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The expression of TNFalpha, IL1beta, and IL32 was the same during the days post-transfection between WT-YMHD and sC69*-YMHD. 2019 Frontiers in microbiology Result HBV C69X 113 118 S 113 114 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The expression of viral proteins and RNAs from the transfected plasmids would show similar levels for WT and sC69*. 2019 Frontiers in microbiology Result HBV C69X 109 114 S 109 110 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The Impact of the sC69* Mutant on Innate Immune Response in HepG2-NTCP Cell Line. 2019 Frontiers in microbiology Result HBV C69X 18 23 S 18 19 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The Impact of the sC69* Mutant on Innate Immune Response in the HLCs Model. 2019 Frontiers in microbiology Result HBV C69X 18 23 S 18 19 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The levels of HBV pgRNA and total RNA of sC69* + pLMS was similar to those of WT (Figure 3B). 2019 Frontiers in microbiology Result HBV C69X 41 46 S 41 42 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The Negative Impact of the sC69* Mutant on Viral Infection Could Be Rescued by Co-expression of WT HBs. 2019 Frontiers in microbiology Result HBV C69X 27 32 S;S 99;27 102;28 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* Mutant Attenuates the Innate Immune Response During Poly (I:C) Treatment. 2019 Frontiers in microbiology Result HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* not only inhibits viral secretion, but also results in HBs locating around the hepatocyte nuclear (Supplementary Figure S1D). 2019 Frontiers in microbiology Result HBV C69X 4 9 S;S 65;4 68;5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Therefore, we could exclude the possibility that the less induction of innate immune response were caused by the less replication of sC69* mutant. 2019 Frontiers in microbiology Result HBV C69X 133 138 S 133 134 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. This showed that the frequency of sC69* mutant varied in different CHB patients, including HBeAg-positive untreated patients (3.67%, 12/327), HBeAg-negative untreated patients (11.90%, 5/42) and LMV-treated patients (3.03%, 2/66) (Table 2). 2019 Frontiers in microbiology Result HBV C69X 34 39 C;C;S 91;142;34 96;147;35 Chronic Hepatitis B 67 70 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Thus, the sC69* + pLMS and WT were used in the following experiments. 2019 Frontiers in microbiology Result HBV C69X 10 15 S 10 11 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To ascertain whether sC69* could affect innate immune responses, we infected HepG2-NTCP cells in transwell system and quantified mRNA levels of innate immunity related genes (Figure 2A). 2019 Frontiers in microbiology Result HBV C69X 21 26 S 21 22 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To determine whether sC69* mutant could impact virion infection and spread, we modified the experimental system by using the transwell plate, in which the transfection-produced virions were generated in the upper insert and penetrated to the bottom well containing HepG2-NTCP cells (Figure 1A). 2019 Frontiers in microbiology Result HBV C69X 21 26 S 21 22 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To examine whether sC69* attenuates ISGs expression at early stage or late stage (IFNs mediated signaling) of ISGs induction, we stimulated WT and sC69* + pLMS infected HepG2-NTCP cells with 500 U/ml IFNbeta during the infection and measured the expression of pgRNA, HBV total RNA and ISGs levels by RT-qPCR (Figure 4A). 2019 Frontiers in microbiology Result HBV C69X;C69X 19;147 24;152 RT;S;S 300;19;147 302;20;148 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To exclude the viral replication influence on the induction of innate immune response, we did RT mutation of HBV WT and sC69* from YMDD to YMHD (Supplementary Figure S4A). 2019 Frontiers in microbiology Result HBV C69X 120 125 RT;S;P 94;120;131 96;121;135 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. To study whether the sC69* mutant could affect innate immune responses; we carried out transwell-based infection experiment. 2019 Frontiers in microbiology Result HBV C69X 21 26 S 21 22 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We grouped the patients into sC69 WT and sC69* groups (Table 1). 2019 Frontiers in microbiology Result HBV C69X 41 46 S;S 29;41 30;42 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We showed before that the sC69* inhibits virion replication and secretion which can be rescued by co-expressing WT HBs to facilitate this mutant survival, indicating that WT surface proteins can package the sC69* mutant genome and allow the mutant to persist (Supplementary Figures S1B,C). 2019 Frontiers in microbiology Result HBV C69X;C69X 26;207 31;212 S;S;S;S 115;26;207;174 118;27;208;181 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We stimulated HepG2-NTCP cells with 10 mug/ml poly (I:C) during HBV WT and sC69* + pLMS infection (Figure 3A). 2019 Frontiers in microbiology Result HBV C69X 75 80 S 75 76 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We transfected WT-YMHD and sC69*-YMHD into HepG2 cells and detect HBV pgRNA and ISGs expression at days 0.5, 1, 2, 3, 5, and 7 post-transfection. 2019 Frontiers in microbiology Result HBV C69X 27 32 S 27 28 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. 11/36 (30.6%) strains contained T/G1727A/C mutation in core upstream regulatory sequence, while A1762T/G1764A mutations were observed in 6 (16.7%) sequences. 2019 BMC infectious diseases Result HBV G1764A;G1727A;T1727A;T1727C;G1727C;A1762T 103;32;32;32;32;96 109;42;42;42;42;102 C 55 59 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Combinations of mutations T/G1727A with 1762/1764 were found in OBI092. 2019 BMC infectious diseases Result HBV G1727A;T1727A 26;26 34;34 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. In genotype C, vaccine escape related mutations T47K (13.0%), T116 N (4.3%), I126T (8.7%), Q129R (8.7%) and G145A/R (17.4%) were found. 2019 BMC infectious diseases Result HBV T47K;T116N;I126T;Q129R;G145A;G145R 48;62;77;91;108;108 52;68;82;96;115;115 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. No cysteine or typical P120L substitutions of OBI in the MHR were found in NDRs. 2019 BMC infectious diseases Result HBV P120L 23 28 Occult Hepatitis B 46 49 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. P120Q (4.3%), T123A (4.3%), I126S, M133 T (8.7%), F134 L (4.3%) substitutions were found which might potentially affect HBsAg detection. 2019 BMC infectious diseases Result HBV P120Q;T123A;I126S;M133T;F134L 0;14;28;35;50 5;19;33;41;56 S 120 125 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. P120Q/S (8.7%) and Q129H (4.3%) substitutions were detected and recognized to have a major impact on HBsAg detection, while Y100S (8.7%) substitution was observed responsible in OBIs for lack of excretion of HBsAg. 2019 BMC infectious diseases Result HBV P120Q;P120S;Q129H;Y100S 0;0;19;124 7;7;24;129 S;S 101;208 106;213 Occult Hepatitis B 178 182 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Previously reported HBV vaccine escape variants carrying point nucleotide mutations in the MHR (aa 124-147) of genotype B were also identified including T116 N (4.3%), P120S (4.3%), T126A (8.7%), Q129R/H (17.3%), D144A/E (8.7%) and G145A/R (21.7%). 2019 BMC infectious diseases Result HBV T116N;P120S;T126A;Q129R;Q129H;D144A;D144E;G145A;G145R 153;168;182;196;196;213;213;232;232 159;173;187;203;203;220;220;239;239 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. T/G1727A with G1896A and T/G1727C with G1896A were presented in OBI100/OBI228 and OBI74/OBI185, respectively. 2019 BMC infectious diseases Result HBV G1727A;G1727C;T1727A;T1727C;G1896A;G1896A 0;25;0;25;14;39 8;33;8;33;20;45 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. The ATG start codon was abolished by a point mutation (ntA1814C/T) in three cases; and the ntG1896A mutation introducing a stop signal was present in 10 (27.8%) sequences. 2019 BMC infectious diseases Result HBV A1814C;A1814T;G1896A 56;56;92 65;65;99 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. A high proportion (61.0%, 16/26) of G1896A mutation occurred in the PC region. 2019 Mediterranean journal of hematology and infectious diseases Result HBV G1896A 36 42 Precore 68 70 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. A1762T and G1764A were frequently detected together in 23.0% (6/26) of the isolates. 2019 Mediterranean journal of hematology and infectious diseases Result HBV A1762T;G1764A 0;11 6;17 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Also, AST was significantly higher among patients with F8L HBV mutants (P=0.001) (Table 3). 2019 Mediterranean journal of hematology and infectious diseases Result HBV F8L 55 58 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Five (5) mutations were detected within the surface gene in the patients (F8L, T118M, E164D, T189I, and W196L). 2019 Mediterranean journal of hematology and infectious diseases Result HBV F8L;T118M;E164D;T189I;W196L 74;79;86;93;104 77;84;91;98;109 S 44 51 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. However, none of the patients with A1762T/G1764A mutation carried the G1764T/C1766G mutant (Table 2). 2019 Mediterranean journal of hematology and infectious diseases Result HBV G1764A;C1766G;A1762T;G1764T 42;77;35;70 48;83;41;76 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. In the BCP region, the most common mutations were A1762T (30.0%, 8/26) and G1764T (30.0%, 8/26), followed by G1764A (26.0%, 7/26), C1766G (26.0%, 7/26), C1766T (11.5%, 3/26). 2019 Mediterranean journal of hematology and infectious diseases Result HBV A1762T;G1764T;G1764A;C1766G;C1766T 50;75;109;131;153 56;81;115;137;159 BCP 7 10 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Similarly, G1764T and C1766G were frequently seen together in 26.0% (7/26) of cases. 2019 Mediterranean journal of hematology and infectious diseases Result HBV G1764T;C1766G 11;22 17;28 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The frequency of mutations in the MHR was seen in 18.0% (6/33) of isolates (T118M, E164D). 2019 Mediterranean journal of hematology and infectious diseases Result HBV T118M;E164D 76;83 81;88 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The G1899A mutation was found in 6 (23.0%) isolates and had concomitant G1896A change. 2019 Mediterranean journal of hematology and infectious diseases Result HBV G1899A;G1896A 4;72 10;78 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The most common amino acid change found within HBsAg was W196L in 13 (39.0%) isolates. 2019 Mediterranean journal of hematology and infectious diseases Result HBV W196L 57 62 S 47 52 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. There was no significant relationship between BCP, pre-core and surface mutations with HBV viral load, HBeAg and liver enzymes (Table 4), except an association between C1766G and HBeAg negativity which was significant (P=0.04). 2019 Mediterranean journal of hematology and infectious diseases Result HBV C1766G 168 174 BCP;C;C;Precore;S 46;103;179;51;64 49;108;184;59;71 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. 1a) and A1838G (HBc gene I > V; HBx gene: STOP > STOP; LRT p = 1.3 x 10-81. 2019 Scientific reports Result HBV A1838G 8 14 C;X 16;32 19;35 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Across the viral genome, the most significant associations were observed between the viral load and two non-synonymous variants C1817T (HBc gene Q > STOP; HBx gene C > C; likelihood ratio test [LRT] p = 1.7 x 10-33. 2019 Scientific reports Result HBV C1817T 128 134 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Although G1896A frequently disrupts the production of HBeAg via the introduction of a premature stop codon, other mutations are likely to achieve a similar clinical effect via different molecular means. 2019 Scientific reports Result HBV G1896A 9 15 C 54 59 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Although we identified C1817T association with viral load while controlling for HBeAg status, our findings do not exclude the possibility that this variant could have pleiotropic effects on multiple clinical factors. 2019 Scientific reports Result HBV C1817T 23 29 C 80 85 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. As a result of lower viral load, patients with high frequency of C1817T and A1838G experienced earlier viral suppression while on treatment (LRT p < 1.0 x 10-6 for weeks 4, 8, 12, 24, and 48). 2019 Scientific reports Result HBV C1817T;A1838G 65;76 71;82 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Aside from C1817T and A1838G variants, it is worth mentioning that C1653T, G1896A, and G1899A displayed the next most significant association with viral load in the discovery patient cohort (LRT p = 6 x 10-8, p = 6.7 x 10-8, and p = 2.3 x 10-7, respectively). 2019 Scientific reports Result HBV C1817T;A1838G;C1653T;G1896A;G1899A 11;22;67;75;87 17;28;73;81;93 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Aside from its previously mentioned role in the epsilon region of the pgRNA, G1896A introduces a stop codon in the precore region abolishing HBeAg production. 2019 Scientific reports Result HBV G1896A 77 83 C;Precore 141;115 146;122 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. At this cutoff patients with high frequency of C1817T and A1838G had median viral loads nearly three orders of magnitude lower (reduction by 2.8 log10IU/mL of serum HBV DNA) than patients without or with low frequency of these variants (Wilcoxon rank sum test, p < 10-5. 2019 Scientific reports Result HBV C1817T;A1838G 47;58 53;64 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Both C1817T and A1838G associations were validated in an independent patient cohort (N = 365; LRT p = 1.2 x 10-17 and p < 5.2 x 10-31, respectively; Supplementary. 2019 Scientific reports Result HBV C1817T;A1838G 5;16 11;22 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Despite deep sequencing coverage at the G1896A locus (mediancoverage = 8949), a substantial portion of 24% (22% excluding HBV genotype A, see Discussion) of HBeAg-negative patients had undetectable frequency of G1896A variant. 2019 Scientific reports Result HBV G1896A;G1896A 40;211 46;217 C 157 162 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. For example, variant G1899A induces Gly to Asp change (Gly/Asp29) in a loop at the dimer interface interacting with the same residue from the other dimer at a distance of ~6 A. 2019 Scientific reports Result HBV G1899A 21 27 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. HBeAg is the product of precore mRNA which nearly completely overlaps pregenomic (pg) RNA, suggesting an effect of C1817T on both the precore mRNA and pgRNA transcription. 2019 Scientific reports Result HBV C1817T 115 121 C;Precore;Precore 0;24;134 5;31;141 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. In fact, a classification model based solely on G1896A frequency attains only a relatively modest performance predicting HBeAg status with a low true negative rate (Specificity = 0.60, AUC = 0.81). 2019 Scientific reports Result HBV G1896A 48 54 C 121 126 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Indeed, C1817T is additionally associated with HBeAg status in our data as well (LRT p = 2.8 x 10-12). 2019 Scientific reports Result HBV C1817T 8 14 C 47 52 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. More importantly, we found that G1896A is not a necessary variant determining patient's HBeAg status. 2019 Scientific reports Result HBV G1896A 32 38 C 88 93 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Next, we assessed the predictive power of additional variants by building a random-forest classifier using a total of 37 significant variants, including G1896A (see methods for viral variant selection). 2019 Scientific reports Result HBV G1896A 153 159 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Our data therefore suggest that, in the absence of G1896A, combinations of other variants are likely interfering with HBeAg production or protein structure resulting in HBeAg negative phenotype. 2019 Scientific reports Result HBV G1896A 51 57 C;C 118;169 123;174 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Our unbiased approach led us to the discovery of additional variants highly associated with patient's HBeAg status: G1899A, A1838G, T2045A, G2345A, G2352A, T2441C, A2189C, T2443C, C1962A, G2237C, and others (LRT; p < 9.55 x 10-13. 2019 Scientific reports Result HBV G1899A;A1838G;T2045A;G2345A;G2352A;T2441C;A2189C;T2443C;C1962A;G2237C 116;124;132;140;148;156;164;172;180;188 122;130;138;146;154;162;170;178;186;194 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Regardless of HBeAg status, however, C1817T and A1838G were both highly associated with viral load. 2019 Scientific reports Result HBV C1817T;A1838G 37;48 43;54 C 14 19 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Specifically, C1653T alters the binding site of the CAAT enhancer-binding protein of the alpha-box within the HBV enhancer II region, which is known to transcriptionally regulate the pgRNA. 2019 Scientific reports Result HBV C1653T 14 20 Enh II 114 125 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. The variant with the strongest association was G1896A (LRT; p = 5.43 x 10-69. 2019 Scientific reports Result HBV G1896A 47 53 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. This observation is largely explained by the aforementioned fact that 24% of HBeAg-negative patients lacked G1896A whereas 7.3% of HBeAg-positive patients had G1896A at higher than 0.66 in frequency. 2019 Scientific reports Result HBV G1896A;G1896A 108;159 114;165 C;C 77;131 82;136 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. To further evaluate the relevance of G1896A in conjunction with other variants in determining patient HBeAg status, we built several classification models to assess the collective predictive power and rank the significance of each variant. 2019 Scientific reports Result HBV G1896A 37 43 C 102 107 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Variant G2237C corresponds to Glu/Gln142 located at the end of an alpha-helix, forming a strong salt-bridge interaction with Arg141 and stabilizing the domain structure in this region. 2019 Scientific reports Result HBV G2237C 8 14 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Variants G1896A and G1899A, on the other hand, impact the base pairing of the stem structure within the epsilon region of the pgRNA, affecting the secondary RNA structure and consequently the encapsidation of the pgRNA, a crucial step prior to the generation of the rcDNA. 2019 Scientific reports Result HBV G1896A;G1899A 9;20 15;26 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. While the association between G1896A and patient HBeAg status is highly significant, the presence of G1896A alone cannot completely explain patient HBeAg status. 2019 Scientific reports Result HBV G1896A;G1896A 30;101 36;107 C;C 49;148 54;153 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. In addition, the rate of G1986A preC mutation was significant higher in patients with rt269I (49.61%) than those with rt269L (28.83%, p < 0.01). 2019 Frontiers in immunology Result HBV G1986A 25 31 Precore;RT;RT 32;86;118 36;88;120 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. In double mutations in BCP, only the G1764A mutation, but not the A1762T, was significantly prevalent in patients with rt269I of both our cohort and GenBank. 2019 Frontiers in immunology Result HBV G1764A;A1762T 37;66 43;72 BCP;RT 23;119 26;121 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. Of the various HBV mutations, G1896A mutations on the pre-core region (preC mutation) and A1762T/G1764A double mutations on the basal core promoter (BCP) lead to HBeAg negative infection that are significantly related to liver disease progression. 2019 Frontiers in immunology Result HBV G1764A;G1896A;A1762T 97;30;90 103;36;96 BCP;BCP;C;Precore;Precore 128;149;162;71;54 147;152;167;75;62 Liver disease 221 234 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. The Higher Frequency of preC Mutation (G1896A) in Patients With rt269I Infections Is Responsible for the Higher Frequency of HBeAg Negative Infections. 2019 Frontiers in immunology Result HBV G1896A 39 45 C;Precore;RT 125;24;64 130;28;66 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. These results suggest that the high frequency of G1986A preC mutation is responsible for HBeAg negative infections in patients with genotype C rt269I infections. 2019 Frontiers in immunology Result HBV G1986A 49 55 C;Precore;RT 89;56;143 94;60;145 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. 2), among the 16 isolates from our study located in cluster c, 15 isolates had the A1762T/G1764A mutation and 12 isolates had combination mutation (Table 3). 2019 Scientific reports Result HBV G1764A;A1762T 90;83 96;89 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Based on the presence or absence of the mutations of pre-S deletion, G1613A, C1653T, T1753V, A1762T/G1764A, Pre-C W28 stop codon, and P130, these 340 genotype C1 strains were classified in 48 patterns. 2019 Scientific reports Result HBV G1764A;W28X;G1613A;C1653T;T1753V;A1762T 100;114;69;77;85;93 106;122;75;83;91;99 Precore;PreS 108;53 113;58 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Combination mutation at T1753V and A1762T/G1764A was most frequent. 2019 Scientific reports Result HBV G1764A;T1753V;A1762T 42;24;35 48;30;41 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. double mutation at A1762T/G1764A was confirmed in 160 strains (160/340, 47.1%), almost a half of the 340 strains (Table 3). 2019 Scientific reports Result HBV G1764A;A1762T 26;19 32;25 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. For the isolates of genotype B2 and B4, only the genotype B4 isolate had a mutation at G1613A. 2019 Scientific reports Result HBV G1613A 87 93 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. In details, patterns 1 to 9 represented combination mutation at C1653T and A1762T/G1764A (32/340 9.4%), patterns 10 and 11 at C1653T or T1753V and A1762T/G1764A (4/340 1.25%), and patterns 12 to 23 at T1753V and A1762T/G1764A (77/340 22.6%). 2019 Scientific reports Result HBV G1764A;G1764A;G1764A;C1653T;A1762T;C1653T;T1753V;A1762T;T1753V;A1762T 82;154;219;64;75;126;136;147;201;212 88;160;225;70;81;132;142;153;207;218 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. In patients with LC/HCC, the rates of Pre-S deletion, G1613A, and Core P130 mutation were 4.8% (1/21), 52.4% (11/21) and 38.1% (8/21) respectively. 2019 Scientific reports Result HBV G1613A 54 60 C;PreS 66;38 70;43 Hepatocellular carcinoma;Liver cirrhosis 20;17 23;19 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. In patterns 24 to 32, 47 strains of double mutation at A1762T/G1764A were recognized (47/340 13.8%). 2019 Scientific reports Result HBV G1764A;A1762T 62;55 68;61 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. In patterns 33 to 48, single mutation at G1613A, C1653T, T1753V, or Core P130 was observed in 18, 2, 4 and 18 strains, respectively (Supplementary Table 1). 2019 Scientific reports Result HBV G1613A;C1653T;T1753V 41;49;57 47;55;63 C 68 72 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Mutation at G1613A was found in five isolates. 2019 Scientific reports Result HBV G1613A 12 18 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Of these, five at C1653T and A1762T/G1764A and nine at T1753V and A1762T/G1764A were recognized. 2019 Scientific reports Result HBV G1764A;G1764A;C1653T;A1762T;T1753V;A1762T 36;73;18;29;55;66 42;79;24;35;61;72 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Strains with single mutation at G1613A, C1653T, T1753V, or Core P130 were not confirmed in patients with LC/HCC. 2019 Scientific reports Result HBV G1613A;C1653T;T1753V 32;40;48 38;46;54 C 59 63 Hepatocellular carcinoma;Liver cirrhosis 108;105 111;107 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The double mutation at A1762T/G1764A was recognized in 18 of the isolates in genotype C1 (18/24 75.0% Table 2). 2019 Scientific reports Result HBV G1764A;A1762T 30;23 36;29 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The rates of combination mutation at C1653T or T1753V and A1762T/G1764A were also raised significantly according to liver disease progression (Among 3 groups P < 0.001; posthoc pairwise ASC vs CH P < 0.001, ASC vs LC/HCC P < 0.001, CH vs LC/HCC P < 0.001. 2019 Scientific reports Result HBV G1764A;C1653T;T1753V;A1762T 65;37;47;58 71;43;53;64 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The rates of retaining double mutation at A1762T/G1764A in ASC, patients with chronic hepatitis, and patients with LC/HCC were 28.9% (28/97), 49.0% (73/149), and 100% (21/21), respectively. 2019 Scientific reports Result HBV G1764A;A1762T 49;42 55;48 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 78;118;115 95;121;117 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. There was no solitary mutation at C1653T or T1753V. 2019 Scientific reports Result HBV C1653T;T1753V 34;44 40;50 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Above this [K+] region is where the final scattered intensities for D2N/D4N and WT reached the same plateau, indicating that most dimers had formed into capsids. 2018 ACS omega Result HBV D4N;D2N 72;68 75;71 Capsid 153 160 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. After reaching equilibrium, the 1.0 mg mL-1 D2N/D4N-0.2 M K+ solution had 44% of dimer proteins assembled into capsids, as determined by the elution peak area ratio of capsids over the total contribution from proteins, obtained from size exclusion chromatography (SEC). 2018 ACS omega Result HBV D4N;D2N 48;44 51;47 Capsid;Capsid 111;168 118;175 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. At pH 7.5, the effective surface charge density of the WT dimer was -0.40 charges nm-2 (dimer surface area is ~36.3 nm2), whereas that of D2N/D4N was lowered to -0.29 charges nm-2. 2018 ACS omega Result HBV D4N;D2N 142;138 145;141 S;S 25;94 32;101 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Charge numbers for both WT and D2N/D4N dimers within pH 6.6-9.6 were calculated (Table 1) using protein calculator 3.4 . 2018 ACS omega Result HBV D4N;D2N 35;31 38;34 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Equivalent Charge Density Led to Identical Capsid Assembly Process for WT and D2N/D4N. 2018 ACS omega Result HBV D4N;D2N 82;78 85;81 Capsid 43 49 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. In terms of association energy per contact, the DeltaGcontact was calculated as -3.01 and -3.18 kcal mol-1 for WT and D2N/D4N at the low salt concentration (0.2 M KCl), respectively. 2018 ACS omega Result HBV D4N;D2N 122;118 125;121 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Increasing K+ concentration to 0.2 M enabled rapid association of D2N/D4N dimers, especially at higher protein concentrations (Figure 2c). 2018 ACS omega Result HBV D4N;D2N 70;66 73;69 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Scattered light intensity monitored by SLS revealed that D2N/D4N dimers assembled much faster and reached a higher final scattering intensity than WT Cp149 dimers (Figure 2c,d). 2018 ACS omega Result HBV D4N;D2N 61;57 64;60 C 150 152 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The CSC of D2N/D4N solution increased from <0.1 to 0.6 M of K+ when protein concentration dropped from 120 to 20 muM. 2018 ACS omega Result HBV D4N;D2N 15;11 18;14 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The CSC of D2N/D4N was always slightly lower than that of WT. 2018 ACS omega Result HBV D4N;D2N 15;11 18;14 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The impact from mutation was excluded because the overall structures of WT and D2N/D4N mutants were the same, demonstrated by their overlapped circular dichroism (CD) and fluorescence spectra in Figure S1D,E, and the mutated sites were not involved in dimer-dimer association (Figure S1). 2018 ACS omega Result HBV D4N;D2N 83;79 86;82 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The lower charge density of D2N/D4N dimers resulted in weaker electrostatic repulsion between dimers, which promoted the capsid formation and more capsids were formed under the same condition. 2018 ACS omega Result HBV D4N;D2N 32;28 35;31 Capsid;Capsid 121;147 127;154 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Therefore, the higher scattering intensity indicated that more capsids were formed from D2N/D4N dimers under the same condition. 2018 ACS omega Result HBV D4N;D2N 92;88 95;91 Capsid 63 70 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Therefore, the hydrophobic interaction should be the same for both the WT and D2N/D4N. 2018 ACS omega Result HBV D4N;D2N 82;78 85;81 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Under the high salt condition (0.7 M KCl), however, the DeltaGcontact of WT and D2N/D4N assembly became much closer by 53%, being -3.56 and -3.65 kcal mol-1, respectively (calculation details in the Supporting Information). 2018 ACS omega Result HBV D4N;D2N 84;80 87;83 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Under the same buffer condition and pH, D2N/D4N assembly was always more kinetically favored than WT due to its fewer charges (Figure 5a). 2018 ACS omega Result HBV D4N;D2N 44;40 47;43 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. When 0.7 M K+ was added, the portions of Cp1492 (1.0 mg mL-1) assembled into capsids at equilibrium are 87% (WT) and 89% (D2N/D4N) (Figure 4a). 2018 ACS omega Result HBV D4N;D2N 126;122 129;125 Capsid;C 77;41 84;43 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. When K+ was increased to 0.5 M, the difference between WT and D2N/D4N capsid formation still existed but became smaller (Figure 2d). 2018 ACS omega Result HBV D4N;D2N 66;62 69;65 Capsid 70 76 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. Within this [K+] region, D2N/D4N formed more capsids than WT. 2018 ACS omega Result HBV D4N;D2N 29;25 32;28 Capsid 45 52 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. A closer examination of the Southern blot profiles of HBV replicative intermediates revealed reproducibly the lack or reduction of the full-length RC form in mutant I97L (highlighted by a red asterisk in. 2019 Journal of virology Result HBV I97L 165 169 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Again, as highlighted by a red asterisk, fully mature full-length RC form in mutant I97L appeared to be greatly diminished. 2019 Journal of virology Result HBV I97L 84 88 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Again, relative to WT HBV, we observed a nearly 2-fold-lower level of viral DNA of mutant I97L at 3 dpi with 30 mug of DNA per mouse. 2019 Journal of virology Result HBV I97L 90 94 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Again, we observed lower levels of intrahepatic viral DNA of mutant I97L, relative to the WT HBV, at 3 days, 1 week, and 2 weeks postinjection. 2019 Journal of virology Result HBV I97L 68 72 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. As described in the introduction, we observed previously an immature secretion phenotype of the HBc variant I97L in the tissue culture system. 2019 Journal of virology Result HBV I97L 108 112 C 96 99 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. As expected, the single mutant I97L secreted predominantly immature HBV genomes, including SS DNA. 2019 Journal of virology Result HBV I97L 31 35 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. At 1 week postinjection (right panel), the DNA level of mutant I97L became further reduced than that of WT HBV as determined by Southern blotting, despite the fact that mutant I97L displayed stronger signals of viral RNA, capsid particles, and serum HBeAg. 2019 Journal of virology Result HBV I97L;I97L 63;176 67;180 Capsid;C 222;250 228;255 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. At 3 days postinjection, extracellular viral DNA signals of mutants I97L and I97L/P130T were much stronger than those of WT and mutant P130T (compare lanes 1 and 3 versus lanes 2 and 4. 2019 Journal of virology Result HBV P130T;I97L;I97L;P130T 82;68;77;135 87;72;81;140 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. At 3 dpi (upper panel), similar levels of intracellular SS DNAs were observed between the single mutant I97L and the double mutant I97L/P130T. 2019 Journal of virology Result HBV P130T;I97L;I97L 136;104;131 141;108;135 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. At 3 dpi with 14 mug of HBV plasmid DNA (left panel), DNA replicative intermediates of mutant I97L were already weaker than those of WT, while the cytoplasmic viral RNA and intrahepatic capsid particles were comparable between WT and mutant I97L on the agarose gels. 2019 Journal of virology Result HBV I97L;I97L 94;241 98;245 Capsid 186 192 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Because very weak or no RC DNA signals were detected at weeks 1 and 2, we compared the differences of intracellular SS DNA between WT and I97L strains. 2019 Journal of virology Result HBV I97L 138 142 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. both mutants I97L and I97L/P130T appeared to be deficient in the fully mature, full-length RC DNA molecule (red asterisk lanes 2 and 4. 2019 Journal of virology Result HBV P130T;I97L;I97L 27;13;22 32;17;26 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. By Southern blotting, we detected an abundant amount of immature viral genomes in the virion fractions of mutant I97L, but not in WT HBV (compare lanes 1 and 3 in. 2019 Journal of virology Result HBV I97L 113 117 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Characterization of mutant I97L in immunodeficient mice. 2019 Journal of virology Result HBV I97L 27 31 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Consistent with the previously reported hypermaturation phenotype based on the HepG2 cell culture system, the single mutant P130T displayed a more predominant signal intensity of the fully matured RC form DNA than did WT and the other mutants at day 3. 2019 Journal of virology Result HBV P130T 124 129 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Consistent with these viral DNA results, the intracellular level of capsid particles of mutant I97L was significantly reduced relative to the WT HBV at 2 weeks postinjection (bottom panel). 2019 Journal of virology Result HBV I97L 95 99 Capsid 68 74 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Fig2D showed a decreased level of intracellular viral DNA of mutant I97L at day 3 postinjection. 2019 Journal of virology Result HBV I97L 68 72 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. For easier comparison of the kinetics in the disappearance of HBV DNA between WT and I97L, we adjusted the amount of the input plasmids by using 10 mug of WT and 30 mug of I97L DNAs. 2019 Journal of virology Result HBV I97L;I97L 85;172 89;176 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Full-length RC DNA generated in vitro by mutant I97L in an endogenous polymerase reaction. 2019 Journal of virology Result HBV I97L 48 52 P 70 80 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Furthermore, these data suggest that the lower level of mutant I97L DNA was not due to any decrease in viral RNA, capsid expression, or transfection efficiencies in hydrodynamic delivery. 2019 Journal of virology Result HBV I97L 63 67 Capsid 114 120 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Genome hypermaturation of HBc mutant P130T correlated with prolonged persistence of viral DNA. 2019 Journal of virology Result HBV P130T 37 42 C 26 29 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Here, in the in vivo setting in BALB/c mice, overall reduction by at least 2.37-fold in I97L total viral DNA synthesis (measurements of full-length RC plus full-length SS DNAs) was observed, with the most striking contrast in the high-MW RC DNA between WT and mutant I97L. 2019 Journal of virology Result HBV I97L;I97L 88;267 92;271 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Here, the more rapid decline of I97L viral DNAs is entirely consistent with the previous results from various mouse models. 2019 Journal of virology Result HBV I97L 32 36 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, at 1 or 2 weeks postinjection, the secreted mutant I97L DNA disappeared rapidly and exhibited much lower DNA signals than did WT HBV. 2019 Journal of virology Result HBV I97L 60 64 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, at 2 weeks postinjection (right panel), DNA signals of mutant I97L were undetectable, when a significant amount of WT viral DNA remained apparent. 2019 Journal of virology Result HBV I97L 71 75 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, at 2 weeks postinjection, serum HBeAg of mutant I97L was slightly lower than that of the WT. 2019 Journal of virology Result HBV I97L 57 61 C 41 46 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, the I97L/P130T double mutant exhibited only a minor, yet reproducible effect on the upshifted viral DNA profile: from lower-MW SS DNA to higher-MW RC DNA (compare lanes 2 and 4). 2019 Journal of virology Result HBV P130T;I97L 18;13 23;17 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, the opposite was observed at 1 week postinjection, when almost no viral DNA signal was detected in the sera from mice injected with mutants I97L or I97L/P130T (compare lanes 5 and 7 to lanes 6 and 8. 2019 Journal of virology Result HBV P130T;I97L;I97L 162;149;157 167;153;161 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, the rescue efficiency of intracellular RC DNA of mutant I97L by P130T is insignificant (RC/SS ratio of 0.46 versus 0.52). 2019 Journal of virology Result HBV I97L;P130T 65;73 69;78 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In contrast to the differential kinetics in HBV DNA persistence between WT and mutant I97L, the levels of serum HBeAg remained similar throughout the time course. 2019 Journal of virology Result HBV I97L 86 90 C 112 117 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In contrast, mutants I97L and I97L/P130T contained reduced amounts of intracellular mature genome and were less persistent than WT HBV. 2019 Journal of virology Result HBV P130T;I97L;I97L 35;21;30 40;25;34 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In other words, an I97L/P130T double mutant in HepG2 cells behaved like WT HBV in preferential secretion of virions containing mature genome. 2019 Journal of virology Result HBV P130T;I97L 24;19 29;23 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In other words, the total viral DNA of I97L appeared to be 3-fold further reduced than that of the WT HBV, suggesting that the viral DNA level of I97L is relatively less persistent than the WT HBV. 2019 Journal of virology Result HBV I97L;I97L 39;146 43;150 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In summary, mutant P130T with genome hypermaturation appeared to be more persistent than WT HBV. 2019 Journal of virology Result HBV P130T 19 24 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In summary, the poor replication and persistence of viral DNA of mutant I97L were likely not due to any differential innate or adaptive immune responses to mutant versus WT HBV. 2019 Journal of virology Result HBV I97L 72 76 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In the latter case (right panel), intracellular nucleocapsids of mutant I97L are exported prematurely before their DNA replicative intermediates have a chance to reach the full-length genome size. 2019 Journal of virology Result HBV I97L 72 76 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Inefficient rescue of I97L immature secretion by an HBc mutation P130T. 2019 Journal of virology Result HBV I97L;P130T 22;65 26;70 C 52 55 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Interestingly, as summarized in Table 1, the prolonged persistence of intracellular viral DNA of mutant P130T is very well correlated with its phenotype of genome hypermaturation (see Discussion). 2019 Journal of virology Result HBV P130T 104 109 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It is particularly striking that, at week 1, the RC DNA signal of mutant P130T was much stronger than those in the WT HBV. 2019 Journal of virology Result HBV P130T 73 78 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It is reminiscent of HBc mutant F97L, which exhibited a pleiotropic phenotype, including both a cis-defect in viral DNA synthesis and a trans-defect in virion secretion (; see also the Discussion). 2019 Journal of virology Result HBV F97L 32 36 C 21 24 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It remains unclear whether this phenotype could be in part due to a cis-defect in viral DNA synthesis (e.g., an intrinsic deficiency in making the full-length plus-strand DNA) or is entirely due to an overly efficient envelopment and export of immature capsids of mutant I97L. 2019 Journal of virology Result HBV I97L 271 275 Capsid 253 260 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. More rapid clearance of intracellular mutant I97L DNA. 2019 Journal of virology Result HBV I97L 45 49 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L exhibited a reduced level of intracellular relaxed circular DNA. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. mutant I97L exhibited an ~4-fold-lower level of total intracellular viral DNAs (full-length RC plus full-length SS) than WT HBV. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L is deficient in the fully mature full-length RC DNA, as highlighted by a red asterisk in. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. mutant I97L released into blood circulation an excessive amount of immature HBV genomes, including both lower-MW RC and SS viral DNA. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L secreted more immature HBV genomes than its parental wild-type HBV in BALB/c mice. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. mutant I97L secreted strong signals of immature genomes on day 3 postinjection. 2019 Journal of virology Result HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutation I97L was dominant over mutation P130T, since the latter could not successfully reverse the rapid decline of both intracellular and extracellular HBV DNA in the double mutant I97L/P130T at later time points postinjection. 2019 Journal of virology Result HBV P130T;I97L;P130T;I97L 188;9;41;183 193;13;46;187 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Of note, the EPR assay did not compare kinetically the efficiencies of viral DNA synthesis between WT and I97L. 2019 Journal of virology Result HBV I97L 106 110 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. On the other hand, the RC DNA signals (*) from the double mutant I97L/P130T were slightly stronger than from the I97L single mutant. 2019 Journal of virology Result HBV P130T;I97L;I97L 70;65;113 75;69;117 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Our results found only marginal difference in HBc expression between WT and mutant I97L. 2019 Journal of virology Result HBV I97L 83 87 C 46 49 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Overall, host innate immunity does not seem to play a role in the lower level of viral replication of HBc mutant I97L. 2019 Journal of virology Result HBV I97L 113 117 C 102 105 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Overall, the intracellular HBV DNA of mutant I97L indeed declined more rapidly than that of WT HBV. 2019 Journal of virology Result HBV I97L 45 49 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Previously, we observed no apparent deficiency of intracellular viral DNA replication of mutant I97L in cell culture. 2019 Journal of virology Result HBV I97L 96 100 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Previously, we reported another frequent, naturally occurring proline-to-threonine mutation at HBc amino acid 130 (P130T) in human hepatomas in Taiwan. 2019 Journal of virology Result HBV P130T 115 120 C 95 98 Hepatocellular carcinoma 131 140 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Relative to that of WT HBV, at 3 day or 1 week postinjection, the single mutant P130T exhibited an extracellular DNA profile with a 2-fold-increased RC/SS DNA ratio, indicative of a hypermaturation phenotype. 2019 Journal of virology Result HBV P130T 80 85 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Since we used a high dose of mutant I97L plasmid DNA (30 mug of DNA/mouse) in. 2019 Journal of virology Result HBV I97L 36 40 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Taken together, the immature virion secretion of mutant I97L is not due to the contamination from naked core particles in vivo, since they were not detected here. 2019 Journal of virology Result HBV I97L 56 60 C 104 108 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. the averaged transfection efficiencies (SEAP activities) between WT and I97L experimental groups were comparable to each other. 2019 Journal of virology Result HBV I97L 72 77 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The difference in the viral DNA levels between WT and mutant I97L could originate from either the decreased synthesis or increased secretion or degradation of mutant I97L viral DNA. 2019 Journal of virology Result HBV I97L;I97L 61;166 65;170 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. the full-length RC form (*) of both mutants I97L and I97L/P130T can be achieved by an endogenous polymerase reaction (EPR) in vitro by using nucleocapsids purified from intracellular lysates or extracellular virions (see Materials and Methods). 2019 Journal of virology Result HBV P130T;I97L;I97L 58;53;44 64;57;48 P 97 107 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. the HBV DNA of mutant P130T was clearly more persistent than those of the WT, mutant I97L, and double mutant I97L/P130T strains. 2019 Journal of virology Result HBV P130T;P130T;I97L;I97L 114;22;85;109 119;27;89;113 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The lack of fully matured full-length RC form in mutant I97L is highlighted by a red asterisk in. 2019 Journal of virology Result HBV I97L 56 60 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. the possibility that the lower level of mutant I97L viral DNA at 2 weeks postinjection was caused by the high-dose DNA induced innate immunity cannot be excluded. 2019 Journal of virology Result HBV I97L 47 52 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The ratio of the averaged signal intensities of total viral DNAs (full-length RC plus full-length SS) between WT and I97L was approximately 2.7 to 1 on day 3, but this ratio shifted to approximately 8 to 1 on week 1. 2019 Journal of virology Result HBV I97L 117 121 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The serum HBeAg was higher for mutant I97L due to the 3-fold-higher dose of input plasmid DNA at 1 to 3 dpi. 2019 Journal of virology Result HBV I97L 38 42 C 10 15 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The substitution at HBc amino acid 97 of mutant I97L could represent an immune escape mutation since it coincides with potent T-cell epitopes. 2019 Journal of virology Result HBV I97L 48 52 C 20 23 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This adjustment successfully generated near-equal signal intensities by Southern blotting between WT HBV and mutant I97L at 3 dpi. 2019 Journal of virology Result HBV I97L 116 120 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This P130T mutant displayed a hypermaturation phenotype by accumulating more abundant amounts of full-length RC form DNA and is highly efficient in rescuing the immature secretion phenotype of mutant I97L in the human hepatoblastoma HepG2 cell line. 2019 Journal of virology Result HBV P130T;I97L 5;200 10;204 Hepatocellular carcinoma 218 232 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This result indicated that neither intracellular nor extracellular phenotypic defects in the full-length RC form of mutant I97L are due to an inability to generate in vitro the full-length genome. 2019 Journal of virology Result HBV I97L 123 127 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This result strongly supports the notion that the viral DNA associated with mutant I97L virions is less persistent than that of WT HBV at later time points postinjection. 2019 Journal of virology Result HBV I97L 83 87 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To compare the in vivo expressions of viral proteins between WT and mutant I97L, we performed Western blot analysis using liver samples from mice sacrificed on 3 dpi. 2019 Journal of virology Result HBV I97L 75 79 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To distinguish between these two possibilities, we performed endogenous polymerase reactions using capsids prepared from four different sources of HBV: WT, I97L, P130T, and I97L/P130T. 2019 Journal of virology Result HBV P130T;I97L;P130T;I97L 178;156;162;173 183;160;167;177 Capsid;P 99;72 106;82 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To examine the intracellular viral DNA replication between WT and mutant I97L in the injected mouse liver, we extracted viral DNA from the freshly dissected liver and performed Southern blot analysis (100 mg liver mass/lane. 2019 Journal of virology Result HBV I97L 73 77 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To examine the potential role of adaptive immunity in the lower level of viral DNA in mutant I97L, we extended our study to NOD/SCID immunodeficient mice, which are deficient in mature T and B cells, and with attenuated NK cells. 2019 Journal of virology Result HBV I97L 93 97 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To examine whether mutation P130T can rescue in vivo the immature secretion of mutant I97L, we performed hydrodynamic delivery and compared the virion secretions from four different plasmids in BALB/c mice: WT, I97L, P130T, and a double mutant I97L/P130T. 2019 Journal of virology Result HBV P130T;P130T;I97L;I97L;P130T;I97L 249;28;86;211;217;244 254;33;90;215;222;248 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To exclude the possibility that the immature genomes of I97L HBV in. 2019 Journal of virology Result HBV I97L 56 60 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To investigate the immature secretion phenotype of mutant I97L in an in vivo experimental setting, we introduced HBV DNA (adr) of wild-type (WT) and mutant I97L into BALB/c mouse liver by hydrodynamic delivery. 2019 Journal of virology Result HBV I97L;I97L 58;156 62;160 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To monitor the transfection efficiency of hydrodynamic delivery, we coinjected WT or I97L plasmids with a control plasmid encoding secretable alkaline phosphatase (SEAP). 2019 Journal of virology Result HBV I97L 85 89 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. We compared the intracellular levels of viral DNAs in livers between WT and mutant I97L at 1 week postinjection. 2019 Journal of virology Result HBV I97L 83 87 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. we detected no naked core particles (1.35 g/cm3) in the sera in all gradient fractions from both WT and mutant I97L injected BALB/c mice. 2019 Journal of virology Result HBV I97L 111 115 C 21 25 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. we examined whether the deficiency in the intracellular viral DNA replication of mutant I97L can be rescued by the mutation P130T. 2019 Journal of virology Result HBV I97L;P130T 88;124 92;129 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. We first compared the viral DNA replications between WT HBV and mutant I97L in the livers of IFNAR-/- mice at 3 days postinjection with equal amounts of plasmid DNAs (30 mug/mouse) by Southern blotting. 2019 Journal of virology Result HBV I97L 71 75 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. By contrast, the A49V point mutation at the transactivation domain was detected significantly more frequently in the LC/HCC samples (26.92%; 7/26) than in the ASC cases (p = 0.01). 2019 Clinical and experimental hepatology Result HBV A49V 17 21 Hepatocellular carcinoma;Liver cirrhosis 120;117 123;119 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. From them, L11Q, N37S and K38R were more prevalent, but L19* (stop codon), M1T, T5P/A, G29A and N32D were also observed with lower prevalence. 2019 Clinical and experimental hepatology Result HBV L19X;M1T;T5P;T5A;L11Q;N37S;K38R;G29A;N32D 56;75;80;80;11;17;26;87;96 60;78;85;85;15;21;30;91;100 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Hence, an impressive substitution at the start codon of pre-S2 (M109T) in 2 ASC samples and a stop codon (L19*) in the pre-S1 region of 3 ASC samples were detected. 2019 Clinical and experimental hepatology Result HBV L19X;M109T 106;64 110;69 PreS1;PreS2 119;56 125;62 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Moreover, an S130F/L mutation in the pre-S2 region of the LC samples (22.22%; 2/9) and a substitution at the start codon of the pre-S2 (Met1R) region in 11.76% (2/17) of the HCC cases were also detected, with a non-significant difference (p = 0.46). 2019 Clinical and experimental hepatology Result HBV S130F;S130L 13;13 20;20 PreS2;PreS2 37;128 43;134 Hepatocellular carcinoma;Liver cirrhosis 174;58 177;60 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Moreover, in the hepatocyte binding site (amino acid residue 10-36 in pre-S1), the L11Q point mutation was detected in 6 ASC samples, which was significantly different from that in the LC/HCC sample (p = 0.02). 2019 Clinical and experimental hepatology Result HBV L11Q 83 87 PreS1 70 76 Hepatocellular carcinoma;Liver cirrhosis 188;185 191;187 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Nucleotide substitutions, including 3,015 GT>A and 3,138 G>T, were found significantly more frequently in 14 and 18 ASC individuals, respectively. 2019 Clinical and experimental hepatology Result HBV G138T 53 60 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. The frequency of certain mutations within B-cell epitopes of the pre-S1 region, including L11Q (p = 0.02), N37S (p = 0.02) and K38R (p = 0.04), was higher in the ASC group compared with that in the LC/HCC group. 2019 Clinical and experimental hepatology Result HBV L11Q;N37S;K38R 90;107;127 94;111;131 PreS1 65 71 Hepatocellular carcinoma;Liver cirrhosis 201;198 204;200 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. The most prevalent substitution event in this group was A49V at the transactivation domain, which was not significantly different between LC (11.11%; 1/9) and HCC (35.29%; 6/17) groups (p = 0.29). 2019 Clinical and experimental hepatology Result HBV A49V 56 60 Hepatocellular carcinoma;Liver cirrhosis 159;138 162;140 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. However, mutation Q16R resulted in decreased HBsAg secretion compared to wt M88 (EC/IC ratio: 0.57 versus 1.2) whereas a significant increase in HBsAg secretion was observed in P38.II (EC/IC ratio: 31 versus 0.5). 2019 Emerging microbes & infections Result HBV Q16R 18 22 S;S 45;145 50;150 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Introduction of the N146D/S/Y mutations in plasmid M88 and P38.II by SDM did not significantly alter the EC and IC HBsAg production pattern, although a slight reduction in HBsAg secretion was observed for P38.II mutants, as reflected by the decreased HBsAg EC/IC ratio compared to that of wt HBsAg (5-8 versus 17) (Figure 3). 2019 Emerging microbes & infections Result HBV N146D;N146S;N146Y 20;20;20 29;29;29 S;S;S;S 115;172;251;292 120;177;256;297 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Mutants N146D/S/Y showed an expected non-glycosylated profile. 2019 Emerging microbes & infections Result HBV N146D;N146S;N146Y 8;8;8 17;17;17 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Mutations Q16R, Q181R and W182R did not substantially modify the total HBsAg production pattern in M88 and P38.II plasmids (Figure 4). 2019 Emerging microbes & infections Result HBV Q16R;Q181R;W182R 10;16;26 14;21;31 S 71 76 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Particularly, mutations removing the N146 glycosylation site (N146D/S/Y) were found in 4.4% (2/45) and 6% (3/50) of OBI genotype B (OBIB) and genotype C (OBIC) sequences, respectively. 2019 Emerging microbes & infections Result HBV N146D;N146S;N146Y 62;62;62 71;71;71 Occult Hepatitis B 116 119 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Particularly, no HBsAg was detected in the supernatants of cultures transfected with mutants L87R and C90R. 2019 Emerging microbes & infections Result HBV L87R;C90R 93;102 97;106 S 17 22 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Seven OBI-specific substitutions introducing an arginine residue in S TMDs were investigated: Q16R in TMD1, C85R, L87R, L88R, and C90R in TMD2, and Q181R and W182R in TMD3. 2019 Emerging microbes & infections Result HBV Q16R;C85R;L87R;L88R;C90R;Q181R;W182R 94;108;114;120;130;148;158 98;112;118;124;134;153;163 S 68 69 Occult Hepatitis B 6 9 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Western blot analysis of transfected cell lysates verified the absence of detectable levels of intra-cellular S protein carrying L87R and C90R mutations (data not shown). 2019 Emerging microbes & infections Result HBV L87R;C90R 129;138 133;142 S 110 111 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. When introduced in M88 and P38.II, mutations C85R, L87R, L88R, and C90R significantly impaired both EC and IC HBsAg production irrespective of the sequence backbone. 2019 Emerging microbes & infections Result HBV C85R;L87R;L88R;C90R 45;51;57;67 49;55;61;71 S 110 115 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. A similar pattern was observed for the W172* mutant. 2019 Viruses Result HBV W172X 39 44 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. The ratio of extracellular to intracellular HBsAg of the D144E mutant was comparable to wildtype HBsAg (107% +- 13% for Architect (p = 0.989) and 116% +- 10% for Strep-tag-ELISA (p = 0.594)). 2019 Viruses Result HBV D144E 57 62 S;S 44;97 49;102 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. Therefore, Huh7-cells were transiently transfected with a plasmid encoding the strep-tagged HBsAg, carrying the wild-type (wt) sequence and the SHB L216* mutation, as well as the SHB D144E and W172* as controls (see Materials and Methods section). 2019 Viruses Result HBV L216X;W172X;D144E 148;193;183 153;198;188 S;S;S 92;144;179 97;147;182 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. We detected significantly lower intracellular (29% +- 15% for Architect (p < 0.0001) and 22% +- 12% for Strep-tag-ELISA (p < 0.0001)) and extracellular concentrations of HBsAg (4.2% +- 6% for Architect (p < 0.0001) and 10% +- 9% for Strep-tag-ELISA (p < 0.0001)) in the case of the L216* mutant vs. 2019 Viruses Result HBV L216X 282 287 S 170 175 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. We detected significantly lower intracellular (35% +- 14% for Architect (p < 0.0001) and 3% +- 4% for Strep-tag-ELISA (p < 0.0001)) and extracellular concentrations of HBsAg (43% +- 40% for Architect (p = 0.012) and 10% +- 12% for Strep-tag-ELISA (p < 0.0001)) in the case of the W172* mutant vs. 2019 Viruses Result HBV W172X 280 285 S 168 173 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. When comparing HBsAg production and secretion of HBsAg D144E mutant compared to HBsAg wildtype, we observed a modestly reduced intracellular HBsAg when measured with Architect (62% +- 17% for Architect (p = 0.005) and 125% +- 23% for Strep-tag-ELISA (p = 0.054)), and a modestly higher extracellular HBsAg when measured with Strep-tag-ELISA (125% +- 23% for Architect (p = 0.347) and 144% +- 32% for Strep-tag-ELISA (p = 0.01)). 2019 Viruses Result HBV D144E 55 60 S;S;S;S;S 15;49;80;141;300 20;54;85;146;305 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among 40 patients treated with low genetic barriers, one of four patients with pre-existing rtM204I variants (1/4, 25.0%) and half of patients without pre-existing rtM204I variants (18/36, 50.0%) achieved CVR at 12 mo of low genetic barriers. 2019 World journal of gastroenterology Result HBV M204I;M204I 94;166 99;171 RT;RT 92;164 94;166 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among 95 patients treated with tenofovir, all seven patients with pre-existing rtM204I variants (7/7, 100%) as well as almost patients without pre-existing rtM204I variants (85/88, 96.6%) achieved CVR at 12 mo of tenofovir. 2019 World journal of gastroenterology Result HBV M204I;M204I 81;158 86;163 RT;RT 79;156 81;158 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among 97 patients treated with entecavir, only one of six patients with pre-existing rtM204I variants (1/6, 16.7%) achieved CVR at 12 mo of entecavir, whereas almost patients without pre-existing rtM204I variants (87/91, 95.6%) achieved CVR at 12 mo entecavir (87/91, 95.6%). 2019 World journal of gastroenterology Result HBV M204I;M204I 87;198 92;203 RT;RT 85;196 87;198 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among all clinical samples, seventeen samples (4.1%) were identified as carrying rtM204I variants and among these samples, nine samples were rtM204I variant exclusively and eight samples were rtM204I variant coexistent with WT. 2019 World journal of gastroenterology Result HBV M204I;M204I;M204I 83;143;194 88;148;199 RT;RT;RT 81;141;192 83;143;194 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among the clinical factors (age, sex, HBeAg status, HBV-DNA titers, HBsAg quantitative levels, AST, ALT, total bilirubin, albumin, prothrombin time, platelet counts, presence of significant fibrosis, LC or HCC), univariate analysis showed that pre-existing rtM204I variants were more frequently detected in patients with significant fibrosis, or patients with HCC. 2019 World journal of gastroenterology Result HBV M204I 259 264 C;S;RT 38;68;257 43;73;259 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 206;360;200 209;363;202 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among the positively identified samples, all of the samples produced a distinct melting peak or peaks with a Tm or Tms being in the diagnostic Tm range for WT or rtM204I. 2019 World journal of gastroenterology Result HBV M204I 164 169 RT 162 164 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among these, in four samples, rtM204I was dominant over WT; in one sample, codominant; in three samples, WT was dominant over rtM204I (Table 3). 2019 World journal of gastroenterology Result HBV M204I;M204I 32;128 37;133 RT;RT 30;126 32;128 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Association between pre-existence of rtM204I variants and patient characteristics. 2019 World journal of gastroenterology Result HBV M204I 39 44 RT 37 39 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Association between the pre-existence of rtM204I variants and antiviral responsiveness. 2019 World journal of gastroenterology Result HBV M204I 43 48 RT 41 43 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Determination of diagnostic Tm range for the identification of WT and rtM204I variants by LNA real-time PCR. 2019 World journal of gastroenterology Result HBV M204I 72 77 RT 70 72 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Identification of WT and rtM204I variants was performed by LNA real-time PCR melting curve analysis by the observation of melting peak formation and specific Tm measurements in the specified channels (Figure 2, Table 2). 2019 World journal of gastroenterology Result HBV M204I 27 32 RT 25 27 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. LNA real-time PCR with samples of rtM204I positive control DNAs (n = 48) in amounts ranging from 24 to 2400000 copies resulted in a 100% positive detection rate and 100% specificity showing a distinct melting peak formation at the FAM channel in all of the rtM204I control DNA samples with Tms ranging from 51.3 to 52.2 C (mean, 51.7 +- 0.2 C) but no significant melting peak formation at the HEX channel (WT detection channel). 2019 World journal of gastroenterology Result HBV M204I;M204I 36;259 41;264 RT;RT 34;257 36;259 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. LNA real-time PCR with samples of WT control DNAs (n = 48) in amounts ranging from 24 to 2400000 copies resulted in a 95.8% positive detection rate and 100% specificity showing a distinct melting peak formation at the HEX channel in all of the WT control DNA samples with Tms ranging from 61.9 to 63.3 C (mean, 62.6 +- 0.4 C) but no significant melting peak formation at the FAM channel (rtM204I detection channel). 2019 World journal of gastroenterology Result HBV M204I 392 397 RT 390 392 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Logistic multivariate analysis showed that pre-existing rtM204I variants were significantly more frequent in patients with significant fibrosis (odd ratio 3.397, 95% confidence interval 1.119-10.319, P = 0.031) (Table 5). 2019 World journal of gastroenterology Result HBV M204I 58 63 RT 56 58 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Logistic multivariate regression analysis revealed that achievement of CVR was reversely associated with higher HBV-DNA titers, treatment with low genetic barrier drugs, and, infection with pre-existing rtM204I variants prior to NAs (odds ratio 0.014, 95% confidence interval 0.002-0.096, P < 0.001; Table 6). 2019 World journal of gastroenterology Result HBV M204I 205 210 RT 203 205 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Of 410 clinical samples tested in duplicate by our LNA real-time PCR method, 403 samples (98.3%) were positively identified as WT and/or rtM204I variants, with two samples found to be mixed with presumably unknown variants with non-typable Tms. 2019 World journal of gastroenterology Result HBV M204I 139 144 RT 137 139 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Overall, thirteen samples carried the rtM204I variant predominantly and one sample co-dominantly with WT. 2019 World journal of gastroenterology Result HBV M204I 40 45 RT 38 40 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Table 7 shows the mean changes in the HBV-DNA levels and cumulative probabilities of CVR in 17 patients with pre-existing rtM204I variants. 2019 World journal of gastroenterology Result HBV M204I 124 129 RT 122 124 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The decrease in HBV-DNA was significantly less prominent in patients infected with pre-existing rtM204I variants than in patients infected without pre-existing rtM204I variants, at 3, 6, 9, and 12 mo of antiviral treatments (all P < 0.05). 2019 World journal of gastroenterology Result HBV M204I;M204I 98;162 103;167 RT;RT 96;160 98;162 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The pre-existing rtM204I variants prior to NAs were detected in 17 of 403 treatment-naive CHB patients (4.2%). 2019 World journal of gastroenterology Result HBV M204I 19 24 RT 17 19 Chronic Hepatitis B 90 93 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The pre-existing rtM204I variants were more frequently detected in subjects with higher FIB-4 scores. 2019 World journal of gastroenterology Result HBV M204I 19 24 RT 17 19 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The results of direct PCR sequencing of thirty clinical samples randomly chosen among positively identified samples by LNA real-time PCR had results identical to those of our LNA real-time PCR assay, proving its reliability for screening for pre-existing rtM204I variants from treatment naive CHB patients (Figure 3). 2019 World journal of gastroenterology Result HBV M204I 257 262 RT 255 257 Chronic Hepatitis B 293 296 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The third sample that showed three melting peaks was revealed to have an additional codon for isoleucine of rtM204I. 2019 World journal of gastroenterology Result HBV M204I 110 115 RT 108 110 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. Among them, mutation rtM204I associated with LAM and LdT had the highest proportion, 38.33%; mutation rtL180M associated with LAM, LdT, and ETV accounted for 19.30%; mutation rtM204V associated with LAM, LdT, and ETV accounted for 12.97%; and other mutations accounted for no more than 10%. 2019 Scientific reports Result HBV M204I;L180M;M204V 23;104;177 28;109;182 RT;RT;RT 21;102;175 23;104;177 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. Combinational mutation occurrences were mainly L180M + M204I/V (33/79). 2019 Scientific reports Result HBV M204V;L180M;M204I 55;47;55 62;52;62 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. Single site mutation occurrences were mainly M204I (86/126) and M236T (14/126). 2019 Scientific reports Result HBV M204I;M236T 45;64 50;69 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. In addition to previously reported mutations, we also found five variants of the X gene located in the HBV functional region, including L37I, S43P, H86P/R, L98I and T105A, which have not been reported in previous studies and may be specific for Indonesian HBV. 2019 Biomedical reports Result HBV L37I;S43P;H86P;H86R;L98I;T105A 136;142;148;148;156;165 140;146;154;154;160;170 X 81 82 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. Multinomial regression analysis confirmed that K130M/V131I mutations were correlated with CLD progression (OR, 7.629; 95% CI, 1.578-36.884; Table V). 2019 Biomedical reports Result HBV V131I;K130M 53;47 58;52 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The dominant mutations in the basal core promoter (BCP) were K130M/V131I, as found in 12.6% (11/87) of CLD patients. 2019 Biomedical reports Result HBV V131I;K130M 67;61 72;66 BCP;BCP 30;51 49;54 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. There was an association between the K130M/V131I mutations and the progression of CLD (P<0.05), but not for other X gene mutations (P>0.05; Table IV). 2019 Biomedical reports Result HBV V131I;K130M 43;37 48;42 X 114 115 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. There were significant differences in viral load levels in HBV-infected patients who had X gene mutations, as well as the R87W/G, I127L/T/N/S and K130M/V131I mutation (P<0.05). 2019 Biomedical reports Result HBV V131I;I127L;I127T;I127N;I127S;R87W;R87G;K130M 152;130;130;130;130;122;122;146 157;141;141;141;141;128;128;151 X 89 90 HBV infections 59 71 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. All the mutations were synonymous, except T528C which resulted in an amino acid change (Met125Thr) in the 'a' determinant of the S protein. 2019 Scientific reports Result HBV T528C;M125T 42;88 47;97 S;S 107;129 121;130 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Analysis of the S gene amplicon sequences from 10 patients identified 10 mutations - 8 mutations common to all patients (C373T, C493A, C505T, C514A, T528C, A616G, T619C, T667C), whereas 2 mutations, T364C and A541G were specific to patients 8 and 11 respectively. 2019 Scientific reports Result HBV C373T;C493A;C505T;C514A;T528C;A616G;T619C;T667C;T364C;A541G 121;128;135;142;149;156;163;170;199;209 126;133;140;147;154;161;168;175;204;214 S 16 17 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. In core gene region - G2095A (Arg94Leu) in B cell in patient 4, A2070G (Glu86Arg) in B cell in patient 31 and T1934A (Ser41Thr) in tumor cells in patient 38. 2019 Scientific reports Result HBV G2095A;R94L;A2070G;E86R;T1934A;S41T 22;30;64;72;110;118 28;38;70;80;116;126 C 3 7 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. In X gene region - T1590G (Phe73Val) in B cell in patients 10 and 11, C1504T (Ala44Val) in patient 36, T1809G (Ser146Ala) and T1812C (Ser147Pro) in patient 37. 2019 Scientific reports Result HBV T1590G;F73V;C1504T;A44V;T1809G;S146A;T1812C;S147P 19;27;70;78;103;111;126;134 25;35;76;86;109;120;132;143 X 3 4 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. The four core gene amplicons revealed 11 mutations, with two mis-sense mutations A2100C (Asp96Thr) and C2115T (Ala101Val). 2019 Scientific reports Result HBV A2100C;D96T;C2115T;A101V 81;89;103;111 87;97;109;120 C 9 13 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. Six of these (sL127I, sA128V, sG130S, sM133T, sF134I, and S140T) were located in the 'a' determinant region, among which three immune escape mutants (IEMs) (sY100C, sA128V, and sM133T) were identified. 2020 International journal of infectious diseases Result HBV L127I;A128V;G130S;M133T;F134I;Y100C;A128V;M133T;S140T 14;22;30;38;46;157;165;177;58 20;28;36;44;52;163;171;183;63 S;S;S;S;S;S;S;S;S 86;14;22;30;38;46;157;165;177 100;15;23;31;39;47;158;166;178 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. These included the previously reported mutations rtL91I, rtM129L, rtW153R, rtS213T, rtV214A, rtN238T, rtN248H, and rtI269L (Yamani et al.,; Choi et al.,; Shaha et al.,; Ababneh et al.,). 2020 International journal of infectious diseases Result HBV L91I;M129L;W153R;S213T;V214A;N238T;N248H;I269L 51;59;68;77;86;95;104;117 55;64;73;82;91;100;109;122 RT;RT;RT;RT;RT;RT;RT;RT 49;57;66;75;84;93;102;115 51;59;68;77;86;95;104;117 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. The mutation patterns were sI110L + sS193L, sP120L + + sT123N + sT126I + sA128V + sY134H + sD144E + +sG145A, sT118A+sP127T, sI110L+sP120T+sD144A+ +sG145R and sP120R+sC121Y+sT131I + sS132P. 2019 Polish journal of microbiology Result HBV I110L;S193L;P120L;T123N;T126I;A128V;Y134H;D144E;G145A;T118A;P120T;D144A;P120R;C121Y;S132P;P127T;I110L;G145R;T131I 27;36;44;55;64;73;82;91;101;109;131;138;158;165;181;116;124;147;172 33;42;50;61;70;79;88;97;107;115;137;144;164;171;187;122;130;153;178 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 27;36;44;55;64;73;82;91;101;109;116;124;131;138;147;158;165;172;181 28;37;45;56;65;74;83;92;102;110;117;125;132;139;148;159;166;173;182 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. Twenty-five patients (36.7%) had secondary/compensatory mutations and the mutations patterns (rtL91I, rtQ149K, rtQ215H/P/S and rtN238D) were depicted in Table II. 2019 Polish journal of microbiology Result HBV L91I;Q215H;Q215P;Q215S;Q149K;N238D 96;113;113;113;104;129 100;122;122;122;109;134 RT;RT;RT;RT 94;102;111;127 96;104;113;129 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. The most prevalent pol gene mutation was rtQ215H/P/S and it falls in the compensatory mutation category. 2019 Polish journal of microbiology Result HBV Q215H;Q215P;Q215S 43;43;43 52;52;52 P;RT 19;41 22;43 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. However, some mutations (H9Y, N13H, I91L, I269L, and V278I) were found in the RT domain that are not associated with drug resistance, according to Geno2pheno:hbv. 2020 International journal of molecular sciences Result HBV H9Y;N13H;I91L;I269L;V278I 25;30;36;42;53 28;34;40;47;58 RT 78 80 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Mutational analysis at the nucleotide level showed only two mutations, C2964A and C3062T, in the preS1 region of BD2 HBV; no mutations were found in the preS2 region, consistent with previous findings (Figure 2). 2020 International journal of molecular sciences Result HBV C2964A;C3062T 71;82 77;88 PreS1;PreS2 97;153 102;158 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Only one putative NA-resistant mutation, I91L, was found, and no primary, secondary, pre-treatment, or drug-resistant mutations were observed in the RT domain of Pol. 2020 International journal of molecular sciences Result HBV I91L 41 45 P;RT 162;149 165;151 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Small HBsAg showed the following mutations: N3S, V18G, E44G, M47T, S53L, V159A, A177V, S210N, and I213L; none of these are associated with HBsAg escape, though the N3S mutant is associated with an increased risk of HCC. 2020 International journal of molecular sciences Result HBV N3S;N3S;V18G;E44G;M47T;S53L;V159A;A177V;S210N;I213L 44;164;49;55;61;67;73;80;87;98 47;167;53;59;65;71;78;85;92;103 S;S 6;139 11;144 Hepatocellular carcinoma 215 218 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. In fact, M184V in HIV-1 (or M204V in HBV) is not reportedly associated with TDF/TAF resistance. 2020 Scientific reports Result HBV M204V 28 33 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. One possible solution to overcome M184V/I (M204V/I in HBV) resistance is to decrease composition for NRTIs that do not rely on the interactions with Met184. 2020 Scientific reports Result HBV M204V;M204I 43;43 50;50 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. Previous in vitro antiviral assays have demonstrated that 4'-cyano-containing NRTIs, such as CAdA and CdG, show slightly decreased but moderate activity against HBV with M204V in RT. 2020 Scientific reports Result HBV M204V 170 175 RT 179 181 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. The corresponding M204V/I mutation in HBV RT has also been identified as a key mutation highly affecting HBV's sensitivity to 3TC and ETV, and in particular, triple mutations M204V/L180M/S202G render HBV completely resistant to both 3TC and ETV. 2020 Scientific reports Result HBV S202G;M204V;M204V;M204I;L180M 187;18;175;18;181 192;25;180;25;186 RT 42 44 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. These interactions may contribute to enzymatic stability of HIV-1 RT, and thus Q182G is unlikely to be suitable for helping understand the mechanism of HBV's resistance to 3TC and ETV due to S202G in HBV RT. 2020 Scientific reports Result HBV S202G 191 196 RT;RT 66;204 68;206 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. These results strongly suggest that HBV's resistance to 3TC and ETV (with M204V/L180M in HBV RT) is reasonably well simulated using an HIV-1 with HBV-associated 3MB mutations. 2020 Scientific reports Result HBV M204V;L180M 74;80 79;85 RT 93 95 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Although above Phos-tag analysis indicated that S162 is the major site of the Pin1-binding phosphorylation site (Figure 1B), we found that a single site-directed mutant (S162A) still interacted with Pin1 with relatively lower binding activity. 2020 Frontiers in cell and developmental biology Result HBV S162A 170 175 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Amounts of HBV DNA and HBcAg, but not HBeAg devoid of Pin1-binding site, were significantly reduced in the case of the T160A/S162A virus relative to the WT virus (Figures 6D-F). 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 125;119 130;124 C;C 23;38 28;43 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Cells expressing either HA-tagged WT HBc or the T160A/S162A mutant were processed for the immunoblot analysis with anti-pHBc or anti-HA antibody. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 54;48 59;53 C 37 40 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Cycloheximide analysis demonstrated that the HBc-T160A/S162A mutant was conspicuously destabilized relative to WT HBc (Figure 3F), confirming that Pin1 indeed regulates the HBc stability by interacting with the phosphorylated Thr160-Pro and Ser162-Pro motifs. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A;T160P;S162P 55;49;226;241 60;54;236;251 C;C;C 45;114;173 48;117;176 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. HepG2 cells were transfected with an HBV molecular clone (either WT or T160A/S162A), and supernatants were collected to analyze HBV DNA and HBcAg. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 77;71 82;76 C 140 145 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. HepG2 cells were transfected with plasmid encompassing HA-HBc or its mutants (T160A, S162A, or T160A/S162A), and then subjected to GST pull-down assay. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A;S162A;T160A 101;78;85;95 106;83;90;100 C 58 61 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Notably, HBc harboring a double mutation (T160A/S162A) completely lost the ability to bind GST-Pin1 (Figure 2E). 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 48;42 53;47 C 9 12 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Notably, the T160A/S162A double mutant yielded a much lower molecular weight band, implying that both sites are phosphorylated within HBc (Figure 1B). 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 19;13 24;18 C 134 137 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. On the other hand, HBc harboring a T160A or S162A mutation yielded relatively lower molecular weight bands than WT HBc and other site-directed mutants (S155A and S170A). 2020 Frontiers in cell and developmental biology Result HBV T160A;S162A;S155A;S170A 35;44;152;162 40;49;157;167 C;C 19;115 22;118 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. Since mutation in both sites (T160A/S162A) completely abolished its Pin1-binding, these results indicate that Thr160 is an another Pin1 binding-phosphorylated residue. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 36;30 41;35 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. To further delineate the biological importance of the Pin1-HBc interaction, we tested the efficiency of virus production of HBV encoding WT HBc or its T160A/S162A mutant. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 157;151 162;156 C;C 59;140 62;143 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. To further delineate the functional implication of the Pin1-HBc interaction, we investigated the protein stability of the T160A/S162A mutant, which is unable to bind Pin1. 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 128;122 133;127 C 60 63 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. To this end, we generated recombinant GST-Pin1 and the WW domain mutant (W34A), which lacks pSer/Thr-Pro binding activity. 2020 Frontiers in cell and developmental biology Result HBV W34A 73 77 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. We found that a single site-directed mutation (T160A and S162A) resulted in the prominent reduction of co-precipitated HBc with GST-Pin1 (Figure 2E). 2020 Frontiers in cell and developmental biology Result HBV T160A;S162A 47;57 52;62 C 119 122 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. We observed phosphorylation of HBc only in WT HBc, but not in the T160A/S162A mutant (Figure 1C). 2020 Frontiers in cell and developmental biology Result HBV S162A;T160A 72;66 77;71 C;C 31;46 34;49 32084506 7-Deaza-7-fluoro modification confers on 4'-cyano-nucleosides potent activity against entecavir/adefovir-resistant HBV variants and favorable safety. We then analyzed the interactions of ETV-TP and CdFA-TP with HBV-RT, in which three amino acid substitutions associated with HBV's resistance to ETV (L180M/S202G/M204V) have been introduced (RTETV-R). 2020 Antiviral research Result HBV S202G;M204V;L180M 156;162;150 161;167;155 RT 65 67 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. In particular, the additional N-Glycosylation sites in HBsAg MHR derive from a single aa substitution in 3 patients (T115N, T117N, and T123N, respectively) and from the insertion of 114N-ins in a single patient. 2020 Viruses Result HBV T115N;T117N;T123N 117;124;135 122;129;140 S 55 60 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. In particular, the N-linked glycosylation sites 114Nins, T117N, T115N, and T123N showed a 68%, 62%, 56%, and 45% decrease in extracellular HBsAg amount (p-values ranging from 0.05 to 0.01), respectively (Figure 1A). 2020 Viruses Result HBV T117N;T115N;T123N 57;64;75 62;69;80 S 139 144 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. In the remaining patient, the pattern of mutations S113N+T131N+M133T was observed, resulting in the introduction of 2 different glycosylation sites. 2020 Viruses Result HBV S113N;T131N;M133T 51;57;63 56;62;68 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Notably, for the triple mutant S113N+T131N+M133T, an 80% decrease in extracellular HBsAg amount was observed (p < 0.01). 2020 Viruses Result HBV S113N;T131N;M133T 31;37;43 36;42;48 S 83 88 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. In addition, 5 patients with sustained HBeAg-positive and HBV DNA >3 log10 IU/mL until the end of the follow-up period, who presented 100% rtM204I/V mutation at baseline, were also included for kinetics analysis of rtM204I/V in serum HBV DNA/RNA during the interferon rescue period. 2021 Hepatology (Baltimore, Md.) Result HBV M204I;M204V;M204I;M204V 141;141;217;217 148;148;224;224 C;RT;RT 39;139;215 44;141;217 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. In brief, for the EFFORT study, 299 patients were included in the MONO group and 77 of them developed VB as well as the rtM204I/V mutation. 2021 Hepatology (Baltimore, Md.) Result HBV M204I;M204V 122;122 129;129 RT 120 122 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Population sequencing of serum HBV DNA confirmed that all of the 9 patients bore 100% rtM204I/V LAMR mutation at week 104 of the EFFORT study or at baseline of the ML18376 study. 2021 Hepatology (Baltimore, Md.) Result HBV M204I;M204V 88;88 95;95 RT 86 88 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Population sequencing revealed that LAMR variant rtM204I/V in serum DNA emerged between weeks 64 and 88 in all 5 patients evaluated. 2021 Hepatology (Baltimore, Md.) Result HBV M204I;M204V 51;51 58;58 RT 49 51 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Remarkably, a significant percentage of rtM204I/V LAMR mutant (40%-90%) was found in serum HBV RNA, intrahepatic viral RNA, and cccDNA at the corresponding time points in biopsy samples in all 7 patients. 2021 Hepatology (Baltimore, Md.) Result HBV M204I;M204V 42;42 49;49 RT 40 42 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. The result showed that the optimized T5 exonuclease digestion can efficiently exclude an excess (40-fold) of LAMR rtM204V rcDNA that was spiked in a Hirt DNA extract containing WT cccDNA. 2021 Hepatology (Baltimore, Md.) Result HBV M204V 116 121 RT 114 116 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Again, the strongest decrease (91%) in HBsAg secretion factor was observed for the pair S204N + L205P (Figure 4(B)). 2020 Emerging microbes & infections Result HBV S204N;L205P 88;96 93;101 S 39 44 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. All the mutations associated with HBsAg<1000IU/ml (with the exception of Y206C) were found significantly correlated in pairs with other HBsAg C-terminus mutations. 2020 Emerging microbes & infections Result HBV Y206C 73 78 S;S 34;136 39;141 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. All the pairs of mutations (with the exception of Y206F + V194A) significantly decreased the amount of extracellular HBsAg compared to wt (P values ranging from 0.022 to <0.001) paralleling their association with lower HBsAg levels in vivo (Figure 4(A)). 2020 Emerging microbes & infections Result HBV Y206F;V194A 50;58 55;63 S;S 117;219 122;224 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. By stratifying 228 HBeAg-negative genotype D infected patients according to HBsAg levels, 5 specific mutations (V190A, S204N, Y206C, Y206F and S210N) resulted significantly correlated with HBsAg<1000IU/ml (Figure 2). 2020 Emerging microbes & infections Result HBV V190A;S204N;Y206C;Y206F;S210N 112;119;126;133;143 117;124;131;138;148 C;S;S 19;76;189 24;81;194 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. For the pair of mutations S204N + L205P, a 99% decrease was observed (Figure 4(A)). 2020 Emerging microbes & infections Result HBV S204N;L205P 26;34 31;39 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Furthermore, some pairs of mutations (V190A + F220L, S204N + L205P, S204N + F220L) were also associated with lower median (IQR) serum HBV-DNA (Figure 3(B)). 2020 Emerging microbes & infections Result HBV V190A;F220L;S204N;L205P;S204N;F220L 38;46;53;61;68;76 43;51;58;66;73;81 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. In particular, V190A and S210N were both specifically correlated with F220L (Phi = 0.30, P = 0.003 for both), while S204N showed positive correlation with L205P (Phi = 0.25) (Table 2). 2020 Emerging microbes & infections Result HBV V190A;S210N;F220L;S204N;L205P 15;25;70;116;155 20;30;75;121;160 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Interestingly, among the above-mentioned HBsAg mutations, S204N was the only detected with higher prevalence in patients with HBsAg<1000IU/ml than in those with HBsAg>1000IU/ml in HBV genotype A (100% for HBsAg<1000IU/ml versus 12.9% for HBsAg>1000IU/ml, P = 0.003) (Table S4. 2020 Emerging microbes & infections Result HBV S204N 58 63 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Notably, for the mutational pairs S204N + L205P, Y206F + S210R, Y206F + S204T and Y206F + M197T, the decrease in HBsAg release was significant also compared to the corresponding single mutation S204N (P < 0.001) or Y206F (P = 0.007, P = 0.001 and <0.0001, respectively) (Figure 4(A)). 2020 Emerging microbes & infections Result HBV S204N;L205P;Y206F;S210R;Y206F;S204T;Y206F;M197T;S204N;Y206F 34;42;49;57;64;72;82;90;194;215 39;47;54;62;69;77;87;95;199;220 S 113 118 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Similarly, considering the overall population of patients infected with HBV-genotype E, 6 patients were characterized by the presence of S204N (Table S4. 2020 Emerging microbes & infections Result HBV S204N 137 142 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. The single mutation S204N and S210N determined a 31% and 23% decrease in HBsAg release compared to wt (P = 0.004 and P = 0.001, respectively). 2020 Emerging microbes & infections Result HBV S204N;S210N 20;30 25;35 S 73 78 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Y206F showed multiple positive correlations with different HBsAg C-terminus mutations: V194A (phi = 0.23), M197T (phi = 0.32), S204T (phi = 0.26) and S210R (phi = 0.33) (Table 2). 2020 Emerging microbes & infections Result HBV Y206F;V194A;M197T;S204T;S210R 0;87;107;127;150 5;92;112;132;155 S 59 64 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Compare to reference sequences of genotype D and genotype C, several nucleotide (amino acid) positions changed in nearly all the HBV/CD1 and HBV/CD2 sequences, such as A942T(aaL613QH for HBV/CD1 and aaH613K for HBV/CD2), T1485A and T3210A(aaS272TN) in P gene, T1485C(aaS38P) in X gene. 2020 Virology journal Result HBV A942T;T1485A;T3210A;T1485C 168;221;232;260 173;227;238;266 P;X 252;278 253;279 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. In addition, T1753C, another mutation in BCP, was found at a frequency of 4.6% in CD1 and 18.4% in CD2 (P = 0.003). 2020 Virology journal Result HBV T1753C 13 19 BCP 41 44 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. In the level of nucleotide, the double mutations A1762T/G1764A in the BCP region of HBV (nt1742-1849) were frequently observed in HBV/CD sequences (50/179, 27.9%). 2020 Virology journal Result HBV G1764A;A1762T 56;49 62;55 BCP 70 73 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Nucleotide mutations, including A1984G, T150AC, A2735C, C2523G, A37G, C2712AT, and C1653T were dramatically different in CD1 and CD2, though these mutations were in the same recombination regions (genotype C or genotype D fragment). 2020 Virology journal Result HBV A1984G;T150A;T150C;A2735C;C2523G;A37G;C2712A;C2712T;C1653T 32;40;40;48;56;64;70;70;83 38;46;46;54;62;68;77;77;89 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Other mutations, including stop codon mutation G1896A, were identically detected in CD1 and CD2 isolates. 2020 Virology journal Result HBV G1896A 47 53 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. Analysis of polymerase gene sequences from baseline and follow-up samples showed the presence of resistance-associated mutations in 5 of these 6 patients, including L180M, A181T, M204I, and M204V (Table 5). 2020 Viruses Result HBV L180M;A181T;M204I;M204V 165;172;179;190 170;177;184;195 P 12 22 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. At baseline, patient ZA164 was HBsAg-positive with 7.67 x 103 IU/mL HBV DNA and the M204I variant. 2020 Viruses Result HBV M204I 84 89 S 31 36 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. At the final visit at 6 months, HBV DNA level had dropped to 2.42 x 103 IU/mL, the M204I variant was not detectable, and the patient was still HBsAg-positive. 2020 Viruses Result HBV M204I 83 88 S 143 148 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. Patient ZA113 had the L180M mutation and the L180M + M204V mutations at the 12- and 18-month follow-up visits, respectively, with HBV viremia increasing from 1.99 x 104 IU/mL at baseline to 7.08 x 106 at the 18-month follow-up. 2020 Viruses Result HBV L180M;L180M;M204V 22;45;53 27;50;58 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. Patient ZA131 was HBsAg-positive with undetectable HBV DNA levels at baseline, which increased to 3.39 x 102 IU/mL at 6 months with the M204I variant being detected. 2020 Viruses Result HBV M204I 136 141 S 18 23 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. An important point is that there are changes in exchange throughout the HBV Cp dimer when the tyrosine at position 132 is mutated to an alanine, consistent with the idea that this is an allosterically regulated protein. 2020 ACS chemical biology Result HBV Y132A 94 143 C 76 78 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. At later time points, the chassis has more exchange in the wCp149-Y132A mutant indicating that this region has a less stable secondary structure in the mutant. 2020 ACS chemical biology Result HBV Y132A 66 71 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. If an allosteric network connects the inter-dimer interface to the intra-dimer interface, we reasoned there should be differences in dynamics between the mutant Cp149-Y132A dimers and the wild type Cp149 dimers. 2020 ACS chemical biology Result HBV Y132A 167 172 C;C 161;198 163;200 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In support of this hypothesis, we observed by HDX-MS that the Y132A mutation led to differences in exchange that propagated throughout the entire structure (Figure 5, panel A; Supplemental movie 2 and 4). 2020 ACS chemical biology Result HBV Y132A 62 67 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In the HBV dimer, the site of the Y132A mutation was more flexible in the mutant and the chassis and fulcrum were more stable in the mutant. 2020 ACS chemical biology Result HBV Y132A 34 39 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In the wCp149 dimer, the residues near the Y132A mutation had an increase in exchange at early time points, but at later time points shows no difference in exchange when compared to wild type (Figure 5, panel A; Supplemental movies 3 and 5). 2020 ACS chemical biology Result HBV Y132A 43 48 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The hCp149-Y132A dimer was not significantly different from hCp149 dimer. 2020 ACS chemical biology Result HBV Y132A 11 16 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The hCp149-Y132A dimer was the least stable based on the changes in intensity from 20V to 120V followed by the hCp149, the wCp149-Y132A, and finally the wCp149. 2020 ACS chemical biology Result HBV Y132A;Y132A 11;130 16;135 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The similar melting temperatures between the wild type dimers and the mutant dimers indicates that the Y132A mutation has little effect on the overall thermal stability of the dimer. 2020 ACS chemical biology Result HBV Y132A 103 108 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The spike tip showed more exchange at earlier time points in the hCp149 dimer, but at three hours this trend switched and the hCp149-Y132A mutant took up more deuterium overall. 2020 ACS chemical biology Result HBV Y132A 133 138 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The spike tip shows more exchange in the wCp149-Y132A mutant than in the wCp149 dimer indicating that the mutation destabilizes the hydrogen bond network on the other side of the protein. 2020 ACS chemical biology Result HBV Y132A 48 53 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The Y132A mutation lowered the intra-dimer interface stability for both human and woodchuck dimers. 2020 ACS chemical biology Result HBV Y132A 4 9 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Thermal stability melting curves were generated for the dimers: hCp149, hCp149-Y132A, wCp149, and wCp149-Y132A. 2020 ACS chemical biology Result HBV Y132A;Y132A 79;105 84;110 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. This suggests that the spike has at least two populations of amides, fast and slow exchanging, that respond differently to the distal Y132A mutation. 2020 ACS chemical biology Result HBV Y132A 134 139 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. The results of our amino acid sequences of the preS/S gene compared to consensus genes showed several mutations at position L109R, T113S, K122R, T126N, N131T, F134Y, P142L, W163R and R169P of the major hydrophilic region (MHR). 2020 Heliyon Result HBV L109R;T113S;K122R;T126N;N131T;F134Y;P142L;W163R;R169P 124;131;138;145;152;159;166;173;183 129;136;143;150;157;164;171;178;188 PreS;S 47;52 51;53 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Among the two later cases, there were 3 classical mt including rtM204V/I (primary drug resistance mt) and rtL180M (compensatory/secondary mt). 2020 Diagnostics (Basel, Switzerland) Result HBV M204I;M204V;L180M 65;65;108 72;72;113 RT;RT 63;106 65;108 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Among these above 94 cases, there were 11 cases carrying additional mt that are not related to drug resistance, such as rtI187V (+ rtV207M) x 2 cases, rtI187V (+ rtS213T), rtI187V (+ rtP237T), rtI187V (+ rtL229V), rtI187V (+ rtV207M + rtS213T + rtS256G), rtK212T (+ rtV207I + rtV207M), rtV253I (+ rtV207M), rtV253I (+ rtN238A) x 2 cases, and rtL235V (+ rtV207M + rtL229V). 2020 Diagnostics (Basel, Switzerland) Result HBV I187V;I187V;I187V;I187V;I187V;N238A;V207M;S213T;P237T;L229V;V207M;S213T;S256G;K212T;V207I;V207M;V253I;V207M;V253I;L235V;V207M;L229V 122;153;174;195;216;320;133;164;185;206;227;237;247;257;268;278;288;299;309;344;355;365 127;158;179;200;221;325;138;169;190;211;232;242;252;262;273;283;293;304;314;349;360;370 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 120;131;151;162;172;183;193;204;214;225;235;245;255;266;276;286;297;307;318;342;353;363 122;133;153;164;174;185;195;206;216;227;237;247;257;268;278;288;299;309;320;344;355;365 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. During analysis of the sequencing chromatograms for 92 cases having NA drug-resistance-associated mt, we found 2 representative cases carrying mt rtV207I (G750A) and mt rtV207I (G750T) which have the minor (mt) peaks constituting <= 20% of major (wt) peaks at rt positions. 2020 Diagnostics (Basel, Switzerland) Result HBV V207I;V207I;G750A;G750T 148;171;155;178 153;176;160;183 RT;RT;RT 146;169;260 148;171;262 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Figure 3 shows nucleotide peaks of conventional PCR and COLD-PCR products using templates as the mt:wt mixture controls of the wt and individual mt including rtA194T, rtM204I, and rtN236T locating at the respective domains B, C, and D of HBV RT. 2020 Diagnostics (Basel, Switzerland) Result HBV N236T;A194T;M204I 182;160;169 187;165;174 RT;RT;RT;RT 158;167;180;242 160;169;182;244 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. In addition, 23 cases had only mt that are not related to drug resistance, such as rtI187V x 20 cases, rtV253I, rtS256C, and rtI187V + rtN248H. 2020 Diagnostics (Basel, Switzerland) Result HBV N248H;I187V;V253I;S256C;I187V 137;85;105;114;127 142;90;110;119;132 RT;RT;RT;RT;RT 83;103;112;125;135 85;105;114;127;137 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. In contrast, the COLD-PCR method successfully enriched the mt population, resulting in higher mt peaks and a 5% mt/wt ratio detection level for the rtA194T (G709A), rtM204I (G741T), and rtN236T (A836C) mt. 2020 Diagnostics (Basel, Switzerland) Result HBV A194T;M204I;N236T;G709A;G741T;A836C 150;167;188;157;174;195 155;172;193;162;179;200 RT;RT;RT 148;165;186 150;167;188 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. More specifically, 85 cases (59.9%) had mt causing a single amino acid substitution associated with LMV and/or ADF resistance, the most frequent being rtV207M (54 cases; 38.0%), followed by rtN238T (14 cases; 9.9%); rtN238A (8 cases; 5.6%); rtV207L (2 cases; 1.4%); rtS213T (2 cases; 1.4%); rtS256G (2 cases; 1.4%); and rtL229V, rtP237T, and rtN238K in 1 case each (0.7%). 2020 Diagnostics (Basel, Switzerland) Result HBV V207M;N238T;N238A;N238K;V207L;S213T;S256G;L229V;P237T 153;192;218;344;243;268;293;322;331 158;197;223;349;248;273;298;327;336 RT;RT;RT;RT;RT;RT;RT;RT;RT 151;190;216;241;266;291;320;329;342 153;192;218;243;268;293;322;331;344 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Multiple-point mt associated with LMV or ADF resistance were observed in 9 cases (6.3%), 6 cases carried double mt (rtV207M + rtS213T; rtV207M + rtL229V; rtV207M + rtI233V; rtV207I + rtV207M x 2 cases; rtN238A + rtS256G), 2 cases carried triple mt (rtL180M + rtM204I + rtN238T; rtV207M + rtS213T + rtS256G), and 1 case carried quadruple mt (rtL180M + rtM204V + rtV207I + rtV207M). 2020 Diagnostics (Basel, Switzerland) Result HBV N238A;M204V;V207M;S213T;V207M;L229V;V207M;I233V;V207I;V207M;S256G;L180M;M204I;N238T;V207M;S213T;S256G;L180M;V207I;V207M 204;353;118;128;137;147;156;166;175;185;214;251;261;271;280;290;300;343;363;373 209;358;123;133;142;152;161;171;180;190;219;256;266;276;285;295;305;348;368;378 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 116;126;135;145;154;164;173;183;202;212;249;259;269;278;288;298;341;351;361;371 118;128;137;147;156;166;175;185;204;214;251;261;271;280;290;300;343;353;363;373 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Our data confirms that the two samples are really positive mt rtV207I (G750A) and mt rtV207I (G750T). 2020 Diagnostics (Basel, Switzerland) Result HBV V207I;V207I;G750A;G750T 64;87;71;94 69;92;76;99 RT;RT 62;85 64;87 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. the intensities of fluorescent curves in both samples were much higher than that of the control (0.88 vs. 0.46 for G750A; 1.32 vs. 0.85 for G750T) and that the Ct聽values of both samples were smaller than that of the control (26.14 vs. 33.96 for mt G750A; 25.51 vs. 28.47 for G750T). 2020 Diagnostics (Basel, Switzerland) Result HBV G750A;G750T;G750T;G750A 115;140;275;248 120;145;280;253 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. As expected, HBeAg expression differed with the greatest levels in the wild-type HBV and clearly reduced levels in the A1762T/G1764A double mutant (Figure 1A). 2020 Frontiers in microbiology Result HBV G1764A;A1762T 126;119 132;125 C 13 18 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Further, an evaluation of APOBEC3G protein levels by immunoblot showed increased amounts in wild type compared to the mock and HBV X/BCP/PC variants (Figure 3A) which was confirmed with densitometry analysis (p-values: vs. mock = 0.0414; vs. G1896A = 0.0205; vs. A1762T/G1764A = 0.0058). 2020 Frontiers in microbiology Result HBV G1764A;G1896A;A1762T 270;242;263 276;248;269 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Interestingly, the A1762T/G1764A double mutation HBV has consistently higher levels of supernatant HBV DNA (p-value = 0.0363) and HBV RNA (p-value = 0.0220) in comparison to G1896A HBV variant. 2020 Frontiers in microbiology Result HBV G1764A;A1762T;G1896A 26;19;174 32;25;180 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. It is interesting to note that both of the X/BCP/PC variants lead to suppression of this cytokine in comparison to wild-type (p-values: vs. G1896A = 0.0509; vs. A1762T/G1764A = 0.0157;聽Figure 3C). 2020 Frontiers in microbiology Result HBV G1764A;G1896A;A1762T 168;140;161 174;146;167 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Similarly, the analyzed cytokines/chemokines were comparable in the individuals with predominantly G1896A variant (Supplementary Figures S6, S7). 2020 Frontiers in microbiology Result HBV G1896A 99 105 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. In the present study, the rt134 and rt153 variants led to the concomitant occurrence of "a" determinant mutations, including sT126A (n=5), sT126S (n=2), sT126N (n=1), and sG145R (n=1). 2020 Infection and drug resistance Result HBV T126A;T126S;T126N;G145R 125;139;153;171 131;145;159;177 RT;RT;S;S;S;S 26;36;125;139;153;171 28;38;126;140;154;172 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Primary and/or secondary DR variants were found in 7.3% (15/206) of patients, and included rtL80I/V, rtI169T, rtV173L, rtL180M, rtA181T/V, rtM204I/V, and rtN236T. 2020 Infection and drug resistance Result HBV L80I;L80V;I169T;V173L;L180M;A181T;A181V;M204I;M204V;N236T 93;93;103;112;121;130;130;141;141;156 99;99;108;117;126;137;137;148;148;161 RT;RT;RT;RT;RT;RT;RT 91;101;110;119;128;139;154 93;103;112;121;130;141;156 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. Because the entire S gene is embedded within the viral polymerase gene, some viral polymerase mutations that confer drug resistance can cause amino acid sequence changes in HBsAg; major ones include E164D, W172L, L173F, I195M and W196L/S/V. 2020 PloS one Result HBV W196L;W196S;W196V;E164D;W172L;L173F;I195M 230;230;230;199;206;213;220 239;239;239;204;211;218;225 S;P;P;S 173;55;83;19 178;65;93;20 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. C149R was not detectable by any of the three antibodies, suggesting a critical role of this cysteine residue in the expression of S antigens. 2020 PloS one Result HBV C149R 0 5 S 130 131 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. D144A and D144E also shared this feature. 2020 PloS one Result HBV D144A;D144E 0;10 5;15 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. G145K and G145R, well-known immune escape mutants, both showing low expression, also showed a consistent binding to Lenvervimab. 2020 PloS one Result HBV G145K;G145R 0;10 5;15 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. In contrast, the polyclonal anti-HBsAg antibody signal was severely reduced in several mutants within the 2nd loop of 'a' determinant, such as K141I, P142L/S, D144A/E, G145K/R, N146S and T148I. 2020 PloS one Result HBV K141I;P142L;P142S;D144A;D144E;G145K;G145R;N146S;T148I 143;150;150;159;159;168;168;177;187 148;157;157;166;166;175;175;182;192 S;S 119;33 133;38 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. It was notable that K141E and K141I, despite their difference in expression levels (i.e., anti-HA antibody signals), both bind coherently to Lenvervimab. 2020 PloS one Result HBV K141E;K141I 20;30 25;35 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. N146S showed a comparable binding to both antibodies. 2020 PloS one Result HBV N146S 0 5 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. The most common and stable one is G145R, the postvaccination immune escape mutant first found in a child born from a carrier mother. 2020 PloS one Result HBV G145R 34 39 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. We also found that Lenvervimab does not bind K160N. 2020 PloS one Result HBV K160N 45 50 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. We found that these mutations, either alone or in combination of doubles, do not affect Lenvervimab binding with the exceptions of E164A/D/G/V (Fig 6). 2020 PloS one Result HBV E164A;E164D;E164G;E164V 131;131;131;131 142;142;142;142 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. rtM204I/sW196* Resulted in an Enhanced Transactivation of Proto-Oncogenes, Increased Cell Proliferation, and Decreased Apoptosis, but Did Not Elicit an Endoplasmic Reticulum (ER) Stress Response. 2020 International journal of molecular sciences Result HBV W196X;M204I 8;2 14;7 RT;S 0;8 2;9 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. rtM204I/sW196* Resulted in More Anchorage-Independent Growth and Enhanced Mouse Xenograft Tumorigenesis. 2020 International journal of molecular sciences Result HBV W196X;M204I 8;2 14;7 RT;S 0;8 2;9 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The rtM204I/sW196* (YIDDst) plasmid was constructed via a PCR-based site-directed mutagenesis method, and the sequence was confirmed by Sanger sequencing, as shown in Figure 1A. 2020 International journal of molecular sciences Result HBV W196X;M204I 12;6 18;11 RT;S 4;12 6;13 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Additional substitutions were observed in the upper regulatory region (URR) and BCP regions: patient 2C carried the HBV URR mutant G1728A and BCP mutant G1764T/C1766G, and HBV from patients 6C and 7C carried BCP T1768A and URR C1678T mutants, respectively. 2020 PloS one Result HBV C1766G;G1728A;G1764T;T1768A;C1678T 160;131;153;212;227 166;137;159;218;233 BCP;BCP;BCP 80;142;208 83;145;211 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Amino acid changes including rtL80I, rtV173L, rtL180M, rtV191I and rtM204I/V in the reverse transcriptase (RT) region of the pol gene, and sE164D, sW182*, sI195M and sW196LS in the overlapping small HBsAg (SHB) region were identified in all eight children. 2020 PloS one Result HBV L80I;V173L;L180M;V191I;M204I;M204V;E164D;W182X;I195M 31;39;48;57;69;69;139;147;155 35;44;53;62;76;76;145;153;161 S;P;RT;RT;RT;RT;RT;RT;RT;S;S;S;S;S 199;125;84;29;37;46;55;67;107;139;147;155;166;206 204;128;105;31;39;48;57;69;109;140;148;156;167;209 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Pre-C genomic changes were found in three samples: G1862T in sample 2C, and mixed populations of stop codon G1896A mutant and wild-type virus (W28*W) in samples 3C and 6C. 2020 PloS one Result HBV W28X;G1862T;G1896A 143;51;108 147;57;114 Precore 0 5 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. However, patient No.6 was found to have mutations of Gln129Arg (Q129R), Thr131Asn (T131N), Met133Ser (M133S), Phe134Leu (F134L) and Asp144Glu (D144E) in the "a" determinant of HBsAg (Figure 2, Table 3). 2020 International journal of medical sciences Result HBV Q129R;Q129R;T131N;T131N;M133S;M133S;F134L;F134L;D144E;D144E 53;64;72;83;91;102;110;121;132;143 62;69;81;88;100;107;119;126;141;148 S 176 181 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. A multivariate analysis showed that age and the coexistence of ADV-r/LAM-r mutations were independently associated with the sA159V mutation. 2020 World journal of gastroenterology Result HBV A159V 124 130 S 124 125 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Clinical incidence and features of the sA159V mutation. 2020 World journal of gastroenterology Result HBV A159V 39 45 S 39 40 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Five representative sA159V-positive patients with available serial serum samples were subjected to clonal analysis of HBV RT/S genes. 2020 World journal of gastroenterology Result HBV A159V 20 26 RT;S 122;20 124;21 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In both patients, the sA159V mutant existed before virological breakthrough (samples C-S1 and D-S1), and sA159V-containing ADV-resistant mutants were dominant in samples C-S2 and D-S2 at virological breakthrough (Figure 1C and D). 2020 World journal of gastroenterology Result HBV A159V;A159V 22;105 28;111 S;S 22;105 23;106 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In contrast, LAM-resistant mutants (M2-M5) and ETV-resistant mutants (M6-M7) were highly resistant to LAM, regardless of the presence or absence of the sA159V mutation in the viral genome (Figure 5A). 2020 World journal of gastroenterology Result HBV A159V 152 158 S 152 153 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In contrast, the detection rate of sA159G did not differ significantly between the two patient groups (1.25% (87/6982) vs 1.48% (185/12458), P > 0.05). 2020 World journal of gastroenterology Result HBV A159G 35 41 S 35 36 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In particular, mutations were detected in 67/63/168 of 298 sQ101H/K/R-positive patients, 39/2/76 of 117 sS114A/L/T-positive patients, 5/5/15/3/1/2 of 31 sT118A/K/M/R/S/V-positive patients, 3/0/0/23/81 of 107 sP120A/L/Q/S/T-positive patients, 94/58/0/214 of 366 sT/I126A/N/P/S-positive patients, 14/46/136 of 196 sM133I/L/T-positive patients, 1/8 of 9 sC137W/Y-positive patients, 77/46 of 123 sG145A/R-positive patients, and 87/136 of 223 sA159G/V-positive patients. 2020 World journal of gastroenterology Result HBV T126A;T126N;T126P;T126S;I126A;I126N;I126P;I126S;Q101H;Q101K;Q101R;S114A;S114L;S114T;T118A;T118K;T118M;T118R;T118S;T118V;P120A;P120L;P120Q;P120S;P120T;M133I;M133L;M133T;C137W;C137Y;G145A;G145R;A159G;A159V 261;261;261;261;261;261;261;261;59;59;59;104;104;104;153;153;153;153;153;153;209;209;209;209;209;313;313;313;351;351;392;392;438;438 275;275;275;275;275;275;275;275;69;69;69;114;114;114;169;169;169;169;169;169;222;222;222;222;222;322;322;322;359;359;400;400;446;446 S;S;S;S;S;S;S;S;S 59;104;153;208;261;312;351;392;438 60;105;154;209;262;313;352;393;439 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In sample A-S3, sA159V+rtL180M+rtM204V+rtT184L was the most abundant (Figure 1A). 2020 World journal of gastroenterology Result HBV L180M;M204V;T184L;A159V 25;33;41;16 30;38;46;22 RT;RT;RT;S 23;31;39;16 25;33;41;17 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In tested clones of sample A-S1, WT, sA159V, sQ129R, and rtM204I detection rates were 80%, 10%, 5%, and 5%, respectively. 2020 World journal of gastroenterology Result HBV M204I;A159V;Q129R 59;37;45 64;43;51 RT;S;S 57;37;45 59;38;46 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Patient B had seven sA159V-containing mutants in samples B-S1 and B-S2 during ETV therapy. 2020 World journal of gastroenterology Result HBV A159V 20 26 S 20 21 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Resistant mutants were subsequently suppressed by ETV+ADV, whereas the sA159V mutation was observed in sample B-S3 (Figure 1B). 2020 World journal of gastroenterology Result HBV A159V 71 77 S 71 72 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Restricted by the scale of the study, sA159V was selected as a representative immune escape-associated mutation for further analyses. 2020 World journal of gastroenterology Result HBV A159V 38 44 S 38 39 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. sA159V+rtL180M+rtM204V (35%), rtL180M+rtM204V (35%), sA159V+rtM204I (15%), sA159V+rtL180M+rtM204I (5%), sA159V+rtM204V (5%), and rtM204I (5%). 2020 World journal of gastroenterology Result HBV L180M;M204V;L180M;M204V;M204I;L180M;M204I;M204V;M204I;A159V;A159V;A159V;A159V 9;17;32;40;62;84;92;113;131;0;53;75;104 14;22;37;45;67;89;97;118;136;6;59;81;110 RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S 7;15;30;38;60;82;90;111;129;0;53;75;104 9;17;32;40;62;84;92;113;131;1;54;76;105 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Samples from Patient E included three sA159V-containing ETV/LAM-resistant mutants (sample E-S2) when the virological response was inadequate upon ETV+TDF therapy (Figure 1E). 2020 World journal of gastroenterology Result HBV A159V 38 44 S 38 39 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The clinical features of the sA159V-positive and sA159V-negative patients are summarized in Table 3. 2020 World journal of gastroenterology Result HBV A159V;A159V 29;49 35;55 S;S 29;49 30;50 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The detection rate of sA159V was significantly higher in patients with resistance mutations than in patients lacking resistance mutations [1.95% (136/6982) vs 1.08% (134/12458), P < 0.05]. 2020 World journal of gastroenterology Result HBV A159V 22 28 S 22 23 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The sA159V-positive patients had higher rates of coexisting drug-resistance mutations than the sA159V-negative patients. 2020 World journal of gastroenterology Result HBV A159V;A159V 4;95 10;101 S;S 4;95 5;96 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. These mutations were sQ101H/K/R, sS114A/L/T, sT118A/K/M/R/S/V, sP120A/L/Q/S/T, sT/I126A/N/P/S, sM133I/L/T, sC137W/Y, sG145A/R, and sA159G/V. 2020 World journal of gastroenterology Result HBV T126A;T126N;T126P;T126S;I126A;I126N;I126P;I126S;Q101H;Q101K;Q101R;S114A;S114L;S114T;T118A;T118K;T118M;T118R;T118S;T118V;P120A;P120L;P120Q;P120S;P120T;M133I;M133L;M133T;C137W;C137Y;G145A;G145R;A159G;A159V 80;80;80;80;80;80;80;80;21;21;21;33;33;33;45;45;45;45;45;45;63;63;63;63;63;95;95;95;107;107;117;117;131;131 93;93;93;93;93;93;93;93;31;31;31;43;43;43;61;61;61;61;61;61;77;77;77;77;77;105;105;105;115;115;125;125;139;139 S;S;S;S;S;S;S;S;S 21;33;45;63;79;95;107;117;131 22;34;46;64;80;96;108;118;132 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Three sA159V-containing resistant mutants had significantly higher replication capacities than their sA159V-lacking counterparts (M2 vs M3, M4 vs M5, M6 vs M7, all P < 0.05) (Figure 4). 2020 World journal of gastroenterology Result HBV A159V;A159V 6;101 12;107 S;S 6;101 7;102 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Three sA159V-containing resistant mutants had significantly lower HBsAg levels than their sA159V-lacking counterparts (M2 vs M3, M4 vs M5, M6 vs M7, all P < 0.05) (Figure 3). 2020 World journal of gastroenterology Result HBV A159V;A159V 6;90 12;96 S;S;S 66;6;90 71;7;91 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. In addition, polymorphism I195V within the S gene for all the samples was also detected in OBI individuals belonging to genotype A1 (Table II, Figs 2-3). 2020 Memorias do Instituto Oswaldo Cruz Result HBV I195V 26 31 S 43 44 Occult Hepatitis B 91 94 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. One escape mutation (T123A) associated with OBI in one sample was observed. 2020 Memorias do Instituto Oswaldo Cruz Result HBV T123A 21 26 Occult Hepatitis B 44 47 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. After the implementation of GCAC1809-1812TTCT in addition to A1762T/G1764A (Figure 5C), the RNA secondary structure was stabilized by a hairpin structure and the MFE decreased approximately to the WT level (-69.1 kcal/mol; GC content of 46%). 2020 JCI insight Result HBV G1764A;A1762T 68;61 74;67 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Although this mutation was found in 66% (226 of 340) of the samples with A1762T/G1764A, in samples without A1762T/G1764A, the GCAC1809-1812TTCT variant was detected only in 3% (7 of 220) of the samples (Figure 1B). 2020 JCI insight Result HBV G1764A;G1764A;A1762T;A1762T 80;114;73;107 86;120;79;113 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. An HBV genome was isolated from a serum sample of 1 patient infected with HBV GTA harboring both A1762T/G1764A and GCAC1809-1812TTCT and this genome was cloned as a 1.2-mer into pUC vector. 2020 JCI insight Result HBV G1764A;A1762T 104;97 110;103 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. As described above, GCAC1809-1812TTCT is highly prevalent in inactive carriers and strongly associated with BCP double mutation A1762T/G1764A. 2020 JCI insight Result HBV G1764A;A1762T 135;128 141;134 BCP 108 111 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Besides a high prevalence of A1762T/G1764A in 61% (340 of 560) of the samples, we observed that additional mutations in the Kozak sequence at position nt1809-1812 directly preceding the precore start codon were found in 51% (283 of 560) of the samples (Figure 1A). 2020 JCI insight Result HBV G1764A;A1762T 36;29 42;35 Precore 186 193 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. GCAC1809-1812TTCT in combination with BCP double mutation A1762T/G1764A was associated with significantly lower HBV DNA levels (2.51 log IU/mL vs. 2020 JCI insight Result HBV G1764A;A1762T 65;58 71;64 BCP 38 41 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. GCAC1809-1812TTCT was highly prevalent in inactive carriers and strongly associated with BCP double mutation A1762T/G1764A. 2020 JCI insight Result HBV G1764A;A1762T 116;109 122;115 BCP 89 92 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Here, we observed that HBeAg levels were moderately but not significantly decreased in cells expressing genomes with the BCP double mutation A1762T/G1764A located in the promoter region (BCP1 and BCP3). 2020 JCI insight Result HBV G1764A;A1762T 148;141 154;147 BCP;BCP;BCP;C 121;187;196;23 124;190;199;28 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. However, the introduction of GCAC1809-1812TTCT without A1762T/G1764A (Figure 5D) resulted in a calculated MFE (-69.2 kcal/mol; GC content of 47%), which is comparable to the thermodynamic stability of the WT sequence. 2020 JCI insight Result HBV G1764A;A1762T 62;55 68;61 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. in comparison with A1762T/G1764A without GCAC1809-1812TTCT and in comparison with samples without any of these mutations (Figure 1D). 2020 JCI insight Result HBV G1764A;A1762T 26;19 32;25 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. In contrast, A1762T/G1764A alone without GCAC1809-1812TTCT was not associated with changes in HBV DNA levels. 2020 JCI insight Result HBV G1764A;A1762T 20;13 26;19 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. In contrast, non-TTCT mutations at position nt1809-1812 were not associated with the BCP double mutation A1762T/G1764A (Figure 1B). 2020 JCI insight Result HBV G1764A;A1762T 112;105 118;111 BCP 85 88 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Overall, the A1762T/G1764A mutation was found in the vast majority of samples (65%, 81 of 125). 2020 JCI insight Result HBV G1764A;A1762T 20;13 26;19 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. The calculated MFE of the A1762T/G1764A containing pgRNA appeared to be higher (-66.7 kcal/mol; GC content of 47%) in comparison with pgRNA lacking this mutation (-68.9 kcal/mol; GC content of 48%). 2020 JCI insight Result HBV G1764A;A1762T 33;26 39;32 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. The presence of GCAC1809-1812TTCT was strongly associated with the coexistence of BCP double mutation A1762T/G1764A (Figure 1B). 2020 JCI insight Result HBV G1764A;A1762T 109;102 115;108 BCP 82 85 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. The specificity of the blot was proven by using an additional genome containing the precore double mutation G1896A/G1899A, which was used as an additional HBeAg negative control, and by using an HBeAg positive WT genome as a positive control (Figure 3A). 2020 JCI insight Result HBV G1899A;G1896A 115;108 121;114 C;C;Precore 155;195;84 160;200;91 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. These data suggest that while the introduction of A1762T/G1764A leads to a slight destabilization of the pgRNA secondary structure, GCAC1809-1812TTCT might restore the thermodynamic stability of the pgRNA. 2020 JCI insight Result HBV G1764A;A1762T 57;50 63;56 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. We calculated that the RNA secondary structure of the A1762T/G1764A containing pgRNA is thermodynamically less stable with an increase in the minimum free energy (MFE) value of 2.2 kcal/mol compared with the WT pgRNA secondary structure (Figure 5, A and B). 2020 JCI insight Result HBV G1764A;A1762T 61;54 67;60 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. With respect to our clinical data, the variants harboring the GCAC1809-1812TTCT mutation (TTCT1-3) contain the additional A1762T/G1764A mutation. 2020 JCI insight Result HBV G1764A;A1762T 129;122 135;128 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. A steric hindrance between HBV RT deoxynucleoside triphosphate (dNTP) binding pocket and ETV-TP was illustrated in the molecular model of HBV RT containing rtM204V, while the introduction of rtL229V modified the conformation of side chain, thus to presumably cause an alteration of the spatial relationship between HBV RT and ETV-TP (Figure 5(A-D)). 2020 Emerging microbes & infections Result HBV M204V;L229V 158;193 163;198 RT;RT;RT;RT;RT 31;142;156;191;319 33;144;158;193;321 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. After scrutinizing the frequency of mutations within these sites, only two NA-r mutations, ntG700A (rtV191I, P = 0.014) and ntC671T (rtA181T/V, P = 0.048) from treatment-naive and post-treatment samples, respectively, were identified as genotype-specific mutations (Figure 3(C-D)). 2020 Emerging microbes & infections Result HBV A181T;A181V;V191I;G700A;C671T 135;135;102;92;125 142;142;107;98;131 RT;RT 100;133 102;135 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. As a result, mutated RT of both rtM204V and rtM204V + rtL229V showed restricted binding affinity to LMV-TP, since binding at lower potential energy creates a more stable structure. 2020 Emerging microbes & infections Result HBV M204V;M204V;L229V 34;46;56 39;51;61 RT;RT;RT;RT 21;32;44;54 23;34;46;56 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. As a result, the frequency of rtL229V/M/F among the post-treatment populations tended to be significantly higher than that among treatment-naive ones (P = 0.029), which indicated a similar distribution as compared with the other four primary and secondary resistance mutations (Figure 4(B)). 2020 Emerging microbes & infections Result HBV L229V;L229M;L229F 32;32;32 41;41;41 RT 30 32 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Binding energy to ETV-TP slightly increased by HBV RT containing rtM204V, while this RT with an addition of rtL229V displayed a binding energy rise of 0.29, suggesting that the introduction of the rtL229V mutation accompanied by rtM204V might restrict ETV-TP binding site to further cause a resistance to ETV. 2020 Emerging microbes & infections Result HBV M204V;L229V;L229V;M204V 67;110;199;231 72;115;204;236 RT;RT;RT;RT;RT;RT 51;65;85;108;197;229 53;67;87;110;199;231 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Effects of rtL229V on HBV replication and antiviral susceptibility. 2020 Emerging microbes & infections Result HBV L229V 13 18 RT 11 13 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Figure 5 displays the three-dimensional structure of the wild-type HBV RT and the HBV RT binding domain harboring different mutations of rtM204V and rtM204V + rtL229V. 2020 Emerging microbes & infections Result HBV M204V;M204V;L229V 139;151;161 144;156;166 RT;RT;RT;RT;RT 71;86;137;149;159 73;88;139;151;161 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Five AA sites identified with the significantly elevated entropy levels were rtL180M, rtA181T/V/I, rtM204I/V/L, rtL229V/M/F, rtN236T/I, four of which had been widely known already as classical resistance mutation. 2020 Emerging microbes & infections Result HBV A181T;A181V;A181I;M204I;M204V;M204L;L229V;L229M;L229F;N236T;N236I;L180M 88;88;88;101;101;101;114;114;114;127;127;79 97;97;97;110;110;110;123;123;123;134;134;84 RT;RT;RT;RT;RT 77;86;99;112;125 79;88;101;114;127 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Five mutations: ntA753T/G, ntC876T, ntA894G/C occurred with the rates up to more than 10% in both treatment-naive group and post-treatment group. 2020 Emerging microbes & infections Result HBV A753T;A753G;C876T;A894G;A894C 17;17;28;37;37 25;25;34;45;45 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. For instance, ntA753T/G, ntC787A/G, ntA805C/T, ntA894G/C were significantly more correlated with genotype B (P < 0.05), while ntC/T724G, ntT820C, ntC837T, ntT840C, ntA852G, ntC873T, ntC876T were significantly more associated with genotype C (P < 0.05). 2020 Emerging microbes & infections Result HBV T724G;A753T;A753G;C787A;C787G;A805C;A805T;A894G;A894C;T820C;C837T;T840C;A852G;C873T;C876T 128;15;15;26;26;37;37;48;48;138;147;156;165;174;183 135;23;23;34;34;45;45;56;56;144;153;162;171;180;189 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. From these measurements we concluded that rtL229V mutants inhibited the antiviral susceptibility of LMV at a consistent level with the other classical LMV-resistance mutation, and further conferred resistance to ETV when accompanied by the additional rtM204V mutation simultaneously. 2020 Emerging microbes & infections Result HBV L229V;M204V 44;253 49;258 RT;RT 42;251 44;253 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Most of the patients with the colocalization of rtM204V/I + rtL229 V/M/F mutations experienced significant virological breakthrough (increased HBV DNA level of 2.3~7.9 log10 IU/ml, patients with low drug compliance excluded) and had a history of prolonged LMV exposure prior to the detection of the resistance mutations. 2020 Emerging microbes & infections Result HBV M204V;M204I;L229V;L229M;L229F 50;50;62;62;62 57;57;72;72;72 RT;RT 48;60 50;62 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Only 1.1% (3 of 285, rtA181T/rtM204V/rtL180M + rtM204I) of HBV isolates harboring classical primary or secondary resistance mutation were observed among treatment-naive patients. 2020 Emerging microbes & infections Result HBV A181T;M204V;L180M;M204I 23;31;39;49 28;36;44;54 RT;RT;RT;RT 21;29;37;47 23;31;39;49 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Plasmid expression vectors harboring single mutation rtL229V, rtM204V and combination mutation rtL229V + rtM204V were constructed by site-directed mutagenesis from the wild-type plasmid. 2020 Emerging microbes & infections Result HBV L229V;M204V;L229V;M204V 55;64;97;107 60;69;102;112 RT;RT;RT;RT 53;62;95;105 55;64;97;107 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Putative resistance mutations were observed at 8 AA sites among the panel of treatment-naive patients; they were rtV191I, rtS213T, rtV214A, rtE218D, rtL229V, rtI233V, rtN238S, rtS/C256G. 2020 Emerging microbes & infections Result HBV C256G;N238S;S256G;V191I;S213T;V214A;E218D;L229V;I233V 178;169;178;115;124;133;142;151;160 185;174;185;120;129;138;147;156;165 RT;RT;RT;RT;RT;RT;RT;RT 113;122;131;140;149;158;167;176 115;124;133;142;151;160;169;178 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Starting with the rtL229V single mutation, resistance to LMV began to appear and increased >1000-fold (IC50>10 muMu) in contrast to wild-type (Table S4). 2020 Emerging microbes & infections Result HBV L229V 20 25 RT 18 20 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Table 2 displays the rtL229V/M/F isolates with the characteristics of genotype, drug usage, viral load and the virological response to drug. 2020 Emerging microbes & infections Result HBV L229V;L229M;L229F 23;23;23 32;32;32 RT 21 23 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The classical NA-r mutations rtL180M (ntT/C667A) and rtM204V/I (ntA739G or ntG741T/A), were treatment-specific and were preferentially present in post-treatment patients. 2020 Emerging microbes & infections Result HBV C667A;M204V;M204I;L180M;A739G;G741T;G741A 40;55;55;31;65;76;76 47;62;62;36;71;84;84 RT;RT 29;53 31;55 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The decreased susceptibility to ETV with rtL229V + rtM204V was 25.7-fold as compared with the wild-type, which could be recognized as drug resistance, but was relatively weaker than that observed with rtL229V or rtM204V-transfected cells exposed to LMV. 2020 Emerging microbes & infections Result HBV M204V;L229V;L229V;M204V 53;43;203;214 58;48;208;219 RT;RT;RT;RT 41;51;201;212 43;53;203;214 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The level of HBsAg, HBeAg, and HBV DNA from Bel-7404 cells transfected with the rtL229V mutants was significantly lower than that of those with the wild-type plasmid, suggesting that the presence of the rtL229V single mutation might reduce viral replication and production of HBV antigen. 2020 Emerging microbes & infections Result HBV L229V;L229V 82;205 87;210 C;S;RT;RT 20;13;80;203 25;18;82;205 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The results from 285 samples revealed that 14 nucleotide sites might be genotype-dependent within HBV RT region, that is, T or C at nt667 and nt864, C or T at nt724 and nt843, A or T at nt791, nt855 and nt861, G or A at nt793 and nt799, G or T at nt796,A or G at nt834, C or A at nt841, A or C at nt849 and nt853 were significantly correlated with genotype B or genotype C respectively (P < 0.0001) (supplementary data: Table S1). 2020 Emerging microbes & infections Result HBV T796A 242 254 RT 102 104 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The results revealed a relatively higher frequency of the mutation rtL229V (5/10, 50%) than rtL229M or rtL229F, and a correlation between rt229 substitutions and AA changes at rt204 or rt180 (6/10, 60%). 2020 Emerging microbes & infections Result HBV L229V;L229M;L229F 69;94;105 74;99;110 RT;RT;RT;RT;RT;RT 67;92;103;138;176;185 69;94;105;140;178;187 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The rtM204V + rtL229V mutants impaired HBV DNA at similar levels to the rtL229V single mutants, while no significance was observed in HBsAg and HBeAg decrease between the combination mutants and wild-type (Figure 6(A)). 2020 Emerging microbes & infections Result HBV M204V;L229V;L229V 6;16;74 11;21;79 C;S;RT;RT;RT 144;134;4;14;72 149;139;6;16;74 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. There was no in-vitro resistance to ETV for either single mutation rtL229V or rtM204V, which had IC50 values of 0.008 and 0.020 muM (1.0-fold and 2.5-fold), respectively. 2020 Emerging microbes & infections Result HBV M204V;L229V 80;69 85;74 RT;RT 67;78 69;80 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. To assess the efficacy of rtL229V mutation, in-vitro assays for wild-type HBV and mutants were performed. 2020 Emerging microbes & infections Result HBV L229V 28 33 RT 26 28 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. To investigate the clinical profile of rtL229 substitution, we analyzed the rtL229V/M/F isolates from a cohort of 214 post-treatment patients. 2020 Emerging microbes & infections Result HBV L229V;L229M;L229F 78;78;78 87;87;87 RT;RT 39;76 41;78 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. As HBV genotype G permanently harbours C1817T and G1896A nonsense mutations in the precore region, this genotype should be incapable of HBeAg production. 2021 Emerging microbes & infections Result HBV C1817T;G1896A 39;50 45;56 C;Precore 136;83 141;90 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. HBV strains harbouring G1896A could not produce detectable HBeAg in cell cultures. 2021 Emerging microbes & infections Result HBV G1896A 23 29 C 59 64 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. However, both Elecsys and Architect HBeAg assays showed positive reactivity in samples from viral vectors with G1896A mutation, whereas the NTR-HBeAg assay exhibited completed negative results for these samples (Figure 4B and C). 2021 Emerging microbes & infections Result HBV G1896A 111 117 C;C 36;144 41;149 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. In addition, among these patients, 16 were infected with HBV strain harbouring basic core promoter (BCP) mutation A1762T/G1764A, whereas the remaining 45 patients were infected with BCP wild-type strain. 2021 Emerging microbes & infections Result HBV G1764A;A1762T 121;114 127;120 BCP;BCP;BCP 79;100;182 98;103;185 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. None of these HBV clones harbour G1896A mutation. 2021 Emerging microbes & infections Result HBV G1896A 33 39 33357228 Viral hepatitis B and C in HIV-exposed South African infants. Both sequences harboured the double A1762T/G1764A BCP mutation. 2020 BMC pediatrics Result HBV G1764A;A1762T 43;36 49;42 BCP 50 53 33357228 Viral hepatitis B and C in HIV-exposed South African infants. Sequence analysis revealed the M204I mutation in the reverse transcriptase domain of the polymerase gene in the Durban sample while the Cape Town sample harboured the double A1762T/G1764A BCP mutation in the core gene. 2020 BMC pediatrics Result HBV G1764A;M204I;A1762T 181;31;174 187;36;180 BCP;C;P;RT 188;208;89;53 191;212;99;74 33357228 Viral hepatitis B and C in HIV-exposed South African infants. The "Week 0" Cape Town sample showed a similar serological profile to the "Week 48" sample from the same child and also had the double A1762T/G1764A BCP mutation. 2020 BMC pediatrics Result HBV G1764A;A1762T 142;135 148;141 BCP 149 152 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. C1653T, T1753V and A1762T/G1764A were highly frequent in genotype G (95, 95, and 97.5%, respectively), followed by genotype C (12, 18.1, and 46.1%, respectively), while Pre-S deletions prevailed in genotype C (3.3%) (Table 1). 2020 Frontiers in microbiology Result HBV G1764A;C1653T;T1753V;A1762T 26;0;8;19 32;6;14;25 PreS 169 174 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. In particular, significant differences in the frequency of G145R were observed within genotypes C and D, with the highest rates recorded for subgenotypes C6-C15 and D2 (34 and 8.2%, P < 0.001 for both; Tables 2-6). 2020 Frontiers in microbiology Result HBV G145R 59 64 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Notably, G145R was only detected in genotypes G (5.0%), D (2.5%), C (2.1%), and B (0.2%) (P < 0.001) (Table 1). 2020 Frontiers in microbiology Result HBV G145R 9 14 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Overall, rtL180M, rtA181T/V, rtT184G/S, rtS202G/I, rtM204I, rtM204V, rtN236T, and rtM250V were more frequently detected in genotypes A (13.9%), C (0.8%), D (0.1%), H (3.8%), G (25%), A (13.1%), B (0.7%), and C (0.1%), respectively. 2020 Frontiers in microbiology Result HBV A181T;A181V;T184G;T184S;S202G;S202I;M250V;L180M;M204I;M204V;N236T 20;20;31;31;42;42;84;11;53;62;71 27;27;38;38;49;49;89;16;58;67;76 RT;RT;RT;RT;RT;RT;RT;RT 9;18;29;40;51;60;69;82 11;20;31;42;53;62;71;84 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Significant differences in A1762T/G1764A rates were found within genotypes B, C, D, and F, with subgenotypes B2, C6-C15, D1 and F1 showing the highest rates (17.7, 56.3, 28.3, and 29.3%, respectively). 2020 Frontiers in microbiology Result HBV G1764A;A1762T 34;27 40;33 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. The frequencies of C1653T, T1753V and A1762T/G1764A (double mutant) and Pre-S deletions in different HBV genotypes are shown in Table 1. 2020 Frontiers in microbiology Result HBV G1764A;C1653T;T1753V;A1762T 45;19;27;38 51;25;33;44 PreS 72 77 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. The most common substitutions were I/T126S (1.8%), G145R (1.2%), M133T (1.2%), Q129R (1.0%), I/T126A (0.8%), and P120T (0.8%). 2020 Frontiers in microbiology Result HBV T126S;T126A;I126S;I126A;G145R;M133T;Q129R;P120T 35;93;35;93;51;65;79;113 42;100;42;100;56;70;84;118 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. These major mutations were more frequent in genotypes A (P120T, 3.2%), B (I/T126A, 2.8%; Q129R, 2.2%), C (I/T126S, 3.9%; M133T, 1.9%), and G (G145R, 5.0%). 2020 Frontiers in microbiology Result HBV T126A;I126A;P120T;Q129R;I126S;T126S;M133T;G145R 74;74;57;89;106;106;121;142 81;81;62;94;112;112;126;147 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. Amino acid substitutions were detected in the following frequency: rtM204V/I (9/31; 29.0%), rtL180M (8/31; 25.8%), rtV173L (7/31; 22.5%). 2021 Virology journal Result HBV M204V;M204I;L180M;V173L 69;69;94;117 76;76;99;122 RT;RT;RT 67;92;115 69;94;117 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. No single mutation was detected while all amino acid substitutions were detected in combinations as rtL180M + rtV173L + rtM204V (n = 7/10), rtV173L + rtM204V (1/10), rtL180M + rtM204I (1/10), and rtL180M + rtM204V + rtS202I (1/10). 2021 Virology journal Result HBV L180M;V173L;M204V;V173L;M204V;L180M;M204I;L180M;M204V;S202I 102;112;122;142;152;168;178;198;208;218 107;117;127;147;157;173;183;203;213;223 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 100;110;120;140;150;166;176;196;206;216 102;112;122;142;152;168;178;198;208;218 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. One of the individuals showing the DRM combination rtM204V/I + rtL180M + rtS202I was an ART-naive HIV/HBV/HDV-positive patient (Table 2. 2021 Virology journal Result HBV M204V;M204I;L180M;S202I 53;53;65;75 60;60;70;80 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. As shown in Table 2, 45.5% (5/11, 45.5%) S regions in 11 HBV-B isolates had N40S mutations. 2021 BMC infectious diseases Result HBV N40S 76 80 S 41 42 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. In addition, immune escape mutants containing Q129H, T131I/T, G145R, and E164V were also found in these S sequences. 2021 BMC infectious diseases Result HBV T131T;Q129H;T131I;G145R;E164V 53;46;53;62;73 60;51;60;67;78 S 104 105 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Several mutations associated with the interference of HBsAg detection, such as mutations in the major hydrophilic region (MHR), including Q129H, T131I, M133L/S/T, F134L, T143M, and G145R, and mutations outside the MHR, including Y100C, L175S, and Y103I, were found in S genes among HBV-infected blood donors. 2021 BMC infectious diseases Result HBV M133L;M133S;M133T;T131I;Q129H;F134L;T143M;G145R;Y100C;L175S;Y103I 152;152;152;145;138;163;170;181;229;236;247 161;161;161;150;143;168;175;186;234;241;252 S;S 54;268 59;269 HBV infections 282 294 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. The A1762T and G1764A mutations were found in two cases. 2021 BMC infectious diseases Result HBV A1762T;G1764A 4;15 10;21 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. The most common mutations in the BCP region (nt1742-1849) and pre-C region were A1752G and A1846T. 2021 BMC infectious diseases Result HBV A1752G;A1846T 80;91 86;97 BCP;Precore 33;62 36;67 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Twenty-one mutations were identified in the core upstream regulatory sequence (nt1678-1741) from 16 samples, and T1719G occurred in 93.8% (15/16) samples. 2021 BMC infectious diseases Result HBV T1719G 113 119 C 44 48 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. As shown in Figure 5f, unlike attenuated replication level, clones carrying rtT301A mutation showed relatively higher levels of intracellular HBV RNA. 2021 International journal of molecular sciences Result HBV T301A 78 83 RT 76 78 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. As similar results were obtained from both Huh7 and HepG2, the effect of rtT301A mutation maybe comparable among hepatoma cell lines, implying that that the naturally occurring novel rtT301A mutation impaired the replication competence and increased resistance to tenofovir. 2021 International journal of molecular sciences Result HBV T301A;T301A 75;185 80;190 RT;RT 73;183 75;185 Hepatocellular carcinoma 113 121 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Collectively, regardless of mutant construct, the rtT301A mutation decreased replication capacity and increased tenofovir resistance. 2021 International journal of molecular sciences Result HBV T301A 52 57 RT 50 52 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Concerning the characteristics of Huh7 and HepG2 cells that may contribute to their unique capacity to support viral replication, the effect of rtT301A mutation on HBV DNA replication was further evaluated in normal liver cell line (L-02). 2021 International journal of molecular sciences Result HBV T301A 146 151 RT 144 146 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Despite the impaired replication ability of rtT301A mutants harboring CYELMVI mutations, this mutant population was present in significant amount in CHB patients treated with TDF (Table 1). 2021 International journal of molecular sciences Result HBV T301A 46 51 RT 44 46 Chronic Hepatitis B 149 152 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Effect of Patient-Derived HBV RT Mutants Harboring the rtT301A Mutation on Replication Capacity and Tenofovir Resistance in Hepatoma Cell Lines. 2021 International journal of molecular sciences Result HBV T301A 57 62 RT;RT 30;55 32;57 Hepatocellular carcinoma 124 132 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. However, the levels of HBsAg and HBeAg in culture supernatants of transfected Huh7 cells were not altered by tenofovir treatment, indicating that regardless of low replication capacity, production of viral RNAs and antigens of each clone were not affected by the rtT301A substitution. 2021 International journal of molecular sciences Result HBV T301A 265 270 C;S;RT 33;23;263 38;28;265 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Impaired Replication Ability of rtT301A Mutants in Hepatoma Cell Lines Is Restored in PHHs. 2021 International journal of molecular sciences Result HBV T301A 34 39 RT 32 34 Hepatocellular carcinoma 51 59 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In addition, we examined the effect of the rtT301A mutant on the replication of WT HBV (Figure 6b). 2021 International journal of molecular sciences Result HBV T301A 45 50 RT 43 45 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In particular, Clones 1-29 and 4-7 showed slightly increased resistance to tenofovir (Figure 3d), suggesting that the rtT301A substitution may diminish replication capability and increase tenofovir resistance simultaneously. 2021 International journal of molecular sciences Result HBV T301A 120 125 RT 118 120 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Interestingly, as shown in Figure 5b, HBV DNA replication ability was lost in all clones containing the rtT301A mutation. 2021 International journal of molecular sciences Result HBV T301A 106 111 RT 104 106 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Interestingly, clonal analysis from all four sample collections revealed that 72.7% (8 out of 11 clones) of CYELMVI mutants harbored a novel rtT301A (A) substitution (Table 1). 2021 International journal of molecular sciences Result HBV T301A 143 148 RT 141 143 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. More importantly, regardless of the rtT301A mutation, there was no significant difference in replication levels among four patient-derived mutants (i.e., Clones 1-23, 1-29, 4-7, and 4-8). 2021 International journal of molecular sciences Result HBV T301A 38 43 RT 36 38 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Next, we asked whether WT polymerase (WT Pol) can rescue the replication-defective rtT301A mutant. 2021 International journal of molecular sciences Result HBV T301A 85 90 P;P;RT 41;26;83 44;36;85 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Next, we examined whether the defective replication of the rtT301A mutant is due to impeded viral transcription. 2021 International journal of molecular sciences Result HBV T301A 61 66 RT 59 61 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. One possibility is that the rtT301A mutant pgRNA could be encapsidated along with WT Pol, therefore explaining the abundance of the rtT301A mutant in patient serum. 2021 International journal of molecular sciences Result HBV T301A;T301A 30;134 35;139 P;RT;RT 85;28;132 88;30;134 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Quantitative real-time PCR also showed that considerable reduction in the replication ability of clones containing the rtT301A mutation commonly occurred in Huh7 and HepG2 cells (Figure 5d). 2021 International journal of molecular sciences Result HBV T301A 121 126 RT 119 121 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Surprisingly, clones carrying the rtT301A mutation significantly restored viral replication in PHHs (Figure 7a). 2021 International journal of molecular sciences Result HBV T301A 36 41 RT 34 36 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Surprisingly, supplementation of WT Pol restored the replication of rtT301A mutant to some extent, whereas it reduced the replication of WT HBV. 2021 International journal of molecular sciences Result HBV T301A 70 75 P;RT 36;68 39;70 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The impact of the rtT301A mutation in different HBV backbones on replication ability and drug resistance were compared by plotting the fold resistance (IC50 and IC70) vs. 2021 International journal of molecular sciences Result HBV T301A 20 25 RT 18 20 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The observed effect of rtT301A mutation on replication was comparable in both hepatoma cell lines. 2021 International journal of molecular sciences Result HBV T301A 25 30 RT 23 25 Hepatocellular carcinoma 78 86 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The replication of WT virus was not affected at all by the presence of rtT301A mutant virus, indicating that the rtT301A mutant Pol did not inhibit the function of WT Pol and may not act as a dominant-negative molecule. 2021 International journal of molecular sciences Result HBV T301A;T301A 73;115 78;120 P;P;RT;RT 128;167;71;113 131;170;73;115 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The role of the novel rtT301A mutation was investigated using three representative clones (Clones 1-29, 4-7, and 4-8) carrying tenofovir-resistant mutations (CYELMVI), of which Clones 1-29 and 4-7 carried an additional rtT301A mutation (Figure 3a). 2021 International journal of molecular sciences Result HBV T301A;T301A 24;221 29;226 RT;RT 22;219 24;221 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The rtT301A Mutation Decreases Replication Capacity and Increases Tenofovir Resistance in Hepatoma Cell Lines. 2021 International journal of molecular sciences Result HBV T301A 6 11 RT 4 6 Hepatocellular carcinoma 90 98 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The WT Polymerase (WT Pol) Partially Rescued the Replication Defect of the rtT301A Mutant. 2021 International journal of molecular sciences Result HBV T301A 77 82 P;P;RT 22;7;75 25;17;77 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Therefore, loss of HBsAg level in Clone 4-7, which has two additional mutations in polymerase compared to Clone 1-29, may be attributed to the S34P or/and W199R mutations in the corresponding surface gene. 2021 International journal of molecular sciences Result HBV S34P;W199R 143;155 147;160 S;P;S 19;83;192 24;93;199 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Therefore, since rtT301A mutation was frequently accompanied by tenofovir-resistant mutations (CYELMVI) while distinct viral breakthrough did not occur, we sought to identify the effect of this particular substitution in RT sequence on HBV replication ability and drug susceptibility. 2021 International journal of molecular sciences Result HBV T301A 19 24 RT;RT 17;221 19;223 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. This is probably caused by the accumulation of RNA transcripts due to the impaired RT activity of rtT301A containing mutants. 2021 International journal of molecular sciences Result HBV T301A 100 105 RT;RT 83;98 85;100 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. To confirm that the rtT301A mutation is associated with viral replication and tenofovir resistance, we introduced the rtT301A mutation into three replicons: WT, CYEI, and CYELMVI HBV 1.2mers (Figure 5a). 2021 International journal of molecular sciences Result HBV T301A;T301A 22;120 27;125 RT;RT 20;118 22;120 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. To examine the effect of rtT301A mutation on the level of HBV transcripts, Northern blot analysis was carried out in Huh7 cell line. 2021 International journal of molecular sciences Result HBV T301A 27 32 RT 25 27 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. To further evaluate the effect of rtT301A mutation on tenofovir resistance, IC50 as well as IC70 values of WT and mutant clones were determined by quantitative real-time PCR (Figure 5g) and summarized in Table 3. 2021 International journal of molecular sciences Result HBV T301A 36 41 RT 34 36 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. To rule out the possibility that the effect of rtT301A mutation shown in Huh7 cell is not cell-type specific, we performed similar experiments in HepG2 cells. 2021 International journal of molecular sciences Result HBV T301A 49 54 RT 47 49 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. To test this, the rtT301A mutant was co-transfected with increasing dose of the WT Pol construct (Figure 6a). 2021 International journal of molecular sciences Result HBV T301A 20 25 P;RT 83;18 86;20 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Finally, in the presence of the quadruple mutant A12S/P33S/P46S/T36D, there was a 25.6% reduction in HBV DNA (4[3.7-4.1] logIU/mL), which accounted for a 1.4-log drop in HBV viremia relative to the wt virus (p = 0.00012). 2021 Scientific reports Result HBV T36D;P46S;P33S;A12S 64;59;54;49 68;63;58;53 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Furthermore, a reduction of 18.5% (4.3 [4.1-4.6] logIU/mL) occurred in the presence of the quadruple mutant A12S/P33S/P46S/T36G (p = 0.047). 2021 Scientific reports Result HBV T36G;P33S;P46S;A12S 123;113;118;108 127;117;122;112 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. However, in the case of genotype D, the A12S, P33S, P46S, and T36A/D/G mutations were more highly represented in one specific group, CI patients. 2021 Scientific reports Result HBV T36A;T36D;T36G;A12S;P33S;P46S 62;62;62;40;46;52 70;70;70;44;50;56 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Of note, the A12S/P33S/P46S/T36D pattern presented a DeltaDeltag lower than the pattern with T36G (DeltaDeltag of - 1.4 and - 1.85 for respectively, T36D and T36G), indicating greater instability. 2021 Scientific reports Result HBV P46S;T36D;P33S;A12S;T36G;T36D;T36G 23;28;18;13;93;149;158 27;32;22;17;97;153;162 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Specifically, HBV DNA showed a > 14% decrease in the presence of the double mutant A12S/P33S and the triple mutant A12S/P33S/P46S (median [Q1-Q3] 4.4 [4.3-4.7] logIU/mL, and 4.6 [4.5-4.9] logIU/mL, respectively, versus 5.3 [5.1-5.8] for wt HBV). 2021 Scientific reports Result HBV P33S;P33S;P46S;A12S;A12S 88;120;125;83;115 92;124;129;87;119 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. An assessment of the distribution of HBV precore/core region specific mutations among the HBV genotypes in Table 2 showed that there exists a significant statistical difference between the occurrence of G1862C, G1888A, and G1899A specific mutations among the HBV subgenotype A1 and genotype D infected participants (P < 0.05, Fisher's exact test). 2021 International journal of health sciences Result HBV G1862C;G1888A;G1899A 203;211;223 209;217;229 C;Precore 49;41 53;48 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. However, a trend toward statistical significance was observed in the difference between the median of HBV DNA and AFP levels among the participants with the G1899A mutation (P = 0.057 and P = 0.056, respectively), where a higher median value was observed among those with the mutant strains for both HBV DNA and AFP levels [Tables 3 and 4]. 2021 International journal of health sciences Result HBV G1899A 157 163 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. A number of studies have reported that preC-W28Stop, a preC 1896 mutation, is significantly related to liver disease progression. 2021 Microorganisms Result HBV W28X 44 51 Precore;Precore 39;55 43;59 Liver disease 103 116 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. C-Q182K/* (C2444A/T or A2445G mutation), of which the frequency tended to be higher in rt269I strains than in rt269L strains (q = 0.068), has been reported to be significantly related to HCC in Korean chronic patients infected with genotype C2. 2021 Microorganisms Result HBV Q182K;C2444A;C2444T;A2445G 2;11;11;23 9;19;19;29 C;RT;RT 0;87;110 1;89;112 Hepatocellular carcinoma 187 190 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. F141L in PreS2 has been reported to be significantly related to HCC progression in Korean chronic patients by inducing cell cycle progression by downregulating the p53 and p21 pathways and upregulating CDK4 and cyclin A. 2021 Microorganisms Result HBV F141L 0 5 PreS2 9 14 Hepatocellular carcinoma 64 67 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Indeed, a previous study reported that C-I97F/L (A2189T/C or C2191T mutation) was the preC/C type found the most frequently in HCC patients in Korean chronic patients infected with genotype C2. 2021 Microorganisms Result HBV I97F;I97L;A2189T;A2189C;C2191T 41;41;49;49;61 47;47;57;57;67 C;Precore;C 39;86;91 40;90;92 Hepatocellular carcinoma 127 130 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Of note, of the seven types, the following three rt269I signature types, rtN139K/H, rtM204I/V and rtI224V, have been reported to be NAr RT mutation types related to clinical severity, including HCC or liver cirrhosis . 2021 Microorganisms Result HBV N139K;N139H;M204I;M204V;I224V 75;75;86;86;100 82;82;93;93;105 RT;RT;RT;RT;RT 49;73;84;98;136 51;75;86;100;138 Hepatocellular carcinoma;Liver cirrhosis 194;201 197;216 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Of the four rt269I signature types, I84T/M/L/V in PreS1 has been reported to be frequently found in HBV occult cases. 2021 Microorganisms Result HBV I84T;I84M;I84L;I84V 36;36;36;36 46;46;46;46 PreS1;RT 50;12 55;14 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Of these, the frequency in all four types but one rt269L signature type (I68T in the S region) was significantly or tended to be higher in rt269I HBV strains than in rt269L. 2021 Microorganisms Result HBV I68T 73 77 RT;RT;RT;S 50;139;166;85 52;141;168;86 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Of these, three NS mutations, V/L5M, S101P/A and V131I, and one, T36P/S/A, were rt269I and rt269L signature types, respectively. 2021 Microorganisms Result HBV L5M;V5M;T36P;T36S;T36A;S101P;S101A;V131I 30;30;65;65;65;37;37;49 35;35;73;73;73;44;44;54 RT;RT 80;91 82;93 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. rtM204I, a YMDD motif mutation whose frequency was significantly higher in rt269I than in rt269L (q = 0.009), can lead to resistance to various drugs, including lamivudine (LMV), and it is the most frequently encountered preexisting NAr mutation worldwide. 2021 Microorganisms Result HBV M204I 2 7 RT;RT;RT;P 0;75;90;11 2;77;92;15 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. T36P/S/A, a rt269L signature type that is more prevalent in rt269I strains than in rt269L strains (q < 0.001), has been reported to be higher in HCC patients, which enables the escape of the host immune response, possibly due to its location at the B epitope. 2021 Microorganisms Result HBV T36P;T36S;T36A 0;0;0 8;8;8 RT;RT;RT 12;60;83 14;62;85 Hepatocellular carcinoma 145 148 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. The C-I97F/L in the C region, of which the frequency was significantly higher in rt269I strains than in rt269L strains (q = 0.047), is well known as the most frequently encountered HBcAg mutation, as mentioned in several studies leading to an immature secretion phenotype due to defective nucleocapsid assembly. 2021 Microorganisms Result HBV I97F;I97L 6;6 12;12 C;C;C;RT;RT 4;20;181;81;104 5;21;186;83;106 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. The L213I/S in the S region, which tended to be higher in rt269I HBV strains than in rt269L (q = 0.054), has been reported to be related to disease progression in chronic patients). 2021 Microorganisms Result HBV L213I;L213S 4;4 11;11 RT;RT;S 58;85;19 60;87;20 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. The preC-W28Stop, known as a preC mutation at 1896 nt, leads to premature termination of HBeAg, resulting in HBeAg-negative infection in chronic patients with its mutation, of which the frequency was significantly higher in rt269I strains than in rt269L strains (q < 0.001). 2021 Microorganisms Result HBV W28X 9 16 C;C;Precore;Precore;RT;RT 89;109;4;29;224;247 94;114;8;33;226;249 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. The rt269L signature type, I68T in the S region, which is significantly prevalent in the rt269L versus rt269I type (q = 0.004), has been reported to be an HCC-independent risk factor in chronic Chinese patients with genotype C infections. 2021 Microorganisms Result HBV I68T 27 31 RT;RT;RT;S 4;89;103;39 6;91;105;40 Hepatocellular carcinoma 155 158 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. V/L5M, which tended to be higher in rt269I strains than in rt269L strains, has been reported to be significantly related to HCC progression and HBeAg-negative serostatus in chronic patients with genotype C2 infections). 2021 Microorganisms Result HBV L5M;V5M 0;0 5;5 C;RT;RT 144;36;59 149;38;61 Hepatocellular carcinoma 124 127 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. V131I also leads to one of the double mutations in the overlapping basal core promoter (1764 G to A), which is significantly prevalent in rt269I strains versus rt269L (q = 0.004) and has also been reported to be related to HBsAg-negative serostatus and HCC progression in chronic patients. 2021 Microorganisms Result HBV V131I 0 5 BCP;S;RT;RT 67;223;138;160 86;228;140;162 Hepatocellular carcinoma 253 256 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. We found a total of five types of signature NS mutations in the S ORF (I84T/M/L/V and A90T/V in PreS1, F141L in PreS2, and I68T and L213I/S in S). 2021 Microorganisms Result HBV I84T;I84M;I84L;I84V;A90T;A90V;F141L;I68T;L213I;L213S 71;71;71;71;86;86;103;123;132;132 81;81;81;81;92;92;108;127;139;139 PreS1;PreS2;S;S 96;112;64;143 101;117;65;144 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. We found a total of four types of signature NS mutations in the X ORF (V/L5M, T36P/S/A, S101P/A and V131I). 2021 Microorganisms Result HBV L5M;V5M;T36P;T36S;T36A;S101P;S101A;V131I 71;71;78;78;78;88;88;100 76;76;86;86;86;95;95;105 X 64 65 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. We found a total of seven types of signature NS mutations in the Pol region (three types in RT, one type in the terminal protein (TP) region, two types in the spacer region and one type in the RNaseH region), of which all seven (rtN139K/H, rtM204I/V and rtI224V in RT, D16A/E/N/V in TP, S314P and F321L in Spacer and D828A/V in the RNaseH region) were rt269I signature types. 2021 Microorganisms Result HBV N139K;N139H;M204I;M204V;I224V;D16A;D16E;D16N;D16V;S314P;F321L;D828A;D828V 231;231;242;242;256;269;269;269;269;287;297;317;317 238;238;249;249;261;279;279;279;279;292;302;324;324 P;RT;RT;RT;RT;RT;RT 65;92;229;240;254;265;352 68;94;231;242;256;267;354 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. We found a total of three types of signature NS mutations in the preC/C region (one in the preC region: preC-W28Stop, two in the C region: C-I97F/L (A2189T/C or C2191T mutation) and C-Q182K/* (C2444A/T or A2445G mutation)). 2021 Microorganisms Result HBV W28X;I97F;I97L;A2189T;A2189C;C2191T;Q182K;C2444A;C2444T;A2445G 109;141;141;149;149;161;184;193;193;205 116;147;147;157;157;167;191;201;201;211 C;C;C;Precore;Precore;Precore;C 129;139;182;91;104;65;70 130;140;183;95;108;69;71 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Branches with VEM G145R were estimated to emerge around the year 1930 (95% HPD 1866-1958). 2021 Journal of viral hepatitis Result HBV G145R 18 23 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Compared to all other genotypes, genotype C had the highest prevalence of individual RAMs S106C/G, DH/N134E and I269L, and Asia had the highest prevalence of these individual RAMs S106C/G, DH/N134E and I269L compared to other continents, Figure S4. 2021 Journal of viral hepatitis Result HBV N134E;N134E;S106C;S106G;I269L;S106C;S106G;I269L 99;189;90;90;112;180;180;202 107;197;97;97;117;187;187;207 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. G145A/R had an overall prevalence of 1.3% (37/2837) and had the highest prevalence in genotype C at 2.2% (24/1102; p = 0.002), and in Asia at 1.6% (34/2109; p = 0.009); this is the best recognized VEM (Figure 2A). 2021 Journal of viral hepatitis Result HBV G145A;G145R 0;0 7;7 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Genotype C had the highest prevalence of all of these mutations, apart from L80I/M/V which is most common in Genotype D (although the difference is not statistically significant) (Figure 1B). 2021 Journal of viral hepatitis Result HBV L80I;L80M;L80V 76;76;76 84;84;84 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. However, four sequences (KF214668, KF214671, KF214673 and KF214676) with RAM I269L and one sequence (KF214659) with VEM S/T143M were sampled from Asia in 1963, and one sequence (HQ700441) with RAM L180M was sampled from Oceania in 1984, demonstrating that relevant mutations can arise without exposure to treatment or vaccination. 2021 Journal of viral hepatitis Result HBV T143M;S143M;I269L;L180M 120;120;77;197 127;127;82;202 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. In genotype B, all sequences containing the A194T variant clustered together (Bayes factor, BF, support >100; n = 4 sequences). 2021 Journal of viral hepatitis Result HBV A194T 44 49 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. In genotype C, there were clusters of RAMs S106C (BF > 100, n = 5 sequences), R153Q (BF > 100, n = 3 sequences) and I129L (BF > 100, n = 34 sequences). 2021 Journal of viral hepatitis Result HBV S106C;R153Q;I129L 43;78;116 48;83;121 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. L180M and M204I/V were both present in all genotypes and continents that we analysed (Figure 1B, C). 2021 Journal of viral hepatitis Result HBV L180M;M204I;M204V 0;10;10 5;17;17 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. M133I/L/T and Q129H/N/R had the highest prevalence in genotype B and M133I/L/T had the highest prevalence in Asia, also being present in >3% of the sequences (Figure 2B and 2C). 2021 Journal of viral hepatitis Result HBV M133I;M133L;M133T;Q129H;Q129N;Q129R;M133I;M133L;M133T 0;0;0;14;14;14;69;69;69 9;9;9;23;23;23;78;78;78 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. M204I/V had the highest overall prevalence at 3.8% (109/2838) (Figure 1A). 2021 Journal of viral hepatitis Result HBV M204I;M204V 0;0 7;7 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Other VEMs that had an overall prevalence of >1% were T118A/R/V, M133I/L/T, A128V, Q129H/N/R, G145A/R, P120S/T and S/T143L/M (Figure 2A). 2021 Journal of viral hepatitis Result HBV T143M;T118A;M133I;M133L;M133T;Q129H;Q129N;Q129R;T143L;T118R;T118V;S143L;S143M;A128V;G145A;G145R;P120S;P120T 115;54;65;65;65;83;83;83;115;54;54;115;115;76;94;94;103;103 124;63;74;74;74;92;92;92;124;63;63;124;124;81;101;101;110;110 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. RAM H/Y9H is wild type in genotypes A-E. 2021 Journal of viral hepatitis Result HBV H9H;Y9H 4;4 9;9 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. RAMs H126Y and R/W153W, which contribute to TFV resistance when combined with >=3 other RAMs, are wild type in genotype A. 2021 Journal of viral hepatitis Result HBV W153W;R153W;H126Y 15;15;5 22;22;10 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. RAMs L80I/M/V, V173L, L180M, A181T/V and T184X are common to 3TC, ETV and/or TFV. 2021 Journal of viral hepatitis Result HBV L80I;L80M;L80V;V173L;L180M;A181T;A181V;T184X 5;5;5;15;22;29;29;41 13;13;13;20;27;36;36;46 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Some sequences containing both M204V and L180M formed a cluster in genotype B (BF = 54.99, n = 4 sequences) and some with M204I formed a cluster in genotype D (BF > 100, n = 3 sequences). 2021 Journal of viral hepatitis Result HBV M204V;L180M;M204I 31;41;122 36;46;127 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. T118A/R/V, A128V and S/T143L/M had the highest prevalence in genotype D and in Europe, being present >3% of the sequences. 2021 Journal of viral hepatitis Result HBV S143L;S143M;T143L;T143M;T118A;T118R;T118V;A128V 21;21;21;21;0;0;0;11 30;30;30;30;9;9;9;16 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. The estimated time of emergence of branches with RAMs M204V+L180M was around the year 1945 (95% HPD 1897-1971). 2021 Journal of viral hepatitis Result HBV M204V;L180M 54;60 59;65 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. The overall prevalence of ETV resistance predicted by this data set, determined by the presence of RAMs M204I/V+L180M, was 2.4% (67/2838); other combinations of ETV drug-resistant mutations were uncommon (all <0.6%); Figure S3. 2021 Journal of viral hepatitis Result HBV M204I;M204V;L180M 104;104;112 111;111;117 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Vaccine escape mutations K141E/I/R was not present in our data set. 2021 Journal of viral hepatitis Result HBV K141E;K141I;K141R 25;25;25 34;34;34 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. We considered the distribution of 12 RAMs (S106C/G, D134E, R153W/Q, V173L, L180M, A181T/V, A194T, A200V, M204I/V, L217R, L229V/W and I269L) and eight VEMs (C139S, S/T140I, P142S, S/T143L/M, D144A/E/G/N, G145A/E/R, K141A/I/R and C147S) across the branches of ML phylogenetic trees. 2021 Journal of viral hepatitis Result HBV T140I;S143L;S143M;T143L;T143M;D144A;D144E;D144G;D144N;G145A;G145E;G145R;K141A;K141I;K141R;S140I;S106C;S106G;D134E;R153W;R153Q;V173L;L180M;A181T;A181V;A194T;A200V;M204I;M204V;L217R;L229V;L229W;I269L;C139S;P142S;C147S 163;179;179;179;179;190;190;190;190;203;203;203;214;214;214;163;43;43;52;59;59;68;75;82;82;91;98;105;105;114;121;121;133;156;172;228 170;188;188;188;188;201;201;201;201;212;212;212;223;223;223;170;50;50;57;66;66;73;80;89;89;96;103;112;112;119;128;128;138;161;177;233 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Classification of P5T-HBc + P2, L60V-HBc + P2 and F97L-HBc + P2 confirmed a similar variability of the spikes. 2021 Microorganisms Result HBV P5T;L60V;F97L 18;32;50 21;36;54 C;C;C 22;37;55 25;40;58 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. EM maps and pdb models of WT-HBc and F97L-HBc without bound peptides have been determined previously. 2021 Microorganisms Result HBV F97L 37 41 C;C 29;42 32;45 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Fitting of the isotherms gave a stoichiometry of n = 0.5 for P5T-HBc, WT-HBc and F97L-HBc, suggesting that each HBc dimer in the capsid bound one peptide. 2021 Microorganisms Result HBV P5T;F97L 61;81 64;85 Capsid;C;C;C;C 129;65;73;86;112 135;68;76;89;115 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. For L60V-HBc, we could not determine a meaningful stoichiometry (Figure 2d) and fixed the stoichiometry to n = 0.5 for determining the KD and H. 2021 Microorganisms Result HBV L60V 4 8 C 9 12 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Here, L60V-HBc showed somewhat larger differences, which affected the spikes surrounding the 5-fold symmetry axes (AB spikes) more than those surrounding the 3-fold symmetry axes (CD spikes). 2021 Microorganisms Result HBV L60V 6 10 C 11 14 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. In the center of the CD spike, F97 in chain D adopted two alternate rotamer conformations (Figure 7b) similar as observed for L60V-HBc without bound peptide (Figure 3). 2021 Microorganisms Result HBV L60V 126 130 C 131 134 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. L60V-HBc was the most stable variant with the highest transition temperature Tm (Tm(L60V-HBc) > Tm(WT-HBc) > Tm(F97L) > Tm(P5T)) (Figure 1). 2021 Microorganisms Result HBV P5T;L60V;L60V;F97L 123;0;84;112 126;4;88;116 C;C;C 5;89;102 8;92;105 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Next, we built models into the maps of L60V-HBc and P5T-HBc. 2021 Microorganisms Result HBV L60V;P5T 39;52 43;55 C;C 44;56 47;59 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. One noticeable difference between the consensus models was at the position of F97, which is spatially close to P5T and L60V. 2021 Microorganisms Result HBV P5T;L60V 111;119 114;123 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Similar observations were previously reported for HBc-F97L and HBc-WT and suggested that the spikes are more mobile than the rest of the capsids. 2021 Microorganisms Result HBV F97L 54 58 Capsid;C;C 137;50;63 144;53;66 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Structures of the low-secretion variants HBc-P5T and HBc-L60V have not been reported previously and were determined for the first time in this study. 2021 Microorganisms Result HBV P5T;L60V 45;57 48;61 C;C 41;53 44;56 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The alternate orientation of F97 in L60V-HBc increases the adjacent hydrophobic pocket similar to the smaller side-chain in F97L-HBc does, which also points away from the dimer axis (Figure 3g). 2021 Microorganisms Result HBV L60V;F97L 36;124 40;128 C;C 41;129 44;132 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The KDs were similar for WT-HBc and P5T-HBc (KD_WT = 68 +- 4 microM, KD_P5 T = 74 +- 5 microM), but according to Student's t-test significantly larger for L60V-HBc and F97L-HBc (KD_L60V = 127 +- 19 microM, and 155 +- 14 microM). 2021 Microorganisms Result HBV P5T;L60V;F97L;L60V 36;155;168;180 39;159;172;185 C;C;C;C 28;40;160;173 31;43;163;176 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The Low-Level Secretion Phenotype Mutation L60V, but Not the Mutation P5T Mobilizes the F97 Side-Chain in the Center of the Spikes. 2021 Microorganisms Result HBV L60V;P5T 43;70 47;73 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The maps of P5T-HBc and L60V-HBc were almost indistinguishable from WT maps (local cross-correlation > 0.9) except at regions close to the mutated residues (local correlation < 0.9, Figure 3). 2021 Microorganisms Result HBV P5T;L60V 12;24 15;28 C;C 16;29 19;32 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The overall resolutions were 3.2 A with B-factors of 139 A2 (P5T-HBc) and 158 A2 (L60V-HBc), respectively (Table S3 and Supplemental Information S2). 2021 Microorganisms Result HBV P5T;L60V 61;82 64;86 C;C 65;87 68;90 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The stoichiometry of n = 0.5 was also justified by the subsequent analysis of the electron microscopic data (see below) that showed one peptide per dimeric spike in L60V-HBc. 2021 Microorganisms Result HBV L60V 165 169 C 170 173 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Therefore, we determined structures for WT-HBc, F97L-HBc, P5T-HBc and L60V-HBc with bound peptides (Table S2). 2021 Microorganisms Result HBV P5T;F97L;L60V 58;48;70 61;52;74 C;C;C;C 43;53;62;75 46;56;65;78 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. We purified P5T-HBc, L60V-HBc, WT-HBc and F97L-HBc by ammonium sulfate precipitation followed by a sucrose density step gradient. 2021 Microorganisms Result HBV P5T;L60V;F97L 12;21;42 15;25;46 C;C;C;C 16;26;34;47 19;29;37;50 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. While in WT-HBc and P5T-HBc, the phenylalanine side-chain of F97 pointed towards the dimer axis, in L60V-HBc, it had an additional alternate position pointing away from the dimer axis (Figure 3g). 2021 Microorganisms Result HBV P5T;L60V 20;100 23;104 C;C;C 12;24;105 15;27;108 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. While L60V-HBc, WT-HBc and F97L-HBc had similar transition temperatures between 91 C and 95 C, the transition temperature of P5T-HBc was much lower (TM = 86 C), showing that the mutation P5T weakens the stability of the whole capsid substantially. 2021 Microorganisms Result HBV P5T;P5T;L60V;F97L 127;190;6;27 130;193;10;31 Capsid;C;C;C;C 229;11;19;32;131 235;14;22;35;134 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. As shown in Figure 3, the proportion of maternal HBV DNA load >=103 IU/mL at delivery was 71.4% in the rtM204I >= 20% group, which was similar to that in the rtM204I < 20% group (71.4% vs. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I;M204I 105;160 110;165 RT;RT 103;158 105;160 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. As shown in Table 3, 34.3% (25/73) patients had rtM204I mutation and 27.4% (20/73) had rtM204 V mutation. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I;M204V 50;89 55;95 RT;RT 48;87 50;89 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. At primary drug resistance mutation sites, rtM204I/V associated with resistance to LAM and TBV, also known as classical YMDD mutation, presented in 41.1% (30/73) of patients before TBV treatment and 9.6% of patients had mutation frequencies greater than 20%; RtA181 T/V was in 5.5% (4/73) of patients, involved in the LAM, TBV, and ADV shared resistance pathway; and rtN236 T/A mutation, which was reported to decrease the sensitivity to TDF, presented in 53.4% (39/73) pregnant women and 5.5% of patients had mutation frequencies greater than 20%. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I;M204V;N236T;N236A 45;45;369;369 52;52;377;377 RT;RT;RT;P 43;259;367;120 45;261;369;124 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. At the compensatory mutation sites, 15.1% (11/73) participants had L80I/V mutation that is associated with resistance to LAM. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV L80I;L80V 67;67 73;73 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. However, rtI169 T, rtA194 T, rtV173 L, rtL180 M, rtL82 M, rtS85 A, rtV207I, rtL217 R, and rtS/C256G mutations were not present before TBV treatment. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV C256G;I169T;A194T;V173L;L180M;L82M;S85A;V207I;L217R;S256G 92;11;21;31;41;51;60;69;78;92 99;17;27;37;47;56;65;74;84;99 RT;RT;RT;RT;RT;RT;RT;RT;RT 9;19;29;39;49;58;67;76;90 11;21;31;41;51;60;69;78;92 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. In addition, the patients were further divided into high mutation group (the frequency of rtM204I >= 20%, 10%, and 5%) and low mutation group (the frequency < 20%, 10%, and 5%) before the TBV treatment. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I 92 97 RT 90 92 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Multibase mutations combined with rtM204I/V were analyzed; rtM204I + rtN236 T and rtM204 V + rtN236 T appeared to be the most common ones (16.4% and 17.8%, resp.). 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I;M204V;M204I;N236T;M204V;N236T 36;36;61;71;84;95 43;43;66;77;90;101 RT;RT;RT;RT;RT 34;59;69;82;93 36;61;71;84;95 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. No change was found in the frequencies of rtM204I mutation before and after (0.34 +- 0.23 vs. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I 44 49 RT 42 44 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. RtM204I/V + rtL80I/V and rtM204I + rtA181 T/V may affect the sensitivity to LAM, TBV, and ADV; they also presented but the proportions of the mutations were low (Table 3). 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV L80I;L80V;M204I;A181T;A181V 14;14;27;37;37 20;20;32;45;45 RT;RT;RT;RT 0;12;25;35 2;14;27;37 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Similar trend was observed in groups with 10% (72.7% vs. 72.1%,聽P=0.968) and 5% frequency of rtM204I (62.5% vs. 75.0%,聽P=0.325). 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I 95 100 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. The frequency of rtM204I was not significantly higher in patients with HBV DNA load >=103 IU/mL than that of patients with HBV DNA <103 IU/mL at delivery (0.13 +- 0.12 vs. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I 19 24 RT 17 19 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. The proportions of patients with rtN236 T/A mutation have no difference with those of patients with rtM204I/V mutation (41.1% vs. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV N236T;N236A;M204I;M204V 35;35;102;102 43;43;109;109 RT;RT 33;100 35;102 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Two patients who accepted LAM before pregnancy had preexisting rtM204I mutation. 2021 The Canadian journal of infectious diseases & medical microbiology Result HBV M204I 65 70 RT 63 65 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Both real-time PCR and direct sequencing protocols indicated that 13 out of the 32 samples (40.625%) were M204V-positive. 2021 Journal of clinical and translational hepatology Result HBV M204V 106 111 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Eighteen samples (56.25%) were identified as M204V-negative by both real-time PCR and direct sequencing. 2021 Journal of clinical and translational hepatology Result HBV M204V 45 50 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. None of the samples were found to be M204V false positives. 2021 Journal of clinical and translational hepatology Result HBV M204V 37 42 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. One sample (3.125%) was identified as M204V-positive by direct sequencing, whereas the real-time PCR results could not be evaluated. 2021 Journal of clinical and translational hepatology Result HBV M204V 38 43 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. Overall, the sensitivity of real-time PCR for detecting the M204V mutation was 92.86% (13/14), with a specificity of 100%. 2021 Journal of clinical and translational hepatology Result HBV M204V 60 65 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. The specificity and sensitivity of the probes were confirmed via the amplification of positive serum samples, which had been verified as containing the M204V/I mutation via Sanger sequencing. 2021 Journal of clinical and translational hepatology Result HBV M204I;M204V 152;152 159;159 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. We designed two different probes for 204 nucleotide mutations, to ensure the presence of a mutation, and subsequently designed two specific probes each for M204V or M204I. 2021 Journal of clinical and translational hepatology Result HBV M204V;M204I 156;165 161;170 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. In total, the sQ129H IEM was detected in 18.2% (n = 8/44) of the individuals with available sequence. 2021 Viruses Result HBV Q129H 14 20 S 14 15 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Other mutations detected on the Pol gene sequences were N248H (2.6%; n = 7); E263D (19.4%; n = 6); K11R (6.5%; n = 2); S53I (19.4%; n = 6); and one (3.2%) each of L77V, D134H, V56M, and D271N mutations, none of which has been reported in HBV genotype E, and the significance of this is not yet known. 2021 Viruses Result HBV N248H;E263D;K11R;S53I;L77V;D134H;V56M;D271N 56;77;99;119;163;169;176;186 61;82;103;123;167;174;180;191 P 32 35 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Out of the 31 Pol gene sequences obtained, a predominance of the M336L mutation (96.8%; n = 30) was observed. 2021 Viruses Result HBV M336L 65 70 P 14 17 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The mutational analysis of the partial HBs and Pol gene sequences revealed the presence of the escape mutation Q129H in eight HBV isolates sequenced in this study (Figure 3). 2021 Viruses Result HBV Q129H 111 116 S;P 39;47 42;50 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The sequences with accession numbers MZ398363 (BD-021), MZ398364 (BD-042), MZ398365 (BD-043), MZ398366 (BD-040) and MZ398367 (BD-048) MZ368887 (BD-026B), MZ368888 (BD-056B), and MN819056 (PH-069) have the sQ129H mutation on the HBs part. 2021 Viruses Result HBV Q129H 205 211 S;S 228;205 231;206 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. The following mutation pairs were observed: T115S (3/20, 15%), P120T/S (3/20, 15%), T126S (1/20, 5%), Q129R (2/20, 10%), M133T (2/20, 10%), S143L (5/20, 25%), D144E/A (3/20, 15%), and G145R/A (4/20, 20%) (Table 3). 2021 Infection and drug resistance Result HBV T115S;P120T;P120S;T126S;Q129R;M133T;S143L;D144E;D144A;G145R;G145A 44;63;63;84;102;121;140;159;159;184;184 49;70;70;89;107;126;145;166;166;191;191 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. Mutation rtM204V conferring resistance to 3CT occurred predominantly at 26.7% in all the patients followed by rtL180M (20.0%) and rtV173L at 13.3%. 2021 International journal of health sciences Result HBV M204V;L180M;V173L 11;112;132 16;117;137 RT;RT;RT 9;110;130 11;112;132 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. On the other hand, 5 patients (11.1%) had rtM204V mutations with rtV173L and rtL180M secondary mutations [Table 2]. 2021 International journal of health sciences Result HBV M204V;V173L;L180M 44;67;79 49;72;84 RT;RT;RT 42;65;77 44;67;79 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. Six patients (13.3%) had rtV173L multiple mutations at rtM204V with rtL180M secondary mutation. 2021 International journal of health sciences Result HBV V173L;M204V;L180M 27;57;70 32;62;75 RT;RT;RT 25;55;68 27;57;70 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. Triple nucleoside analog linked to mutation existed at rtM204V with secondary mutation at rtL180M and mutation rtV173L. 2021 International journal of health sciences Result HBV M204V;L180M;V173L 57;92;113 62;97;118 RT;RT;RT 55;90;111 57;92;113 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. A similar profile was observed for the density gradient of I97L-HBV/NL, a peak of HBsAg at fraction 13 and 2 peaks of NL DNA at fractions of 13 and 17 (Figure 3E, upper panels). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 59 63 S 82 87 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. At the end of the observation, the number of patients who achieved ALT within the normal range was higher in the HBV-I97L-infected group than in the HBV-I97wt-infected group. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 117 121 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. At the peak fraction of infectivity, the mean infectivity titer adjusted by NL DNA was 165.0 +- 3.3 and 49.9 +- 5.4 (relative light units [RLU]/copy) for I97wt- and I97L-HBV/NL, respectively (Table 3). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 165 169 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Because concentrated culture media containing the same amount of HBV DNA were applied to these density gradients, the HBV DNA titers in the 2 peaks were comparable (fractions 14 and 16 for HBV-I97wt and fractions 13 and 16 for HBV-I97L). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 231 235 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. By using the purified viruses HBV-I97wt and -I97L, the efficiencies of the steps of attachment, internalization, and cccDNA synthesis were analyzed. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 45 49 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Clinical Characteristics and Transition of HBV DNA and HBsAg Levels in Patients Infected With HBV-I97wt or HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 111 115 S 55 60 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Detection of HBV DNA Species in Cell Culture-Generated HBV-I97wt and -I97L. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 70 74 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L in the HBV Reporter Virus Infection System. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 11 15 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L on Cell Culture-Generated HBV. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 11 15 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L on Interaction Between HBc and L-HBs. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 11 15 C;S 39;49 42;52 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L Substitution on cccDNA Synthesis. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 11 15 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. For the density gradient of HBV-I97L, the highest amount of RC was also detected in the peak fraction of HBV DNA (fraction 13), but the ratio of the band density of RC/SS in fraction 13 was 1.33. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 32 36 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBeAg-negative patients (n = 77; Figure 1) were divided into 2 groups according to the amino acid, isoleucine (HBV-I97wt) or leucine (HBV-I97L), at position 97 in the HBc region. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 138 142 C;C 167;0 170;5 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBsAg levels in the culture medium were comparable between I97wt-HBV/NL and I97L-HBV/NL. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 76 80 S 0 5 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBV-I97L and HBV-I97wt were transfected into HepG2 cells, and the production of HBV proteins and infectious viruses was assessed. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 4 8 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. HBVcc of HBV-I97wt and HBV-I97L were also analyzed by iodixanol density gradient, applying the same amount of HBV DNA to compare the infectivity (Figure 4B and C). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 27 31 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. However, the efficiency of cccDNA synthesis after infection with HBV-I97L was significantly lower than that after infection with HBV-I97wt (Figure 7B). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 69 73 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. However, the level of core-associated HBV DNA was significantly lower in the HBV-I97L-transfected cells than in HBV-I97wt-transfected cells when measured by real-time PCR with the HBs set (Figure 7D, left). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 81 85 C;S 22;180 26;183 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In contrast, HBsAg and HBV DNA became undetectable in 11 (27.5%) and 14 (35.0%) patients with HBV-I97L, respectively. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 98 102 S 13 18 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In the case of I97L-HBV/NL, the amount of HBcrAg in fraction 16 decreased, with another peak at fraction 13. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 15 19 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In the density gradients of HBV-I97wt and HBV-I97L, HBsAg peaked at fraction 13, but the HBsAg level in the peak fraction of HBV-I97L was higher than that of HBV-I97wt because of the presence of more HBsAg in the culture medium of HBV-I97L containing the same amount of HBV DNA. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L;I97L 46;129;235 50;133;239 S;S;S 52;89;200 57;94;205 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Infection with the same amount from the fractions of these gradients revealed lower infectivity for I97L-HBV/NL than for I97wt-HBV/NL (Figure 3D and E, lower panels). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 100 104 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Levels of HBsAg and HBV DNA were significantly lower in patients with HBV-I97L than in those with HBV-I97wt (P = .029 and <.0001, respectively). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 74 78 S 10 15 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. On the other hand, in the density gradient of HBV-I97L, the amount of HBV DNA in both peak fractions of HBsAg (fraction 13) and HBcrAg (fraction 16) was higher when using the HBx set than the HBc set (Figure 6C, right). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 50 54 C;S;X 192;104;175 195;109;178 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Similarly, fraction 14 of HBV-I97L showed the peak infectivity, and the number of HBV-positive cells was 1.64 x 102 +- 2.36 x 101, indicating approximately 3-fold lower infectivity than that of HBV-I97wt (Figure 4B and C, lower panel). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 30 34 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Specifically, the HBV DNA titer in the HBV-I97wt and HBV-I97L density gradient fractions was examined by real-time PCR, with primer and probe sets targeting the HBc region (HBc set) and the HBx region (HBx set). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 57 61 C;C;X;X 161;173;190;202 164;176;193;205 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Taken together, our data indicated that the amino acid substitution I97L is associated with the reduction of plus-strand HBV DNA synthesis and the production of immature virions with single-stranded DNA. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 68 72 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The annual reduction in HBsAg in patients with HBV-I97L was -0.25 +- 0.28 log IU/mL and was significantly greater than that in those with HBV-I97wt (-0.12 +- 0.22 log IU/mL; P = .029). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 51 55 S 24 29 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The annual reduction in HBV DNA in the patients with HBV-I97L was -0.36 +- 0.53 log copies/mL and was also significantly greater than that in those with HBV-I97wt (-0.12 +- 0.44 log copies/mL; P = .030). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 57 61 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The culture medium level of hepatitis B core-related antigen (HBcrAg) was higher for I97L-HBV/NL than for I97wt-HBV/NL, whereas the NL DNA titer was lower in I97L-HBV/NL than in I97wt-HBV/NL (Figure 3B). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 85;158 89;162 C 40 44 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The effects of I97L on the cell culture-generated HBV (HBVcc) were also evaluated. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 15 19 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The efficiencies of pgRNA transcription were similar between the molecular clones of HBV-I97wt and -I97L (Figure 7C). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 100 104 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The efficiency of cccDNA synthesis in I97L-transfected cells was also substantially lower than that in I97wt-transfected cells (Figure 7E). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 38 42 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The extracellular and intracellular HBsAg levels of HBV-I97L-transfected cells were similar to those of HBV-I97wt-transfected cells (Figure 4A, left). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 56 60 S 36 41 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The extracellular HBcrAg level of HBV-I97L-transfected cells was significantly higher than that of HBV-I97wt-transfected cells, although intracellular HBcrAg levels of these clone-transfected cells were comparable (Figure 4A, middle). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 38 42 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The extracellular HBV DNA level of HBV-I97L-transfected cells was significantly lower than that of HBV-I97wt-transfected cells (Figure 4A, right). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 39 43 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The highest infectivity titers that normalized with GEq were observed at fraction 14 of HBV-I97wt (1.44 x 10-3 count/GEq) and at fraction 15 of HBV-I97L (3.89 x 10-4 count/GEq). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 148 152 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The NanoLuc signal generated by the interaction was significantly higher in the I97L-HBc-LgBiT transfected cells than that in the I97wt-HBc-LgBiT transfected cells (Figure 5B). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 80 84 C;C 85;136 88;139 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The NL DNA level in the peak fraction was lower for I97L-HBV/NL than for I97wt-HBV/NL, depending on the difference in NL DNA titer in the culture media. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 52 56 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The plasmid of I97L-HBc-LgBiT that expresses the fusion protein of HBc with the I97L substitution and LgBiT was also prepared. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 15;80 19;84 C;C 20;67 23;70 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The ratio of HBc/HBx was significantly lower in I97L-transfected cells than that in I97wt-transfected cells. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 48 52 C;X 13;17 16;20 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The ratio of the HBcrAg level in fraction 13 to fraction 16 was higher for HBV-I97L than HBV-I97wt, suggesting higher levels of envelope-interacted HBcrAg for HBV-I97L than HBV-I97wt. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 79;163 83;167 S 128 136 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. These data suggested that the amount of HBc protein that interacts with HBsAg increased for I97L-HBV/NL. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 92 96 C;S 40;72 43;77 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. These rates of undetectable HBsAg and HBV DNA levels were significantly higher in patients with HBV-I97L than in those with HBV-I97wt (P = .028 and .012, respectively). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 100 104 S 28 33 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Thirty-seven patients were included in the HBV-I97wt-infected group, and 40 patients were included in the HBV-I97L-infected group (Table 1). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 110 114 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. To assess the effects of amino acid substitution I97L in the HBc region on the HBV life cycle, we used an infection system with recombinant HBV reporter virus (HBV/NL) encoding NanoLuc luciferase (NL). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 49 53 C 61 64 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. To assess the effects of I97L on the HBV life cycle, we evaluated the efficiency of each step in HBV infection. 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 25 29 HBV infections 97 110 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. To confirm the efficient interaction between I97L-HBc and HBs proteins, we used the NanoLuc Binary Technology (NanoBiT). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 45 49 C;S 50;58 53;61 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. To evaluate the underlying mechanisms of the difference in infectivity between these clones, we compared HBV DNA species in the fractions from iodixanol density gradients of HBV-I97wt and -I97L by Southern blotting (Figure 6A). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 189 193 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. We assessed the HBV DNA species of core-associated HBV DNA by Southern blotting and found a predominance of SS in I97L-transfected cells in comparison with I97wt-transfected cells (Figure 7D, middle). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L 114 118 C 35 39 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. We introduced I97L into the replication-competent HBV genotype C molecular clone, and the clone generated (HBV-I97L) was compared with the genotype C wild-type molecular clone (HBV-I97wt). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 14;111 18;115 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. We prepared 2 kinds of encapsidation signal-lacking plasmids (HBV-dE) containing I97wt and I97L and transfected them with the encapsidation competent-reporter plasmid (HBV-NL) into HepG2 cells to obtain the HBV reporter viruses I97wt-HBV/NL and I97L-HBV/NL (Figure 3A). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 91;245 95;249 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. When infected with I97wt-HBV/NL and I97L-HBV/NL at 20 genome equivalents (GEq) per cell, NL activity was substantially (approximately 4-fold) lower in I97L-HBV/NL-infected cells than in I97wt-HBV/NL-infected cells (Figure 3C). 2021 Cellular and molecular gastroenterology and hepatology Result HBV I97L;I97L 36;151 40;155 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. 5 of the 7 sites were missense mutations, including 356S>A (T192G), 444S>P (T456C), 807D>V (A1546T), 10R>K (G2337A) on P gene, and 331A>V (C659T) on the S gene (Table 7). 2021 Computational and structural biotechnology journal Result HBV T456C;T192G;S444P;S356A;G2337A;D807V;C659T;A331V;A1546T;R10K 76;60;68;52;108;84;139;131;92;101 81;65;74;58;114;90;144;137;98;106 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. In the group of patients undergoing treatment, strains of HBV with resistance mutations (rtM204V/I/S) associated or not with compensatory mutations (rtL180M, rtV173L) were identified in 13.9% (5/36) of the analyzed samples. 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Result HBV M204V;M204I;M204S;L180M;V173L 91;91;91;151;160 100;100;100;156;165 RT;RT;RT 89;149;158 91;151;160 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. In the group of patients who were not undergoing treatment, 1.1% (1/90) of the samples presented resistance mutations (rtM204V) to LAM, ADF and FTC, as well as partial resistance to ETV, in addition to a mutation (rtA181T) that confers partial resistance in vitro, but does not imply in vivo resistance to TDF. 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Result HBV A181T;M204V 216;121 221;126 RT;RT 119;214 121;216 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. One sample (1.1%) presented a compensatory mutation (rtV/F/L/M207I), which typically appears after other primary variants of resistance to LAM; and 26.7% (24/90) of the samples showed potential resistance mutations for ADF (rtV214A, rtL217R, rtP237H, rtN238T, rtQ215S, and rtI233V). 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Result HBV F207I;L207I;M207I;V207I;V214A;L217R;P237H;N238T;Q215S;I233V 55;55;54;55;226;235;244;253;262;275 66;66;66;66;231;240;249;258;267;280 RT;RT;RT;RT;RT;RT;RT 53;224;233;242;251;260;273 55;226;235;244;253;262;275 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. Strains with partial resistance mutations for ETV (rtM204V/I/S) or potentially associated with resistance to ADF (rtV214A, rtL217R, rtQ215S, rtN238T, and rtP237H) were identified in 13.9% (5/36) and 19.4% (7/36) of the samples, respectively. 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Result HBV M204V;M204I;M204S;V214A;L217R;Q215S;N238T;P237H 53;53;53;116;125;134;143;156 62;62;62;121;130;139;148;161 RT;RT;RT;RT;RT;RT 51;114;123;132;141;154 53;116;125;134;143;156 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. In contrast, the map of HBc-F97L (EMDB 4417 and all maps generated in this study (Table 1), (Figure 6) were reconstructed from HBc-CLP purifications without TX100 (and any other detergents) and did not show a pocket factor. 2021 Viruses Result HBV F97L 28 32 C;C 24;127 27;130 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Interestingly, in the absence of TX100, the side chain densities of Leu-97 in chains A and D (Figure 6c, L97*) pointed towards the center of the spike similar as Phe-97 in "conformation 1" of wt HBc whereas the densities of Leu-97 in chains B and C pointed towards the side of the spike similar as Phe-97 in "conformation 2" of wt HBc (Figure 4). 2021 Viruses Result HBV L97X 105 109 C;C 195;331 198;334 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Intrigued by the changes in the rotamer conformation of Phe-97, we revisited the mutant HBc-F97L, which is a naturally occurring variant with an immature secretion phenotype. 2021 Viruses Result HBV F97L 92 96 C 88 91 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Next, we looked at the mutants HBc-P5T and HBc-L60V, which have a low secretion phenotype. 2021 Viruses Result HBV P5T;L60V 35;47 38;51 C;C 31;43 34;46 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Previous studies have shown that CLPs of both mutants are structurally almost indistinguishable from wt HBc with the exception that Phe-97 adopts both alternate rotamer conformations with similar occupancy in HBc-L60V. 2021 Viruses Result HBV L60V 213 217 C;C 104;209 107;212 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. The maps of both mutants with added TX100 showed TX100 in the hydrophobic pockets at the same positions as in wt HBc and in HBc-F97L (Figure 7). 2021 Viruses Result HBV F97L 128 132 C;C 113;124 116;127 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. Thus, we suspected that this earlier map represents HBc-F97L in a TX100 bound state, which is plausible as TX100 was used during cell lysis. 2021 Viruses Result HBV F97L 56 60 C 52 55 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. We added TX100 to the detergent-free purified HBc-F97L CLPs followed by electron cryo-microscopy and image processing. 2021 Viruses Result HBV F97L 50 54 C 46 49 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Accordingly, extracellular particle-associated HBV DNA was clearly detected for the WT but not the W3S or W3S (N146G) mutant (Figure 2E, right). 2021 Viruses Result HBV W3S;W3S;N146G 99;106;111 102;109;116 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. As shown in Figure 1C, the HBeAg and preS1 (LS) expressions in the cells and HBeAg from the medium were not very different among the wild type (WT) and mutants (W3S, and W3S [N146G]), whereas the HBsAg expression from the mutants could not be detected by ELISA (Figure 1C) as reported. 2021 Viruses Result HBV W3S;W3S;N146G 161;170;175 164;173;180 C;C;S;PreS1 27;77;196;37 32;82;201;42 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Comparison of HBs and Pol Amino Acids Sequences of HBV-WT (adr4) and W3S. 2021 Viruses Result HBV W3S 69 72 S;P 14;22 17;25 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Figure 1D shows the almost comparable expression of LS and the massive glycosylation of W3S LS. 2021 Viruses Result HBV W3S 88 91 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In order to test the physicochemical properties of WT and W3S particles, CsCl density gradient ultracentrifugation of the virion and/or the HBs particles from the transfected cell culture medium was performed; twelve fractions were collected from the top; and the densities, the preS1 ELISA and the quantity of particle-associated HBV DNA are shown (Figure 3A,B). 2021 Viruses Result HBV W3S 58 61 S;PreS1 140;279 143;284 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In the case of intracellular particle-associated HBV DNA, the maturated HBV replicative intermediates as RC-DNA (RC) and/or double-stranded linear DNA (DSL) were more abundantly detected in W3S and W3S (N146G) (Figure 2E, left), suggesting that the maturation of HBV genome replication should progress with accumulation in the cell. 2021 Viruses Result HBV W3S;W3S;N146G 190;198;203 193;201;208 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Interestingly, the inverse was found for extracellular virion production, which was decreased in W3S and especially in W3S (N146G) at either 5 or 7 days post-transfection (Figure 2D). 2021 Viruses Result HBV W3S;W3S;N146G 97;119;124 100;122;129 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Next, we tested the replication and virion production efficiency of the W3S mutant HBV compared to the WT. 2021 Viruses Result HBV W3S 72 75 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. On the other hand, we could not show the density of glycosylation-deficient HBV (pHB-W3S [N146G]) from the medium of transfected cells because there was almost no virus secretion into the extracellular space (data not shown). 2021 Viruses Result HBV W3S;N146G 85;90 88;95 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Several amino acid mutations in the RT region of the HBVpol were found in the W3S, since the HBs sequence was overlapped with RT (Figure 1A,B, and the bottom). 2021 Viruses Result HBV W3S 78 81 S;RT;RT 93;36;126 96;38;128 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Taken together, these results indicate that W3S virions were produced at a similar pattern in CsCl density profiles to that of the wild type, and glycosylation itself affected HBV virion secretion, as reported previously. 2021 Viruses Result HBV W3S 44 47 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The large S (LS) protein in the lysate was monitored with Western blot analysis, since we had no reliable anti-S antibody in hand and W3S HBsAg was unlikely to be detected. 2021 Viruses Result HBV W3S 134 137 S;S;S 138;4;111 143;11;112 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The large S from W3S (N146G) canceled the glycosylation (Figure 1D). 2021 Viruses Result HBV W3S;N146G 17;22 20;27 S 4 11 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The Physicochemical Properties of the WT and W3S Dane Particles Are Basically Identical. 2021 Viruses Result HBV W3S 45 48 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The pol RT K152R mutation was due to the construction of glycosylation-deficient HBsAg N146G (Figure 1B). 2021 Viruses Result HBV K152R;N146G 11;87 16;92 S;P;RT 81;4;8 86;7;10 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The results demonstrated that WT and W3S virions could be produced at a density of 1.20 to 1.25 g/mL. 2021 Viruses Result HBV W3S 37 40 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The results showed that intracellular core-associated DNA had a tendency to be increased in W3S and W3S (N146G) compared with the WT, at either 5 or 7 days post-transfection (Figure 2D). 2021 Viruses Result HBV W3S;W3S;N146G 92;100;105 95;103;110 C 38 42 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. There was no difference in HBeAg expression among WT, W3S and W3S (N146G), in either the medium or cytoplasm (indicated as cell), at either 5 or 7 days after transfection (Figure 2A,B). 2021 Viruses Result HBV W3S;W3S;N146G 54;62;67 57;65;72 C 27 32 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. These results suggested that the W3S HBsAg should be massively glycosylated at N146 even under replication condition, which was consistent with our previous report. 2021 Viruses Result HBV W3S 33 36 S 37 42 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. To examine this, we constructed an HBV replication-competent plasmid pHB-W3S, which was thought to be massively glycosylated on the HBs with several RT mutations (Figure 1B), and the plasmid pHB-W3S (N146G), which was glycosylation-deficient with the same RT mutations as pHB-W3S on the backbone of pHB-WT (adr4, X01587.1) with exception at K152R (Figure 1B). 2021 Viruses Result HBV W3S;W3S;W3S;N146G;K152R 73;195;276;200;341 76;198;279;205;346 S;RT;RT 132;149;256 135;151;258 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. We reported a diagnostic escape HBs sequence (W3S) in which two mutations, P120K and T123D close to the "a" determinant, were responsible for the escape. 2021 Viruses Result HBV W3S;P120K;T123D 46;75;85 49;80;90 S 32 35 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. 3A and B), suggesting that core-envelope interaction could be normal for mutants CTP and M198P. 2021 Journal of biomedical science Result HBV M198P 89 94 C;S 27;32 31;40 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. By native agarose gel, followed by Western and Southern blot analyses, we observed again significant reduction in the secretion of virion-associated core protein and virion-associated viral DNA of mutant W196P and M198P (lane 3 and 5. 2021 Journal of biomedical science Result HBV W196P;M198P 204;214 209;219 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Drug-resistant polymerase mutant YIDD contains envelope mutations W196L/S. 2021 Journal of biomedical science Result HBV W196S;W196L 66;66 73;73 S;P;P 47;15;33 55;25;37 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Interestingly, in lane 4, the core protein and viral DNA phenotypes of mutant M197P are almost indistinguishable from those of WT HBV. 2021 Journal of biomedical science Result HBV M197P 78 83 C 30 34 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Interestingly, we noted that mutant W196L exhibited significantly increased secretion of genome-containing virions. 2021 Journal of biomedical science Result HBV W196L 36 41 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Next, we performed complementation assay by cotransfecting HuH-7 cells with each of these three envelope protein expression vectors and the pol-null M198P plasmid. 2021 Journal of biomedical science Result HBV M198P 149 154 S;P 96;140 104;143 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. None of these mutants, including mutants CTP, M198P, and W196P, are predicted to have altered the loop size of CYL-II by bioinformatic analysis [software TMHMM v2.0 (http://www.cbs.dtu.dk/services/TMHMM/)]. 2021 Journal of biomedical science Result HBV M198P;W196P 46;57 51;62 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Only the triple mutant CTP and the single mutant M198P are severely deficient in virion secretion (red asterisk, right panel. 2021 Journal of biomedical science Result HBV M198P 49 54 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. relative to the WT control, mutants CTP and M198P had reduced levels of small, middle and large envelope proteins, despite their respective core protein levels are similar to each other. 2021 Journal of biomedical science Result HBV M198P 44 49 C;S 140;90 144;104 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. The defect in genome-containing virion secretion of mutant M198P can be successfully rescued only by cotransfection with the small S envelope expression vector, but not by the L and M expression vectors. 2021 Journal of biomedical science Result HBV M198P 59 64 S 125 141 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. To find out which specific amino acid change of these three clustering CTP mutations is responsible for the lack of virion secretion, we compared virion secretion among single envelope mutations W196C, M197T, and M198P (left panel. 2021 Journal of biomedical science Result HBV W196C;M197T;M198P 195;202;213 200;207;218 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Viral DNA synthesis can only be detected in mutant M197T by Southern blot analysis. 2021 Journal of biomedical science Result HBV M197T 51 56 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. We detected no apparent difference in the subcellular envelope protein HBs and core protein HBc between wild type HBV, triple mutant CTP and single mutant M198P. 2021 Journal of biomedical science Result HBV M198P 155 160 C;S;C;S 79;54;92;71 83;62;95;74 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. we engineered three replicons containing single mutation W196P, M197P, and M198P in the small loop of the HBsAg envelope. 2021 Journal of biomedical science Result HBV W196P;M197P;M198P 57;64;75 62;69;80 S;S 112;106 120;111 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. We found no apparent difference in virion secretion between WT-HBV, mutant W196S, and a control mutant W196F. 2021 Journal of biomedical science Result HBV W196S;W196F 75;103 80;108 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. We therefore examined the virion secretion of a highly common polymerase mutant YIDD, which contains corresponding envelope mutations W196L or W196S (from tryptophan to leucine or serine). 2021 Journal of biomedical science Result HBV W196L;W196S 134;143 139;148 S;P;P 115;62;80 123;72;84 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. While mutant M197T has a moderate reduction in empty virion secretion, triple mutant AAA and single mutant W196C exhibited a level of empty virion secretion similar to that of wild type (WT) HBV. 2021 Journal of biomedical science Result HBV M197T;W196C 13;107 18;112 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. While the lamivudine-resistant mutations corresponding to sW196L/S inhibited secretion of HDV particles, it remains unclear if HBV virion secretion is also affected by the drug resistant polymerase mutants. 2021 Journal of biomedical science Result HBV W196S;W196L 58;58 66;66 P;S 187;58 197;59 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Among these E2 mutations, E2G was significantly frequent in the OBIs compared with the control group (p < 0.05), while no significant difference was found regarding other types of E2 mutation between the two groups (p > 0.05) (Table 1). 2021 Frontiers in microbiology Result HBV E2G 26 29 Occult Hepatitis B 64 68 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Compared with pHBV1.3C (median, 0.030 IOD/pixel), the fluorescence density of pHBV1.3C-E2A-transfected cells (median, 0.048 IOD/pixel) was significantly higher (1.6-fold vs. 2021 Frontiers in microbiology Result HBV E2A 87 90 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. extracellular), while pHBV1.3C-E2D was significantly decreased than extracellular (91.2% vs. 2021 Frontiers in microbiology Result HBV E2D 31 34 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Hence, pHBV1.3B/C-E2G/A could decrease HBsAg secretion, whereas pHBV1.3C-E2D promoted HBsAg secretion. 2021 Frontiers in microbiology Result HBV E2D 73 76 S;S 39;86 44;91 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. However, no significant changing was found in pHBV1.3C-E2D (median, 0.023 IOD/pixel) (Figure 3B). 2021 Frontiers in microbiology Result HBV E2D 55 58 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Immunofluorescence density analysis showed that, compared with pHBV1.3B (median, 0.040 IOD/pixel), the pHBV1.3B-E2G-transfected cells (median, 0.097 IOD/pixel) and pHBV1.3B-E2A-transfected cells (median, 0.061 IOD/pixel) were significantly higher (1.5-2.4-fold vs. 2021 Frontiers in microbiology Result HBV E2G;E2A 112;173 115;176 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Mutation E2G/A/V/D were identified in 1.1-11.2% of the genotype B OBIs, and E2G/A/D were identified in 3.3-13.3% of the genotype C OBIs (Table 1). 2021 Frontiers in microbiology Result HBV E2G;E2A;E2V;E2D;E2G;E2A;E2D 9;9;9;9;76;76;76 18;18;18;18;83;83;83 Occult Hepatitis B;Occult Hepatitis B 66;131 70;135 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Notably, unlike pHBV1.3B-E2G, which could cause HBsAg intracellular accumulation (246.7% vs. 2021 Frontiers in microbiology Result HBV E2G 25 28 S 48 53 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Overall, E2 mutations (E2G/A/V/D) existed in 21.8% (26/119) of the OBI subjects, while no E2 mutation was found in the control group. 2021 Frontiers in microbiology Result HBV E2G;E2A;E2V;E2D 23;23;23;23 32;32;32;32 Occult Hepatitis B 67 70 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. pHBV1.3B) (p < 0.0001), while pHBV1.3B-E2V (median, 0.027 IOD/pixel) and pHBV1.3B-E2D (median, 0.031 IOD/pixel) were significantly lower (p < 0.05) (Figure 3A). 2021 Frontiers in microbiology Result HBV E2V;E2D 39;82 42;85 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. pHBV1.3B) (p < 0.05), pHBV1.3C-E2G could lead to a very significant HBsAg decrease both extracellularly (0.5% vs. 2021 Frontiers in microbiology Result HBV E2G 31 34 S 68 73 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The intracellular relative HBsAg level of pHBV1.3B-E2G significantly increased by 146.7%, while other E2 mutations significantly decreased by 24.3-88.8% (p < 0.05) (Figures 1A,B and Supplementary Table 2). 2021 Frontiers in microbiology Result HBV E2G 51 54 S 27 32 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The positive fluorescent cells transfected with pHBV1.3C-E2G were too few to involve in the fluorescence density analysis. 2021 Frontiers in microbiology Result HBV E2G 57 60 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The results showed that there are typical N-terminal signal peptides in S proteins with E2G/A mutations in genotypes B and C, with a typical cleavage site (CS) for peptidase at positions 27 and 28 (Supplementary Figure 2). 2021 Frontiers in microbiology Result HBV E2G;E2A 88;88 93;93 S 72 73 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The staining of pHBV1.3B-E2V/D or pHBV1.3C-E2D-transfected cells was similar to that of genotype-matched pHBV1.3B/C. 2021 Frontiers in microbiology Result HBV E2V;E2D;E2D 25;25;43 30;30;46 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Fourteen triple nucleotide mutations were found among which the more frequent mutation in LC and HCC groups were A110S/K, Y111E, and F112L while K91W/R and R96C were found in the lowest frequency (Figs 6-8). 2022 PloS one Result HBV A110S;A110K;Y111E;F112L;K91W;K91R;R96C 113;113;122;133;145;145;156 120;120;127;138;151;151;160 Hepatocellular carcinoma;Liver cirrhosis 97;90 100;92 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Moreover, some non-reported mutations such as E109A/Y (43.75%), A110S/K (37.5%), Y111D/E (50%), and F112L (43.75%) were also found in high frequency in HCC and LC (14.28%, 14.28%, 28.2% and 42.8% respectively) patients as compared to CHB (12.8%, 15.2%, 16.8% and 16% respectively) (Figs 2 and 3). 2022 PloS one Result HBV E109A;E109Y;A110S;A110K;Y111D;Y111E;F112L 46;46;64;64;81;81;100 53;53;71;71;88;88;105 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 152;234;160 155;237;162 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Nine single nucleotide mutations were found in the Enh-II region, including the highest incidence rate of mutation L108D, Y111D, K113E in HCC as compared to other groups. 2022 PloS one Result HBV L108D;Y111D;K113E 115;122;129 120;127;134 Hepatocellular carcinoma 138 141 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Non-reported mutations such as E109A/Y (43.75%), A110S/K (37.5%), Y111D/E (50%), F112L (43.75%) were found in high frequency in the HCC group as compared to other groups (Table 2). 2022 PloS one Result HBV E109A;E109Y;A110S;A110K;Y111D;Y111E;F112L 31;31;49;49;66;66;81 38;38;56;56;73;73;86 Hepatocellular carcinoma 132 135 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Sequencing and data analysis showed the highest frequency of S101F (62.2%), A102V/R/G/I (56.25%), and M103L/A (68.75%) mutation in HCC and 57.1%, 42.8%, and 28.52% respectively in LC as compared to 16%, 15.2%, and 18.4% respectively in CH patients. 2022 PloS one Result HBV S101F;A102V;A102R;A102G;A102I;M103L;M103A 61;76;76;76;76;102;102 66;87;87;87;87;109;109 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 131;236;180 134;238;182 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Similarly, 9 double nucleotide mutations were also detected in different regions of the Enh-II region having A102G, M103A, and K118I in HCC compared to CH and LC. 2022 PloS one Result HBV A102G;M103A;K118I 109;116;127 114;121;132 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 136;152;159 139;154;161 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. One patient had the double resistance polymerase mutation rtM204V/I-rtL180M, in both serum and DBS. 2022 Scientific reports Result HBV M204V;M204I;L180M 60;60;70 67;67;75 P;RT;RT 38;58;68 48;60;70 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Clone 1-2 harbored 7 mutations (AIHILAT: rtT38A (A), rtV191I (I), rtN226H (H), rtV266I (I), rtQ267L (L), rtS317A (A) and rtA329T (T)) (Figure 2a). 2022 Biomedicines Result HBV T38A;V191I;N226H;V266I;Q267L;S317A;A329T 43;55;68;81;94;107;123 47;60;73;86;99;112;128 RT;RT;RT;RT;RT;RT;RT 41;53;66;79;92;105;121 43;55;68;81;94;107;123 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. HBV RT rtL180M and rtM204V Mutations Are Associated with BFV Resistance. 2022 Biomedicines Result HBV L180M;M204V 9;21 14;26 RT;RT;RT 4;7;19 6;9;21 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Since the previous reports showed that two mutations (rtL180M or rtM204V) are associated with resistance to NA drugs such as LMV and ETV, the MVLIM mutant clone were divided into four distinct clones (LIM, MV, M, and V) to further screen the mutation that is responsible for BFV resistance. 2022 Biomedicines Result HBV L180M;M204V 56;67 61;72 RT;RT 54;65 56;67 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Taken together, these observations indicated that rtL180M and/or rtM204V substitution contributed to development of BFV resistance. 2022 Biomedicines Result HBV L180M;M204V 52;67 57;72 RT;RT 50;65 52;67 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. The replication-defective rtM204V mutation was compensated by rtL180M mutation. 2022 Biomedicines Result HBV M204V;L180M 28;64 33;69 RT;RT 26;62 28;64 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. This phenomenon is consistent with previous report, demonstrating that the rtL180M mutation in HBV polymerase is commonly accompanied by rtM204V or rtM204I mutations. 2022 Biomedicines Result HBV L180M;M204V;M204I 77;139;150 82;144;155 P;RT;RT;RT 99;75;137;148 109;77;139;150 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. This result is consistent to the previous reports that rtL180M and rtM204V mutations are associated with ETV resistance. 2022 Biomedicines Result HBV L180M;M204V 57;69 62;74 RT;RT 55;67 57;69 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. When compared to the WT, Clone 1-1 harbored 10 mutations (IRHEKMVLIM: rtV23I (I), rtH55R (R), rtY124H (H), rtD134E (E), rtN139K (K), rtL180M (M), rtM204V (V), rtQ267L (L), rtL269I (I) and rtL336M (M)). 2022 Biomedicines Result HBV V23I;H55R;N139K;Y124H;D134E;L180M;M204V;Q267L;L269I;L336M 72;84;122;96;109;135;148;161;174;190 76;88;127;101;114;140;153;166;179;195 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 70;82;94;107;120;133;146;159;172;188 72;84;96;109;122;135;148;161;174;190 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. When the rtM204V mutation was accompanied by rtL180M, the replicative capacity was increased, demonstrating the complementary function of rtL180M mutation. 2022 Biomedicines Result HBV M204V;L180M;L180M 11;47;140 16;52;145 RT;RT;RT 9;45;138 11;47;140 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Data in Table 4 indicate that both wild-type rHBsAg and the rHBsAg G145R mutant caused a statistically significant stimulation of the production of IFN-gamma, TNF-alpha, and IL-10, but no effect on IFN-alpha production. 2022 Vaccines Result HBV G145R 67 72 S;S 45;60 51;66 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. However, the CD69 activation induced by the rHBsAg G145R mutant was weaker compared with wild-type rHBsAg. 2022 Vaccines Result HBV G145R 51 56 S;S 44;99 50;105 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast to wild-type rHBsAg, rHBsAg with the G145R mutation caused a statistically significant production of IL-2, and while the amount of secreted IL-2 was low with the average concentration of 22 pg/mL, it was comparable to the level of IL-2 response to PHA stimulation (21 pg/mL). 2022 Vaccines Result HBV G145R 49 54 S;S 25;33 31;39 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, rHBsAg with the G145R mutation significantly suppressed PHA-induced activation of the CD69 molecule on B cells, NK cells, and CD8+ T cells. 2022 Vaccines Result HBV G145R 29 34 S 13 19 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. On the other hand, costimulation with wild-type or mutant rHBsAg along with PHA increased the IL-2 level 3.15 times for wild-type rHBsAg (p = 0.0035) and 1.28 times for the G145R mutant HBsAg (p = 0.4004), compared to stimulation with these antigens alone. 2022 Vaccines Result HBV G145R 173 178 S;S;S 186;58;130 191;64;136 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. rHBsAg with the G145R mutation had no statistically significant effect on the expression of activation markers on PBMC from healthy donors except the expression of CD69 on all tested cells. 2022 Vaccines Result HBV G145R 16 21 S 0 6 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Table 2 and Figure 1, Figure 2 and Figure 3 summarize the data on the expression of activation markers on PBMC after antigenic stimulation with wild-type rHBsAg (ayw2) or rHBsAg with the G145R mutation (ayw2). 2022 Vaccines Result HBV G145R 187 192 S;S 154;171 160;177 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Table 4 and Figure 4 summarize the levels of cytokine response of PBMC from healthy donors to wild-type rHBsAg (ayw2) and rHBsAg G145R mutant (ayw2) stimulation. 2022 Vaccines Result HBV G145R 129 134 S;S 104;122 110;128 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Taken together, the results indicate a major difference in immunogenicity between wild-type HBsAg and HBsAg with the G145R mutation, both in the spectrum and level of cytokine production and in the expression profile of activation markers on the surface of immunocompetent cells. 2022 Vaccines Result HBV G145R 117 122 S;S;S 92;102;246 97;107;253 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The effects of wild-type rHBsAg (ayw2) and rHBsAg with the G145R mutation (ayw2) on PHA-induced activation of PBMC from healthy donors were also evaluated, and the results are summarized in Table 2. 2022 Vaccines Result HBV G145R 59 64 S;S 25;43 31;49 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Thus, 4 out of 20 donors responded to wild-type rHBsAg, while 18 out of 20 donors responded to the rHBsAg G145R mutant. 2022 Vaccines Result HBV G145R 106 111 S;S 48;99 54;105 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Thus, PBMC of healthy donors responded to stimulation with the rHBsAg G145R mutant with the production of IL-2 approximately 4.5 times more often compared with wild-type rHBsAg. 2022 Vaccines Result HBV G145R 70 75 S;S 63;170 69;176 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Thus, the immunosuppressive effect of the G145R mutant is stronger than that of the wild-type HBsAg. 2022 Vaccines Result HBV G145R 42 47 S 94 99 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Under the same conditions, the rHBsAg G145R mutant added along with PHA had a small trend to increase the IFN-gamma level relative to PHA (1.1 times, p = 0.2466), but this IFN-gamma level was significantly higher compared with stimulation with the rHBsAg G145R mutant alone (1.8 times, p = 0.0337). 2022 Vaccines Result HBV G145R;G145R 38;255 43;260 S;S 31;248 37;254 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. A1762T/G1764A, T1674G, C1653T, T1674G, and T1753C were all identified as independent risk factors of HCC occurrence in our previous cohort study. 2022 Frontiers in oncology Result HBV G1764A;A1762T;T1674G;C1653T;T1674G;T1753C 7;0;15;23;31;43 13;6;21;29;37;49 Hepatocellular carcinoma 101 104 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. In this cohort of HBV-infected patients, combo mutation A1762T/G1764A+C1653T+T1674G, A1762T/G1764A+T1674G+T1753C, and A1762T/G1764A+C1653T+T1753C were all significantly associated with an increased risk of HCC, with an age- and gender-adjusted HR (95% CI) of 1.81 (1.42-2.32), 1.54 (1.11-2.14), and 1.83 (1.32-2.53), respectively ( Figure 1 ). 2022 Frontiers in oncology Result HBV G1764A;G1764A;G1764A;T1674G;C1653T;A1762T;T1674G;A1762T;T1753C;C1653T;A1762T;T1753C 63;92;125;77;70;56;99;85;106;132;118;139 69;98;131;83;76;62;105;91;112;138;124;145 Hepatocellular carcinoma;HBV infections 206;18 209;30 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. The combo mutation A1762T/G1764A+C1653T+T1674G and A1762T/G1764A+T1674G+T1753C were then selected for the following experiments because of higher frequencies in the HBV-infected population. 2022 Frontiers in oncology Result HBV G1764A;G1764A;C1653T;T1674G;A1762T;A1762T;T1674G;T1753C 26;58;33;40;19;51;65;72 32;64;39;46;25;57;71;78 HBV infections 165 177 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. The frequencies of combo mutations A1762T/G1764A+C1653T+T1674G, A1762T/G1764A+T1674G+T1753C, and A1762T/G1764A+C1653T+T1753C in the baseline sera of the HBV-infected population were 10.38%, 7.78%, and 4.4%, respectively. 2022 Frontiers in oncology Result HBV G1764A;G1764A;G1764A;T1674G;C1653T;A1762T;T1674G;A1762T;T1753C;C1653T;A1762T;T1753C 42;71;104;56;49;35;78;64;85;111;97;118 48;77;110;62;55;41;84;70;91;117;103;124 HBV infections 153 165 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. This study investigated four HBx mutants (nt.1374-1838) carrying the HCC-risk mutations: M1, A1762T/G1764A alone; M2, A1762T/G1764A+T1674G+T1753C; M3, A1762T/G1764A+C1653T+T1674G, and Ct-HBx (nt. 2022 Frontiers in oncology Result HBV G1764A;G1764A;G1764A;A1762T;A1762T;T1753C;T1674G;A1762T;T1674G;C1653T 100;125;158;93;118;139;132;151;172;165 106;131;164;99;124;145;138;157;178;171 X;X 29;187 32;190 Hepatocellular carcinoma 69 72 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Moreover, a G to A substitution at nucleotide position 1896 (G1896A) was detected in the pre-C region of one sample (HB55) (S2 Fig), this sample was negative for HBeAg. 2022 PloS one Result HBV G1896A;G1896A 61;12 67;59 C;Precore 162;89 167;94 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Of note, A168V and T127P were detected in the HBsAg of the occult HBV strain (HB51). 2022 PloS one Result HBV A168V;T127P 9;19 14;24 S 46 51 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Of these, T1753A and A1761C mutations were detected in one sample (HB55); and G1764T/A, C1766G/T, and C1773T mutations were detected in two samples (HB35 and HB55). 2022 PloS one Result HBV G1764A;C1766T;T1753A;A1761C;G1764T;C1766G;C1773T 78;88;10;21;78;88;102 86;96;16;27;86;96;108 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Seven amino acid substitutions were detected in HBsAg of strains isolated from pregnant women, including the conversion of Ile Leu at amino acid 110 (I110L), Thr Pro at amino acid 127 (T127P), Asp Glu at amino acid 144 (D144E), Ser Ala at amino acid 154 (S154A), Gly Ala at amino acid 159 (G159A), Ala Gly at amino acid 166 (A166G) and Ala Val at amino acid 168 (A168V) of HBsAg (S1 Fig and Table 2). 2022 PloS one Result HBV I110L;I110L;T127P;D144E;S154A;G159A;A166G;A168V;T127P;D144E;S154A;G159A;A166G;A168V 123;152;160;197;234;271;308;348;189;226;263;300;337;377 150;157;187;226;261;298;335;375;194;231;268;305;342;382 S;S 48;387 53;392 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. T1753A, A1761C, and G1764A mutations caused the conversion of Ile Asn at amino acid 127 (I127N), Lys Gln at amino acid 130 (K130Q), and Val Leu at amino acid 131 (V131L) of the X protein, respectively (S3 Fig). 2022 PloS one Result HBV T1753A;A1761C;G1764A;I127N;K130Q;V131L;I127N;K130Q;V131L 0;8;20;91;128;169;62;99;140 6;14;26;96;133;174;89;126;167 X 183 184 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. T1753A, A1761C, G1764T/A, C1766G/T, and C1773T mutations were detected in the BCP region. 2022 PloS one Result HBV G1764A;C1766T;T1753A;A1761C;G1764T;C1766G;C1773T 16;26;0;8;16;26;40 24;34;6;14;24;34;46 BCP 78 81 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. Mutation analysis of this patient's HBV showed there were three mutants (S143T, D144G, and G145R) in the S gene region, and the mutant of site 1896 in the pre-Core region coexisted with the wild type (G1896A/G), but no mutation in the pre-S1, pre-S2, and BCP gene regions (Details shown in Table 3). 2022 Frontiers in microbiology Result HBV G1896G;S143T;D144G;G145R;G1896A 201;73;80;91;201 209;78;85;96;209 BCP;Precore;PreS1;PreS2;S 255;155;235;243;105 258;163;241;249;106 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Among them, 4 point-mutations W4P/R/Y, S5L/T, A90T/S/G, and L108V/I were observed with the significantly higher rates in the HCC group compared to non-HCC group: W4P/R/Y (12.2% vs 2%, p = 0.005), S5L/T (6.1% vs 1%, p = 0.055), A90T/S/G (6.1% vs 0.5%, p = 0.026) and L108V/I (6.1% vs 0.5%, p = 0.026) (Table 2). 2022 PloS one Result HBV A90T;A90S;A90G;W4P;W4R;W4Y;S5L;S5T;A90T;A90S;A90G;W4P;W4R;W4Y;S5L;S5T;L108V;L108I;L108V;L108I 227;227;227;30;30;30;39;39;46;46;46;162;162;162;196;196;60;60;266;266 235;235;235;37;37;37;44;44;54;54;54;169;169;169;201;201;67;67;273;273 Hepatocellular carcinoma;Hepatocellular carcinoma 125;151 128;154 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Exceptionally, 13 S mutations presented the higher distributions (p<0.1) in the HCC group: F20S (8.2% vs 1%, p = 0.015), D33G (4.1% vs 0%, p = 0.039), (T47A/E/V/K (18.4% vs 7.1%, p = 0.025), R79H (6.1% vs 0%, p = 0.007), L88P (4.1% vs 0%, p = 0.039), P120S/T (on the MHR region, 16.3% vs 6.6%, p = 0.042), G145R (6.1% vs 1%, p = 0.055), S174N (6.1% vs 0.5%, p = 0.026), V190A (6.1% vs 0.5%, p = 0.026), P203R (8.2% vs 2%, p = 0.052), Y206H/F/C (6.1% vs 1.5%, p = 0.094), L209V/S/G (6.1% vs 1%, p = 0.055) and F212Y/L/C (8.2% vs 0.5%, p = 0.006), (Table 4). 2022 PloS one Result HBV T47A;T47E;T47V;T47K;Y206H;Y206F;Y206C;L209V;L209S;L209G;F212Y;F212L;F212C;F20S;D33G;R79H;L88P;P120S;P120T;G145R;S174N;V190A;P203R 152;152;152;152;434;434;434;471;471;471;509;509;509;91;121;191;221;251;251;306;337;370;403 162;162;162;162;443;443;443;480;480;480;518;518;518;95;125;195;225;258;258;311;342;375;408 S 18 19 Hepatocellular carcinoma 80 83 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Only F141V/L/I was found with a significantly higher rate in the HCC group (18.4% vs 9.6%, p = 0.08). 2022 PloS one Result HBV F141V;F141L;F141I 5;5;5 14;14;14 Hepatocellular carcinoma 65 68 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S174N (S) had the highest OR (29.73) with positive predictive value (PPV), negative predictive value (NPV), sentitivity (SEN), specificity (SPE) for predicting HCC respectively, 75%, 81.1%, 6.1%, 99.5%. 2022 PloS one Result HBV S174N 0 5 S 7 8 Hepatocellular carcinoma 160 163 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The final multivariable analysis for related factors to HCC had included gender, age group, HBeAg marker and 6 mutations (PreS1 W4P/R/Y and five S point-mutations as F20S, T47A/E/V/K, P120S/T, S174N, P203R) on Table 5. 2022 PloS one Result HBV T47A;T47E;T47V;T47K;W4P;W4R;W4Y;P120T;S174N;F20S;P120S;P203R 172;172;172;172;128;128;128;184;193;166;184;200 182;182;182;182;135;135;135;191;198;170;191;205 C;PreS1;S 92;122;145 97;127;146 Hepatocellular carcinoma 56 59 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The mutations with a rate over 30% were N51Y/T/S/Q/P 30.4%, V68T/S/I 44.9%, and T/N87S/T/P 46.2%; from 10 to <30% were Q10K/H/R (16.2%), H48Y/N (13.8%), E/D54A/N (25.1%), I/N56H/W (25.9%), K57Q/K (25.1%), A60V (25.5%), D/A62S/T (25.1%), G73S/N (24.3%), and V95A (24.3%); and from 5 to <10% were G35R/K (8.5%), and I84V/M/L (7.7%). 2022 PloS one Result HBV E54A;E54N;D54A;D54N;I56H;I56W;N56H;N56W;D62S;D62T;A62S;A62T;V68T;V68S;V68I;Q10K;Q10H;Q10R;I84V;I84M;I84L;N51Y;N51T;N51S;N51Q;N51P;T87S;T87T;T87P;N87S;N87T;N87P;H48Y;H48N;K57Q;K57K;A60V;G73S;G73N;V95A;G35R;G35K 153;153;153;153;171;171;171;171;219;219;219;219;60;60;60;119;119;119;314;314;314;40;40;40;40;40;80;80;80;80;80;80;137;137;189;189;205;237;237;257;295;295 161;161;161;161;179;179;179;179;227;227;227;227;68;68;68;127;127;127;322;322;322;52;52;52;52;52;90;90;90;90;90;90;143;143;195;195;209;243;243;261;301;301 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The point-mutations on the S gene that owned the rates of >30% of the population were: S53L (37.7%), A184V/G (39.3%), and S210K/N/R/S (39.3%); from 15 to <30% were L21S (29.1%), G44E/V (18.6%), I126T/N/S (21.1%), and M198I/M (18.2%); and from 5 to <15% were V14A/G/Q (10.1%), N40S/K (6.9%), T47A/E/V/K (9.3%), P/L49R/H (5.7%), P62Q/L (9.7%), C76Y/T/W (10.5%), Y100C/F (5.3%), P120S/T (8.5%), R122K (8.9%), M133T/S/L/I (7.7%), Y161F/S (10.1%), T189I (5.3%), S204R/N (10.1%), I208T/S (5.7%), L213I/M (7.3%), and V224A (11.7%). 2022 PloS one Result HBV P49R;P49H;L49R;L49H;S210K;S210N;S210R;S210S;I126T;I126N;I126S;V14A;T47A;T47E;T47V;T47K;C76Y;C76T;C76W;M133T;M133S;M133L;M133I;V14G;V14Q;P120T;S53L;A184V;A184G;L21S;G44E;G44V;M198I;M198M;N40S;N40K;P62Q;P62L;Y100C;Y100F;P120S;R122K;Y161F;Y161S;T189I;S204R;S204N;I208T;I208S;L213I;L213M;V224A 310;310;310;310;122;122;122;122;194;194;194;258;291;291;291;291;342;342;342;406;406;406;406;258;258;376;87;101;101;164;178;178;217;217;276;276;327;327;360;360;376;392;426;426;443;457;457;474;474;490;490;510 318;318;318;318;133;133;133;133;203;203;203;266;301;301;301;301;350;350;350;417;417;417;417;266;266;383;91;108;108;168;184;184;224;224;282;282;333;333;367;367;383;397;433;433;448;464;464;481;481;497;497;515 S 27 28 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The point-mutations with the rates of over 30% were T125S/N/P (30.8%), I150T (42.5%), and V158A (36%); from 10 to <30% of population were M120V/I (11.3%) and F141V/L/I (11.3%); and from 5 to <10% of population were Q121R/K (5.3%), T164I/D/S (6.1%), and F165S/L (5.7%). 2022 PloS one Result HBV T164I;T164D;T164S;F141V;F141L;F141I;T125S;T125N;T125P;I150T;V158A;M120V;M120I;Q121R;Q121K;F165S;F165L 231;231;231;158;158;158;52;52;52;71;90;138;138;215;215;253;253 240;240;240;167;167;167;61;61;61;76;95;145;145;222;222;260;260 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The result found eight variables that composed of males (OR = 4.51, 95%CI 1.78-11.4, p = 0.001), age >=40 (OR = 5.5, 95%CI 2.06-14.68, p = 0.001), HBeAg negative (OR = 2.46, 95%CI 1.1-5.53, p = 0.029) and 5 point-mutations such as W4P/R/Y (OR = 11.56, 95%CI 1.99-67.05, p = 0.006), T47A/E/V/K (OR = 3.67, 95%CI 1.19-11.29, p = 0.023), P120S/T (OR = 3.38, 95%CI 1.09-10.49, p = 0.035), S174N (OR = 29.73, 95%CI 2.12-417.07, p = 0.012) and P203S (OR = 8.45, 95%CI 1.43-50.06, p = 0.019) had significant relations with HCC (Table 6). 2022 PloS one Result HBV T47A;T47E;T47V;T47K;W4P;W4R;W4Y;P120T;P120S;S174N;P203S 282;282;282;282;231;231;231;335;335;385;438 292;292;292;292;238;238;238;342;342;390;443 C 147 152 Hepatocellular carcinoma 516 519 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. They were one mutation on the PreS1 region: W4P/R/Y (OR = 5.48, 95%CI 1.32-22.83) and 5 mutations on the S region: F20S (OR = 9.72, 95%CI 1.55-61.06), T47A/E/V/K (OR = 2.91, 95%CI 1.04-8.13), P120S/T (OR = 4.26, 95%CI 1.58-11.52), S174N (OR = 18.21, 95%CI 1.77-187.65), and P203R (OR = 9.72, 95%CI 1.55-61.06) (Table 5). 2022 PloS one Result HBV T47A;T47E;T47V;T47K;W4P;W4R;W4Y;P120T;F20S;P120S;S174N;P203R 151;151;151;151;44;44;44;192;115;192;231;274 161;161;161;161;51;51;51;199;119;199;236;279 PreS1;S 30;105 35;106 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. No deletion/insertion event was found in the sequences when compared with reference ones, but rare stop codon mutations such as L101* and L76* were also detected. 2022 Clinical and experimental hepatology Result HBV L101X;L76X 128;138 133;142 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The G29D substitution detected in 32% (25/73) of the subjects was the second one, but its frequency among the studied groups was also not significant (p = 0.19). 2022 Clinical and experimental hepatology Result HBV G29D 4 8 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The stop codon of W28* was detected in 55% (40/73) of the patients, which was the most frequent change in the precore sequence, but the difference among the groups was not significant (p = 0.69). 2022 Clinical and experimental hepatology Result HBV W28X 18 22 Precore 110 117 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. M204V/I: 48.8%, plus L180M: 33.3% +- L80V: 28.8% and V173L: 42.2%:a profile suggestive for LAM resistance (with all mutations, except for M204V, also being associated with telbivudine resistance, and the combination of L180M, M204V, andV173L being associated with entecavir (ETV) resistance. 2022 Medicina (Kaunas, Lithuania) Result HBV M204V;M204I;L80V;V173L;L180M;M204V;L180M;M204V 0;0;37;53;21;138;219;226 7;7;41;58;26;143;224;231 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. N236T: 28.8% and A181T/V: 15.5%:a profile suggestive for ADV resistance (and associated with reduced susceptibility to TDF/TAF). 2022 Medicina (Kaunas, Lithuania) Result HBV N236T;A181T;A181V 0;17;17 5;24;24 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. There were no significant differences in the distribution of RAMs in patients infected with different HBV genotypes, except for the compensatory L80V mutation and the adefovir (ADV) resistance mutation N236T, which were more frequently found in HBV genotype A infections (p = 0.032 and p = 0.004, respectively), as shown in Table 3. 2022 Medicina (Kaunas, Lithuania) Result HBV L80V;N236T 145;202 149;207 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. Sequencing of the HBV polymerase revealed two common lamivudine resistant mutations - rtL180M and rtM204V. 2006 Comparative hepatology Conclusion HBV L180M;M204V 88;100 93;105 P;RT;RT 22;86;98 32;88;100 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. Two adefovir resistant mutations, rtA181T and rtN236T, were detected, whereas previous lamivudine resistant mutations, rtL180M and rtM204V, were absent. 2006 Comparative hepatology Conclusion HBV A181T;N236T;L180M;M204V 36;48;121;133 41;53;126;138 RT;RT;RT;RT 34;46;119;131 36;48;121;133 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Upward shifting favors the binding of LdT without enforcing M204 for induced fit effect, and also helps in binding to mutant M204V HBV, while M204I does not support LdT binding due to steric clash. 2008 Antiviral research Conclusion HBV M204V;M204I 125;142 130;147 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. A sequence analysis of 20 independent clones propagated from liver revealed the presence of a homogeneous preC mutated population showing the A1896G stop codon and the A1899G substitution, which stabilised the epsilon structure better, thus avoiding a possible decrease in viral replication; only three clones had a divergent sequence with additional nucleotide point mutations. 2009 Journal of medical case reports Conclusion HBV A1896G;A1899G 142;168 148;174 Precore 106 110 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. Genetically related preC mutants harbouring the A1896G substitution, which prevents the formation of the preC protein, were found in 19 clones propagated from PBMCs. 2009 Journal of medical case reports Conclusion HBV A1896G 48 54 Precore;Precore 20;105 24;109 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. Notably, all of the clones from the different compartments had the preC stop codon mutant and the point mutation A1899G. 2009 Journal of medical case reports Conclusion HBV A1899G 113 119 Precore 67 71 19946588 Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report. The point mutation A1899G, which further stabilises the structure of the epsilon region by pairing with T1855, was invariably detected in PBMCs and plasma (Figure 2). 2009 Journal of medical case reports Conclusion HBV A1899G 19 25 20573234 Infection with hepatitis B virus carrying novel pre-S/S gene mutations in female siblings vaccinated at birth: two case reports. It was discovered that the mother had a novel mutation at the pre-S2 region (psT168A), while the amino acid sequence in the S region was identical to that of the reference sequence. 2010 Journal of medical case reports Conclusion HBV P168A;S168A;T168A 77;77;77 84;84;84 PreS2;S 62;124 68;125 20573234 Infection with hepatitis B virus carrying novel pre-S/S gene mutations in female siblings vaccinated at birth: two case reports. Of these substitutions, four (sL97S, sL98S, sG102R, and sA159P) were novel. 2010 Journal of medical case reports Conclusion HBV L97S;L98S;G102R;A159P 30;37;44;56 35;42;50;62 S;S;S;S 30;37;44;56 31;38;45;57 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. Especially this latter mutation rtM204K and the mutation in the direct neighbourhood of the so called YMDD motif, the rtV207 M exchange, may be considered as novel mutations. 2010 Virology journal Conclusion HBV M204K;V207M 34;120 39;126 RT;RT;P 32;118;102 34;120;106 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1776A mutation was statistically responsible for HBeAg negativity. 2010 BMC infectious diseases Conclusion HBV G1776A 0 6 C 50 55 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. G1896A was indicated to be associated with liver disease progression independent of the infection history. 2010 BMC infectious diseases Conclusion HBV G1896A 0 6 Liver disease 43 56 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In conclusion, our data show that HBc protein with hot-spot mutations (L60V, S87G and I97L) can also inhibit MxA gene expression and different mutations have different effect in Huh7 cells; compared to WT HBc protein and the other two mutated proteins (L60V or S87G), HBc protein with the I97L mutation plays an especial role in suppressing transcription and promoter activity of the MxA gene induced by IFN-alpha. 2010 Virology journal Conclusion HBV L60V;S87G;I97L;L60V;S87G;I97L 71;77;86;253;261;289 75;81;90;257;265;293 C;C;C 34;205;268 37;208;271 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. In conclusion, antigenic index analysis and de novo prediction of tertiary conformation of the three HBsAg variants (T123A, M133L, and T143M) found in Indonesian blood donor samples with undetectable HBsAg revealed that T143M substitution altered the antigenicity most significantly compared to the other two mutation patterns and the other known variants. 2010 Virology journal Conclusion HBV T123A;M133L;T143M;T143M 117;124;135;220 122;129;140;225 S;S 101;200 106;205 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Further studies analyzing the complete genome of HBV strains with the Y100C substitution may elucidate whether this mutation affects HBV replication or if there are mutations in other HBV genomic region that could explain the association of these variants with occult hepatitis B infection. 2011 Hepatitis research and treatment Conclusion HBV Y100C 70 75 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Our findings indicated that Y100C substitution alone did not negatively affect the detection and/or secretion of HBsAg. 2011 Hepatitis research and treatment Conclusion HBV Y100C 28 33 S 113 118 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Since previous studies have described that Y100C variation of the small S protein was frequently detected in the absence of HBsAg and was statistically associated with occult infection, the potential influence of this substitution in the occurrence of this peculiar type of chronic hepatitis B was investigated here. 2011 Hepatitis research and treatment Conclusion HBV Y100C 43 48 S;S 124;66 129;73 Occult Hepatitis B;Chronic Hepatitis B 168;274 184;293 21694884 New approaches in the management of chronic hepatitis B: role of tenofovir. The rtA194T mutation in association with LAM-resistance may confer resistance to TDF, although both in vivo and in vitro studies regarding this mutation demonstrate conflicting results. 2009 Infection and drug resistance Conclusion HBV A194T 6 11 RT 4 6 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. After 2 years under such therapy, this viral population was completely replaced by mutation rtM204I -homogenously exhibiting lamivudine resistance. 2011 BMC infectious diseases Conclusion HBV M204I 94 99 RT 92 94 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. Once lamivudine therapy was reintroduced, and until entecavir plus tenofovir were administered, the dual lamivudine resistance-associated mutations rtL180M and rtM204I were invariably detected. 2011 BMC infectious diseases Conclusion HBV L180M;M204I 150;162 155;167 RT;RT 148;160 150;162 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The HBV genomic characterization at preC-C level showed the presence of A1762T and G1764A double mutation that was early detected when the patient was untreated, remaining in this condition during the entire follow-up. 2011 BMC infectious diseases Conclusion HBV A1762T;G1764A 72;83 78;89 C;Precore 41;36 42;40 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The T1753C mutation was also consistently detected. 2011 BMC infectious diseases Conclusion HBV T1753C 4 10 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. These rtA200V and rtI253V variants remained present during entecavir therapy, and were also detected in samples sequenced after breakthrough during entecavir therapy. 2011 BMC infectious diseases Conclusion HBV A200V;I253V 8;20 13;25 RT;RT 6;18 8;20 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. Under the latter therapeutic scheme, only ephemerally and with minor contribution (~5%), the A181T and T184L lamivudine-adefovir and entecavir resistance-associated mutations were detected, respectively. 2011 BMC infectious diseases Conclusion HBV A181T;T184L 93;103 98;108 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. When this therapy was interrupted for 6 months, quasispecies composition almost exclusively consisted of wild-type pol nucleotide sequences, except for a minor contribution (< 10%) showing the adefovir resistance-associated mutation I233V. 2011 BMC infectious diseases Conclusion HBV I233V 233 238 P 115 118 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. By analyzing the clinical variables, virological parameters, and clinical use of rescue agents in LAM-resistant mutants, we found older age, cirrhosis, and rtA181T mutation are significantly associated with occurrence of HCC in the subsequent courses of antiviral therapy. 2011 BMC cancer Conclusion HBV A181T 158 163 RT 156 158 Liver cirrhosis;Hepatocellular carcinoma 141;221 150;224 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A single G1613A mutation was associated with future emergence of HCC that could be a marker for predicting HCC development. 2011 BMC cancer Conclusion HBV G1613A 9 15 Hepatocellular carcinoma;Hepatocellular carcinoma 65;107 68;110 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. Two mutations in the core promoter region, G1613A and C1653T, were associated with hepatocarcinogenesis. 2011 BMC cancer Conclusion HBV G1613A;C1653T 43;54 49;60 Core promoter 21 34 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. However, the G145R mutant was present as a minor population in children and adults. 2012 BMC research notes Conclusion HBV G145R 13 18 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. Our prediction model enabled to identify the impact of rtI233V mutation which has been debated in the recent years. 2013 Bioinformation Conclusion HBV I233V 57 62 RT 55 57 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. The rtI233V amino acid substitution did not show to alter the catalytic sites and adefovir binding. 2013 Bioinformation Conclusion HBV I233V 6 11 RT 4 6 23423477 Impact of rtI233V mutation in hepatitis B virus polymerase protein and adefovir efficacy: Homology modeling and molecular docking studies. we show that rtI233V mutation cannot affect the antiviral efficacy of adefovir. 2013 Bioinformation Conclusion HBV I233V;I233V 15;16 20;22 RT 13 15 23679074 Late HBsAg seroreversion of mutated hepatitis B virus after bone marrow transplantation. Surprisingly, in both samples (genotype D) two identical mutations (D144E and G145R, described in literature as HBsIE mutations) were identified. 2013 BMC infectious diseases Conclusion HBV D144E;G145R 68;78 73;83 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. Also the basal core promoter region of HBV genome was not sequenced in this study, therefore, the prevalence of A1762T and G1764A mutations could not be determined. 2013 Journal of medical virology Conclusion HBV A1762T;G1764A 112;123 118;129 BCP 9 28 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Drug-resistant YMDD mutations caused a significant reduction in the antigenicity of immune-escaped HBsAg, particularly for the most common mutant sG145K. 2013 Virology journal Conclusion HBV G145K 146 152 S;S;P 99;146;15 104;147;19 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. Several immune-epitope mutants, such as S45T/A, N131T, I194V, and S207N in S, were detected in all isolates and needed to explore their role in HBV infection. 2013 TheScientificWorldJournal Conclusion HBV S45T;S45A;N131T;I194V;S207N 40;40;48;55;66 46;46;53;60;71 S 75 76 HBV infections 144 157 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Few mutations in X gene (T36A and G50R) showed high frequency of association with HCC, however further studies are required to validate the findings. 2014 PloS one Conclusion HBV T36A;G50R 25;34 29;38 X 17 18 Hepatocellular carcinoma 82 85 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Further, there were no substitutions that could be associated with reduced TDF susceptibility (rtA181V/T, rtN236T, or rtA194T) in April 2013. 2014 Drug design, development and therapy Conclusion HBV A181V;A181T;A194T;N236T 97;97;120;108 104;104;125;113 RT;RT;RT 95;106;118 97;108;120 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. HBV DNA levels gradually increased, and LAM-resistant virus emerged (reverse transcriptase [rt] M204I). 2014 Drug design, development and therapy Conclusion HBV M204I 96 101 RT;RT 69;92 90;94 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. In comparison with those at the start of TDF therapy, the amino acid substitutions changed from rtL180M, rtT184M, and rtM204V to rtL180M, rtS202G, and rtM204V, and no other amino acid substitutions apart from these in the rt region were observed. 2014 Drug design, development and therapy Conclusion HBV L180M;T184M;M204V;L180M;S202G;M204V 98;107;120;131;140;153 103;112;125;136;145;158 RT;RT;RT;RT;RT;RT;RT 96;105;118;129;138;151;222 98;107;120;131;140;153;224 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. In June 2010 (week 3 of ETV retreatment), amino acid substitutions of rtL180M, rtT184I, and rtM204V (ETV resistance substitutions) were simultaneously detected. 2014 Drug design, development and therapy Conclusion HBV L180M;T184I;M204V 72;81;94 77;86;99 RT;RT;RT 70;79;92 72;81;94 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. In October 2007 (after switching from LAM to ETV), an amino acid substitution of the rt gene, rtM204I (LAM resistance substitution), was detected. 2014 Drug design, development and therapy Conclusion HBV M204I 96 101 RT;RT 85;94 87;96 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Moreover, amino acid substitutions of rtL180M, rtS202G, and rtM204V (ETV resistance substitutions) emerged during ETV treatment in February 2009. 2014 Drug design, development and therapy Conclusion HBV L180M;S202G;M204V 40;49;62 45;54;67 RT;RT;RT 38;47;60 40;49;62 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Moreover, amino acid substitutions of rtL180M, rtT184M, and rtM204V coexisted with the above mutants at the end of June 2010 (week 6 of ETV retreatment). 2014 Drug design, development and therapy Conclusion HBV L180M;T184M;M204V 40;49;62 45;54;67 RT;RT;RT 38;47;60 40;49;62 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Since April 2013 (month 31 of TDF and ETV treatment), amino acid substitutions of rtL180M, rtS202G, and rtM204V have emerged and have been found to be associated with an increase in serum HBV DNA (Figure 2). 2014 Drug design, development and therapy Conclusion HBV L180M;S202G;M204V 84;93;106 89;98;111 RT;RT;RT 82;91;104 84;93;106 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Treatment was switched from LAM to ETV (0.5 mg/day) in October 2007 (HBV DNA 3.9 log copies/mL) following the emergence of ETV-resistant virus (rtL180M, rtS202G, and rtM204V) and higher elevation in HBV DNA. 2014 Drug design, development and therapy Conclusion HBV L180M;S202G;M204V 146;155;168 151;160;173 RT;RT;RT 144;153;166 146;155;168 25374716 Death from Liver Failure despite Lamivudine Prophylaxis during R-CHOP Chemotherapy due to Rapid Emergence M204 Mutations. Genotyping with the INNO-LIPA assay confirmed L80I, M80V, and M204V/S mutations, conferring lamivudine resistance. 2013 Case reports in hepatology Conclusion HBV L80I;M80V;M204V;M204S 46;52;62;62 50;56;69;69 25374716 Death from Liver Failure despite Lamivudine Prophylaxis during R-CHOP Chemotherapy due to Rapid Emergence M204 Mutations. HBeAg remained negative, and genotyping with the INNO-LIPA assay confirmed L80I and M204I mutations, conferring lamivudine resistance. 2013 Case reports in hepatology Conclusion HBV L80I;M204I 75;84 79;89 C 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Additionally, three nonsynonymous mutations were found in the ORF S, S region, T1387C, T1640C, and A1512T; whereas 6 amino acid substitutions (rtL108P, rtR110G, rtL180M, rtR192C, rtT150S and rtI187V) were found in the RT domain. 2014 Virology journal Conclusion HBV L108P;R110G;L180M;R192C;T150S;I187V;T1387C;T1640C;A1512T 145;154;163;172;181;193;79;87;99 150;159;168;177;186;198;85;93;105 RT;RT;RT;RT;RT;RT;RT;S;S 143;152;161;170;179;191;218;66;69 145;154;163;172;181;193;220;67;70 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Our data showing an inhibitory effect of estrogen in tumor formation in male nude mice suggest that estrogen or estrogenic compounds have therapeutic potential in patients with W4P-LHB-induced HCC. 2015 Molecular cancer Conclusion HBV W4P 177 180 S 181 184 Hepatocellular carcinoma 193 196 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The novel HBV preS1 mutation W4P may contribute to HCC development in men with chronic hepatitis B in an IL-6-dependent manner. 2015 Molecular cancer Conclusion HBV W4P 29 32 PreS1 14 19 Hepatocellular carcinoma;Chronic Hepatitis B 51;79 54;98 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. In particular, the HBc-R154G particles displayed the lowest degree of cell binding ability. 2015 Journal of nanobiotechnology Conclusion HBV R154G 23 28 C 19 22 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The HBc-R154G particles showed a clear decrease in the binding ability to a heparan sulfate proteoglycan, as well as a decrease in the cellular uptake capacity. 2015 Journal of nanobiotechnology Conclusion HBV R154G 8 13 C 4 7 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. The HBV BCP/PC mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF. 2015 Virology journal Conclusion HBV T1753V;A1762T;G1764A;C1766T;T1768A;A1846T;G1896A;G1899A 25;33;41;49;57;65;73;84 31;39;47;55;63;71;79;90 BCP;C;Precore 8;99;12 11;104;14 Acute on chronic liver failure 157 165 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. In conclusion, findings of this study demonstrated that ETV monotherapy and ETV plus ADV therapy were clinically effective and comparable as rescue therapy for HBV rtA181V/T mutants alone. 2016 Saudi journal of gastroenterology Conclusion HBV A181V;A181T 166;166 173;173 RT 164 166 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Large-scale, long-term studies of rescue therapy for HBV rtA181V/T mutants alone should be conducted, and therapeutic plans for achievement of further antiviral efficacy for HBV rtA181V/T mutants alone should be established and recommended. 2016 Saudi journal of gastroenterology Conclusion HBV A181V;A181T;A181V;A181T 59;59;180;180 66;66;187;187 RT;RT 57;178 59;180 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Then, an independent case-control study revealed that the A2159G and A2189Y mutations were independent risk factors for HCC in chronic HBV-infected subjects in Qidong. 2016 International journal of molecular sciences Conclusion HBV A2159G;A2189Y 58;69 64;75 Hepatocellular carcinoma;HBV infections 120;135 123;147 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Compared with non-HCC clones, the HCC clones showed higher prevalence of T1753C and G1896A mutations, and preS deletions, especially those removing a neutralizing epitope in the preS2 domain. 2017 Virus research Conclusion HBV T1753C;G1896A 73;84 79;90 PreS;PreS2 106;178 110;183 Hepatocellular carcinoma;Hepatocellular carcinoma 34;18 37;21 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Our results indicated that ETV is efficient in rescuing rtA181T/V mutation CHB patients and HBV DNA level could predict viral clearance at the 12th month. 2017 Virology journal Conclusion HBV A181T;A181V 58;58 65;65 RT 56 58 Chronic Hepatitis B 75 78 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. On the other hand, prevalence of G1899A mutations increased from 2.5% to 17.4%. 2017 Emerging infectious diseases Conclusion HBV G1899A 33 39 28418295 Phenotypic and Genotypic Shifts in Hepatitis B Virus in Treatment-Naive Patients, Taiwan, 2008-2012. Over the 5 years of this study, we found an increasing prevalence of G1899A mutations and an increasing concentration of serum HBV DNA in treatment-naive, HBeAg-positive patients. 2017 Emerging infectious diseases Conclusion HBV G1899A 69 75 C 155 160 28445403 Detection of Hepatitis B Virus M204I Mutation by Quantum Dot-Labeled DNA Probe. In this study, we developed a sensitive and simple fluorescent method for detecting HBV M204I mutation. 2017 Sensors (Basel, Switzerland) Conclusion HBV M204I 88 93 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. Additional findings of our study were compatible with previous studies, which claimed that Iranian HBV viruses belong to genotype D and indicated significant association of the preC G1896A mutation with this genotype of HBV. 2017 Electronic physician Conclusion HBV G1896A 182 188 Precore 177 181 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. Finally, the genotypic testing also highlighted the presence of two HBV RT mutations (S135Y and I233V) that are potentially involved in resistance to first-generation nucleos(t)ide RT inhibitors. 2017 BMC infectious diseases Conclusion HBV S135Y;I233V 86;96 91;101 RT;RT 72;181 74;183 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. In the current clinical case, the HBsAg mutation S204R was detected. 2017 BMC infectious diseases Conclusion HBV S204R 49 54 S 34 39 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. The acquisition of a positively-charged amino acid (Arginine [R] at position 204) in this transmembrane domain might alter the HBsAg structure to result in i) HBsAg negativity in the currently available diagnostic test and ii) HBV escape from a high anti-HBs titer. 2017 BMC infectious diseases Conclusion HBV R204R 52 80 S;S;S 255;127;159 258;132;164 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. The test did not reveal the presence of LMV resistance mutations but showed the presence of three mutations in HbsAg: T127P, F170FL and S204R. 2017 BMC infectious diseases Conclusion HBV T127P;S204R 118;136 123;141 S 111 116 28806922 Hepatitis B reactivation characterized by HBsAg negativity and anti-HbsAg antibodies persistence in haematopoietic stem cell transplanted patient after lamivudine withdrawal. This concept agrees with a previous study, which showed that the viral clones encoding S204R (lysine [S] substitution with arginine [R] at position 204) and G145R (glycine [G] substitution with arginine [R] at position 145) exhibited an approximately 60% viral secretion defect compared with the wild-type. 2017 BMC infectious diseases Conclusion HBV S204R;G145R;R204R;R145R 87;157;123;194 92;162;151;222 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. Interestingly, the G1896A and A1762T/G1764A mutations, although associated with fulminant hepatitis B development in other studies, were found at low frequency in ACLF patients compared to non-ACLF/HBeAg negative hepatitis CHB patients. 2017 Virology journal Conclusion HBV G1764A;G1896A;A1762T 37;19;30 43;25;36 C 198 203 Acute on chronic liver failure;Fulminant Hepatitis B 163;80 167;99 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The emergence of sW172* mutant coding truncated mutant HBsAg may increase possibility of HBV tumorigenesis, and its mechanism may be associated with down-regulated expression of TGFBI in TGF-beta/Smad signaling pathway. 2018 Virology journal Conclusion HBV W172X 17 23 S;S 55;17 60;18 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The present study demonstrated that HBV DNA genomic mutations in A1762T/G1764A and Pre S deletion were associated with worse prognosis and early recurrence for HBV-HCC patients after surgery. 2018 Cancer management and research Conclusion HBV G1764A;A1762T 72;65 78;71 PreS 83 88 Hepatocellular carcinoma 164 167 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Eight mutations in RT region, rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V, and rtM309K were significantly associated with progression of HCC in treatment-naive patients. 2018 World journal of gastroenterology Conclusion HBV L80I;D134N;N139K;N139T;N139H;Y141F;M204I;M204V;M309K;F221Y;I224V 32;40;49;49;49;62;71;71;104;82;91 36;45;58;58;58;67;78;78;109;87;96 RT;RT;RT;RT;RT;RT;RT;RT;RT 19;30;38;47;60;69;80;89;102 21;32;40;49;62;71;82;91;104 Hepatocellular carcinoma 160 163 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. We found eight mutations and amino acid substitutions in the S protein, including the most common vaccine escape mutation G145R (Figure 4). 2018 World journal of hepatology Conclusion HBV G145R 122 127 S 61 62 30142581 In situ, amplification-free double-stranded mutation detection at 60 copies/ml with thousand-fold wild type in urine. Using HBVDM and KRAS G12V as model mutations, it was shown that with such a cooling scheme in a flow PEPS was able to detect double-stranded mutations with 70% detection efficiency or better at concentrations ranging 10-19M - 10-16M against single-stranded DNA detection at the same concentrations as validated by in situ detection of fluorescent reporter microspheres (FRMs) following the double stranded mutation detections as well as microscopic visualization of FRMs following the FRMs detection. 2018 Biosensors & bioelectronics Conclusion HBV G12V 21 25 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Especially, in vitro studies suggest that SPII G120A might play a positive role in up-regulating the HBV total RNA to increase the HBsAg and HBV DNA levels. 2019 Viruses Conclusion HBV G120A 47 52 S;S promoter II 131;42 136;46 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Finally, we identified several novel mutations, such as C18T, A115C, G120A and A138G, which could regulate the SPII promoter activity and HBsAg levels. 2019 Viruses Conclusion HBV C18T;A115C;G120A;A138G 56;62;69;79 60;67;74;84 S;S promoter II 138;111 143;115 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. In conclusion, despite several limitations, our present study demonstrated for the first time the possibility that mutations in the pre-S1 promoter region, especially the G2765A substitution in the Sp1 region, reduce the expression of L protein and regulate biological character of virus, leading to a low viral load and less severe disease in chronic HBV infection. 2019 Virology journal Conclusion HBV G2765A 171 177 S;S1 promoter;S1 promoter 235;132;198 244;147;201 Chronic HBV infection 344 365 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, sC69* could possibly inhibit the innate immune response compared to the WT, allowing the virus to escape immune surveillance. 2019 Frontiers in microbiology Conclusion HBV C69X 13 18 S 13 14 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* substitution could impact viral infection and be rescued when coexisting with WT. 2019 Frontiers in microbiology Conclusion HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We found that sC69* usually coexists with WT HBV. 2019 Frontiers in microbiology Conclusion HBV C69X 14 19 S 14 15 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Furthermore, the present data indicate a high rate of G1896A mutant in the PC region among Iranian CHB patients and a negative correlation between the emergence of A1762T/G1764A mutation and G1764T/C1766G mutant in the BCP region. 2019 Mediterranean journal of hematology and infectious diseases Conclusion HBV G1764A;C1766G;G1896A;A1762T;G1764T 171;198;54;164;191 177;204;60;170;197 BCP;Precore 219;75 222;77 Chronic Hepatitis B 99 102 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. A mutant D2N/D4N dimer with exactly the same structural conformation as WT Cp1492 but with four fewer negative charges at neutral pH was designed to probe the effect of charge. 2018 ACS omega Conclusion HBV D4N;D2N 13;9 16;12 C 75 77 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The kinetic and thermodynamic outcomes of capsid formation were identical for the WT and D2N/D4N dimers when they were charge matched, confirming that the capsid formation was controlled by the effective surface charge density (macroion-macroion repulsion) and the charge screening effect macroion-counterion interaction). 2018 ACS omega Conclusion HBV D4N;D2N 93;89 96;92 Capsid;Capsid;S 42;155;204 48;161;211 31542053 Hepatitis B virus reactivation sustained by a hepatitis B virus surface antigen immune-escape mutant isolate in a patient who was hepatitis B core antibody positive during treatment with sofosbuvir and velpatasvir for hepatitis C virus infection: a case report. In contrast, by analyzing the S region, two relevant mutations, P120S and T126I, localized in the major hydrophilic region, an immune-active HBsAg domain, were found. 2019 Journal of medical case reports Conclusion HBV P120S;T126I 64;74 69;79 S;S 141;30 146;31 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Although P56L, I68V, and I68T were detected as a minor population in the three umbilical cord samples, there was no variant in the "a" determinant region of HBsAg gene from the three umbilical cord samples. 2019 BMC infectious diseases Conclusion HBV P56L;I68V;I68T 9;15;25 13;19;29 S 157 162 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Although the direct sequencing showed that G145A was present as a major population in the mother's nails, the deep sequencing showed that G145A (34.8%) was present as a minor population in her nails. 2019 BMC infectious diseases Conclusion HBV G145A;G145A 43;138 48;143 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Both D144A and G145A were reported to be VEMs. 2019 BMC infectious diseases Conclusion HBV D144A;G145A 5;15 10;20 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Except for the S40 N variant, there was no variant as a major population in HBsAg gene from the umbilical cords and serum. 2019 BMC infectious diseases Conclusion HBV S40N 15 20 S 76 81 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. G44E, G102C, and Y161F were detected in the serum of the 1st-born, the umbilical cord of the 1st-born, and the umbilical cord of the 3rd-born child, respectively. 2019 BMC infectious diseases Conclusion HBV G44E;G102C;Y161F 0;6;17 4;11;22 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. G44E, P56L, F93S, C107Y, L110P, S117 N, T118K, D144A and W167 L were detected in only one sample. 2019 BMC infectious diseases Conclusion HBV G44E;P56L;F93S;C107Y;L110P;S117N;T118K;D144A;W167L 0;6;12;18;25;32;40;47;57 4;10;16;23;30;38;45;52;63 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. However, D144A (2.5%) and G145A (11.2%), which were located in the "a" determinant region, were detected as a minor population in the serum of the 2nd-born child. 2019 BMC infectious diseases Conclusion HBV D144A;G145A 9;26 14;31 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. However, G145A mutant was detected in the nails of the 2nd-born child. 2019 BMC infectious diseases Conclusion HBV G145A 9 14 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. I68T was detected in both the serum and nails of the 1st-born and 2nd-born children. 2019 BMC infectious diseases Conclusion HBV I68T 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. I68V was detected as a minor population in all seven samples. 2019 BMC infectious diseases Conclusion HBV I68V 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Locked nucleic acid-based probe real-time PCR for G145A mutant. 2019 BMC infectious diseases Conclusion HBV G145A 50 55 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Of the 10 minor variants, four (I110L, S113 T, K122Q, and T143S) were detectable in all of the umbilical cord samples and all serum samples. 2019 BMC infectious diseases Conclusion HBV I110L;S113T;K122Q;T143S 32;39;47;58 37;45;52;63 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Of the 11 variants, T126A and T143S were located in the "a" determinant region. 2019 BMC infectious diseases Conclusion HBV T126A;T143S 20;30 25;35 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Of the 13 variants, only T114S was detected as a major population in all of the samples from umbilical cords, serum, and nails. 2019 BMC infectious diseases Conclusion HBV T114S 25 30 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. P120S was detected in the serum of the mother and 1st-born child of Family 1. 2019 BMC infectious diseases Conclusion HBV P120S 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Similar to the deep sequencing, the LNA-based probe real-time PCR did not detect G145A mutant in the umbilical cord samples of Family 2. 2019 BMC infectious diseases Conclusion HBV G145A 81 86 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T126A and T143S have been reported as VEMs. 2019 BMC infectious diseases Conclusion HBV T126A;T143S 0;10 5;15 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T126A was detected in the umbilical cord (9.2%) and serum (7.0%) of the 1st-born child, and T143S was detected in all three umbilical cords (1st-born: 1.7%, 2nd-born: 1.7%, 3rd-born: 1.8%) and in three serum samples (mother: 2.0%, 1st-born: 2.0% 2nd-born: 2.0%). 2019 BMC infectious diseases Conclusion HBV T126A;T143S 0;92 5;97 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T126A was detected in the umbilical cord and serum of this 1st-born child. 2019 BMC infectious diseases Conclusion HBV T126A 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The following locked nucleic acid (LNA)-based probes (nt 582-591) designed for discrimination between the glycine to alanine at the 145th amino acid of HBsAg (G145A mutant: nucleotide position at 588: G C) and the wild-type were used for the real-time PCR. 2019 BMC infectious diseases Conclusion HBV G145A 159 164 S 152 157 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The G145A mutation is shown in. 2019 BMC infectious diseases Conclusion HBV G145A 4 9 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The levels of G145A mutant were 3.8 log copies/mL in the mother's nails, 7.0 log copies/mL in the serum of the 2nd-born child, and 3.3 log copies/mL in the nails of the 2nd-born child. 2019 BMC infectious diseases Conclusion HBV G145A 14 19 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The quantification of G145A mutant in family 2. 2019 BMC infectious diseases Conclusion HBV G145A 22 27 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The quantification of G145A mutant showed that G145A was present as a major population in the nails of the mother and as a minor population in the serum and nails of the 2nd-born child. 2019 BMC infectious diseases Conclusion HBV G145A;G145A 22;47 27;52 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The wild-type and G145A mutant-type DNA extracted from serum were quantified according to the recombinant plasmid wild-type controls and the G145A mutant-type (nucleotide position at 588: G C) controls, respectively. 2019 BMC infectious diseases Conclusion HBV G145A;G145A 18;141 23;146 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. There was thus a discrepancy in the population of G145A mutant from the nails of the mother of Family 2 between the direct sequencing and the deep sequencing. 2019 BMC infectious diseases Conclusion HBV G145A 50 55 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. These findings suggest that the G145A mutant exists as a minor population in the 2nd-born child. 2019 BMC infectious diseases Conclusion HBV G145A 32 37 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. To re-evaluate the populations of G145A mutant in the umbilical cords, serum, and nails of Family 2, we performed an LNA-based probe real-time PCR. 2019 BMC infectious diseases Conclusion HBV G145A 34 39 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. V47A was also detected in all samples except for the umbilical cord of the 1st-born child. 2019 BMC infectious diseases Conclusion HBV V47A 0 4 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. preS1 C2964A, RT domain I91L, and small HBsAg N3S mutations were found, all of which have clinical importance. 2020 International journal of molecular sciences Conclusion HBV N3S;C2964A;I91L 46;6;24 49;12;28 S;PreS1;RT 40;0;14 45;5;16 32080249 Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine. Our structures also explain a common mechanism for 3TC/ETV resistance by severe steric clash between the M184V/I (M204V/I in HBV) side-chain and the oxathiolane/methylene of bound 3TC-TP/ETV-TP. 2020 Scientific reports Conclusion HBV M204V;M204I 114;114 121;121 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Our data strongly suggest that the Y132A mutation alters the ensemble of conformations present in solution. 2020 ACS chemical biology Conclusion HBV Y132A 35 40 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. This implies that the hCp149-Y132A dimer does not sample the assembly active conformation. 2020 ACS chemical biology Conclusion HBV Y132A 29 34 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. This research attempted to investigate several new substitution sites (T126N, N131T, P142L, and S207N) identified in two HBV S proteins. 2020 Heliyon Conclusion HBV T126N;N131T;P142L;S207N 71;78;85;96 76;83;90;101 S 125 126 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Downregulated TGFbi not only contributes to oncogenicity in sW196*-transfected cells, but also in other preS/S* (sW172* and sW182*) cells, suggesting a common oncogenic mechanism shared by the surface truncation mutants; some may emerge during NA antiviral therapy. 2020 International journal of molecular sciences Conclusion HBV W196X;W172X;W182X 60;113;124 66;119;130 PreS;S;S;S;S;S 104;109;60;113;124;193 108;110;61;114;125;200 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The HBV preS/S C-terminal truncation mutant sW196*, which may be selected in NA (3TC, Telbivudine, or Entecavir)-resistant rtM204I strains, potentially confers cell transformation and tumorigenesis ability through altered (up- or down-regulated) cellular transcriptions that orchestrate in different cancer-promoting sectors. 2020 International journal of molecular sciences Conclusion HBV M204I;W196X 125;44 130;50 PreS;S;RT;S 8;13;123;44 12;14;125;45 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. In the molecular analysis, we for the first time demonstrate the mutations of Gln129Arg (Q129R) and Met133Ser (M133S) in the "a" determinant of HBsAg in an OBI patient. 2020 International journal of medical sciences Conclusion HBV Q129R;Q129R;M133S;M133S 78;89;100;111 87;94;109;116 S 144 149 Occult Hepatitis B 156 159 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. G1896A converts codon 28 from tryptophan (TGG) to a stop codon (TAG) and terminates the translation of the HBeAg precursor . 2020 Wellcome open research Conclusion HBV G1896A 0 6 C 107 112 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. Mutations at amino acid level were also seen in surface antigen (V190A and T127P), both of which have been associated with CHB-AR in the context of immunosuppression ( Table 1). 2020 Wellcome open research Conclusion HBV V190A;T127P 65;75 70;80 S 48 55 Chronic Hepatitis B 123 126 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. The most prevalent minority variant mutations in our HBV sequences were G1896A, G1899A and G1764A (precore/core and basal core promotor sequences respectively) ( Table 1). 2020 Wellcome open research Conclusion HBV G1896A;G1899A;G1764A 72;80;91 78;86;97 BCP;C;Precore 116;107;99 135;111;106 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Further genotypic drug resistance testing found the emergence of rtL180M, rtM204V and rtA194T mutations (confirmed by a second sequencing). 2021 Infection and drug resistance Conclusion HBV L180M;M204V;A194T 67;76;88 72;81;93 RT;RT;RT 65;74;86 67;76;88 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. ETVr-related substitution M204I was detected, but no other mutations were identified (Table II). 2021 Molecular and clinical oncology Conclusion HBV M204I 26 31 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. The current study established a practical quantitative real-time PCR that monitors HBV DNA polymerase gene mutations in patients undergoing treatment with NAs, with particular reference to the M204V mutation. 2021 Journal of clinical and translational hepatology Conclusion HBV M204V 193 198 P 91 101 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The high prevalence of the sQ129H escape mutation detected here points out the need for better screening procedures for HBV-infected individuals in order to avoid the spread of viral strains evading vaccine protection and thus posing a serious threat to the successful elimination of HBV. 2021 Viruses Conclusion HBV Q129H 27 33 S 27 28 HBV infections 120 132 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. Through the analysis of 11,088 HBV genomes and 1637 HPV-16 genomes, some valuable mutations, including the T350G of HBV and the C659T of HPV-16, were detected. 2021 Computational and structural biotechnology journal Conclusion HBV C659T 128 133 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Preliminary data suggested that E2G/A may produce a truncated S protein by the formation of N-terminal signal peptide, which might cause the HBsAg secretion impairment in OBI. 2021 Frontiers in microbiology Conclusion HBV E2G;E2A 32;32 37;37 S;S 141;62 146;63 Occult Hepatitis B 171 174 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Subsequently, there are great differences in the underlying mechanism of OBI attributed to the E2G mutations between genotype B and genotype C. 2021 Frontiers in microbiology Conclusion HBV E2G 95 98 Occult Hepatitis B 73 76 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. However, in contrast to wild-type rHBsAg, rHBsAg with the G145R mutation does not affect the expression of CD86 on B cells, and induces IL-2 along with lower production of TNF-alpha, IL-10, and IFN-gamma. 2022 Vaccines Conclusion HBV G145R 58 63 S;S 34;42 40;48 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In addition, the development of antibodies after vaccination of humans with a multivalent vaccine containing HBsAg with the G145R mutation needs to be evaluated. 2022 Vaccines Conclusion HBV G145R 124 129 S 109 114 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The distinct immunogenic properties of the G145R mutant demonstrated in vitro in this study, together with its previously described antigenic and morphological characteristics and the recognized profile of the specific antibody production in vivo, provide strong support toward including the mutant antigen in the composition of HBV vaccines and further exploring the mechanisms of the vaccinal G145R escape mutant interaction with various components of the immune system. 2022 Vaccines Conclusion HBV G145R;G145R 43;395 48;400 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The rHBsAg G145R mutant induces expression of CD69 on B, NK, and T cells (both CD4+ and CD8+), similarly to wild-type rHBsAg, although the effect is weaker. 2022 Vaccines Conclusion HBV G145R 11 16 S;S 4;118 10;124 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. The HBx combo mutation C1653T+T1674G+A1762T/G1764A promotes carcinogenesis via upregulating the expression of PAI1 and CDC20 and inducing cancer-promoting inflammation. 2022 Frontiers in oncology Conclusion HBV G1764A;C1653T;T1674G;A1762T 44;23;30;37 50;29;36;43 X 4 7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The W4P/R/Y (on preS1 region) and T47A/E/V/K, P120S/T, S174N and P203R (on S region) were found related to HCC. 2022 PloS one Conclusion HBV W4P;W4R;W4Y;P120T;T47A;T47E;T47V;T47K;P120S;S174N;P203R 4;4;4;46;34;34;34;34;46;55;65 11;11;11;53;44;44;44;44;53;60;70 PreS1;S 16;75 21;76 Hepatocellular carcinoma 107 110 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Furthermore, more than half of the HBV-infected subjects harbored the stop codon W28* of the precore region that is responsible for the HBeAg negative state. 2022 Clinical and experimental hepatology Conclusion HBV W28X 81 85 C;Precore 136;93 141;100 HBV infections 35 47 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. D110E 2005 Virology journal Table HBV D110E 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. D48N 2005 Virology journal Table HBV D48N 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. K130M 2005 Virology journal Table HBV K130M 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. M130K 2005 Virology journal Table HBV M130K 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. P40S 2005 Virology journal Table HBV P40S 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. R103W 2005 Virology journal Table HBV R103W 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. R87W 2005 Virology journal Table HBV R87W 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. S29P 2005 Virology journal Table HBV S29P 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. S31P 2005 Virology journal Table HBV S31P 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. S33P 2005 Virology journal Table HBV S33P 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. T106P 2005 Virology journal Table HBV T106P 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. T12A 2005 Virology journal Table HBV T12A 0 4 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. V131I 2005 Virology journal Table HBV V131I 0 5 16080797 HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers. V37I 2005 Virology journal Table HBV V37I 0 4 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. A128V 2007 Virology journal Table HBV A128V 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. A159G 2007 Virology journal Table HBV A159G 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. A159P 2007 Virology journal Table HBV A159P 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. E164A 2007 Virology journal Table HBV E164A 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. F158H 2007 Virology journal Table HBV F158H 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. F161S 2007 Virology journal Table HBV F161S 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. F161Y 2007 Virology journal Table HBV F161Y 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. F93I 2007 Virology journal Table HBV F93I 0 4 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. I126T 2007 Virology journal Table HBV I126T 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. I150R 2007 Virology journal Table HBV I150R 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. L162Y 2007 Virology journal Table HBV L162Y 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. N146K 2007 Virology journal Table HBV N146K 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. P127L 2007 Virology journal Table HBV P127L 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. P127V 2007 Virology journal Table HBV P127V 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. P129L 2007 Virology journal Table HBV P129L 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. Q129H 2007 Virology journal Table HBV Q129H 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. R122K 2007 Virology journal Table HBV R122K 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. R160E 2007 Virology journal Table HBV R160E 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. R160K 2007 Virology journal Table HBV R160K 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. R160N 2007 Virology journal Table HBV R160N 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. R169F 2007 Virology journal Table HBV R169F 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. S114T 2007 Virology journal Table HBV S114T 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. S167G 2007 Virology journal Table HBV S167G 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. T113S 2007 Virology journal Table HBV T113S 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. T126I 2007 Virology journal Table HBV T126I 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. V168A 2007 Virology journal Table HBV V168A 0 5 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. Y100N 2007 Virology journal Table HBV Y100N 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. A128V 2007 BMC microbiology Table HBV A128V 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. L127I 2007 BMC microbiology Table HBV L127I 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. L180M 2007 BMC microbiology Table HBV L180M 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. M204I 2007 BMC microbiology Table HBV M204I 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. M204V 2007 BMC microbiology Table HBV M204V 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. T118V 2007 BMC microbiology Table HBV T118V 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. V173L 2007 BMC microbiology Table HBV V173L 0 5 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. Y100C 2007 BMC microbiology Table HBV Y100C 0 5 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. L180M 2008 BMC microbiology Table HBV L180M 0 5 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. M204I 2008 BMC microbiology Table HBV M204I 0 5 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. M204V 2008 BMC microbiology Table HBV M204V 0 5 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. V173L 2008 BMC microbiology Table HBV V173L 0 5 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. A1762T 2008 Journal of the National Cancer Institute Table HBV A1762T 0 6 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. G1764A 2008 Journal of the National Cancer Institute Table HBV G1764A 0 6 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. G1896A 2008 Journal of the National Cancer Institute Table HBV G1896A 0 6 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. L180M 2008 Antiviral research Table HBV L180M 0 5 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. M204I 2008 Antiviral research Table HBV M204I 0 5 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. M204V 2008 Antiviral research Table HBV M204V 0 5 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1499G 2009 Journal of the National Cancer Institute Table HBV A1499G 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1752G 2009 Journal of the National Cancer Institute Table HBV A1752G 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T 2009 Journal of the National Cancer Institute Table HBV A1762T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1898G 2009 Journal of the National Cancer Institute Table HBV A1898G 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1165T 2009 Journal of the National Cancer Institute Table HBV C1165T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1485T 2009 Journal of the National Cancer Institute Table HBV C1485T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1653T 2009 Journal of the National Cancer Institute Table HBV C1653T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1726A 2009 Journal of the National Cancer Institute Table HBV C1726A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1766T 2009 Journal of the National Cancer Institute Table HBV C1766T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1773T 2009 Journal of the National Cancer Institute Table HBV C1773T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1812T 2009 Journal of the National Cancer Institute Table HBV C1812T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1858T 2009 Journal of the National Cancer Institute Table HBV C1858T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1499H 2009 Journal of the National Cancer Institute Table HBV G1499H 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1613A 2009 Journal of the National Cancer Institute Table HBV G1613A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1730C 2009 Journal of the National Cancer Institute Table HBV G1730C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1764A 2009 Journal of the National Cancer Institute Table HBV G1764A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1766A 2009 Journal of the National Cancer Institute Table HBV G1766A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1799C 2009 Journal of the National Cancer Institute Table HBV G1799C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1809T 2009 Journal of the National Cancer Institute Table HBV G1809T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1862T 2009 Journal of the National Cancer Institute Table HBV G1862T 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1888H 2009 Journal of the National Cancer Institute Table HBV G1888H 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1896A 2009 Journal of the National Cancer Institute Table HBV G1896A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1898A 2009 Journal of the National Cancer Institute Table HBV G1898A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1899A 2009 Journal of the National Cancer Institute Table HBV G1899A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1479C 2009 Journal of the National Cancer Institute Table HBV T1479C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1727A 2009 Journal of the National Cancer Institute Table HBV T1727A 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1753V 2009 Journal of the National Cancer Institute Table HBV T1753V 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1765V 2009 Journal of the National Cancer Institute Table HBV T1765V 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1773C 2009 Journal of the National Cancer Institute Table HBV T1773C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T1856C 2009 Journal of the National Cancer Institute Table HBV T1856C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T2170C 2009 Journal of the National Cancer Institute Table HBV T2170C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T2441C 2009 Journal of the National Cancer Institute Table HBV T2441C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T2525C 2009 Journal of the National Cancer Institute Table HBV T2525C 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T2712V 2009 Journal of the National Cancer Institute Table HBV T2712V 0 6 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T31C 2009 Journal of the National Cancer Institute Table HBV T31C 0 4 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. T53C 2009 Journal of the National Cancer Institute Table HBV T53C 0 4 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. A1762T 2010 Journal of viral hepatitis Table HBV A1762T 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. C1766T 2010 Journal of viral hepatitis Table HBV C1766T 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. G1764A 2010 Journal of viral hepatitis Table HBV G1764A 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. G1896A 2010 Journal of viral hepatitis Table HBV G1896A 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. G1899A 2010 Journal of viral hepatitis Table HBV G1899A 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. T1753C/A 2010 Journal of viral hepatitis Table HBV T1753C;T1753A 0;0 8;8 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. T1753V 2010 Journal of viral hepatitis Table HBV T1753V 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. T1754C/G 2010 Journal of viral hepatitis Table HBV T1754C;T1754G 0;0 8;8 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. T1754G 2010 Journal of viral hepatitis Table HBV T1754G 0 6 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. T1768A 2010 Journal of viral hepatitis Table HBV T1768A 0 6 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. L180M 2010 PloS one Table HBV L180M 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. M204V 2010 PloS one Table HBV M204V 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. M250V 2010 PloS one Table HBV M250V 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. S202G 2010 PloS one Table HBV S202G 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. S202I 2010 PloS one Table HBV S202I 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. T184G 2010 PloS one Table HBV T184G 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. T184L 2010 PloS one Table HBV T184L 0 5 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. A1762T 2010 Virology Table HBV A1762T 0 6 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. G1764A 2010 Virology Table HBV G1764A 0 6 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. G1896A 2010 Virology Table HBV G1896A 0 6 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. L180M 2010 Virology Table HBV L180M 0 5 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. M204V 2010 Virology Table HBV M204V 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133I 2010 Virology journal Table HBV M133I 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133I/T 2010 Virology journal Table HBV M133I;M133T 0;0 7;7 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133L 2010 Virology journal Table HBV M133L 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133T 2010 Virology journal Table HBV M133T 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133V 2010 Virology journal Table HBV M133V 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. T123A 2010 Virology journal Table HBV T123A 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. T123N 2010 Virology journal Table HBV T123N 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. T143L 2010 Virology journal Table HBV T143L 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. T143M 2010 Virology journal Table HBV T143M 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181G 2011 Journal of viral hepatitis Table HBV A181G 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181S 2011 Journal of viral hepatitis Table HBV A181S 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181T 2011 Journal of viral hepatitis Table HBV A181T 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181T/S 2011 Journal of viral hepatitis Table HBV A181T;A181S 0;0 7;7 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181T/V 2011 Journal of viral hepatitis Table HBV A181T;A181V 0;0 7;7 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. A181V 2011 Journal of viral hepatitis Table HBV A181V 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. I233V 2011 Journal of viral hepatitis Table HBV I233V 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. L180M 2011 Journal of viral hepatitis Table HBV L180M 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. L217R 2011 Journal of viral hepatitis Table HBV L217R 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. L80I 2011 Journal of viral hepatitis Table HBV L80I 0 4 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. M204I 2011 Journal of viral hepatitis Table HBV M204I 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. M204I/V 2011 Journal of viral hepatitis Table HBV M204I;M204V 0;0 7;7 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. M204V 2011 Journal of viral hepatitis Table HBV M204V 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. M250I 2011 Journal of viral hepatitis Table HBV M250I 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. M250L 2011 Journal of viral hepatitis Table HBV M250L 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. N236T 2011 Journal of viral hepatitis Table HBV N236T 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Q215S 2011 Journal of viral hepatitis Table HBV Q215S 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. S202G 2011 Journal of viral hepatitis Table HBV S202G 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184A 2011 Journal of viral hepatitis Table HBV T184A 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184I 2011 Journal of viral hepatitis Table HBV T184I 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184I/L 2011 Journal of viral hepatitis Table HBV T184I;T184L 0;0 7;7 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184L 2011 Journal of viral hepatitis Table HBV T184L 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184L/A 2011 Journal of viral hepatitis Table HBV T184L;T184A 0;0 7;7 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. T184S 2011 Journal of viral hepatitis Table HBV T184S 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. V173L 2011 Journal of viral hepatitis Table HBV V173L 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. V173M 2011 Journal of viral hepatitis Table HBV V173M 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. V214A 2011 Journal of viral hepatitis Table HBV V214A 0 5 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. V84M 2011 Journal of viral hepatitis Table HBV V84M 0 4 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336C 2011 Virology journal Table HBV A336C 0 5 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. A336T 2011 Virology journal Table HBV A336T 0 5 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. T337C 2011 Virology journal Table HBV T337C 0 5 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. A181T 2011 BMC infectious diseases Table HBV A181T 0 5 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. I233V 2011 BMC infectious diseases Table HBV I233V 0 5 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. L180M 2011 BMC infectious diseases Table HBV L180M 0 5 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. M204I 2011 BMC infectious diseases Table HBV M204I 0 5 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. T184L 2011 BMC infectious diseases Table HBV T184L 0 5 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. G1613A 2011 PloS one Table HBV G1613A 0 6 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. A181T 2011 BMC cancer Table HBV A181T 0 5 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. L180M 2011 BMC cancer Table HBV L180M 0 5 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. M204I 2011 BMC cancer Table HBV M204I 0 5 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. M204V 2011 BMC cancer Table HBV M204V 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A1032C 2011 BMC cancer Table HBV A1032C 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A1053G 2011 BMC cancer Table HBV A1053G 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A1126C 2011 BMC cancer Table HBV A1126C 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A1633G 2011 BMC cancer Table HBV A1633G 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A1762T 2011 BMC cancer Table HBV A1762T 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A2574G 2011 BMC cancer Table HBV A2574G 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A2696G 2011 BMC cancer Table HBV A2696G 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A306G 2011 BMC cancer Table HBV A306G 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A456G 2011 BMC cancer Table HBV A456G 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C1485T 2011 BMC cancer Table HBV C1485T 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C1653T 2011 BMC cancer Table HBV C1653T 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C2444A 2011 BMC cancer Table HBV C2444A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C2586A 2011 BMC cancer Table HBV C2586A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C2919T 2011 BMC cancer Table HBV C2919T 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C3026T 2011 BMC cancer Table HBV C3026T 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C928T 2011 BMC cancer Table HBV C928T 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. C955T 2011 BMC cancer Table HBV C955T 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1356A 2011 BMC cancer Table HBV G1356A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1499A 2011 BMC cancer Table HBV G1499A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1511A 2011 BMC cancer Table HBV G1511A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1613A 2011 BMC cancer Table HBV G1613A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G162A 2011 BMC cancer Table HBV G162A 0 5 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1727A 2011 BMC cancer Table HBV G1727A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G1764A 2011 BMC cancer Table HBV G1764A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G2080A 2011 BMC cancer Table HBV G2080A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. G2783A 2011 BMC cancer Table HBV G2783A 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. T1134C 2011 BMC cancer Table HBV T1134C 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. T1323C 2011 BMC cancer Table HBV T1323C 0 6 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. T3098C 2011 BMC cancer Table HBV T3098C 0 6 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. L180M 2011 BMC research notes Table HBV L180M 0 5 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. M204V 2011 BMC research notes Table HBV M204V 0 5 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. V173L 2011 BMC research notes Table HBV V173L 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. L180M 2011 Hepatitis monthly Table HBV L180M 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. M204I 2011 Hepatitis monthly Table HBV M204I 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. M204V 2011 Hepatitis monthly Table HBV M204V 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. S202C 2011 Hepatitis monthly Table HBV S202C 0 5 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. V173L 2011 Hepatitis monthly Table HBV V173L 0 5 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. 145 Gly to Arg 2012 BMC research notes Table HBV G145R 0 14 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. 587 G to A 2012 BMC research notes Table HBV G587A 0 10 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. A181V 2010 Hepatitis monthly Table HBV A181V 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. H126R 2010 Hepatitis monthly Table HBV H126R 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. H248N 2010 Hepatitis monthly Table HBV H248N 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. L180M 2010 Hepatitis monthly Table HBV L180M 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. L231V 2010 Hepatitis monthly Table HBV L231V 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. L80V 2010 Hepatitis monthly Table HBV L80V 0 4 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. L91I 2010 Hepatitis monthly Table HBV L91I 0 4 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. M204I 2010 Hepatitis monthly Table HBV M204I 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. M204V 2010 Hepatitis monthly Table HBV M204V 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. N236T 2010 Hepatitis monthly Table HBV N236T 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Q215H 2010 Hepatitis monthly Table HBV Q215H 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. R120K 2010 Hepatitis monthly Table HBV R120K 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. S135Y 2010 Hepatitis monthly Table HBV S135Y 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. V173L 2010 Hepatitis monthly Table HBV V173L 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. V207V 2010 Hepatitis monthly Table HBV V207V 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. V555V 2010 Hepatitis monthly Table HBV V555V 0 5 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Y245H 2010 Hepatitis monthly Table HBV Y245H 0 5 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. G1896A 2010 Hepatitis monthly Table HBV G1896A 0 6 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. A1762T 2012 PloS one Table HBV A1762T 0 6 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. A181T/V 2012 PloS one Table HBV A181T;A181V 0;0 7;7 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. G1764A 2012 PloS one Table HBV G1764A 0 6 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. G1896A 2012 PloS one Table HBV G1896A 0 6 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. M250V/I 2012 PloS one Table HBV M250V;M250I 0;0 7;7 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. N236T 2012 PloS one Table HBV N236T 0 5 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. P237H 2012 PloS one Table HBV P237H 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. A181S 2012 PloS one Table HBV A181S 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. A181T 2012 PloS one Table HBV A181T 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. A194T 2012 PloS one Table HBV A194T 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. A200V 2012 PloS one Table HBV A200V 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. G152R 2012 PloS one Table HBV G152R 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. I162T 2012 PloS one Table HBV I162T 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. I169L 2012 PloS one Table HBV I169L 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. I169T 2012 PloS one Table HBV I169T 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. K149N 2012 PloS one Table HBV K149N 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. K154Q 2012 PloS one Table HBV K154Q 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. K154T 2012 PloS one Table HBV K154T 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. L157M 2012 PloS one Table HBV L157M 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. L180M 2012 PloS one Table HBV L180M 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. M204I 2012 PloS one Table HBV M204I 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. M204V 2012 PloS one Table HBV M204V 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. R153Q 2012 PloS one Table HBV R153Q 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. R153W 2012 PloS one Table HBV R153W 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. R167H 2012 PloS one Table HBV R167H 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. S202G 2012 PloS one Table HBV S202G 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. T184A 2012 PloS one Table HBV T184A 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V163I 2012 PloS one Table HBV V163I 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V173L 2012 PloS one Table HBV V173L 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V173M 2012 PloS one Table HBV V173M 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V191I 2012 PloS one Table HBV V191I 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V207I 2012 PloS one Table HBV V207I 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. V207M 2012 PloS one Table HBV V207M 0 5 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. W153Q 2012 PloS one Table HBV W153Q 0 5 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. G1896A 2012 PloS one Table HBV G1896A 0 6 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. G1899A 2012 PloS one Table HBV G1899A 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. A1762T 2012 PloS one Table HBV A1762T 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. A1993T 2012 PloS one Table HBV A1993T 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. C1914G 2012 PloS one Table HBV C1914G 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. G1764A 2012 PloS one Table HBV G1764A 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. G1896A 2012 PloS one Table HBV G1896A 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. G1899A 2012 PloS one Table HBV G1899A 0 6 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. T1753C/G 2012 PloS one Table HBV T1753C;T1753G 0;0 8;8 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. T2077C 2012 PloS one Table HBV T2077C 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. A1757G 2012 PloS one Table HBV A1757G 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. A1762T 2012 PloS one Table HBV A1762T 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1637A 2012 PloS one Table HBV C1637A 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1653T 2012 PloS one Table HBV C1653T 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1766G 2012 PloS one Table HBV C1766G 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1766T 2012 PloS one Table HBV C1766T 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1764A 2012 PloS one Table HBV G1764A 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1764T 2012 PloS one Table HBV G1764T 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1896A 2012 PloS one Table HBV G1896A 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. G1899A 2012 PloS one Table HBV G1899A 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. T1636G 2012 PloS one Table HBV T1636G 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. T1753V 2012 PloS one Table HBV T1753V 0 6 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. T1768A 2012 PloS one Table HBV T1768A 0 6 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. A1762T 2012 PloS one Table HBV A1762T 0 6 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. C1653T 2012 PloS one Table HBV C1653T 0 6 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. G1764A 2012 PloS one Table HBV G1764A 0 6 22962577 Re-evaluation of the carcinogenic significance of hepatitis B virus integration in hepatocarcinogenesis. T1753V 2012 PloS one Table HBV T1753V 0 6 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. E164A 2012 PloS one Table HBV E164A 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. E164D 2012 PloS one Table HBV E164D 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. E164V 2012 PloS one Table HBV E164V 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. P120T 2012 PloS one Table HBV P120T 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. pcG1862T 2012 PloS one Table HBV G1862T 0 8 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Q129H 2012 PloS one Table HBV Q129H 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Q129R 2012 PloS one Table HBV Q129R 0 5 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Y100C 2012 PloS one Table HBV Y100C 0 5 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. A1762T 2013 Virology journal Table HBV A1762T 0 6 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. G1764A 2013 Virology journal Table HBV G1764A 0 6 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. T1753V 2013 Virology journal Table HBV T1753V 0 6 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. D134E 2013 Virology journal Table HBV D134E 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. F221Y 2013 Virology journal Table HBV F221Y 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. I224V 2013 Virology journal Table HBV I224V 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. I91L 2013 Virology journal Table HBV I91L 0 4 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. L229F 2013 Virology journal Table HBV L229F 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. N139E 2013 Virology journal Table HBV N139E 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. N139E/Q 2013 Virology journal Table HBV N139E;N139Q 0;0 7;7 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. N139Q 2013 Virology journal Table HBV N139Q 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Q215E 2013 Virology journal Table HBV Q215E 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Q215H 2013 Virology journal Table HBV Q215H 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Q215P 2013 Virology journal Table HBV Q215P 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Q215S 2013 Virology journal Table HBV Q215S 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. S213T 2013 Virology journal Table HBV S213T 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. T128I 2013 Virology journal Table HBV T128I 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. V191F 2013 Virology journal Table HBV V191F 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. V191I 2013 Virology journal Table HBV V191I 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. W153R 2013 Virology journal Table HBV W153R 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Y124D 2013 Virology journal Table HBV Y124D 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Y124H 2013 Virology journal Table HBV Y124H 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Y124N 2013 Virology journal Table HBV Y124N 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Y126H 2013 Virology journal Table HBV Y126H 0 5 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Y126R 2013 Virology journal Table HBV Y126R 0 5 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. G2A 2013 Virology journal Table HBV G2A 0 3 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. M204I 2013 Iranian journal of microbiology Table HBV M204I 0 5 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. M204V 2013 Iranian journal of microbiology Table HBV M204V 0 5 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. A3120G/T 2013 PloS one Table HBV A3120G;A3120T 0;0 8;8 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. C1730G 2013 PloS one Table HBV C1730G 0 6 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. C2875A 2013 PloS one Table HBV C2875A 0 6 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. C76A 2013 PloS one Table HBV C76A 0 4 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. G1896A 2013 PloS one Table HBV G1896A 0 6 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. T1674C/G 2013 PloS one Table HBV T1674C;T1674G 0;0 8;8 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. T1753V 2013 PloS one Table HBV T1753V 0 6 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. A181T/V 2013 Hepatitis monthly Table HBV A181T;A181V 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. A194T 2013 Hepatitis monthly Table HBV A194T 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. A200V/P 2013 Hepatitis monthly Table HBV A200V;A200P 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. C256G 2013 Hepatitis monthly Table HBV C256G 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. F166L 2013 Hepatitis monthly Table HBV F166L 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. I169T 2013 Hepatitis monthly Table HBV I169T 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. I233V 2013 Hepatitis monthly Table HBV I233V 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. I91L 2013 Hepatitis monthly Table HBV I91L 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. L180M 2013 Hepatitis monthly Table HBV L180M 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. L217R 2013 Hepatitis monthly Table HBV L217R 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. L229G/V 2013 Hepatitis monthly Table HBV L229G;L229V 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. L80V 2013 Hepatitis monthly Table HBV L80V 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. L82M 2013 Hepatitis monthly Table HBV L82M 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. M204I/V 2013 Hepatitis monthly Table HBV M204I;M204V 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. M250V 2013 Hepatitis monthly Table HBV M250V 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. N139D/K 2013 Hepatitis monthly Table HBV N139D;N139K 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. N236T 2013 Hepatitis monthly Table HBV N236T 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. N238K/D 2013 Hepatitis monthly Table HBV N238K;N238D 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. P237H 2013 Hepatitis monthly Table HBV P237H 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Q215S 2013 Hepatitis monthly Table HBV Q215S 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. S202I/G 2013 Hepatitis monthly Table HBV S202I;S202G 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. S213T 2013 Hepatitis monthly Table HBV S213T 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. S53N 2013 Hepatitis monthly Table HBV S53N 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. S85A 2013 Hepatitis monthly Table HBV S85A 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. T128I/N 2013 Hepatitis monthly Table HBV T128I;T128N 0;0 7;7 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. T184G 2013 Hepatitis monthly Table HBV T184G 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. T54N 2013 Hepatitis monthly Table HBV T54N 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. V173L 2013 Hepatitis monthly Table HBV V173L 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. V191I 2013 Hepatitis monthly Table HBV V191I 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. V207I 2013 Hepatitis monthly Table HBV V207I 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. V214A 2013 Hepatitis monthly Table HBV V214A 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. V84M 2013 Hepatitis monthly Table HBV V84M 0 4 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. W153Q 2013 Hepatitis monthly Table HBV W153Q 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Y126C 2013 Hepatitis monthly Table HBV Y126C 0 5 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Y245H 2013 Hepatitis monthly Table HBV Y245H 0 5 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. G1896A 2013 PloS one Table HBV G1896A 0 6 24031448 Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen. G1896A 2009 Brazilian journal of microbiology Table HBV G1896A 0 6 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. G145K 2013 Virology journal Table HBV G145K 0 5 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. G145R 2013 Virology journal Table HBV G145R 0 5 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. T118M 2013 Virology journal Table HBV T118M 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. L180M 2013 Virology journal Table HBV L180M 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. M204I 2013 Virology journal Table HBV M204I 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. M204V 2013 Virology journal Table HBV M204V 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. M250L 2013 Virology journal Table HBV M250L 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. V173L 2013 Virology journal Table HBV V173L 0 5 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. V173M 2013 Virology journal Table HBV V173M 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. I195M 2013 Virology journal Table HBV I195M 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. I195T 2013 Virology journal Table HBV I195T 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. M204V 2013 Virology journal Table HBV M204V 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. Q129P 2013 Virology journal Table HBV Q129P 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. T126P 2013 Virology journal Table HBV T126P 0 5 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. V207L 2013 Virology journal Table HBV V207L 0 5 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. A1762T 2013 PloS one Table HBV A1762T 0 6 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. G1757A 2013 PloS one Table HBV G1757A 0 6 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. G1764A 2013 PloS one Table HBV G1764A 0 6 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. G1896A 2013 PloS one Table HBV G1896A 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. A1762T 2013 Hepatitis monthly Table HBV A1762T 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. A1846T 2013 Hepatitis monthly Table HBV A1846T 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. C1913A 2013 Hepatitis monthly Table HBV C1913A 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. G1764A 2013 Hepatitis monthly Table HBV G1764A 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. G1896A 2013 Hepatitis monthly Table HBV G1896A 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. G1899A 2013 Hepatitis monthly Table HBV G1899A 0 6 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. T1753C/A 2013 Hepatitis monthly Table HBV T1753C;T1753A 0;0 8;8 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. L180M 2013 Hepatitis monthly Table HBV L180M 0 5 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Q267H 2013 Hepatitis monthly Table HBV Q267H 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. A181T 2014 Hepatitis monthly Table HBV A181T 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. L180M 2014 Hepatitis monthly Table HBV L180M 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. L180V 2014 Hepatitis monthly Table HBV L180V 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. M204I 2014 Hepatitis monthly Table HBV M204I 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. M250L 2014 Hepatitis monthly Table HBV M250L 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. M250V 2014 Hepatitis monthly Table HBV M250V 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. N236T 2014 Hepatitis monthly Table HBV N236T 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. S202I 2014 Hepatitis monthly Table HBV S202I 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. T184G 2014 Hepatitis monthly Table HBV T184G 0 5 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. V173L 2014 Hepatitis monthly Table HBV V173L 0 5 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. A181T 2014 PloS one Table HBV A181T 0 5 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. L180M 2014 PloS one Table HBV L180M 0 5 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. M204I 2014 PloS one Table HBV M204I 0 5 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. M204Q 2014 PloS one Table HBV M204Q 0 5 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. T184I 2014 PloS one Table HBV T184I 0 5 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. M204I 2014 PloS one Table HBV M204I 0 5 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. A1762T 2014 PloS one Table HBV A1762T 0 6 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. G1764A 2014 PloS one Table HBV G1764A 0 6 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. G1896A 2014 PloS one Table HBV G1896A 0 6 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. G1899A 2014 PloS one Table HBV G1899A 0 6 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A144H 2014 PloS one Table HBV A144H 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A160S 2014 PloS one Table HBV A160S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A181G 2014 PloS one Table HBV A181G 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A21S 2014 PloS one Table HBV A21S 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A223S 2014 PloS one Table HBV A223S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A31S 2014 PloS one Table HBV A31S 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A329P 2014 PloS one Table HBV A329P 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. A342C 2014 PloS one Table HBV A342C 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. C185M 2014 PloS one Table HBV C185M 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. C77G 2014 PloS one Table HBV C77G 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. D263E 2014 PloS one Table HBV D263E 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. D31A 2014 PloS one Table HBV D31A 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. D45L 2014 PloS one Table HBV D45L 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. E126R 2014 PloS one Table HBV E126R 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. E64N 2014 PloS one Table HBV E64N 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. F122L 2014 PloS one Table HBV F122L 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. F19X 2014 PloS one Table HBV F19X 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. G32R 2014 PloS one Table HBV G32R 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. G50R 2014 PloS one Table HBV G50R 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. H94Y 2014 PloS one Table HBV H94Y 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. I169N 2014 PloS one Table HBV I169N 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. I233V 2014 PloS one Table HBV I233V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. I253V 2014 PloS one Table HBV I253V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. K130N 2014 PloS one Table HBV K130N 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L209V 2014 PloS one Table HBV L209V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L213I 2014 PloS one Table HBV L213I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L308A 2014 PloS one Table HBV L308A 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L30F 2014 PloS one Table HBV L30F 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L336M 2014 PloS one Table HBV L336M 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L69L 2014 PloS one Table HBV L69L 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L98C 2014 PloS one Table HBV L98C 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. M103D 2014 PloS one Table HBV M103D 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. M129L 2014 PloS one Table HBV M129L 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. M204V 2014 PloS one Table HBV M204V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. M250V 2014 PloS one Table HBV M250V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. M30L 2014 PloS one Table HBV M30L 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. N236I 2014 PloS one Table HBV N236I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. N248H 2014 PloS one Table HBV N248H 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. N337F 2014 PloS one Table HBV N337F 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. N76Q 2014 PloS one Table HBV N76Q 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. P11S 2014 PloS one Table HBV P11S 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. P145Q 2014 PloS one Table HBV P145Q 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. P159Q 2014 PloS one Table HBV P159Q 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. P34H 2014 PloS one Table HBV P34H 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Q184S 2014 PloS one Table HBV Q184S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Q211H 2014 PloS one Table HBV Q211H 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Q215S 2014 PloS one Table HBV Q215S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Q344P 2014 PloS one Table HBV Q344P 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Q87H 2014 PloS one Table HBV Q87H 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. R172Q 2014 PloS one Table HBV R172Q 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. R32G 2014 PloS one Table HBV R32G 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S11P 2014 PloS one Table HBV S11P 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S12T 2014 PloS one Table HBV S12T 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S150V 2014 PloS one Table HBV S150V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S202I 2014 PloS one Table HBV S202I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S204R 2014 PloS one Table HBV S204R 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S207N 2014 PloS one Table HBV S207N 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S210M 2014 PloS one Table HBV S210M 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S31A 2014 PloS one Table HBV S31A 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S33P 2014 PloS one Table HBV S33P 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S74X 2014 PloS one Table HBV S74X 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. S81R 2014 PloS one Table HBV S81R 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T118V 2014 PloS one Table HBV T118V 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T120N 2014 PloS one Table HBV T120N 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T127P 2014 PloS one Table HBV T127P 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T138Q 2014 PloS one Table HBV T138Q 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T36A 2014 PloS one Table HBV T36A 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T49S 2014 PloS one Table HBV T49S 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. T70X 2014 PloS one Table HBV T70X 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V105I 2014 PloS one Table HBV V105I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V116I 2014 PloS one Table HBV V116I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V133Y 2014 PloS one Table HBV V133Y 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V163I 2014 PloS one Table HBV V163I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V173L 2014 PloS one Table HBV V173L 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V190L 2014 PloS one Table HBV V190L 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V341S 2014 PloS one Table HBV V341S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V37L 2014 PloS one Table HBV V37L 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. V47G 2014 PloS one Table HBV V47G 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y135S 2014 PloS one Table HBV Y135S 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y161I 2014 PloS one Table HBV Y161I 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y305A 2014 PloS one Table HBV Y305A 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y335N 2014 PloS one Table HBV Y335N 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y339T 2014 PloS one Table HBV Y339T 0 5 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Y54H 2014 PloS one Table HBV Y54H 0 4 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A799G 2014 PloS one Table HBV A799G 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A942S 2014 PloS one Table HBV A942S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A987G 2014 PloS one Table HBV A987G 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C256S 2014 PloS one Table HBV C256S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C294T 2014 PloS one Table HBV C294T 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C300G 2014 PloS one Table HBV C300G 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C314S 2014 PloS one Table HBV C314S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C620S 2014 PloS one Table HBV C620S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C660S 2014 PloS one Table HBV C660S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. C936T 2014 PloS one Table HBV C936T 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. F134S 2014 PloS one Table HBV F134S 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. H271Q 2014 PloS one Table HBV H271Q 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. H617Q 2014 PloS one Table HBV H617Q 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. I224V 2014 PloS one Table HBV I224V 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. I570V 2014 PloS one Table HBV I570V 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. M309K 2014 PloS one Table HBV M309K 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. M655K 2014 PloS one Table HBV M655K 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. P49R 2014 PloS one Table HBV P49R 0 4 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. S204R 2014 PloS one Table HBV S204R 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. S213T 2014 PloS one Table HBV S213T 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. S559T 2014 PloS one Table HBV S559T 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T1055A 2014 PloS one Table HBV T1055A 0 6 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T1069A 2014 PloS one Table HBV T1069A 0 6 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T1071C 2014 PloS one Table HBV T1071C 0 6 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T48M 2014 PloS one Table HBV T48M 0 4 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T555C 2014 PloS one Table HBV T555C 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T766A 2014 PloS one Table HBV T766A 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T843C 2014 PloS one Table HBV T843C 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T870C 2014 PloS one Table HBV T870C 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T895A 2014 PloS one Table HBV T895A 0 5 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. T906R 2014 PloS one Table HBV T906R 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. A128V 2014 PloS one Table HBV A128V 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. F134N 2014 PloS one Table HBV F134N 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. G119R 2014 PloS one Table HBV G119R 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. G130S/R 2014 PloS one Table HBV G130S;G130R 0;0 7;7 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. M133T 2014 PloS one Table HBV M133T 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. P120T 2014 PloS one Table HBV P120T 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. P127T/S 2014 PloS one Table HBV P127T;P127S 0;0 7;7 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. P135L 2014 PloS one Table HBV P135L 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. S143L/M 2014 PloS one Table HBV S143L;S143M 0;0 7;7 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. T118K/A 2014 PloS one Table HBV T118K;T118A 0;0 7;7 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. T125M 2014 PloS one Table HBV T125M 0 5 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. T126I/S 2014 PloS one Table HBV T126I;T126S 0;0 7;7 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. A162G 2014 PloS one Table HBV A162G 0 5 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. A706C 2014 PloS one Table HBV A706C 0 5 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. C3026A 2014 PloS one Table HBV C3026A 0 6 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. T31C 2014 PloS one Table HBV T31C 0 4 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. T531C/G 2014 PloS one Table HBV T531C;T531G 0;0 7;7 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. T53C 2014 PloS one Table HBV T53C 0 4 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. T766A 2014 PloS one Table HBV T766A 0 5 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. L180M 2014 PloS one Table HBV L180M 0 5 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. M204V 2014 PloS one Table HBV M204V 0 5 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. N238D 2014 PloS one Table HBV N238D 0 5 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. V173L 2014 PloS one Table HBV V173L 0 5 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. V214A 2014 PloS one Table HBV V214A 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A1053G 2014 PloS one Table HBV A1053G 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A1762T 2014 PloS one Table HBV A1762T 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A1934T 2014 PloS one Table HBV A1934T 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A2246C 2014 PloS one Table HBV A2246C 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. A2339T 2014 PloS one Table HBV A2339T 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C1653T 2014 PloS one Table HBV C1653T 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C2100A 2014 PloS one Table HBV C2100A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C2289A 2014 PloS one Table HBV C2289A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C2340G 2014 PloS one Table HBV C2340G 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C528T 2014 PloS one Table HBV C528T 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. C534T 2014 PloS one Table HBV C534T 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. E113Q 2014 PloS one Table HBV E113Q 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. F221Y 2014 PloS one Table HBV F221Y 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. G1764A 2014 PloS one Table HBV G1764A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. G1862T 2014 PloS one Table HBV G1862T 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. G1896A 2014 PloS one Table HBV G1896A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. G2237C 2014 PloS one Table HBV G2237C 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. H94Y 2014 PloS one Table HBV H94Y 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. I116L 2014 PloS one Table HBV I116L 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. I127T 2014 PloS one Table HBV I127T 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. K130M 2014 PloS one Table HBV K130M 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. L12V 2014 PloS one Table HBV L12V 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. L213I 2014 PloS one Table HBV L213I 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. P130Q 2014 PloS one Table HBV P130Q 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. S35T 2014 PloS one Table HBV S35T 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. S98T 2014 PloS one Table HBV S98T 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T1050G 2014 PloS one Table HBV T1050G 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T1050G/A 2014 PloS one Table HBV T1050G;T1050A 0;0 8;8 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T125M 2014 PloS one Table HBV T125M 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T127L 2014 PloS one Table HBV T127L 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T12S 2014 PloS one Table HBV T12S 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T147C 2014 PloS one Table HBV T147C 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T1753C 2014 PloS one Table HBV T1753C 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T1858C 2014 PloS one Table HBV T1858C 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T2003A 2014 PloS one Table HBV T2003A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T3139A 2014 PloS one Table HBV T3139A 0 6 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T67N 2014 PloS one Table HBV T67N 0 4 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. T791A 2014 PloS one Table HBV T791A 0 5 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. V131I 2014 PloS one Table HBV V131I 0 5 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. C149R 2014 PloS one Table HBV C149R 0 5 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. G159R 2014 PloS one Table HBV G159R 0 5 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. G50A 2014 PloS one Table HBV G50A 0 4 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. L158G 2014 PloS one Table HBV L158G 0 5 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. Q101H 2014 PloS one Table HBV Q101H 0 5 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. S31N 2014 PloS one Table HBV S31N 0 4 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. S31T 2014 PloS one Table HBV S31T 0 4 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A1392G 2014 Virology journal Table HBV A1392G 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A1512T 2014 Virology journal Table HBV A1512T 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A1623G 2014 Virology journal Table HBV A1623G 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A577G 2014 Virology journal Table HBV A577G 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A697T 2014 Virology journal Table HBV A697T 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. A808G 2014 Virology journal Table HBV A808G 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. C1602A 2014 Virology journal Table HBV C1602A 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. C1638T 2014 Virology journal Table HBV C1638T 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. C787A 2014 Virology journal Table HBV C787A 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. C823T 2014 Virology journal Table HBV C823T 0 5 25471066 Occult hepatitis B virus infection among blood donors in Colombia. T1387C 2014 Virology journal Table HBV T1387C 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. T1640C 2014 Virology journal Table HBV T1640C 0 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. T572C 2014 Virology journal Table HBV T572C 0 5 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. A1762T 2014 Hepatitis monthly Table HBV A1762T 0 6 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. G1764A 2014 Hepatitis monthly Table HBV G1764A 0 6 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. G1896A 2014 Hepatitis monthly Table HBV G1896A 0 6 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. A123A 2014 PloS one Table HBV A123A 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. A211A 2014 PloS one Table HBV A211A 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. C256S 2014 PloS one Table HBV C256S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. D144E 2014 PloS one Table HBV D144E 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. D263E 2014 PloS one Table HBV D263E 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. F122I 2014 PloS one Table HBV F122I 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. F221Y 2014 PloS one Table HBV F221Y 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. G145R 2014 PloS one Table HBV G145R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. G258G 2014 PloS one Table HBV G258G 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. H117H 2014 PloS one Table HBV H117H 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. H124Y 2014 PloS one Table HBV H124Y 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. H134H 2014 PloS one Table HBV H134H 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. H94I 2014 PloS one Table HBV H94I 0 4 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I103V 2014 PloS one Table HBV I103V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I110L 2014 PloS one Table HBV I110L 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I163V 2014 PloS one Table HBV I163V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I253V 2014 PloS one Table HBV I253V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I266K 2014 PloS one Table HBV I266K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I86F 2014 PloS one Table HBV I86F 0 4 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. I92T 2014 PloS one Table HBV I92T 0 4 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. K241K 2014 PloS one Table HBV K241K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. K268K 2014 PloS one Table HBV K268K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. K275E 2014 PloS one Table HBV K275E 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L115V 2014 PloS one Table HBV L115V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L145M 2014 PloS one Table HBV L145M 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L168L 2014 PloS one Table HBV L168L 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L213F 2014 PloS one Table HBV L213F 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L213I 2014 PloS one Table HBV L213I 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L217R 2014 PloS one Table HBV L217R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L260L 2014 PloS one Table HBV L260L 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L91I 2014 PloS one Table HBV L91I 0 4 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. L93F 2014 PloS one Table HBV L93F 0 4 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. M309K 2014 PloS one Table HBV M309K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. N248H 2014 PloS one Table HBV N248H 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. N279T 2014 PloS one Table HBV N279T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. P127S 2014 PloS one Table HBV P127S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. P203Q 2014 PloS one Table HBV P203Q 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. P237T 2014 PloS one Table HBV P237T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Q101Q 2014 PloS one Table HBV Q101Q 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Q215Q 2014 PloS one Table HBV Q215Q 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R110G 2014 PloS one Table HBV R110G 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R153K 2014 PloS one Table HBV R153K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R153Q 2014 PloS one Table HBV R153Q 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R242R 2014 PloS one Table HBV R242R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R274K 2014 PloS one Table HBV R274K 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R280R 2014 PloS one Table HBV R280R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. R289R 2014 PloS one Table HBV R289R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S113S 2014 PloS one Table HBV S113S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S136S 2014 PloS one Table HBV S136S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S137T 2014 PloS one Table HBV S137T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S143T 2014 PloS one Table HBV S143T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S154S 2014 PloS one Table HBV S154S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S155S 2014 PloS one Table HBV S155S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S204R 2014 PloS one Table HBV S204R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S207N 2014 PloS one Table HBV S207N 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S210R 2014 PloS one Table HBV S210R 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S210S 2014 PloS one Table HBV S210S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S213T 2014 PloS one Table HBV S213T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S219P 2014 PloS one Table HBV S219P 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. S259S 2014 PloS one Table HBV S259S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. T115T 2014 PloS one Table HBV T115T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. T125M 2014 PloS one Table HBV T125M 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. T126S 2014 PloS one Table HBV T126S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. T189I 2014 PloS one Table HBV T189I 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. T222S 2014 PloS one Table HBV T222S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. V142V 2014 PloS one Table HBV V142V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. V208V 2014 PloS one Table HBV V208V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. V214D 2014 PloS one Table HBV V214D 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. V253V 2014 PloS one Table HBV V253V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. V286V 2014 PloS one Table HBV V286V 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y134F 2014 PloS one Table HBV Y134F 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y135F 2014 PloS one Table HBV Y135F 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y135H 2014 PloS one Table HBV Y135H 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y135S 2014 PloS one Table HBV Y135S 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y200F 2014 PloS one Table HBV Y200F 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y206L 2014 PloS one Table HBV Y206L 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y206T 2014 PloS one Table HBV Y206T 0 5 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Y252Y 2014 PloS one Table HBV Y252Y 0 5 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. A1679G 2015 Hepatitis monthly Table HBV A1679G 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. A1752G 2015 Hepatitis monthly Table HBV A1752G 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. A1762T 2015 Hepatitis monthly Table HBV A1762T 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. A1775G 2015 Hepatitis monthly Table HBV A1775G 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. C1856T 2015 Hepatitis monthly Table HBV C1856T 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. G1721A 2015 Hepatitis monthly Table HBV G1721A 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. G1757A 2015 Hepatitis monthly Table HBV G1757A 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. G1764A 2015 Hepatitis monthly Table HBV G1764A 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. G1896A 2015 Hepatitis monthly Table HBV G1896A 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. G1899A 2015 Hepatitis monthly Table HBV G1899A 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. T1753G 2015 Hepatitis monthly Table HBV T1753G 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. T1758C 2015 Hepatitis monthly Table HBV T1758C 0 6 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. T1858C 2015 Hepatitis monthly Table HBV T1858C 0 6 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. G1896A 2015 Hepatitis monthly Table HBV G1896A 0 6 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. G1899A 2015 Hepatitis monthly Table HBV G1899A 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. A1752G 2015 PloS one Table HBV A1752G 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. A1762T 2015 PloS one Table HBV A1762T 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. A1846T 2015 PloS one Table HBV A1846T 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. G1764A 2015 PloS one Table HBV G1764A 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. G1896A 2015 PloS one Table HBV G1896A 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. G1899A 2015 PloS one Table HBV G1899A 0 6 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. T1753V 2015 PloS one Table HBV T1753V 0 6 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. A1762T 2015 PloS one Table HBV A1762T 0 6 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. G1764A 2015 PloS one Table HBV G1764A 0 6 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. G1896A 2015 PloS one Table HBV G1896A 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A1846T 2015 PloS one Table HBV A1846T 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A1846T/G 2015 PloS one Table HBV A1846T;A1846G 0;0 8;8 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A2159G 2015 PloS one Table HBV A2159G 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A2159G/C 2015 PloS one Table HBV A2159G;A2159C 0;0 8;8 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A2189C 2015 PloS one Table HBV A2189C 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A2189T 2015 PloS one Table HBV A2189T 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. A2189T/C 2015 PloS one Table HBV A2189T;A2189C 0;0 8;8 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. C1913A 2015 PloS one Table HBV C1913A 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. C1913A/G 2015 PloS one Table HBV C1913A;C1913G 0;0 8;8 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. G1896A 2015 PloS one Table HBV G1896A 0 6 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. G1913A/G 2015 PloS one Table HBV G1913A;G1913G 0;0 8;8 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. G285A 2015 PloS one Table HBV G285A 0 5 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. T216C 2015 PloS one Table HBV T216C 0 5 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. A3054T 2015 Chinese medical journal Table HBV A3054T 0 6 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. C3116T 2015 Chinese medical journal Table HBV C3116T 0 6 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. C256G/S 2015 Hepatitis monthly Table HBV C256G;C256S 0;0 7;7 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. L91I 2015 Hepatitis monthly Table HBV L91I 0 4 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. N238H/T 2015 Hepatitis monthly Table HBV N238H;N238T 0;0 7;7 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. Y54N/H 2015 Hepatitis monthly Table HBV Y54N;Y54H 0;0 6;6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. A1762T 2015 Virology journal Table HBV A1762T 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. A1846T 2015 Virology journal Table HBV A1846T 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. C1766T 2015 Virology journal Table HBV C1766T 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1764A 2015 Virology journal Table HBV G1764A 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1862T 2015 Virology journal Table HBV G1862T 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1896A 2015 Virology journal Table HBV G1896A 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. G1899A 2015 Virology journal Table HBV G1899A 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. T1753V 2015 Virology journal Table HBV T1753V 0 6 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. T1768A 2015 Virology journal Table HBV T1768A 0 6 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. A200V 2015 Hepatitis monthly Table HBV A200V 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. G145R 2015 Hepatitis monthly Table HBV G145R 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. I110V 2015 Hepatitis monthly Table HBV I110V 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. L180M 2015 Hepatitis monthly Table HBV L180M 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. M204I 2015 Hepatitis monthly Table HBV M204I 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. M240I 2015 Hepatitis monthly Table HBV M240I 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. S202I 2015 Hepatitis monthly Table HBV S202I 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. T127P 2015 Hepatitis monthly Table HBV T127P 0 5 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. Y134N 2015 Hepatitis monthly Table HBV Y134N 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. A181T 2015 PloS one Table HBV A181T 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. L180M 2015 PloS one Table HBV L180M 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. L269I 2015 PloS one Table HBV L269I 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. M204I 2015 PloS one Table HBV M204I 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. M204V 2015 PloS one Table HBV M204V 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. M250V 2015 PloS one Table HBV M250V 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. N236T 2015 PloS one Table HBV N236T 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. S202G 2015 PloS one Table HBV S202G 0 5 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. T184L 2015 PloS one Table HBV T184L 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. K141R 2015 Virology journal Table HBV K141R 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. P120T/S 2015 Virology journal Table HBV P120T;P120S 0;0 7;7 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. P127T 2015 Virology journal Table HBV P127T 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Q129R 2015 Virology journal Table HBV Q129R 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. S143L/T 2015 Virology journal Table HBV S143L;S143T 0;0 7;7 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T115S 2015 Virology journal Table HBV T115S 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M 2015 Virology journal Table HBV T125M 0 5 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. A1752G 2015 Hepatitis monthly Table HBV A1752G 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. A1762T 2015 Hepatitis monthly Table HBV A1762T 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. C1653T 2015 Hepatitis monthly Table HBV C1653T 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. C1766T 2015 Hepatitis monthly Table HBV C1766T 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. C1858T 2015 Hepatitis monthly Table HBV C1858T 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1764A 2015 Hepatitis monthly Table HBV G1764A 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A 2015 Hepatitis monthly Table HBV G1896A 0 6 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. A1762T 2016 PloS one Table HBV A1762T 0 6 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. G1764A 2016 PloS one Table HBV G1764A 0 6 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. G1896A 2016 PloS one Table HBV G1896A 0 6 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. L180M 2016 PloS one Table HBV L180M 0 5 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. M204I 2016 PloS one Table HBV M204I 0 5 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. M204V 2016 PloS one Table HBV M204V 0 5 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. P120T 2016 PloS one Table HBV P120T 0 5 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. T126I 2016 PloS one Table HBV T126I 0 5 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. A1762T 2016 Oncotarget Table HBV A1762T 0 6 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. G1764A 2016 Oncotarget Table HBV G1764A 0 6 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. A128T 2016 PloS one Table HBV A128T 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. A159G 2016 PloS one Table HBV A159G 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. C121R 2016 PloS one Table HBV C121R 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. C138Y 2016 PloS one Table HBV C138Y 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. C139R/Y 2016 PloS one Table HBV C139R;C139Y 0;0 7;7 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. F158L 2016 PloS one Table HBV F158L 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. G112R 2016 PloS one Table HBV G112R 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. G119R 2016 PloS one Table HBV G119R 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. I218M 2016 PloS one Table HBV I218M 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. L109P 2016 PloS one Table HBV L109P 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. L110I 2016 PloS one Table HBV L110I 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. L173P 2016 PloS one Table HBV L173P 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. L176P 2016 PloS one Table HBV L176P 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. L205V 2016 PloS one Table HBV L205V 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. M103I 2016 PloS one Table HBV M103I 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. M133T 2016 PloS one Table HBV M133T 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. M197T 2016 PloS one Table HBV M197T 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. M198V 2016 PloS one Table HBV M198V 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. P127T 2016 PloS one Table HBV P127T 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. P151L 2016 PloS one Table HBV P151L 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. P49I 2016 PloS one Table HBV P49I 0 4 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. R160N 2016 PloS one Table HBV R160N 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S132P 2016 PloS one Table HBV S132P 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S136P 2016 PloS one Table HBV S136P 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S167L 2016 PloS one Table HBV S167L 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S174G 2016 PloS one Table HBV S174G 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S204R 2016 PloS one Table HBV S204R 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. S210G 2016 PloS one Table HBV S210G 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. T124S/R 2016 PloS one Table HBV T124S;T124R 0;0 7;7 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. T126A 2016 PloS one Table HBV T126A 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. T140I 2016 PloS one Table HBV T140I 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. T45K 2016 PloS one Table HBV T45K 0 4 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. V190I 2016 PloS one Table HBV V190I 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. W182L 2016 PloS one Table HBV W182L 0 5 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. W191R 2016 PloS one Table HBV W191R 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A1122G 2016 Hepatitis monthly Table HBV A1122G 0 6 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A289T 2016 Hepatitis monthly Table HBV A289T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A355G 2016 Hepatitis monthly Table HBV A355G 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A499G 2016 Hepatitis monthly Table HBV A499G 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A574G 2016 Hepatitis monthly Table HBV A574G 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A633G 2016 Hepatitis monthly Table HBV A633G 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A895T 2016 Hepatitis monthly Table HBV A895T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. A967C 2016 Hepatitis monthly Table HBV A967C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C373T 2016 Hepatitis monthly Table HBV C373T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C573T 2016 Hepatitis monthly Table HBV C573T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C592T 2016 Hepatitis monthly Table HBV C592T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C598T 2016 Hepatitis monthly Table HBV C598T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C735T 2016 Hepatitis monthly Table HBV C735T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C936T 2016 Hepatitis monthly Table HBV C936T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. C966T 2016 Hepatitis monthly Table HBV C966T 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G1131A 2016 Hepatitis monthly Table HBV G1131A 0 6 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G285A 2016 Hepatitis monthly Table HBV G285A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G783A 2016 Hepatitis monthly Table HBV G783A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G793A 2016 Hepatitis monthly Table HBV G793A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G942A 2016 Hepatitis monthly Table HBV G942A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G951A 2016 Hepatitis monthly Table HBV G951A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. G961A 2016 Hepatitis monthly Table HBV G961A 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T123C 2016 Hepatitis monthly Table HBV T123C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T454C 2016 Hepatitis monthly Table HBV T454C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T667C 2016 Hepatitis monthly Table HBV T667C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T705C 2016 Hepatitis monthly Table HBV T705C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T820C 2016 Hepatitis monthly Table HBV T820C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T955C 2016 Hepatitis monthly Table HBV T955C 0 5 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. T975C 2016 Hepatitis monthly Table HBV T975C 0 5 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. G145R/A 2016 PloS one Table HBV G145R;G145A 0;0 7;7 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. G145S 2016 PloS one Table HBV G145S 0 5 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. Y206S 2016 PloS one Table HBV Y206S 0 5 27280884 Impact of Universal Hepatitis B Vaccination on Prevalence, Infection-Associated Morbidity and Mortality, and Circulation of Immune Escape Variants in Russia. Y206S/C 2016 PloS one Table HBV Y206S;Y206C 0;0 7;7 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. A1762T 2016 Cancer science Table HBV A1762T 0 6 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. G1764A 2016 Cancer science Table HBV G1764A 0 6 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. T1753V 2016 Cancer science Table HBV T1753V 0 6 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. T1768A 2016 Cancer science Table HBV T1768A 0 6 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. V1753A 2016 Cancer science Table HBV V1753A 0 6 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. F19L 2016 Oncotarget Table HBV F19L 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. F75S 2016 Oncotarget Table HBV F75S 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. G44G/E 2016 Oncotarget Table HBV G44G;G44E 0;0 6;6 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. G76A 2016 Oncotarget Table HBV G76A 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. G91A 2016 Oncotarget Table HBV G91A 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. G99E 2016 Oncotarget Table HBV G99E 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. H114T 2016 Oncotarget Table HBV H114T 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I110L 2016 Oncotarget Table HBV I110L 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I147T 2016 Oncotarget Table HBV I147T 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I165L 2016 Oncotarget Table HBV I165L 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I255T 2016 Oncotarget Table HBV I255T 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I273L 2016 Oncotarget Table HBV I273L 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. I92T 2016 Oncotarget Table HBV I92T 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. L54P 2016 Oncotarget Table HBV L54P 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. N103D 2016 Oncotarget Table HBV N103D 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. N222T 2016 Oncotarget Table HBV N222T 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. N59T 2016 Oncotarget Table HBV N59T 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. P124K 2016 Oncotarget Table HBV P124K 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. P24L 2016 Oncotarget Table HBV P24L 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. P41H 2016 Oncotarget Table HBV P41H 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. P66L 2016 Oncotarget Table HBV P66L 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Q129H 2016 Oncotarget Table HBV Q129H 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Q184H 2016 Oncotarget Table HBV Q184H 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. S59F 2016 Oncotarget Table HBV S59F 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. S98T 2016 Oncotarget Table HBV S98T 0 4 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. T114I 2016 Oncotarget Table HBV T114I 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. T119P 2016 Oncotarget Table HBV T119P 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. T131I 2016 Oncotarget Table HBV T131I 0 5 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. T40S 2016 Oncotarget Table HBV T40S 0 4 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. F249A 2016 Oncotarget Table HBV F249A 0 5 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. L180M 2016 Oncotarget Table HBV L180M 0 5 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. S202G 2016 Oncotarget Table HBV S202G 0 5 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. G145R 2016 Hepatitis monthly Table HBV G145R 0 5 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. A35E 2016 Infectious agents and cancer Table HBV A35E 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. H15Y 2016 Infectious agents and cancer Table HBV H15Y 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. H44L 2016 Infectious agents and cancer Table HBV H44L 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. K13E 2016 Infectious agents and cancer Table HBV K13E 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. K85Q 2016 Infectious agents and cancer Table HBV K85Q 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. N14K 2016 Infectious agents and cancer Table HBV N14K 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. N19T 2016 Infectious agents and cancer Table HBV N19T 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. N29K 2016 Infectious agents and cancer Table HBV N29K 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. P25L 2016 Infectious agents and cancer Table HBV P25L 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. P30Q 2016 Infectious agents and cancer Table HBV P30Q 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. P64S 2016 Infectious agents and cancer Table HBV P64S 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. R38G 2016 Infectious agents and cancer Table HBV R38G 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. R38K 2016 Infectious agents and cancer Table HBV R38K 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. S100V 2016 Infectious agents and cancer Table HBV S100V 0 5 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. S90T 2016 Infectious agents and cancer Table HBV S90T 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. T52R 2016 Infectious agents and cancer Table HBV T52R 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. V49A 2016 Infectious agents and cancer Table HBV V49A 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. V80I 2016 Infectious agents and cancer Table HBV V80I 0 4 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. W42G 2016 Infectious agents and cancer Table HBV W42G 0 4 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Ala128Val 2016 SpringerPlus Table HBV A128V 0 9 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Pro127Thr 2016 SpringerPlus Table HBV P127T 0 9 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Ser143Leu 2016 SpringerPlus Table HBV S143L 0 9 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Thr118Val 2016 SpringerPlus Table HBV T118V 0 9 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Thr125Met 2016 SpringerPlus Table HBV T125M 0 9 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Thr126Ile 2016 SpringerPlus Table HBV T126I 0 9 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. A168V 2016 Virology journal Table HBV A168V 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. E164D 2016 Virology journal Table HBV E164D 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. E164G 2016 Virology journal Table HBV E164G 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. F161Y 2016 Virology journal Table HBV F161Y 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. G159A 2016 Virology journal Table HBV G159A 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. I120L 2016 Virology journal Table HBV I120L 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. L127P 2016 Virology journal Table HBV L127P 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. L180M 2016 Virology journal Table HBV L180M 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. M204V 2016 Virology journal Table HBV M204V 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. Q129H 2016 Virology journal Table HBV Q129H 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. R122K 2016 Virology journal Table HBV R122K 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. S114T 2016 Virology journal Table HBV S114T 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. S140T 2016 Virology journal Table HBV S140T 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. S143T 2016 Virology journal Table HBV S143T 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. S167L 2016 Virology journal Table HBV S167L 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. T131K 2016 Virology journal Table HBV T131K 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. T131N 2016 Virology journal Table HBV T131N 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. T184S 2016 Virology journal Table HBV T184S 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. V173L 2016 Virology journal Table HBV V173L 0 5 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. Y100C 2016 Virology journal Table HBV Y100C 0 5 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. G145K 2016 PloS one Table HBV G145K 0 5 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. G145R 2016 PloS one Table HBV G145R 0 5 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. A1499G 2016 Aging Table HBV A1499G 0 6 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. A1762T 2016 Aging Table HBV A1762T 0 6 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. G1764A 2016 Aging Table HBV G1764A 0 6 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. A158V 2016 PloS one Table HBV A158V 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. A62A 2016 PloS one Table HBV A62A 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. A91V 2016 PloS one Table HBV A91V 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. F200Y 2016 PloS one Table HBV F200Y 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. G127W 2016 PloS one Table HBV G127W 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. I168T 2016 PloS one Table HBV I168T 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. I184I/M 2016 PloS one Table HBV I184I;I184M 0;0 7;7 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. K333Q 2016 PloS one Table HBV K333Q 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. L165F 2016 PloS one Table HBV L165F 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. L267R 2016 PloS one Table HBV L267R 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. L269I 2016 PloS one Table HBV L269I 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. L336S 2016 PloS one Table HBV L336S 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. L84I 2016 PloS one Table HBV L84I 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. M213T 2016 PloS one Table HBV M213T 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. N134N/D 2016 PloS one Table HBV N134N;N134D 0;0 7;7 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. N13S 2016 PloS one Table HBV N13S 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. N337T 2016 PloS one Table HBV N337T 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. N53S 2016 PloS one Table HBV N53S 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. P159T 2016 PloS one Table HBV P159T 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. P173P/Q 2016 PloS one Table HBV P173P;P173Q 0;0 7;7 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. Q316H 2016 PloS one Table HBV Q316H 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. R135K 2016 PloS one Table HBV R135K 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S101L 2016 PloS one Table HBV S101L 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S204N 2016 PloS one Table HBV S204N 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S256C 2016 PloS one Table HBV S256C 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S50F 2016 PloS one Table HBV S50F 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S96S/A 2016 PloS one Table HBV S96S;S96A 0;0 6;6 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. T45A 2016 PloS one Table HBV T45A 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. T5A 2016 PloS one Table HBV T5A 0 3 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. V114I 2016 PloS one Table HBV V114I 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. V184A 2016 PloS one Table HBV V184A 0 5 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. V90A 2016 PloS one Table HBV V90A 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. V90V 2016 PloS one Table HBV V90V 0 4 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. W74L 2016 PloS one Table HBV W74L 0 4 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. A168V 2016 Hepatitis monthly Table HBV A168V 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. C76Y 2016 Hepatitis monthly Table HBV C76Y 0 4 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. D144E 2016 Hepatitis monthly Table HBV D144E 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. E164D 2016 Hepatitis monthly Table HBV E164D 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. F85C 2016 Hepatitis monthly Table HBV F85C 0 4 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. I110L 2016 Hepatitis monthly Table HBV I110L 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. I92T 2016 Hepatitis monthly Table HBV I92T 0 4 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. L104F 2016 Hepatitis monthly Table HBV L104F 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. P127L/T 2016 Hepatitis monthly Table HBV P127L;P127T 0;0 7;7 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. Q129H 2016 Hepatitis monthly Table HBV Q129H 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. S117G 2016 Hepatitis monthly Table HBV S117G 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. S143L 2016 Hepatitis monthly Table HBV S143L 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. S54G 2016 Hepatitis monthly Table HBV S54G 0 4 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. T123V 2016 Hepatitis monthly Table HBV T123V 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. T125M 2016 Hepatitis monthly Table HBV T125M 0 5 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. W165R 2016 Hepatitis monthly Table HBV W165R 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. F134V 2017 PloS one Table HBV F134V 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. G145R 2017 PloS one Table HBV G145R 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. N146G 2017 PloS one Table HBV N146G 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. P120K 2017 PloS one Table HBV P120K 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Q129R 2017 PloS one Table HBV Q129R 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. T123D 2017 PloS one Table HBV T123D 0 5 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. P203Q 2017 Oncotarget Table HBV P203Q 0 5 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. S210R 2017 Oncotarget Table HBV S210R 0 5 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. P120S 2017 World journal of hepatology Table HBV P120S 0 5 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. P120T 2017 World journal of hepatology Table HBV P120T 0 5 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. S143L 2017 World journal of hepatology Table HBV S143L 0 5 28472081 HBV DNA genome co-transfection procedure for the evaluation of relative fitness. D1del 2017 PloS one Table HBV D1del 0 5 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. A128V 2017 PloS one Table HBV A128V 0 5 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. P120X 2017 PloS one Table HBV P120X 0 5 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. T123S 2017 PloS one Table HBV T123S 0 5 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. T126I 2017 PloS one Table HBV T126I 0 5 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. T131N 2017 PloS one Table HBV T131N 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. A186T 2017 PloS one Table HBV A186T 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. E218A 2017 PloS one Table HBV E218A 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. F134Y 2017 PloS one Table HBV F134Y 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. F183C 2017 PloS one Table HBV F183C 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. G185E 2017 PloS one Table HBV G185E 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. I162T 2017 PloS one Table HBV I162T 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. L140P 2017 PloS one Table HBV L140P 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. L175V 2017 PloS one Table HBV L175V 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. L179P 2017 PloS one Table HBV L179P 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. L180M 2017 PloS one Table HBV L180M 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. M129T 2017 PloS one Table HBV M129T 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. M204V 2017 PloS one Table HBV M204V 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. R122K 2017 PloS one Table HBV R122K 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. S105T 2017 PloS one Table HBV S105T 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. S132P 2017 PloS one Table HBV S132P 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. S171P 2017 PloS one Table HBV S171P 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. S207G 2017 PloS one Table HBV S207G 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. S210R 2017 PloS one Table HBV S210R 0 5 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. W172stop 2017 PloS one Table HBV W172X 0 8 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Y126Q 2017 PloS one Table HBV Y126Q 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. A128V 2017 Scientific reports Table HBV A128V 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. D144A 2017 Scientific reports Table HBV D144A 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. D144E 2017 Scientific reports Table HBV D144E 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. D144N 2017 Scientific reports Table HBV D144N 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. F134L 2017 Scientific reports Table HBV F134L 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. G130E 2017 Scientific reports Table HBV G130E 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. G145A 2017 Scientific reports Table HBV G145A 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. G145R 2017 Scientific reports Table HBV G145R 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. I126N 2017 Scientific reports Table HBV I126N 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. I126S 2017 Scientific reports Table HBV I126S 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. M133I 2017 Scientific reports Table HBV M133I 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. M133T 2017 Scientific reports Table HBV M133T 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. P127T 2017 Scientific reports Table HBV P127T 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Q129H 2017 Scientific reports Table HBV Q129H 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. S143L 2017 Scientific reports Table HBV S143L 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. T126A 2017 Scientific reports Table HBV T126A 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. T131N 2017 Scientific reports Table HBV T131N 0 5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. T131P 2017 Scientific reports Table HBV T131P 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. A162G 2017 BMC infectious diseases Table HBV A162G 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. A1762T 2017 BMC infectious diseases Table HBV A1762T 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. A2159G 2017 BMC infectious diseases Table HBV A2159G 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. A2189C 2017 BMC infectious diseases Table HBV A2189C 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. A2962G 2017 BMC infectious diseases Table HBV A2962G 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. A60V/E 2017 BMC infectious diseases Table HBV A60V;A60E 0;0 6;6 28859616 Molecular characterization of hepatitis B virus in Vietnam. A706C 2017 BMC infectious diseases Table HBV A706C 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. C1653T 2017 BMC infectious diseases Table HBV C1653T 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. C1766G 2017 BMC infectious diseases Table HBV C1766G 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. C2964A 2017 BMC infectious diseases Table HBV C2964A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. C3026A 2017 BMC infectious diseases Table HBV C3026A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. G145R 2017 BMC infectious diseases Table HBV G145R 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. G1757A 2017 BMC infectious diseases Table HBV G1757A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. G1764A 2017 BMC infectious diseases Table HBV G1764A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. G1896A 2017 BMC infectious diseases Table HBV G1896A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. G1899A 2017 BMC infectious diseases Table HBV G1899A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. G2203A 2017 BMC infectious diseases Table HBV G2203A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. N38E 2017 BMC infectious diseases Table HBV N38E 0 4 28859616 Molecular characterization of hepatitis B virus in Vietnam. P120S/E 2017 BMC infectious diseases Table HBV P120S;P120E 0;0 7;7 28859616 Molecular characterization of hepatitis B virus in Vietnam. S204R 2017 BMC infectious diseases Table HBV S204R 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. T126A 2017 BMC infectious diseases Table HBV T126A 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. T1753C 2017 BMC infectious diseases Table HBV T1753C 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. T1768A 2017 BMC infectious diseases Table HBV T1768A 0 6 28859616 Molecular characterization of hepatitis B virus in Vietnam. T531C/G 2017 BMC infectious diseases Table HBV T531C;T531G 0;0 7;7 28859616 Molecular characterization of hepatitis B virus in Vietnam. T53C 2017 BMC infectious diseases Table HBV T53C 0 4 28859616 Molecular characterization of hepatitis B virus in Vietnam. T766A 2017 BMC infectious diseases Table HBV T766A 0 5 28859616 Molecular characterization of hepatitis B virus in Vietnam. V184A 2017 BMC infectious diseases Table HBV V184A 0 5 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1470A 2017 Scientific reports Table HBV C1470A 0 6 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1479A 2017 Scientific reports Table HBV C1479A 0 6 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1485T 2017 Scientific reports Table HBV C1485T 0 6 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1575G 2017 Scientific reports Table HBV C1575G 0 6 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. C1653T 2017 Scientific reports Table HBV C1653T 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. A1762T 2017 Memorias do Instituto Oswaldo Cruz Table HBV A1762T 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. G1764A 2017 Memorias do Instituto Oswaldo Cruz Table HBV G1764A 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. G1862T 2017 Memorias do Instituto Oswaldo Cruz Table HBV G1862T 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. G1896A 2017 Memorias do Instituto Oswaldo Cruz Table HBV G1896A 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. G1899A 2017 Memorias do Instituto Oswaldo Cruz Table HBV G1899A 0 6 28902288 Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases. T1753C 2017 Memorias do Instituto Oswaldo Cruz Table HBV T1753C 0 6 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. arginine instead of leucine in residue 109 2017 PloS one Table HBV L109R 0 29 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. G130E 2017 PloS one Table HBV G130E 0 5 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. G145R 2017 PloS one Table HBV G145R 0 5 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. glycine to glutamic acid in position 130 2017 PloS one Table HBV G130E 0 40 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. L109R 2017 PloS one Table HBV L109R 0 5 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. L180M 2017 PloS one Table HBV L180M 0 5 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. M204V 2017 PloS one Table HBV M204V 0 5 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. V173L 2017 PloS one Table HBV V173L 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A146V 2017 Oncotarget Table HBV A146V 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A47S 2017 Oncotarget Table HBV A47S 0 4 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A47T 2017 Oncotarget Table HBV A47T 0 4 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. F132Y 2017 Oncotarget Table HBV F132Y 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. F132Y/I 2017 Oncotarget Table HBV F132Y;F132I 0;0 7;7 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. H94Y 2017 Oncotarget Table HBV H94Y 0 4 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. I127T 2017 Oncotarget Table HBV I127T 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. K130M 2017 Oncotarget Table HBV K130M 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. S42P 2017 Oncotarget Table HBV S42P 0 4 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. V131I 2017 Oncotarget Table HBV V131I 0 5 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. V88F 2017 Oncotarget Table HBV V88F 0 4 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. D480N 2017 PloS one Table HBV D480N 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. D73E 2017 PloS one Table HBV D73E 0 4 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. K143Q 2017 PloS one Table HBV K143Q 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. P249S 2017 PloS one Table HBV P249S 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. R841K 2017 PloS one Table HBV R841K 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. S314P 2017 PloS one Table HBV S314P 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. S663A 2017 PloS one Table HBV S663A 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. T268S 2017 PloS one Table HBV T268S 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. V210I 2017 PloS one Table HBV V210I 0 5 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. V818D 2017 PloS one Table HBV V818D 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. D144V 2018 PloS one Table HBV D144V 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. G130N 2018 PloS one Table HBV G130N 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. G145K 2018 PloS one Table HBV G145K 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. I169L 2018 PloS one Table HBV I169L 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. K141R 2018 PloS one Table HBV K141R 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. L180M 2018 PloS one Table HBV L180M 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. M133I 2018 PloS one Table HBV M133I 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. M204I 2018 PloS one Table HBV M204I 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. M204V 2018 PloS one Table HBV M204V 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. S143T 2018 PloS one Table HBV S143T 0 5 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. V173L 2018 PloS one Table HBV V173L 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A128V 2018 PloS one Table HBV A128V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A166G 2018 PloS one Table HBV A166G 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1676T 2018 PloS one Table HBV A1676T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1727G 2018 PloS one Table HBV A1727G 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1752C/G 2018 PloS one Table HBV A1752C;A1752G 0;0 8;8 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1760C 2018 PloS one Table HBV A1760C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1761C 2018 PloS one Table HBV A1761C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1762T 2018 PloS one Table HBV A1762T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1772C 2018 PloS one Table HBV A1772C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1811C 2018 PloS one Table HBV A1811C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1814C 2018 PloS one Table HBV A1814C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A181V 2018 PloS one Table HBV A181V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. A1850T 2018 PloS one Table HBV A1850T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C137S 2018 PloS one Table HBV C137S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1674T 2018 PloS one Table HBV C1674T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1678T/A 2018 PloS one Table HBV C1678T;C1678A 0;0 8;8 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1703A 2018 PloS one Table HBV C1703A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1766T 2018 PloS one Table HBV C1766T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1799T 2018 PloS one Table HBV C1799T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1810A 2018 PloS one Table HBV C1810A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1816T 2018 PloS one Table HBV C1816T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1845G 2018 PloS one Table HBV C1845G 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. C1858T 2018 PloS one Table HBV C1858T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. D144A 2018 PloS one Table HBV D144A 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. E164D 2018 PloS one Table HBV E164D 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. E164G 2018 PloS one Table HBV E164G 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. E164V 2018 PloS one Table HBV E164V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. F134V 2018 PloS one Table HBV F134V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G119E 2018 PloS one Table HBV G119E 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G130D 2018 PloS one Table HBV G130D 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G130N 2018 PloS one Table HBV G130N 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1719T 2018 PloS one Table HBV G1719T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1757A 2018 PloS one Table HBV G1757A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1763A 2018 PloS one Table HBV G1763A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1764A 2018 PloS one Table HBV G1764A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1775A 2018 PloS one Table HBV G1775A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1862T 2018 PloS one Table HBV G1862T 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1888A/T 2018 PloS one Table HBV G1888A;G1888T 0;0 8;8 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1896A 2018 PloS one Table HBV G1896A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. G1899A 2018 PloS one Table HBV G1899A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. I169L 2018 PloS one Table HBV I169L 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. I195M 2018 PloS one Table HBV I195M 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. I233V 2018 PloS one Table HBV I233V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. K122R 2018 PloS one Table HBV K122R 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. K160N 2018 PloS one Table HBV K160N 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L109I 2018 PloS one Table HBV L109I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L109Q 2018 PloS one Table HBV L109Q 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L180F 2018 PloS one Table HBV L180F 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L180M 2018 PloS one Table HBV L180M 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L229M 2018 PloS one Table HBV L229M 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L80F 2018 PloS one Table HBV L80F 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L80I 2018 PloS one Table HBV L80I 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L80V 2018 PloS one Table HBV L80V 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L82M 2018 PloS one Table HBV L82M 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L82S 2018 PloS one Table HBV L82S 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. L82V 2018 PloS one Table HBV L82V 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. M103I 2018 PloS one Table HBV M103I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. M133I 2018 PloS one Table HBV M133I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. M204I 2018 PloS one Table HBV M204I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. M204V 2018 PloS one Table HBV M204V 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. P120S 2018 PloS one Table HBV P120S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. P120T 2018 PloS one Table HBV P120T 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. P127T 2018 PloS one Table HBV P127T 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. P237T 2018 PloS one Table HBV P237T 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q101H 2018 PloS one Table HBV Q101H 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q129H 2018 PloS one Table HBV Q129H 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q129R 2018 PloS one Table HBV Q129R 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q215H 2018 PloS one Table HBV Q215H 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q215P 2018 PloS one Table HBV Q215P 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q215S 2018 PloS one Table HBV Q215S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Q267L 2018 PloS one Table HBV Q267L 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. R138K 2018 PloS one Table HBV R138K 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. R153W 2018 PloS one Table HBV R153W 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S113T 2018 PloS one Table HBV S113T 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S117Y 2018 PloS one Table HBV S117Y 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S132Y 2018 PloS one Table HBV S132Y 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S143T 2018 PloS one Table HBV S143T 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S219A 2018 PloS one Table HBV S219A 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. S78T 2018 PloS one Table HBV S78T 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T118A 2018 PloS one Table HBV T118A 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T118M 2018 PloS one Table HBV T118M 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T118S 2018 PloS one Table HBV T118S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T125S 2018 PloS one Table HBV T125S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T126I 2018 PloS one Table HBV T126I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T127L 2018 PloS one Table HBV T127L 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T127P 2018 PloS one Table HBV T127P 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T128I 2018 PloS one Table HBV T128I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T128N 2018 PloS one Table HBV T128N 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T143M 2018 PloS one Table HBV T143M 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T148P 2018 PloS one Table HBV T148P 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1741C 2018 PloS one Table HBV T1741C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1753V 2018 PloS one Table HBV T1753V 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1758C 2018 PloS one Table HBV T1758C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1767A 2018 PloS one Table HBV T1767A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1768A 2018 PloS one Table HBV T1768A 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1771C 2018 PloS one Table HBV T1771C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1773C 2018 PloS one Table HBV T1773C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1809G 2018 PloS one Table HBV T1809G 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T1812C 2018 PloS one Table HBV T1812C 0 6 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. T184S 2018 PloS one Table HBV T184S 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V142E 2018 PloS one Table HBV V142E 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V168A 2018 PloS one Table HBV V168A 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V173L 2018 PloS one Table HBV V173L 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V191I 2018 PloS one Table HBV V191I 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V214A 2018 PloS one Table HBV V214A 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. V84A 2018 PloS one Table HBV V84A 0 4 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Y100C 2018 PloS one Table HBV Y100C 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Y134F 2018 PloS one Table HBV Y134F 0 5 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Y161F 2018 PloS one Table HBV Y161F 0 5 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. A60V 2018 Infectious agents and cancer Table HBV A60V 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. E54K 2018 Infectious agents and cancer Table HBV E54K 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. G102R 2018 Infectious agents and cancer Table HBV G102R 0 5 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. G35R 2018 Infectious agents and cancer Table HBV G35R 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. H51P/R 2018 Infectious agents and cancer Table HBV H51P;H51R 0;0 6;6 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. I126S/T 2018 Infectious agents and cancer Table HBV I126S;I126T 0;0 7;7 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. I84T 2018 Infectious agents and cancer Table HBV I84T 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. L213F/I 2018 Infectious agents and cancer Table HBV L213F;L213I 0;0 7;7 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. L21F 2018 Infectious agents and cancer Table HBV L21F 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. L30S 2018 Infectious agents and cancer Table HBV L30S 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. L42F 2018 Infectious agents and cancer Table HBV L42F 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. N123D 2018 Infectious agents and cancer Table HBV N123D 0 5 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Q118R 2018 Infectious agents and cancer Table HBV Q118R 0 5 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. S124F/P 2018 Infectious agents and cancer Table HBV S124F;S124P 0;0 7;7 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. W77R 2018 Infectious agents and cancer Table HBV W77R 0 4 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Y200F/S 2018 Infectious agents and cancer Table HBV Y200F;Y200S 0;0 7;7 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Y206C/H 2018 Infectious agents and cancer Table HBV Y206C;Y206H 0;0 7;7 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. A1762T 2018 Cancer management and research Table HBV A1762T 0 6 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. G1764A 2018 Cancer management and research Table HBV G1764A 0 6 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. G1899A 2018 Cancer management and research Table HBV G1899A 0 6 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. A181T/V 2018 World journal of gastroenterology Table HBV A181T;A181V 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. A194T 2018 World journal of gastroenterology Table HBV A194T 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. A200V 2018 World journal of gastroenterology Table HBV A200V 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. C256G 2018 World journal of gastroenterology Table HBV C256G 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. D134E/N 2018 World journal of gastroenterology Table HBV D134E;D134N 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. E164D 2018 World journal of gastroenterology Table HBV E164D 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. E218D 2018 World journal of gastroenterology Table HBV E218D 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. F158Y 2018 World journal of gastroenterology Table HBV F158Y 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. F166L 2018 World journal of gastroenterology Table HBV F166L 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. F221Y 2018 World journal of gastroenterology Table HBV F221Y 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. G145R 2018 World journal of gastroenterology Table HBV G145R 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. I169T 2018 World journal of gastroenterology Table HBV I169T 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. I195M 2018 World journal of gastroenterology Table HBV I195M 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. I224V 2018 World journal of gastroenterology Table HBV I224V 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. I233V 2018 World journal of gastroenterology Table HBV I233V 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. I91L 2018 World journal of gastroenterology Table HBV I91L 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L180M 2018 World journal of gastroenterology Table HBV L180M 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L217R 2018 World journal of gastroenterology Table HBV L217R 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L229F 2018 World journal of gastroenterology Table HBV L229F 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L229G/V 2018 World journal of gastroenterology Table HBV L229G;L229V 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L80I/V 2018 World journal of gastroenterology Table HBV L80I;L80V 0;0 6;6 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L80V 2018 World journal of gastroenterology Table HBV L80V 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. L82M 2018 World journal of gastroenterology Table HBV L82M 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. M204I/V 2018 World journal of gastroenterology Table HBV M204I;M204V 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. M250I/L 2018 World journal of gastroenterology Table HBV M250I;M250L 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. N139D/E 2018 World journal of gastroenterology Table HBV N139D;N139E 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. N139K/H 2018 World journal of gastroenterology Table HBV N139K;N139H 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. N236T 2018 World journal of gastroenterology Table HBV N236T 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. N238D/S 2018 World journal of gastroenterology Table HBV N238D;N238S 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. P237H 2018 World journal of gastroenterology Table HBV P237H 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Q215E/H 2018 World journal of gastroenterology Table HBV Q215E;Q215H 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. R242A 2018 World journal of gastroenterology Table HBV R242A 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. S202C/G 2018 World journal of gastroenterology Table HBV S202C;S202G 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. S213T 2018 World journal of gastroenterology Table HBV S213T 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. S53N 2018 World journal of gastroenterology Table HBV S53N 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. S85A 2018 World journal of gastroenterology Table HBV S85A 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T128I 2018 World journal of gastroenterology Table HBV T128I 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T128N 2018 World journal of gastroenterology Table HBV T128N 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T184A/C 2018 World journal of gastroenterology Table HBV T184A;T184C 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T38A 2018 World journal of gastroenterology Table HBV T38A 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T38K 2018 World journal of gastroenterology Table HBV T38K 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. T54N 2018 World journal of gastroenterology Table HBV T54N 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. V173L 2018 World journal of gastroenterology Table HBV V173L 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. V191I 2018 World journal of gastroenterology Table HBV V191I 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. V207I 2018 World journal of gastroenterology Table HBV V207I 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. V214A 2018 World journal of gastroenterology Table HBV V214A 0 5 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. V84M 2018 World journal of gastroenterology Table HBV V84M 0 4 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. W153Q/R 2018 World journal of gastroenterology Table HBV W153Q;W153R 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Y124H/D 2018 World journal of gastroenterology Table HBV Y124H;Y124D 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Y126C/R 2018 World journal of gastroenterology Table HBV Y126C;Y126R 0;0 7;7 29713126 Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression. Y245H 2018 World journal of gastroenterology Table HBV Y245H 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. G129R 2018 PLoS neglected tropical diseases Table HBV G129R 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. G145A/R 2018 PLoS neglected tropical diseases Table HBV G145A;G145R 0;0 7;7 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. G145R 2018 PLoS neglected tropical diseases Table HBV G145R 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. I110L 2018 PLoS neglected tropical diseases Table HBV I110L 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. L180M 2018 PLoS neglected tropical diseases Table HBV L180M 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. M204V 2018 PLoS neglected tropical diseases Table HBV M204V 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Q215S 2018 PLoS neglected tropical diseases Table HBV Q215S 0 5 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. V173L 2018 PLoS neglected tropical diseases Table HBV V173L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A173L 2018 Hepatology communications Table HBV A173L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A181C 2018 Hepatology communications Table HBV A181C 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A181V 2018 Hepatology communications Table HBV A181V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A186S 2018 Hepatology communications Table HBV A186S 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A186T 2018 Hepatology communications Table HBV A186T 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A200V 2018 Hepatology communications Table HBV A200V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A329S 2018 Hepatology communications Table HBV A329S 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. A62T 2018 Hepatology communications Table HBV A62T 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. C188L 2018 Hepatology communications Table HBV C188L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. C332Y 2018 Hepatology communications Table HBV C332Y 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. E263A 2018 Hepatology communications Table HBV E263A 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. F273L 2018 Hepatology communications Table HBV F273L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. H13L 2018 Hepatology communications Table HBV H13L 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. H13S 2018 Hepatology communications Table HBV H13S 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. H35N 2018 Hepatology communications Table HBV H35N 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. H9D 2018 Hepatology communications Table HBV H9D 0 3 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. I169L 2018 Hepatology communications Table HBV I169L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. I169V 2018 Hepatology communications Table HBV I169V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. I187V 2018 Hepatology communications Table HBV I187V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. I290L 2018 Hepatology communications Table HBV I290L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. K318R 2018 Hepatology communications Table HBV K318R 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L164F 2018 Hepatology communications Table HBV L164F 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L180M 2018 Hepatology communications Table HBV L180M 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L220I 2018 Hepatology communications Table HBV L220I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L229F 2018 Hepatology communications Table HBV L229F 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L229V 2018 Hepatology communications Table HBV L229V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L229W 2018 Hepatology communications Table HBV L229W 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L247F 2018 Hepatology communications Table HBV L247F 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L80I 2018 Hepatology communications Table HBV L80I 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. L80V 2018 Hepatology communications Table HBV L80V 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. M204I 2018 Hepatology communications Table HBV M204I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. M204V 2018 Hepatology communications Table HBV M204V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. M250V 2018 Hepatology communications Table HBV M250V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N123H 2018 Hepatology communications Table HBV N123H 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N131G 2018 Hepatology communications Table HBV N131G 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N139T 2018 Hepatology communications Table HBV N139T 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N236T 2018 Hepatology communications Table HBV N236T 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N337D 2018 Hepatology communications Table HBV N337D 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N53H 2018 Hepatology communications Table HBV N53H 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N53K 2018 Hepatology communications Table HBV N53K 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. N76K 2018 Hepatology communications Table HBV N76K 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q125K 2018 Hepatology communications Table HBV Q125K 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q215R 2018 Hepatology communications Table HBV Q215R 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q267M 2018 Hepatology communications Table HBV Q267M 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q267N 2018 Hepatology communications Table HBV Q267N 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q267R 2018 Hepatology communications Table HBV Q267R 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q271V 2018 Hepatology communications Table HBV Q271V 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Q316H 2018 Hepatology communications Table HBV Q316H 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. R153Q 2018 Hepatology communications Table HBV R153Q 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. R18K 2018 Hepatology communications Table HBV R18K 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. R242S 2018 Hepatology communications Table HBV R242S 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. R280G 2018 Hepatology communications Table HBV R280G 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. R289S 2018 Hepatology communications Table HBV R289S 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S117Y 2018 Hepatology communications Table HBV S117Y 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S135F 2018 Hepatology communications Table HBV S135F 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S202G 2018 Hepatology communications Table HBV S202G 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S40A 2018 Hepatology communications Table HBV S40A 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S78C 2018 Hepatology communications Table HBV S78C 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. S78T 2018 Hepatology communications Table HBV S78T 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. T118H 2018 Hepatology communications Table HBV T118H 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. T128N 2018 Hepatology communications Table HBV T128N 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. T184A 2018 Hepatology communications Table HBV T184A 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. T184L 2018 Hepatology communications Table HBV T184L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. T184S 2018 Hepatology communications Table HBV T184S 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V142A 2018 Hepatology communications Table HBV V142A 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V142G 2018 Hepatology communications Table HBV V142G 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V142N 2018 Hepatology communications Table HBV V142N 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V173L 2018 Hepatology communications Table HBV V173L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V191I 2018 Hepatology communications Table HBV V191I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V207I 2018 Hepatology communications Table HBV V207I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V208I 2018 Hepatology communications Table HBV V208I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V214A 2018 Hepatology communications Table HBV V214A 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V214I 2018 Hepatology communications Table HBV V214I 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V214L 2018 Hepatology communications Table HBV V214L 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V214P 2018 Hepatology communications Table HBV V214P 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V27A 2018 Hepatology communications Table HBV V27A 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. V84M 2018 Hepatology communications Table HBV V84M 0 4 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. W257H 2018 Hepatology communications Table HBV W257H 0 5 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Y124C 2018 Hepatology communications Table HBV Y124C 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A131P 2018 Frontiers in cellular and infection microbiology Table HBV A131P 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A34T 2018 Frontiers in cellular and infection microbiology Table HBV A34T 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A69S 2018 Frontiers in cellular and infection microbiology Table HBV A69S 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A80I 2018 Frontiers in cellular and infection microbiology Table HBV A80I 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A80T 2018 Frontiers in cellular and infection microbiology Table HBV A80T 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. A80V 2018 Frontiers in cellular and infection microbiology Table HBV A80V 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E113Q 2018 Frontiers in cellular and infection microbiology Table HBV E113Q 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E180A 2018 Frontiers in cellular and infection microbiology Table HBV E180A 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E180G 2018 Frontiers in cellular and infection microbiology Table HBV E180G 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E40D 2018 Frontiers in cellular and infection microbiology Table HBV E40D 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E64D 2018 Frontiers in cellular and infection microbiology Table HBV E64D 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E77D 2018 Frontiers in cellular and infection microbiology Table HBV E77D 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E77Q 2018 Frontiers in cellular and infection microbiology Table HBV E77Q 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. E83D 2018 Frontiers in cellular and infection microbiology Table HBV E83D 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. F24Y 2018 Frontiers in cellular and infection microbiology Table HBV F24Y 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. G29D 2018 Frontiers in cellular and infection microbiology Table HBV G29D 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. I27V 2018 Frontiers in cellular and infection microbiology Table HBV I27V 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. I97F 2018 Frontiers in cellular and infection microbiology Table HBV I97F 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. L116I 2018 Frontiers in cellular and infection microbiology Table HBV L116I 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. M66I 2018 Frontiers in cellular and infection microbiology Table HBV M66I 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. M93V 2018 Frontiers in cellular and infection microbiology Table HBV M93V 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. N67T 2018 Frontiers in cellular and infection microbiology Table HBV N67T 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. P130A 2018 Frontiers in cellular and infection microbiology Table HBV P130A 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. P130Q 2018 Frontiers in cellular and infection microbiology Table HBV P130Q 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Q177K 2018 Frontiers in cellular and infection microbiology Table HBV Q177K 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. R179P 2018 Frontiers in cellular and infection microbiology Table HBV R179P 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S12T 2018 Frontiers in cellular and infection microbiology Table HBV S12T 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S155T 2018 Frontiers in cellular and infection microbiology Table HBV S155T 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S181P 2018 Frontiers in cellular and infection microbiology Table HBV S181P 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S21A 2018 Frontiers in cellular and infection microbiology Table HBV S21A 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S35A 2018 Frontiers in cellular and infection microbiology Table HBV S35A 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S74G 2018 Frontiers in cellular and infection microbiology Table HBV S74G 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. S87G 2018 Frontiers in cellular and infection microbiology Table HBV S87G 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. T147A 2018 Frontiers in cellular and infection microbiology Table HBV T147A 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. V149I 2018 Frontiers in cellular and infection microbiology Table HBV V149I 0 5 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. V91S 2018 Frontiers in cellular and infection microbiology Table HBV V91S 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. V91T 2018 Frontiers in cellular and infection microbiology Table HBV V91T 0 4 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Y38F 2018 Frontiers in cellular and infection microbiology Table HBV Y38F 0 4 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. G1896A 2018 Saudi journal of biological sciences Table HBV G1896A 0 6 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. G1896G 2018 Saudi journal of biological sciences Table HBV G1896G 0 6 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. H221Y 2018 BMC pregnancy and childbirth Table HBV H221Y 0 5 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. K219Q/E 2018 BMC pregnancy and childbirth Table HBV K219Q;K219E 0;0 7;7 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. K70R 2018 BMC pregnancy and childbirth Table HBV K70R 0 4 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. P225H 2018 BMC pregnancy and childbirth Table HBV P225H 0 5 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. T215F 2018 BMC pregnancy and childbirth Table HBV T215F 0 5 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. T215Y 2018 BMC pregnancy and childbirth Table HBV T215Y 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. A181C 2019 Emerging microbes & infections Table HBV A181C 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. A181V 2019 Emerging microbes & infections Table HBV A181V 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. L180M 2019 Emerging microbes & infections Table HBV L180M 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M204I 2019 Emerging microbes & infections Table HBV M204I 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M204V 2019 Emerging microbes & infections Table HBV M204V 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M204V/I 2019 Emerging microbes & infections Table HBV M204V;M204I 0;0 7;7 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M250I 2019 Emerging microbes & infections Table HBV M250I 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M250L 2019 Emerging microbes & infections Table HBV M250L 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. M250V 2019 Emerging microbes & infections Table HBV M250V 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. S202G 2019 Emerging microbes & infections Table HBV S202G 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. T184A 2019 Emerging microbes & infections Table HBV T184A 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. T184I 2019 Emerging microbes & infections Table HBV T184I 0 5 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. T184L 2019 Emerging microbes & infections Table HBV T184L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. A211G 2019 PeerJ Table HBV A211G 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. A38E 2019 PeerJ Table HBV A38E 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. C198R 2019 PeerJ Table HBV C198R 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. D144E 2019 PeerJ Table HBV D144E 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. F122I 2019 PeerJ Table HBV F122I 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. F122L 2019 PeerJ Table HBV F122L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. G152K 2019 PeerJ Table HBV G152K 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H124D 2019 PeerJ Table HBV H124D 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H124Y 2019 PeerJ Table HBV H124Y 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H197P 2019 PeerJ Table HBV H197P 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H216F 2019 PeerJ Table HBV H216F 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H216I 2019 PeerJ Table HBV H216I 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H216L 2019 PeerJ Table HBV H216L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H216P 2019 PeerJ Table HBV H216P 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. H216T 2019 PeerJ Table HBV H216T 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. I163V 2019 PeerJ Table HBV I163V 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. I187L 2019 PeerJ Table HBV I187L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. K154N 2019 PeerJ Table HBV K154N 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. K212G 2019 PeerJ Table HBV K212G 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. K212N 2019 PeerJ Table HBV K212N 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. K32M 2019 PeerJ Table HBV K32M 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L109R 2019 PeerJ Table HBV L109R 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L145M 2019 PeerJ Table HBV L145M 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L180M 2019 PeerJ Table HBV L180M 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L199V 2019 PeerJ Table HBV L199V 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L217F 2019 PeerJ Table HBV L217F 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L217W 2019 PeerJ Table HBV L217W 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. L91I 2019 PeerJ Table HBV L91I 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. M129L 2019 PeerJ Table HBV M129L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. M133L 2019 PeerJ Table HBV M133L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. M204V 2019 PeerJ Table HBV M204V 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N118D 2019 PeerJ Table HBV N118D 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N123D 2019 PeerJ Table HBV N123D 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N131D 2019 PeerJ Table HBV N131D 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N139D 2019 PeerJ Table HBV N139D 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N53K 2019 PeerJ Table HBV N53K 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N53S 2019 PeerJ Table HBV N53S 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. N76D 2019 PeerJ Table HBV N76D 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Q129R 2019 PeerJ Table HBV Q129R 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Q149K 2019 PeerJ Table HBV Q149K 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Q215H 2019 PeerJ Table HBV Q215H 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Q215L 2019 PeerJ Table HBV Q215L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. R110G 2019 PeerJ Table HBV R110G 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. R122K 2019 PeerJ Table HBV R122K 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S109P 2019 PeerJ Table HBV S109P 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S117N 2019 PeerJ Table HBV S117N 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S119P 2019 PeerJ Table HBV S119P 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S137T 2019 PeerJ Table HBV S137T 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S143L 2019 PeerJ Table HBV S143L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S176T 2019 PeerJ Table HBV S176T 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S185I 2019 PeerJ Table HBV S185I 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S202I 2019 PeerJ Table HBV S202I 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S213Q 2019 PeerJ Table HBV S213Q 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S213T 2019 PeerJ Table HBV S213T 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S78T 2019 PeerJ Table HBV S78T 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. S85A 2019 PeerJ Table HBV S85A 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. T128P 2019 PeerJ Table HBV T128P 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. T184A 2019 PeerJ Table HBV T184A 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. T37A 2019 PeerJ Table HBV T37A 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. V173L 2019 PeerJ Table HBV V173L 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. V208I 2019 PeerJ Table HBV V208I 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. V214Y 2019 PeerJ Table HBV V214Y 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. V27A 2019 PeerJ Table HBV V27A 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Y135S 2019 PeerJ Table HBV Y135S 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Y141F 2019 PeerJ Table HBV Y141F 0 5 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Y54G 2019 PeerJ Table HBV Y54G 0 4 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Y54H 2019 PeerJ Table HBV Y54H 0 4 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. C2771T 2019 Virology journal Table HBV C2771T 0 6 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. G2765A 2019 Virology journal Table HBV G2765A 0 6 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. T2768G 2019 Virology journal Table HBV T2768G 0 6 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. T2780C 2019 Virology journal Table HBV T2780C 0 6 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. A181T/V 2019 Scientific reports Table HBV A181T;A181V 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. A200V 2019 Scientific reports Table HBV A200V 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. E218D 2019 Scientific reports Table HBV E218D 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. F221F/Y 2019 Scientific reports Table HBV F221F;F221Y 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. F221Y 2019 Scientific reports Table HBV F221Y 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. H238N 2019 Scientific reports Table HBV H238N 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. H238Q 2019 Scientific reports Table HBV H238Q 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. I169M 2019 Scientific reports Table HBV I169M 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. I224I/V 2019 Scientific reports Table HBV I224I;I224V 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. I224V 2019 Scientific reports Table HBV I224V 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. L180M/Q 2019 Scientific reports Table HBV L180M;L180Q 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. L229F/M 2019 Scientific reports Table HBV L229F;L229M 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. L229M 2019 Scientific reports Table HBV L229M 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. L229V 2019 Scientific reports Table HBV L229V 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. M204I/V 2019 Scientific reports Table HBV M204I;M204V 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. M250L/V 2019 Scientific reports Table HBV M250L;M250V 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. N236T/V 2019 Scientific reports Table HBV N236T;N236V 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. N238A 2019 Scientific reports Table HBV N238A 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. N238H 2019 Scientific reports Table HBV N238H 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. N238N/H 2019 Scientific reports Table HBV N238N;N238H 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. N238T 2019 Scientific reports Table HBV N238T 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. P237S/H 2019 Scientific reports Table HBV P237S;P237H 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. R242D 2019 Scientific reports Table HBV R242D 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. S202G 2019 Scientific reports Table HBV S202G 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. S213T 2019 Scientific reports Table HBV S213T 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. T184K/L 2019 Scientific reports Table HBV T184K;T184L 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. V173L/M 2019 Scientific reports Table HBV V173L;V173M 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. V191I 2019 Scientific reports Table HBV V191I 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. V207I/L 2019 Scientific reports Table HBV V207I;V207L 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. V207I/M 2019 Scientific reports Table HBV V207I;V207M 0;0 7;7 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. V214A 2019 Scientific reports Table HBV V214A 0 5 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Y245F 2019 Scientific reports Table HBV Y245F 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. C256G 2019 Journal of clinical microbiology Table HBV C256G 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. E218D 2019 Journal of clinical microbiology Table HBV E218D 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. E263D 2019 Journal of clinical microbiology Table HBV E263D 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. F200L 2019 Journal of clinical microbiology Table HBV F200L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. F219I 2019 Journal of clinical microbiology Table HBV F219I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. F220L 2019 Journal of clinical microbiology Table HBV F220L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. F227Y 2019 Journal of clinical microbiology Table HBV F227Y 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. F249I 2019 Journal of clinical microbiology Table HBV F249I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. G145R 2019 Journal of clinical microbiology Table HBV G145R 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. G232D 2019 Journal of clinical microbiology Table HBV G232D 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. H238D/S 2019 Journal of clinical microbiology Table HBV H238D;H238S 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. I218L 2019 Journal of clinical microbiology Table HBV I218L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. I224L 2019 Journal of clinical microbiology Table HBV I224L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. I233V 2019 Journal of clinical microbiology Table HBV I233V 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. I282V 2019 Journal of clinical microbiology Table HBV I282V 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. K154Q 2019 Journal of clinical microbiology Table HBV K154Q 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. K275Q 2019 Journal of clinical microbiology Table HBV K275Q 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L157M 2019 Journal of clinical microbiology Table HBV L157M 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L209M 2019 Journal of clinical microbiology Table HBV L209M 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L217H 2019 Journal of clinical microbiology Table HBV L217H 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L217R 2019 Journal of clinical microbiology Table HBV L217R 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L229G/V 2019 Journal of clinical microbiology Table HBV L229G;L229V 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. L229M 2019 Journal of clinical microbiology Table HBV L229M 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. M204I/V 2019 Journal of clinical microbiology Table HBV M204I;M204V 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. M250I/L 2019 Journal of clinical microbiology Table HBV M250I;M250L 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. N236T 2019 Journal of clinical microbiology Table HBV N236T 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. P237H 2019 Journal of clinical microbiology Table HBV P237H 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Q215H 2019 Journal of clinical microbiology Table HBV Q215H 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Q215P/S 2019 Journal of clinical microbiology Table HBV Q215P;Q215S 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Q271K/I 2019 Journal of clinical microbiology Table HBV Q271K;Q271I 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. R153Q 2019 Journal of clinical microbiology Table HBV R153Q 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. R169C 2019 Journal of clinical microbiology Table HBV R169C 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. R242S 2019 Journal of clinical microbiology Table HBV R242S 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S202C/G 2019 Journal of clinical microbiology Table HBV S202C;S202G 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S204R 2019 Journal of clinical microbiology Table HBV S204R 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S204T/R 2019 Journal of clinical microbiology Table HBV S204T;S204R 0;0 7;7 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S210M 2019 Journal of clinical microbiology Table HBV S210M 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S213T 2019 Journal of clinical microbiology Table HBV S213T 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. S219A 2019 Journal of clinical microbiology Table HBV S219A 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V190G 2019 Journal of clinical microbiology Table HBV V190G 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V207I 2019 Journal of clinical microbiology Table HBV V207I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V207L 2019 Journal of clinical microbiology Table HBV V207L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V207M 2019 Journal of clinical microbiology Table HBV V207M 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V214A 2019 Journal of clinical microbiology Table HBV V214A 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V224I 2019 Journal of clinical microbiology Table HBV V224I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V253I 2019 Journal of clinical microbiology Table HBV V253I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. V278I 2019 Journal of clinical microbiology Table HBV V278I 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. W156L 2019 Journal of clinical microbiology Table HBV W156L 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. W172stop 2019 Journal of clinical microbiology Table HBV W172X 0 8 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. W199stop 2019 Journal of clinical microbiology Table HBV W199X 0 8 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. W243G 2019 Journal of clinical microbiology Table HBV W243G 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Y206H 2019 Journal of clinical microbiology Table HBV Y206H 0 5 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Y245H 2019 Journal of clinical microbiology Table HBV Y245H 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. A159V/G 2019 BMC infectious diseases Table HBV A159V;A159G 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. A1762T 2019 BMC infectious diseases Table HBV A1762T 0 6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. E164D/V 2019 BMC infectious diseases Table HBV E164D;E164V 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. E164G/A 2019 BMC infectious diseases Table HBV E164G;E164A 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. F170S 2019 BMC infectious diseases Table HBV F170S 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. F79H 2019 BMC infectious diseases Table HBV F79H 0 4 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. G1727A 2019 BMC infectious diseases Table HBV G1727A 0 6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. G1727C 2019 BMC infectious diseases Table HBV G1727C 0 6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. G1764A 2019 BMC infectious diseases Table HBV G1764A 0 6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. G1896A 2019 BMC infectious diseases Table HBV G1896A 0 6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. I150T 2019 BMC infectious diseases Table HBV I150T 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. I68T 2019 BMC infectious diseases Table HBV I68T 0 4 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. K122R 2019 BMC infectious diseases Table HBV K122R 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. L175S 2019 BMC infectious diseases Table HBV L175S 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. M103I 2019 BMC infectious diseases Table HBV M103I 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. P111T/S 2019 BMC infectious diseases Table HBV P111T;P111S 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. P142L 2019 BMC infectious diseases Table HBV P142L 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. P49H/L 2019 BMC infectious diseases Table HBV P49H;P49L 0;0 6;6 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Q101K 2019 BMC infectious diseases Table HBV Q101K 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Q30K 2019 BMC infectious diseases Table HBV Q30K 0 4 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. R160K/N 2019 BMC infectious diseases Table HBV R160K;R160N 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. S117G/R 2019 BMC infectious diseases Table HBV S117G;S117R 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. S136F 2019 BMC infectious diseases Table HBV S136F 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. S55F 2019 BMC infectious diseases Table HBV S55F 0 4 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. T116A/P 2019 BMC infectious diseases Table HBV T116A;T116P 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. T118K/R 2019 BMC infectious diseases Table HBV T118K;T118R 0;0 7;7 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. V168A 2019 BMC infectious diseases Table HBV V168A 0 5 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. V177A 2019 BMC infectious diseases Table HBV V177A 0 5 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. A1762T 2019 Frontiers in immunology Table HBV A1762T 0 6 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. G1764A 2019 Frontiers in immunology Table HBV G1764A 0 6 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. G1896A 2019 Frontiers in immunology Table HBV G1896A 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. A1762T 2019 Scientific reports Table HBV A1762T 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. C1653T 2019 Scientific reports Table HBV C1653T 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. G1613A 2019 Scientific reports Table HBV G1613A 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. G1764A 2019 Scientific reports Table HBV G1764A 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. G1896A 2019 Scientific reports Table HBV G1896A 0 6 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. T1753V 2019 Scientific reports Table HBV T1753V 0 6 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. I97L 2019 Journal of virology Table HBV I97L 0 4 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. P130T 2019 Journal of virology Table HBV P130T 0 5 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. M204I 2019 World journal of gastroenterology Table HBV M204I 0 5 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1314G 2019 Scientific reports Table HBV A1314G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1320G 2019 Scientific reports Table HBV A1320G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1329A 2019 Scientific reports Table HBV A1329A 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1437G 2019 Scientific reports Table HBV A1437G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1467G 2019 Scientific reports Table HBV A1467G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. A1764G 2019 Scientific reports Table HBV A1764G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ala31Ser 2019 Scientific reports Table HBV A31S 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ala36Thr 2019 Scientific reports Table HBV A36T 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ala44Val 2019 Scientific reports Table HBV A44V 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Arg32Gly 2019 Scientific reports Table HBV R32G 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Arg72Arg 2019 Scientific reports Table HBV R72R 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Arg86His 2019 Scientific reports Table HBV R86H 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Arg94Leu 2019 Scientific reports Table HBV R94L 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. C1450G 2019 Scientific reports Table HBV C1450G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. C1594T 2019 Scientific reports Table HBV C1594T 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. G1464T 2019 Scientific reports Table HBV G1464T 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. G1479A 2019 Scientific reports Table HBV G1479A 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. G1482C 2019 Scientific reports Table HBV G1482C 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. G1630A 2019 Scientific reports Table HBV G1630A 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. G1635A 2019 Scientific reports Table HBV G1635A 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Glu86Arg 2019 Scientific reports Table HBV E86R 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Gly25Gly 2019 Scientific reports Table HBV G25G 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ile131Val 2019 Scientific reports Table HBV I131V 0 9 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Leu169Leu 2019 Scientific reports Table HBV L169L 0 9 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Met130Lys 2019 Scientific reports Table HBV M130K 0 9 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Phe73Val 2019 Scientific reports Table HBV F73V 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Pro26Arg 2019 Scientific reports Table HBV P26R 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser11Pro 2019 Scientific reports Table HBV S11P 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser146Ala 2019 Scientific reports Table HBV S146A 0 9 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser147Pro 2019 Scientific reports Table HBV S147P 0 9 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser22Gly 2019 Scientific reports Table HBV S22G 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser41Thr 2019 Scientific reports Table HBV S41T 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Ser47Ala 2019 Scientific reports Table HBV S47A 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1335C 2019 Scientific reports Table HBV T1335C 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1350C 2019 Scientific reports Table HBV T1350C 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1353G 2019 Scientific reports Table HBV T1353G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1512G 2019 Scientific reports Table HBV T1512G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1762A 2019 Scientific reports Table HBV T1762A 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1809G 2019 Scientific reports Table HBV T1809G 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. T1812C 2019 Scientific reports Table HBV T1812C 0 6 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Thr74Ile 2019 Scientific reports Table HBV T74I 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Val37Leu 2019 Scientific reports Table HBV V37L 0 8 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Val88Ile 2019 Scientific reports Table HBV V88I 0 8 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. C107Y 2019 BMC infectious diseases Table HBV C107Y 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. D144A 2019 BMC infectious diseases Table HBV D144A 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. F93S 2019 BMC infectious diseases Table HBV F93S 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. G102C 2019 BMC infectious diseases Table HBV G102C 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. G145A 2019 BMC infectious diseases Table HBV G145A 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. G44E 2019 BMC infectious diseases Table HBV G44E 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. I110L 2019 BMC infectious diseases Table HBV I110L 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. I68T 2019 BMC infectious diseases Table HBV I68T 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. I68V 2019 BMC infectious diseases Table HBV I68V 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. K122Q 2019 BMC infectious diseases Table HBV K122Q 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. L110P 2019 BMC infectious diseases Table HBV L110P 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. P120S 2019 BMC infectious diseases Table HBV P120S 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. P56L 2019 BMC infectious diseases Table HBV P56L 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T114S 2019 BMC infectious diseases Table HBV T114S 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T118K 2019 BMC infectious diseases Table HBV T118K 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T126A 2019 BMC infectious diseases Table HBV T126A 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. T143S 2019 BMC infectious diseases Table HBV T143S 0 5 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. V47A 2019 BMC infectious diseases Table HBV V47A 0 4 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Y161F 2019 BMC infectious diseases Table HBV Y161F 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. C121Y 2019 Polish journal of microbiology Table HBV C121Y 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. D144E 2019 Polish journal of microbiology Table HBV D144E 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. G145R 2019 Polish journal of microbiology Table HBV G145R 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. I110L 2019 Polish journal of microbiology Table HBV I110L 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. P120T 2019 Polish journal of microbiology Table HBV P120T 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. P127T 2019 Polish journal of microbiology Table HBV P127T 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. S132P 2019 Polish journal of microbiology Table HBV S132P 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. S143T 2019 Polish journal of microbiology Table HBV S143T 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. S144T 2019 Polish journal of microbiology Table HBV S144T 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. S193L 2019 Polish journal of microbiology Table HBV S193L 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. T118A 2019 Polish journal of microbiology Table HBV T118A 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. T126I 2019 Polish journal of microbiology Table HBV T126I 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. T127L 2019 Polish journal of microbiology Table HBV T127L 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. T131I 2019 Polish journal of microbiology Table HBV T131I 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. V173M 2019 Polish journal of microbiology Table HBV V173M 0 5 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. Y100C 2019 Polish journal of microbiology Table HBV Y100C 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. D144E 2019 Polish journal of microbiology Table HBV D144E 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. G119R 2019 Polish journal of microbiology Table HBV G119R 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. L180M 2019 Polish journal of microbiology Table HBV L180M 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. M133I 2019 Polish journal of microbiology Table HBV M133I 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. M204I 2019 Polish journal of microbiology Table HBV M204I 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. M250G/H 2019 Polish journal of microbiology Table HBV M250G;M250H 0;0 7;7 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. P120T 2019 Polish journal of microbiology Table HBV P120T 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. Q101H 2019 Polish journal of microbiology Table HBV Q101H 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. Q129H 2019 Polish journal of microbiology Table HBV Q129H 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. R122K 2019 Polish journal of microbiology Table HBV R122K 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. S143L 2019 Polish journal of microbiology Table HBV S143L 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. S193L 2019 Polish journal of microbiology Table HBV S193L 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. T123N 2019 Polish journal of microbiology Table HBV T123N 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. T131I 2019 Polish journal of microbiology Table HBV T131I 0 5 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. Y134F 2019 Polish journal of microbiology Table HBV Y134F 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. F220L 2020 Emerging microbes & infections Table HBV F220L 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. L205P 2020 Emerging microbes & infections Table HBV L205P 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. M197T 2020 Emerging microbes & infections Table HBV M197T 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. S204N 2020 Emerging microbes & infections Table HBV S204N 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. S204T 2020 Emerging microbes & infections Table HBV S204T 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. S207I 2020 Emerging microbes & infections Table HBV S207I 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. S210N 2020 Emerging microbes & infections Table HBV S210N 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. S210R 2020 Emerging microbes & infections Table HBV S210R 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. V190A 2020 Emerging microbes & infections Table HBV V190A 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. V194A 2020 Emerging microbes & infections Table HBV V194A 0 5 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Y206F 2020 Emerging microbes & infections Table HBV Y206F 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A1516C 2020 Virology journal Table HBV A1516C 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A1762T 2020 Virology journal Table HBV A1762T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A1984G 2020 Virology journal Table HBV A1984G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A2075G 2020 Virology journal Table HBV A2075G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A2189C 2020 Virology journal Table HBV A2189C 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A3057G 2020 Virology journal Table HBV A3057G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A3108G 2020 Virology journal Table HBV A3108G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. A942T 2020 Virology journal Table HBV A942T 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C129T 2020 Virology journal Table HBV C129T 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C1653T 2020 Virology journal Table HBV C1653T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C1990T 2020 Virology journal Table HBV C1990T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C2002T 2020 Virology journal Table HBV C2002T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C2198A 2020 Virology journal Table HBV C2198A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C2523G 2020 Virology journal Table HBV C2523G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C3026T 2020 Virology journal Table HBV C3026T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C3051T 2020 Virology journal Table HBV C3051T 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C3189A 2020 Virology journal Table HBV C3189A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. C930A 2020 Virology journal Table HBV C930A 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. F130L 2020 Virology journal Table HBV F130L 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G1484A 2020 Virology journal Table HBV G1484A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G1613A 2020 Virology journal Table HBV G1613A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G1764A 2020 Virology journal Table HBV G1764A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G1896A 2020 Virology journal Table HBV G1896A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G49A 2020 Virology journal Table HBV G49A 0 4 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G774A 2020 Virology journal Table HBV G774A 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G886A 2020 Virology journal Table HBV G886A 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. G899A 2020 Virology journal Table HBV G899A 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. H613K 2020 Virology journal Table HBV H613K 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. S116G 2020 Virology journal Table HBV S116G 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. S316G 2020 Virology journal Table HBV S316G 0 5 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T1249G 2020 Virology journal Table HBV T1249G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T1351G 2020 Virology journal Table HBV T1351G 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T1485C 2020 Virology journal Table HBV T1485C 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T1633A 2020 Virology journal Table HBV T1633A 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T1753C 2020 Virology journal Table HBV T1753C 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T3098C 2020 Virology journal Table HBV T3098C 0 6 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. T3210A 2020 Virology journal Table HBV T3210A 0 6 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. A181V/T 2020 Infection and drug resistance Table HBV A181V;A181T 0;0 7;7 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. C256G 2020 Infection and drug resistance Table HBV C256G 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. H126Q/Y 2020 Infection and drug resistance Table HBV H126Q;H126Y 0;0 7;7 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. I169T 2020 Infection and drug resistance Table HBV I169T 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. I233V 2020 Infection and drug resistance Table HBV I233V 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. L180M 2020 Infection and drug resistance Table HBV L180M 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. L229V/M 2020 Infection and drug resistance Table HBV L229V;L229M 0;0 7;7 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. L80I/V 2020 Infection and drug resistance Table HBV L80I;L80V 0;0 6;6 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. L82Q 2020 Infection and drug resistance Table HBV L82Q 0 4 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. M204I/V 2020 Infection and drug resistance Table HBV M204I;M204V 0;0 7;7 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N134A/E/H/S 2020 Infection and drug resistance Table HBV N134A;N134E;N134H;N134S 0;0;0;0 11;11;11;11 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N139D 2020 Infection and drug resistance Table HBV N139D 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N139K 2020 Infection and drug resistance Table HBV N139K 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N236T 2020 Infection and drug resistance Table HBV N236T 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N238D 2020 Infection and drug resistance Table HBV N238D 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. N53A/D/H/I 2020 Infection and drug resistance Table HBV N53A;N53D;N53H;N53I 0;0;0;0 10;10;10;10 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. P237S 2020 Infection and drug resistance Table HBV P237S 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Q215H 2020 Infection and drug resistance Table HBV Q215H 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. R153Q 2020 Infection and drug resistance Table HBV R153Q 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. R242S 2020 Infection and drug resistance Table HBV R242S 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. S213T 2020 Infection and drug resistance Table HBV S213T 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. T128A/D/I/N/P 2020 Infection and drug resistance Table HBV T128A;T128D;T128I;T128N;T128P 0;0;0;0;0 13;13;13;13;13 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. T38A 2020 Infection and drug resistance Table HBV T38A 0 4 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. V173L 2020 Infection and drug resistance Table HBV V173L 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. V191I 2020 Infection and drug resistance Table HBV V191I 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. V207I/L/M 2020 Infection and drug resistance Table HBV V207I;V207L;V207M 0;0;0 9;9;9 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. V214A 2020 Infection and drug resistance Table HBV V214A 0 5 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. V84I 2020 Infection and drug resistance Table HBV V84I 0 4 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Y124D/H 2020 Infection and drug resistance Table HBV Y124D;Y124H 0;0 7;7 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Y221C/N/H 2020 Infection and drug resistance Table HBV Y221C;Y221N;Y221H 0;0;0 9;9;9 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. G1728A 2020 PloS one Table HBV G1728A 0 6 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. G1764T/C 2020 PloS one Table HBV G1764T;G1764C 0;0 8;8 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. G1862T 2020 PloS one Table HBV G1862T 0 6 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. G1896A/G 2020 PloS one Table HBV G1896A;G1896G 0;0 8;8 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. I195M 2020 PloS one Table HBV I195M 0 5 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. L180M 2020 PloS one Table HBV L180M 0 5 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. M204I 2020 PloS one Table HBV M204I 0 5 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. M204V 2020 PloS one Table HBV M204V 0 5 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. T1768A 2020 PloS one Table HBV T1768A 0 6 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. V173L 2020 PloS one Table HBV V173L 0 5 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. V191I 2020 PloS one Table HBV V191I 0 5 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. I126A/N/P/S 2020 World journal of gastroenterology Table HBV I126A;I126N;I126P;I126S 0;0;0;0 11;11;11;11 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. T126A/N/P/S 2020 World journal of gastroenterology Table HBV T126A;T126N;T126P;T126S 0;0;0;0 11;11;11;11 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Y134H/L/R/S/V 2020 World journal of gastroenterology Table HBV Y134H;Y134L;Y134R;Y134S;Y134V 0;0;0;0;0 13;13;13;13;13 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. A159V 2020 Memorias do Instituto Oswaldo Cruz Table HBV A159V 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. A194V 2020 Memorias do Instituto Oswaldo Cruz Table HBV A194V 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. E164G 2020 Memorias do Instituto Oswaldo Cruz Table HBV E164G 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. F134I 2020 Memorias do Instituto Oswaldo Cruz Table HBV F134I 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. F220L 2020 Memorias do Instituto Oswaldo Cruz Table HBV F220L 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. L209V 2020 Memorias do Instituto Oswaldo Cruz Table HBV L209V 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. L216F 2020 Memorias do Instituto Oswaldo Cruz Table HBV L216F 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. L21S 2020 Memorias do Instituto Oswaldo Cruz Table HBV L21S 0 4 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. L49R 2020 Memorias do Instituto Oswaldo Cruz Table HBV L49R 0 4 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. P56L 2020 Memorias do Instituto Oswaldo Cruz Table HBV P56L 0 4 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. R24K/R 2020 Memorias do Instituto Oswaldo Cruz Table HBV R24K;R24R 0;0 6;6 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. S174N 2020 Memorias do Instituto Oswaldo Cruz Table HBV S174N 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. S204G 2020 Memorias do Instituto Oswaldo Cruz Table HBV S204G 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. S210I/T 2020 Memorias do Instituto Oswaldo Cruz Table HBV S210I;S210T 0;0 7;7 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. T123A 2020 Memorias do Instituto Oswaldo Cruz Table HBV T123A 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. T57I 2020 Memorias do Instituto Oswaldo Cruz Table HBV T57I 0 4 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. V190A 2020 Memorias do Instituto Oswaldo Cruz Table HBV V190A 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. V224A 2020 Memorias do Instituto Oswaldo Cruz Table HBV V224A 0 5 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. W36L 2020 Memorias do Instituto Oswaldo Cruz Table HBV W36L 0 4 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. L180M 2020 Emerging microbes & infections Table HBV L180M 0 5 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. L229M 2020 Emerging microbes & infections Table HBV L229M 0 5 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. L229V 2020 Emerging microbes & infections Table HBV L229V 0 5 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. M204I 2020 Emerging microbes & infections Table HBV M204I 0 5 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. M204V 2020 Emerging microbes & infections Table HBV M204V 0 5 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. A1762T 2020 Frontiers in microbiology Table HBV A1762T 0 6 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. C1653T 2020 Frontiers in microbiology Table HBV C1653T 0 6 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. G1764A 2020 Frontiers in microbiology Table HBV G1764A 0 6 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. L180M 2020 Frontiers in microbiology Table HBV L180M 0 5 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. T143L 2020 Frontiers in microbiology Table HBV T143L 0 5 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. T1753V 2020 Frontiers in microbiology Table HBV T1753V 0 6 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. L180M 2021 Virology journal Table HBV L180M 0 5 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. M204I 2021 Virology journal Table HBV M204I 0 5 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. M204V 2021 Virology journal Table HBV M204V 0 5 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. S202I 2021 Virology journal Table HBV S202I 0 5 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. V173L 2021 Virology journal Table HBV V173L 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. A128V 2020 Wellcome open research Table HBV A128V 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. A1762T 2020 Wellcome open research Table HBV A1762T 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. C1766T/T 2020 Wellcome open research Table HBV C1766T 0 8 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. C1799G 2020 Wellcome open research Table HBV C1799G 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. G145R 2020 Wellcome open research Table HBV G145R 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. G1764A 2020 Wellcome open research Table HBV G1764A 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. G1896A 2020 Wellcome open research Table HBV G1896A 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. G1899A 2020 Wellcome open research Table HBV G1899A 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. M133I 2020 Wellcome open research Table HBV M133I 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. P120S/T 2020 Wellcome open research Table HBV P120S;P120T 0;0 7;7 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. T118A 2020 Wellcome open research Table HBV T118A 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. T127P 2020 Wellcome open research Table HBV T127P 0 5 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. T1768A 2020 Wellcome open research Table HBV T1768A 0 6 33458253 Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection. V190A 2020 Wellcome open research Table HBV V190A 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1752G 2021 BMC infectious diseases Table HBV A1752G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1762T 2021 BMC infectious diseases Table HBV A1762T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1775G 2021 BMC infectious diseases Table HBV A1775G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1808G 2021 BMC infectious diseases Table HBV A1808G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1846T 2021 BMC infectious diseases Table HBV A1846T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. A1874G 2021 BMC infectious diseases Table HBV A1874G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C1817T 2021 BMC infectious diseases Table HBV C1817T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C1858T 2021 BMC infectious diseases Table HBV C1858T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C1877T 2021 BMC infectious diseases Table HBV C1877T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C1913A 2021 BMC infectious diseases Table HBV C1913A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C64S 2021 BMC infectious diseases Table HBV C64S 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. C76F 2021 BMC infectious diseases Table HBV C76F 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. E164V 2021 BMC infectious diseases Table HBV E164V 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. F134L 2021 BMC infectious diseases Table HBV F134L 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G145R 2021 BMC infectious diseases Table HBV G145R 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1721A 2021 BMC infectious diseases Table HBV G1721A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1757A 2021 BMC infectious diseases Table HBV G1757A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1764A 2021 BMC infectious diseases Table HBV G1764A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1896A 2021 BMC infectious diseases Table HBV G1896A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1915T 2021 BMC infectious diseases Table HBV G1915T 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G96V 2021 BMC infectious diseases Table HBV G96V 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. I150M 2021 BMC infectious diseases Table HBV I150M 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. I86T 2021 BMC infectious diseases Table HBV I86T 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. K122R 2021 BMC infectious diseases Table HBV K122R 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. L49P 2021 BMC infectious diseases Table HBV L49P 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. M103I 2021 BMC infectious diseases Table HBV M103I 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. M131I 2021 BMC infectious diseases Table HBV M131I 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. M133S 2021 BMC infectious diseases Table HBV M133S 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. M133T 2021 BMC infectious diseases Table HBV M133T 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. N40S 2021 BMC infectious diseases Table HBV N40S 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. P46T 2021 BMC infectious diseases Table HBV P46T 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Q129H 2021 BMC infectious diseases Table HBV Q129H 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. S174N 2021 BMC infectious diseases Table HBV S174N 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. S55F 2021 BMC infectious diseases Table HBV S55F 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. S58C 2021 BMC infectious diseases Table HBV S58C 0 4 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T131I 2021 BMC infectious diseases Table HBV T131I 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T143M 2021 BMC infectious diseases Table HBV T143M 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1719G 2021 BMC infectious diseases Table HBV T1719G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1727A 2021 BMC infectious diseases Table HBV T1727A 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1754G 2021 BMC infectious diseases Table HBV T1754G 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1800C 2021 BMC infectious diseases Table HBV T1800C 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1802C 2021 BMC infectious diseases Table HBV T1802C 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. T1815C 2021 BMC infectious diseases Table HBV T1815C 0 6 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Y100C 2021 BMC infectious diseases Table HBV Y100C 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Y161F 2021 BMC infectious diseases Table HBV Y161F 0 5 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Y161H 2021 BMC infectious diseases Table HBV Y161H 0 5 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. A2189T/C,C 2021 Microorganisms Table HBV A2189T;A2189C 0;0 10;10 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. A90T/V 2021 Microorganisms Table HBV A90T;A90V 0;0 6;6 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. C2444A/T,A 2021 Microorganisms Table HBV C2444A;C2444T 0;0 10;10 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. D16A/E/N/V 2021 Microorganisms Table HBV D16A;D16E;D16N;D16V 0;0;0;0 10;10;10;10 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. D828A/V 2021 Microorganisms Table HBV D828A;D828V 0;0 7;7 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. F141L 2021 Microorganisms Table HBV F141L 0 5 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. F321L 2021 Microorganisms Table HBV F321L 0 5 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. G1896A 2021 Microorganisms Table HBV G1896A 0 6 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. I84T/M/L/V 2021 Microorganisms Table HBV I84T;I84M;I84L;I84V 0;0;0;0 10;10;10;10 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. S101P/A 2021 Microorganisms Table HBV S101P;S101A 0;0 7;7 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. S314P 2021 Microorganisms Table HBV S314P 0 5 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. T36P/S/A 2021 Microorganisms Table HBV T36P;T36S;T36A 0;0;0 8;8;8 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. V131I 2021 Microorganisms Table HBV V131I 0 5 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. G145R 2021 Journal of viral hepatitis Table HBV G145R 0 5 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. L180M 2021 Journal of viral hepatitis Table HBV L180M 0 5 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. M204V 2021 Journal of viral hepatitis Table HBV M204V 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. A181T 2021 Journal of clinical and translational hepatology Table HBV A181T 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. A181V 2021 Journal of clinical and translational hepatology Table HBV A181V 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. L180M 2021 Journal of clinical and translational hepatology Table HBV L180M 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. M204I 2021 Journal of clinical and translational hepatology Table HBV M204I 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. M204V 2021 Journal of clinical and translational hepatology Table HBV M204V 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. N236T 2021 Journal of clinical and translational hepatology Table HBV N236T 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. S202G 2021 Journal of clinical and translational hepatology Table HBV S202G 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. T184A 2021 Journal of clinical and translational hepatology Table HBV T184A 0 5 34007795 Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR. T184L 2021 Journal of clinical and translational hepatology Table HBV T184L 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. D144A 2021 Infection and drug resistance Table HBV D144A 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. D144E 2021 Infection and drug resistance Table HBV D144E 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. G145A 2021 Infection and drug resistance Table HBV G145A 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. G145R 2021 Infection and drug resistance Table HBV G145R 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. G145R/A 2021 Infection and drug resistance Table HBV G145R;G145A 0;0 7;7 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. M133T 2021 Infection and drug resistance Table HBV M133T 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. P120S 2021 Infection and drug resistance Table HBV P120S 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. Q129R 2021 Infection and drug resistance Table HBV Q129R 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. S143L 2021 Infection and drug resistance Table HBV S143L 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. T115S 2021 Infection and drug resistance Table HBV T115S 0 5 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. T126S 2021 Infection and drug resistance Table HBV T126S 0 5 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. I97L 2021 Cellular and molecular gastroenterology and hepatology Table HBV I97L 0 4 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. 331A>V 2021 Computational and structural biotechnology journal Table HBV A331V 0 6 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. 356S>AS 2021 Computational and structural biotechnology journal Table HBV S356A 0 7 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. 444S>PS 2021 Computational and structural biotechnology journal Table HBV S444P 0 7 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. 807D>VX 2021 Computational and structural biotechnology journal Table HBV D807V 0 7 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. A1546T 2021 Computational and structural biotechnology journal Table HBV A1546T 0 6 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. C659T 2021 Computational and structural biotechnology journal Table HBV C659T 0 5 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. C669T 2021 Computational and structural biotechnology journal Table HBV C669T 0 5 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. G2337A 2021 Computational and structural biotechnology journal Table HBV G2337A 0 6 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. G2479A 2021 Computational and structural biotechnology journal Table HBV G2479A 0 6 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. T192G 2021 Computational and structural biotechnology journal Table HBV T192G 0 5 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. T456C 2021 Computational and structural biotechnology journal Table HBV T456C 0 5 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. L180M 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Table HBV L180M 0 5 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. M204V 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Table HBV M204V 0 5 34755817 Hepatitis B in the Northwestern region of Sao Paulo State: genotypes and resistance mutations. V173L 2021 Revista do Instituto de Medicina Tropical de Sao Paulo Table HBV V173L 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. A102V/R/G/I 2022 PloS one Table HBV A102V;A102R;A102G;A102I 0;0;0;0 11;11;11;11 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. A110S/K 2022 PloS one Table HBV A110S;A110K 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. A1710G 2022 PloS one Table HBV A1710G 0 6 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. AAA1725GAA 2022 PloS one Table HBV A1725G;A1725A 0;0 10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. AGC1683ATT 2022 PloS one Table HBV A1683A;A1683T;G1683A;G1683T;C1683A;C1683T 0;0;0;0;0;0 10;10;10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. AT1714GC 2022 PloS one Table HBV A1714G;A1714C;T1714G;T1714C 0;0;0;0 8;8;8;8 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. CGT1659TGC 2022 PloS one Table HBV C1659T;C1659G;C1659C;G1659T;G1659G;G1659C;T1659T;T1659G;T1659C 0;0;0;0;0;0;0;0;0 10;10;10;10;10;10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. D107R 2022 PloS one Table HBV D107R 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. D114G 2022 PloS one Table HBV D114G 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. D119N 2022 PloS one Table HBV D119N 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. E109A/Y 2022 PloS one Table HBV E109A;E109Y 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. F112L 2022 PloS one Table HBV F112L 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. F117S 2022 PloS one Table HBV F117S 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. GAA1699GCG 2022 PloS one Table HBV G1699G;G1699C;A1699G;A1699C 0;0;0;0 10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. GAT1728AAC 2022 PloS one Table HBV G1728A;G1728C;A1728A;A1728C;T1728A;T1728C 0;0;0;0;0;0 10;10;10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. GCG1701AGC 2022 PloS one Table HBV G1701A;G1701G;G1701C;C1701A;C1701G;C1701C 0;0;0;0;0;0 10;10;10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. K118E/I 2022 PloS one Table HBV K118E;K118I 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. K91W/R 2022 PloS one Table HBV K91W;K91R 0;0 6;6 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. K95S 2022 PloS one Table HBV K95S 0 4 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. L100G 2022 PloS one Table HBV L100G 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. L108P 2022 PloS one Table HBV L108P 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. M103L/A 2022 PloS one Table HBV M103L;M103A 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. P90F 2022 PloS one Table HBV P90F 0 4 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. R96C 2022 PloS one Table HBV R96C 0 4 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. S101F 2022 PloS one Table HBV S101F 0 5 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. S104I/W 2022 PloS one Table HBV S104I;S104W 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. T106N/I 2022 PloS one Table HBV T106N;T106I 0;0 7;7 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. T1650C 2022 PloS one Table HBV T1650C 0 6 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. T97A 2022 PloS one Table HBV T97A 0 4 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. TAT1704GAT 2022 PloS one Table HBV T1704G;T1704A;T1704T;A1704G;A1704A;A1704T 0;0;0;0;0;0 10;10;10;10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. TTT1707CTG 2022 PloS one Table HBV T1707C;T1707T;T1707G 0;0;0 10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. TTT1722AGC 2022 PloS one Table HBV T1722A;T1722G;T1722C 0;0;0 10;10;10 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. V92A/P 2022 PloS one Table HBV V92A;V92P 0;0 6;6 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Y111D/E 2022 PloS one Table HBV Y111D;Y111E 0;0 7;7 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. A194V 2022 Scientific reports Table HBV A194V 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. A307C 2022 Scientific reports Table HBV A307C 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. D144A 2022 Scientific reports Table HBV D144A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. D271E 2022 Scientific reports Table HBV D271E 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. F134L 2022 Scientific reports Table HBV F134L 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. F296I 2022 Scientific reports Table HBV F296I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. G44E 2022 Scientific reports Table HBV G44E 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. H122Y 2022 Scientific reports Table HBV H122Y 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. H271Q 2022 Scientific reports Table HBV H271Q 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. H35Q 2022 Scientific reports Table HBV H35Q 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I195M 2022 Scientific reports Table HBV I195M 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I208T 2022 Scientific reports Table HBV I208T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I253V 2022 Scientific reports Table HBV I253V 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I53L 2022 Scientific reports Table HBV I53L 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I53S 2022 Scientific reports Table HBV I53S 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I53V 2022 Scientific reports Table HBV I53V 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. I68T 2022 Scientific reports Table HBV I68T 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. K122R 2022 Scientific reports Table HBV K122R 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. K212T 2022 Scientific reports Table HBV K212T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L109R 2022 Scientific reports Table HBV L109R 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L109V 2022 Scientific reports Table HBV L109V 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L110I 2022 Scientific reports Table HBV L110I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L127F 2022 Scientific reports Table HBV L127F 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L180M 2022 Scientific reports Table HBV L180M 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L26R 2022 Scientific reports Table HBV L26R 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L49P 2022 Scientific reports Table HBV L49P 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. L49R 2022 Scientific reports Table HBV L49R 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. M103I 2022 Scientific reports Table HBV M103I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. M129L 2022 Scientific reports Table HBV M129L 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. M133I 2022 Scientific reports Table HBV M133I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. M204V 2022 Scientific reports Table HBV M204V 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. N122H 2022 Scientific reports Table HBV N122H 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. N123D 2022 Scientific reports Table HBV N123D 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. N238T 2022 Scientific reports Table HBV N238T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. N246S 2022 Scientific reports Table HBV N246S 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Q125K 2022 Scientific reports Table HBV Q125K 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Q215H 2022 Scientific reports Table HBV Q215H 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. R110G 2022 Scientific reports Table HBV R110G 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S109P 2022 Scientific reports Table HBV S109P 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S117C 2022 Scientific reports Table HBV S117C 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S135F 2022 Scientific reports Table HBV S135F 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S137T 2022 Scientific reports Table HBV S137T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S159T 2022 Scientific reports Table HBV S159T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S193L 2022 Scientific reports Table HBV S193L 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S204N 2022 Scientific reports Table HBV S204N 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S204R 2022 Scientific reports Table HBV S204R 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S207N 2022 Scientific reports Table HBV S207N 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S207T 2022 Scientific reports Table HBV S207T 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S210R 2022 Scientific reports Table HBV S210R 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S219A 2022 Scientific reports Table HBV S219A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S34L 2022 Scientific reports Table HBV S34L 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S45A 2022 Scientific reports Table HBV S45A 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. S61L 2022 Scientific reports Table HBV S61L 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T118A 2022 Scientific reports Table HBV T118A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T118N 2022 Scientific reports Table HBV T118N 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T189I 2022 Scientific reports Table HBV T189I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T237A 2022 Scientific reports Table HBV T237A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T259A 2022 Scientific reports Table HBV T259A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T259S 2022 Scientific reports Table HBV T259S 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T27R 2022 Scientific reports Table HBV T27R 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. T313A 2022 Scientific reports Table HBV T313A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V112I 2022 Scientific reports Table HBV V112I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V142A 2022 Scientific reports Table HBV V142A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V142I 2022 Scientific reports Table HBV V142I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V163I 2022 Scientific reports Table HBV V163I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V168A 2022 Scientific reports Table HBV V168A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V180A 2022 Scientific reports Table HBV V180A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V184A 2022 Scientific reports Table HBV V184A 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V214G 2022 Scientific reports Table HBV V214G 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V266I 2022 Scientific reports Table HBV V266I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V278I 2022 Scientific reports Table HBV V278I 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. V96A 2022 Scientific reports Table HBV V96A 0 4 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. W153R 2022 Scientific reports Table HBV W153R 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Y100C 2022 Scientific reports Table HBV Y100C 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Y126C 2022 Scientific reports Table HBV Y126C 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Y161F 2022 Scientific reports Table HBV Y161F 0 5 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Y206V 2022 Scientific reports Table HBV Y206V 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. A166G 2022 PloS one Table HBV A166G 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. A168V 2022 PloS one Table HBV A168V 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. D144E 2022 PloS one Table HBV D144E 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. G159A 2022 PloS one Table HBV G159A 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. I110L 2022 PloS one Table HBV I110L 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. S154A 2022 PloS one Table HBV S154A 0 5 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. T127P 2022 PloS one Table HBV T127P 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. A181S 2022 Frontiers in microbiology Table HBV A181S 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. A181T 2022 Frontiers in microbiology Table HBV A181T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. A181V 2022 Frontiers in microbiology Table HBV A181V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. A194M 2022 Frontiers in microbiology Table HBV A194M 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. A194T 2022 Frontiers in microbiology Table HBV A194T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. D144G 2022 Frontiers in microbiology Table HBV D144G 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. G145R 2022 Frontiers in microbiology Table HBV G145R 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. G1896A 2022 Frontiers in microbiology Table HBV G1896A 0 6 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. H238D 2022 Frontiers in microbiology Table HBV H238D 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. H238S 2022 Frontiers in microbiology Table HBV H238S 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. H238T 2022 Frontiers in microbiology Table HBV H238T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. I169T 2022 Frontiers in microbiology Table HBV I169T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. I233V 2022 Frontiers in microbiology Table HBV I233V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L180M 2022 Frontiers in microbiology Table HBV L180M 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L229F 2022 Frontiers in microbiology Table HBV L229F 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L229G 2022 Frontiers in microbiology Table HBV L229G 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L229M 2022 Frontiers in microbiology Table HBV L229M 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L229V 2022 Frontiers in microbiology Table HBV L229V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L229W 2022 Frontiers in microbiology Table HBV L229W 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L80I 2022 Frontiers in microbiology Table HBV L80I 0 4 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. L80V 2022 Frontiers in microbiology Table HBV L80V 0 4 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M204I 2022 Frontiers in microbiology Table HBV M204I 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M204S 2022 Frontiers in microbiology Table HBV M204S 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M204V 2022 Frontiers in microbiology Table HBV M204V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M250I 2022 Frontiers in microbiology Table HBV M250I 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M250L 2022 Frontiers in microbiology Table HBV M250L 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. M250V 2022 Frontiers in microbiology Table HBV M250V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. N236T 2022 Frontiers in microbiology Table HBV N236T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. N236V 2022 Frontiers in microbiology Table HBV N236V 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. P237H 2022 Frontiers in microbiology Table HBV P237H 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. Q215H 2022 Frontiers in microbiology Table HBV Q215H 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. Q215P 2022 Frontiers in microbiology Table HBV Q215P 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. Q215S 2022 Frontiers in microbiology Table HBV Q215S 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. S143T 2022 Frontiers in microbiology Table HBV S143T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. S202C 2022 Frontiers in microbiology Table HBV S202C 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. S202G 2022 Frontiers in microbiology Table HBV S202G 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. S202I 2022 Frontiers in microbiology Table HBV S202I 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. S213T 2022 Frontiers in microbiology Table HBV S213T 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184A 2022 Frontiers in microbiology Table HBV T184A 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184C 2022 Frontiers in microbiology Table HBV T184C 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184F 2022 Frontiers in microbiology Table HBV T184F 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184G 2022 Frontiers in microbiology Table HBV T184G 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184I 2022 Frontiers in microbiology Table HBV T184I 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184L 2022 Frontiers in microbiology Table HBV T184L 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184M 2022 Frontiers in microbiology Table HBV T184M 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. T184S 2022 Frontiers in microbiology Table HBV T184S 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V173L 2022 Frontiers in microbiology Table HBV V173L 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V207I 2022 Frontiers in microbiology Table HBV V207I 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V207L 2022 Frontiers in microbiology Table HBV V207L 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V207M 2022 Frontiers in microbiology Table HBV V207M 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V214A 2022 Frontiers in microbiology Table HBV V214A 0 5 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. V84M 2022 Frontiers in microbiology Table HBV V84M 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A11T 2022 BMC pediatrics Table HBV A11T 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A1480G 2022 BMC pediatrics Table HBV A1480G 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A1511G 2022 BMC pediatrics Table HBV A1511G 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A2092T 2022 BMC pediatrics Table HBV A2092T 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A47T 2022 BMC pediatrics Table HBV A47T 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A895G 2022 BMC pediatrics Table HBV A895G 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. A928T 2022 BMC pediatrics Table HBV A928T 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. C1060A 2022 BMC pediatrics Table HBV C1060A 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. C144T 2022 BMC pediatrics Table HBV C144T 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. C324T 2022 BMC pediatrics Table HBV C324T 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. D36G 2022 BMC pediatrics Table HBV D36G 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. E64D 2022 BMC pediatrics Table HBV E64D 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. G1461C 2022 BMC pediatrics Table HBV G1461C 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. G3039T 2022 BMC pediatrics Table HBV G3039T 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. G68W 2022 BMC pediatrics Table HBV G68W 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. L100I 2022 BMC pediatrics Table HBV L100I 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. L311I 2022 BMC pediatrics Table HBV L311I 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. M267L 2022 BMC pediatrics Table HBV M267L 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. N97K 2022 BMC pediatrics Table HBV N97K 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. P52L 2022 BMC pediatrics Table HBV P52L 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. S256G 2022 BMC pediatrics Table HBV S256G 0 5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. T2198A 2022 BMC pediatrics Table HBV T2198A 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. T3138G 2022 BMC pediatrics Table HBV T3138G 0 6 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. T57I 2022 BMC pediatrics Table HBV T57I 0 4 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. V30L 2022 BMC pediatrics Table HBV V30L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A119V 2022 PloS one Table HBV A119V 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A128V 2022 PloS one Table HBV A128V 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A138D 2022 PloS one Table HBV A138D 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A143V 2022 PloS one Table HBV A143V 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A159V 2022 PloS one Table HBV A159V 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A160T/P 2022 PloS one Table HBV A160T;A160P 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A166V/G 2022 PloS one Table HBV A166V;A166G 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A17E 2022 PloS one Table HBV A17E 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A184V/G 2022 PloS one Table HBV A184V;A184G 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A33F/L 2022 PloS one Table HBV A33F;A33L 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A45T/G 2022 PloS one Table HBV A45T;A45G 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A55S 2022 PloS one Table HBV A55S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A5T 2022 PloS one Table HBV A5T 0 3 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A60V 2022 PloS one Table HBV A60V 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A62S/T 2022 PloS one Table HBV A62S;A62T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A81T 2022 PloS one Table HBV A81T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A90T/S 2022 PloS one Table HBV A90T;A90S 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. A91T/P 2022 PloS one Table HBV A91T;A91P 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. C221Y/R 2022 PloS one Table HBV C221Y;C221R 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. C48S 2022 PloS one Table HBV C48S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. C64Y 2022 PloS one Table HBV C64Y 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. C76Y/T 2022 PloS one Table HBV C76Y;C76T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. C85Y/F 2022 PloS one Table HBV C85Y;C85F 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D114E 2022 PloS one Table HBV D114E 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D133N 2022 PloS one Table HBV D133N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D144E/A 2022 PloS one Table HBV D144E;D144A 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D27G/S 2022 PloS one Table HBV D27G;D27S 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D33G 2022 PloS one Table HBV D33G 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D42N 2022 PloS one Table HBV D42N 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D44H/N 2022 PloS one Table HBV D44H;D44N 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D50N/E 2022 PloS one Table HBV D50N;D50E 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. D54A/N 2022 PloS one Table HBV D54A;D54N 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. E164G 2022 PloS one Table HBV E164G 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. E39K/G 2022 PloS one Table HBV E39K;E39G 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F134Y/V 2022 PloS one Table HBV F134Y;F134V 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F141V/L 2022 PloS one Table HBV F141V;F141L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F162Y 2022 PloS one Table HBV F162Y 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F165S/L 2022 PloS one Table HBV F165S;F165L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F170S 2022 PloS one Table HBV F170S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F19S 2022 PloS one Table HBV F19S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F20S 2022 PloS one Table HBV F20S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F212Y/L 2022 PloS one Table HBV F212Y;F212L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F220Y/L 2022 PloS one Table HBV F220Y;F220L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F25L 2022 PloS one Table HBV F25L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F34Y 2022 PloS one Table HBV F34Y 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F41S 2022 PloS one Table HBV F41S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F67V/L 2022 PloS one Table HBV F67V;F67L 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F80S 2022 PloS one Table HBV F80S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F83S/C 2022 PloS one Table HBV F83S;F83C 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. F93S/C 2022 PloS one Table HBV F93S;F93C 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G102R/K 2022 PloS one Table HBV G102R;G102K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G10R 2022 PloS one Table HBV G10R 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G130R 2022 PloS one Table HBV G130R 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G145R/A 2022 PloS one Table HBV G145R;G145A 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G149E/K 2022 PloS one Table HBV G149E;G149K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G18R 2022 PloS one Table HBV G18R 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G35R/K 2022 PloS one Table HBV G35R;G35K 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G43K 2022 PloS one Table HBV G43K 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G44E/V 2022 PloS one Table HBV G44E;G44V 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G59A 2022 PloS one Table HBV G59A 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. G73S/N 2022 PloS one Table HBV G73S;G73N 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. H128L 2022 PloS one Table HBV H128L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. H48Y/N 2022 PloS one Table HBV H48Y;H48N 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. H51Y/T 2022 PloS one Table HBV H51Y;H51T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I110L/Q 2022 PloS one Table HBV I110L;I110Q 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I126T/N 2022 PloS one Table HBV I126T;I126N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I150T 2022 PloS one Table HBV I150T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I161T/L 2022 PloS one Table HBV I161T;I161L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I195T 2022 PloS one Table HBV I195T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I208T/S 2022 PloS one Table HBV I208T;I208S 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I218L 2022 PloS one Table HBV I218L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I226M/T 2022 PloS one Table HBV I226M;I226T 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I25V/A 2022 PloS one Table HBV I25V;I25A 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I28T 2022 PloS one Table HBV I28T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I31T 2022 PloS one Table HBV I31T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I68T 2022 PloS one Table HBV I68T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I84V/M 2022 PloS one Table HBV I84V;I84M 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. I92T 2022 PloS one Table HBV I92T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. K167T 2022 PloS one Table HBV K167T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. K57Q/K 2022 PloS one Table HBV K57Q;K57K 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L104W 2022 PloS one Table HBV L104W 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L108V/I 2022 PloS one Table HBV L108V;L108I 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L139Q/P 2022 PloS one Table HBV L139Q;L139P 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L13P/V 2022 PloS one Table HBV L13P;L13V 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L15S 2022 PloS one Table HBV L15S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L173P 2022 PloS one Table HBV L173P 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L175S 2022 PloS one Table HBV L175S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L186H 2022 PloS one Table HBV L186H 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L205V 2022 PloS one Table HBV L205V 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L209V/S 2022 PloS one Table HBV L209V;L209S 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L213I/M 2022 PloS one Table HBV L213I;L213M 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L21S 2022 PloS one Table HBV L21S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L222P 2022 PloS one Table HBV L222P 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L22W 2022 PloS one Table HBV L22W 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L32P 2022 PloS one Table HBV L32P 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L42P/R 2022 PloS one Table HBV L42P;L42R 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L45R/F 2022 PloS one Table HBV L45R;L45F 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L49R/H 2022 PloS one Table HBV L49R;L49H 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L74M/V 2022 PloS one Table HBV L74M;L74V 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L75V/M 2022 PloS one Table HBV L75V;L75M 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L77R 2022 PloS one Table HBV L77R 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L85I/H 2022 PloS one Table HBV L85I;L85H 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L88P 2022 PloS one Table HBV L88P 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L95W 2022 PloS one Table HBV L95W 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. L98V 2022 PloS one Table HBV L98V 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. M103T 2022 PloS one Table HBV M103T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. M120V/I 2022 PloS one Table HBV M120V;M120I 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. M133T/S 2022 PloS one Table HBV M133T;M133S 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. M198I/M 2022 PloS one Table HBV M198I;M198M 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. M75T 2022 PloS one Table HBV M75T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N123T/K 2022 PloS one Table HBV N123T;N123K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N147S 2022 PloS one Table HBV N147S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N156T/I 2022 PloS one Table HBV N156T;N156I 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N174S/K 2022 PloS one Table HBV N174S;N174K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N207S 2022 PloS one Table HBV N207S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N40S/K 2022 PloS one Table HBV N40S;N40K 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N40Y/T 2022 PloS one Table HBV N40Y;N40T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N56H/W 2022 PloS one Table HBV N56H;N56W 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N87S/T 2022 PloS one Table HBV N87S;N87T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. N98T/K 2022 PloS one Table HBV N98T;N98K 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P11H 2022 PloS one Table HBV P11H 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P120S 2022 PloS one Table HBV P120S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P120S/T 2022 PloS one Table HBV P120S;P120T 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P127T 2022 PloS one Table HBV P127T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P134H/T 2022 PloS one Table HBV P134H;P134T 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P151H 2022 PloS one Table HBV P151H 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P153L 2022 PloS one Table HBV P153L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P173Q/L 2022 PloS one Table HBV P173Q;P173L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P19S 2022 PloS one Table HBV P19S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P203R 2022 PloS one Table HBV P203R 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P211R 2022 PloS one Table HBV P211R 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P217S/L 2022 PloS one Table HBV P217S;P217L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P32L 2022 PloS one Table HBV P32L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P62Q/L 2022 PloS one Table HBV P62Q;P62L 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P65T 2022 PloS one Table HBV P65T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P67Q 2022 PloS one Table HBV P67Q 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P70S 2022 PloS one Table HBV P70S 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P89R 2022 PloS one Table HBV P89R 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P92L 2022 PloS one Table HBV P92L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. P94T/S 2022 PloS one Table HBV P94T;P94S 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q101K/H 2022 PloS one Table HBV Q101K;Q101H 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q104R/K 2022 PloS one Table HBV Q104R;Q104K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q10K/H 2022 PloS one Table HBV Q10K;Q10H 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q118L 2022 PloS one Table HBV Q118L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q121R/K 2022 PloS one Table HBV Q121R;Q121K 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q129K 2022 PloS one Table HBV Q129K 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q129R/N 2022 PloS one Table HBV Q129R;Q129N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q132I/H 2022 PloS one Table HBV Q132I;Q132H 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q16P 2022 PloS one Table HBV Q16P 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q30R/K 2022 PloS one Table HBV Q30R;Q30K 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q51L 2022 PloS one Table HBV Q51L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Q82L 2022 PloS one Table HBV Q82L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R103T 2022 PloS one Table HBV R103T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R112K 2022 PloS one Table HBV R112K 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R113T 2022 PloS one Table HBV R113T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R122K 2022 PloS one Table HBV R122K 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R135K 2022 PloS one Table HBV R135K 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R137K/Q 2022 PloS one Table HBV R137K;R137Q 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R160K 2022 PloS one Table HBV R160K 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R24K 2022 PloS one Table HBV R24K 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R73H 2022 PloS one Table HBV R73H 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. R79H 2022 PloS one Table HBV R79H 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S101T/L 2022 PloS one Table HBV S101T;S101L 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S109T 2022 PloS one Table HBV S109T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S114T/P 2022 PloS one Table HBV S114T;S114P 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S124T 2022 PloS one Table HBV S124T 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S132P 2022 PloS one Table HBV S132P 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S136F 2022 PloS one Table HBV S136F 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S146F 2022 PloS one Table HBV S146F 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S147G 2022 PloS one Table HBV S147G 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S148L 2022 PloS one Table HBV S148L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S152N 2022 PloS one Table HBV S152N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S167L 2022 PloS one Table HBV S167L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S174N 2022 PloS one Table HBV S174N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S17F/A 2022 PloS one Table HBV S17F;S17A 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S193L 2022 PloS one Table HBV S193L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S204R/N 2022 PloS one Table HBV S204R;S204N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S210K/N 2022 PloS one Table HBV S210K;S210N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S31R 2022 PloS one Table HBV S31R 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S34L 2022 PloS one Table HBV S34L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S38T 2022 PloS one Table HBV S38T 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S53L 2022 PloS one Table HBV S53L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S59N 2022 PloS one Table HBV S59N 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S5L/T 2022 PloS one Table HBV S5L;S5T 0;0 5;5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S61L 2022 PloS one Table HBV S61L 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S78N 2022 PloS one Table HBV S78N 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T113N 2022 PloS one Table HBV T113N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T115N 2022 PloS one Table HBV T115N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T115S/C 2022 PloS one Table HBV T115S;T115C 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T116N 2022 PloS one Table HBV T116N 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T118M 2022 PloS one Table HBV T118M 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T123A/N 2022 PloS one Table HBV T123A;T123N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T125S/N 2022 PloS one Table HBV T125S;T125N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T126N/I 2022 PloS one Table HBV T126N;T126I 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T131N/S 2022 PloS one Table HBV T131N;T131S 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T140I 2022 PloS one Table HBV T140I 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T143M 2022 PloS one Table HBV T143M 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T14I/T 2022 PloS one Table HBV T14I;T14T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T157S 2022 PloS one Table HBV T157S 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T164I/D 2022 PloS one Table HBV T164I;T164D 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T168I 2022 PloS one Table HBV T168I 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T189I 2022 PloS one Table HBV T189I 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T27I 2022 PloS one Table HBV T27I 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T47A/E 2022 PloS one Table HBV T47A;T47E 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T86A/S 2022 PloS one Table HBV T86A;T86S 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. T97I/T 2022 PloS one Table HBV T97I;T97T 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V136A 2022 PloS one Table HBV V136A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V14A 2022 PloS one Table HBV V14A 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V158A 2022 PloS one Table HBV V158A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V168A 2022 PloS one Table HBV V168A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V172A 2022 PloS one Table HBV V172A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V177L 2022 PloS one Table HBV V177L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V180A 2022 PloS one Table HBV V180A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V190A 2022 PloS one Table HBV V190A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V224A 2022 PloS one Table HBV V224A 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V68T/S 2022 PloS one Table HBV V68T;V68S 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V88I/M 2022 PloS one Table HBV V88I;V88M 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V95A 2022 PloS one Table HBV V95A 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. V96G 2022 PloS one Table HBV V96G 0 4 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W122R 2022 PloS one Table HBV W122R 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W156L 2022 PloS one Table HBV W156L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W172C 2022 PloS one Table HBV W172C 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W199L 2022 PloS one Table HBV W199L 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W74S/L 2022 PloS one Table HBV W74S;W74L 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. W77R/G 2022 PloS one Table HBV W77R;W77G 0;0 6;6 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y100C/F 2022 PloS one Table HBV Y100C;Y100F 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y140S/N 2022 PloS one Table HBV Y140S;Y140N 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y161F/S 2022 PloS one Table HBV Y161F;Y161S 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y163F 2022 PloS one Table HBV Y163F 0 5 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y200F/W 2022 PloS one Table HBV Y200F;Y200W 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y206H/F 2022 PloS one Table HBV Y206H;Y206F 0;0 7;7 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Y225F 2022 PloS one Table HBV Y225F 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A131G 2022 Clinical and experimental hepatology Table HBV A131G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A131P 2022 Clinical and experimental hepatology Table HBV A131P 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A54V 2022 Clinical and experimental hepatology Table HBV A54V 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A69G 2022 Clinical and experimental hepatology Table HBV A69G 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A69S 2022 Clinical and experimental hepatology Table HBV A69S 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. A69S/P 2022 Clinical and experimental hepatology Table HBV A69S;A69P 0;0 6;6 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. C61R 2022 Clinical and experimental hepatology Table HBV C61R 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E117G 2022 Clinical and experimental hepatology Table HBV E117G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E14Q 2022 Clinical and experimental hepatology Table HBV E14Q 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E14Q/D 2022 Clinical and experimental hepatology Table HBV E14Q;E14D 0;0 6;6 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E64D 2022 Clinical and experimental hepatology Table HBV E64D 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E77D 2022 Clinical and experimental hepatology Table HBV E77D 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. E77Q 2022 Clinical and experimental hepatology Table HBV E77Q 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. F122S 2022 Clinical and experimental hepatology Table HBV F122S 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. F24Y 2022 Clinical and experimental hepatology Table HBV F24Y 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. F97V 2022 Clinical and experimental hepatology Table HBV F97V 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G153C 2022 Clinical and experimental hepatology Table HBV G153C 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G153S 2022 Clinical and experimental hepatology Table HBV G153S 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G63A 2022 Clinical and experimental hepatology Table HBV G63A 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G63W 2022 Clinical and experimental hepatology Table HBV G63W 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G73VL76V 2022 Clinical and experimental hepatology Table HBV G73V;L76V 0;0 8;8 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G74S 2022 Clinical and experimental hepatology Table HBV G74S 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. G94A 2022 Clinical and experimental hepatology Table HBV G94A 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. H104Y 2022 Clinical and experimental hepatology Table HBV H104Y 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. I105L 2022 Clinical and experimental hepatology Table HBV I105L 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. I139L 2022 Clinical and experimental hepatology Table HBV I139L 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. I59F 2022 Clinical and experimental hepatology Table HBV I59F 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. I59T 2022 Clinical and experimental hepatology Table HBV I59T 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. I80T 2022 Clinical and experimental hepatology Table HBV I80T 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L100R 2022 Clinical and experimental hepatology Table HBV L100R 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L119W 2022 Clinical and experimental hepatology Table HBV L119W 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L143P 2022 Clinical and experimental hepatology Table HBV L143P 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L16I 2022 Clinical and experimental hepatology Table HBV L16I 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L55I 2022 Clinical and experimental hepatology Table HBV L55I 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L68P 2022 Clinical and experimental hepatology Table HBV L68P 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L81I 2022 Clinical and experimental hepatology Table HBV L81I 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L84P/Q 2022 Clinical and experimental hepatology Table HBV L84P;L84Q 0;0 6;6 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. L84Q 2022 Clinical and experimental hepatology Table HBV L84Q 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. M66I 2022 Clinical and experimental hepatology Table HBV M66I 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. M66I/K 2022 Clinical and experimental hepatology Table HBV M66I;M66K 0;0 6;6 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. M66I/L 2022 Clinical and experimental hepatology Table HBV M66I;M66L 0;0 6;6 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. M93L 2022 Clinical and experimental hepatology Table HBV M93L 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. M93V 2022 Clinical and experimental hepatology Table HBV M93V 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. N92H 2022 Clinical and experimental hepatology Table HBV N92H 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P129L 2022 Clinical and experimental hepatology Table HBV P129L 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P130I 2022 Clinical and experimental hepatology Table HBV P130I 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P130L 2022 Clinical and experimental hepatology Table HBV P130L 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P135Q 2022 Clinical and experimental hepatology Table HBV P135Q 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P135T 2022 Clinical and experimental hepatology Table HBV P135T 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P156T 2022 Clinical and experimental hepatology Table HBV P156T 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P25T 2022 Clinical and experimental hepatology Table HBV P25T 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P50A 2022 Clinical and experimental hepatology Table HBV P50A 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. P79Q 2022 Clinical and experimental hepatology Table HBV P79Q 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R127A 2022 Clinical and experimental hepatology Table HBV R127A 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R133G 2022 Clinical and experimental hepatology Table HBV R133G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R151P/S 2022 Clinical and experimental hepatology Table HBV R151P;R151S 0;0 7;7 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R151Q 2022 Clinical and experimental hepatology Table HBV R151Q 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R151S/Q 2022 Clinical and experimental hepatology Table HBV R151S;R151Q 0;0 7;7 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R157E 2022 Clinical and experimental hepatology Table HBV R157E 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R165K 2022 Clinical and experimental hepatology Table HBV R165K 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. R98Q 2022 Clinical and experimental hepatology Table HBV R98Q 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S155F/T 2022 Clinical and experimental hepatology Table HBV S155F;S155T 0;0 7;7 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S155T 2022 Clinical and experimental hepatology Table HBV S155T 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S21G 2022 Clinical and experimental hepatology Table HBV S21G 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S21T 2022 Clinical and experimental hepatology Table HBV S21T 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S26A 2022 Clinical and experimental hepatology Table HBV S26A 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S87G 2022 Clinical and experimental hepatology Table HBV S87G 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. S87T 2022 Clinical and experimental hepatology Table HBV S87T 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T128L 2022 Clinical and experimental hepatology Table HBV T128L 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T12S 2022 Clinical and experimental hepatology Table HBV T12S 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T142M 2022 Clinical and experimental hepatology Table HBV T142M 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T146S 2022 Clinical and experimental hepatology Table HBV T146S 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T147A 2022 Clinical and experimental hepatology Table HBV T147A 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T147S/C 2022 Clinical and experimental hepatology Table HBV T147S;T147C 0;0 7;7 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T67N 2022 Clinical and experimental hepatology Table HBV T67N 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. T91S 2022 Clinical and experimental hepatology Table HBV T91S 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V120A 2022 Clinical and experimental hepatology Table HBV V120A 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V124G 2022 Clinical and experimental hepatology Table HBV V124G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V13L 2022 Clinical and experimental hepatology Table HBV V13L 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V149I 2022 Clinical and experimental hepatology Table HBV V149I 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V27I 2022 Clinical and experimental hepatology Table HBV V27I 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V27L 2022 Clinical and experimental hepatology Table HBV V27L 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. V72W 2022 Clinical and experimental hepatology Table HBV V72W 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. W102G 2022 Clinical and experimental hepatology Table HBV W102G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. W125G 2022 Clinical and experimental hepatology Table HBV W125G 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. W62C 2022 Clinical and experimental hepatology Table HBV W62C 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. W71G 2022 Clinical and experimental hepatology Table HBV W71G 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. W71R 2022 Clinical and experimental hepatology Table HBV W71R 0 4 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Y118F 2022 Clinical and experimental hepatology Table HBV Y118F 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Y132T 2022 Clinical and experimental hepatology Table HBV Y132T 0 5 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Y67S 2022 Clinical and experimental hepatology Table HBV Y67S 0 4 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Prevalence of hepatitis B virus genotype and precore G1896A and BCP A1762T/G1764A mutants by age at recruitment. 2008 Journal of the National Cancer Institute Figure HBV G1764A;G1896A;A1762T 75;53;68 81;59;74 BCP;Precore 64;45 67;52 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. a) Binding mode (3TC-TP in L180M HBV) showing the loosing of one methyl contribution in small hydrophobic pocket of L180M HBV (green) in compare to wild type HBV (red; L180). 2008 Antiviral research Figure HBV L180M;L180M 27;116 32;121 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. a) Binding mode of L-FMAU-TP along with mutant M204V residue showing neglible steric clash. 2008 Antiviral research Figure HBV M204V 47 52 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. a) Binding mode of LdT in mutant M204V HBV superimposed with M204 residue. 2008 Antiviral research Figure HBV M204V 33 38 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. b) Binding mode (3TC-TP in M204V HBV) showing possible steric clash due to bulky V204 (green) in comparision to wild type HBV (M204; red). 2008 Antiviral research Figure HBV M204V 27 32 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. b) Binding mode of L-FMAU-TP along with M204I and L180M residues (dual mutant L180M+M204I HBV) showing the hydrophobic methyl group of M204I is oriented towards hydrophilic group (3'-OH) of L-FMAU-TP. 2008 Antiviral research Figure HBV M204I;L180M;L180M;M204I;M204I 40;50;78;84;135 45;55;83;89;140 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. b) Binding mode of L-FMAU-TP in L180M HBV. 2008 Antiviral research Figure HBV L180M 32 37 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. b) Binding mode of LdT in mutant M204I HBV superimposed with M204 residue showing the different position and orientation of methyl group in wild type and M204I HBV. 2008 Antiviral research Figure HBV M204I;M204I 33;154 38;159 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. b) ETV binding mode in M204V HBV: exocyclic alkene of ETV oriented towards mutated residue V204 (green) showing no significant steric clash. 2008 Antiviral research Figure HBV M204V 23 28 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. Binding mode of 3TC-TP in L180M+M204I mutant HBV. 2008 Antiviral research Figure HBV L180M;M204I 26;32 31;37 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. c) Binding Mode of 3TC-TP in M204V showing partial steric clash by vander waal's surface area. 2008 Antiviral research Figure HBV M204V 29 34 S 81 88 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. c) M204I mutant shows partial steric clash between I204 and exocyclic alkene as shown by vander Waal's surface area. 2008 Antiviral research Figure HBV M204I 3 8 S 103 110 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. d) Binding Mode of 3TC-TP in M204I showing extensive steric clash by vander waal surface area resulting further unfavorable forward movement of 3TC in comparision to wild type HBV. 2008 Antiviral research Figure HBV M204I 29 34 S 81 88 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. d) Binding mode of LdT in L180M HBV showing the absence of one methyl group in the backside binding pocket of LdT due to mutation of L180 (red) to Met180 (green). 2008 Antiviral research Figure HBV L180M 26 31 18765256 Understanding the molecular basis of HBV drug resistance by molecular modeling. In addition, the absence of one methyl group in the hydrophobic pocket due to L180M mutation. 2008 Antiviral research Figure HBV L180M 78 83 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Frequencies of PreS, C1653T, T1753V, or A1762T/G1764A mutations among asymptomatic hepatitis B surface antigen carriers (ASC), patients with chronic hepatitis B (CHB), patients with liver cirrhosis (LC), and patients with hepatocellular carcinoma (HCC) from the pooled data. 2009 Journal of the National Cancer Institute Figure HBV G1764A;C1653T;T1753V;A1762T 47;21;29;40 53;27;35;46 PreS;S 15;95 19;102 Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 141;162;182;222;248;199 160;165;197;246;251;201 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Summary odds ratios (ORs; in case-control studies) or relative risks (RRs; in cohort studies) of hepatocellular carcinoma (HCC) for PreS (A), C1653T (B), T1753V (C), A1762T/G1764A (D), C1858T (E), and G1896A (F) mutations. 2009 Journal of the National Cancer Institute Figure HBV G1764A;C1653T;T1753V;A1762T;C1858T;G1896A 173;142;154;166;185;201 179;148;160;172;191;207 PreS 132 136 Hepatocellular carcinoma;Hepatocellular carcinoma 97;123 121;126 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Four patterns (BCP-/PC-, BCP+/PC-, BCP-/PC+ and BCP+/PC+) were determined based on positivity (+) or negativity (-) for the BCP double mutation A1762T/G1764A and the G1896A PC mutation. 2010 Journal of viral hepatitis Figure HBV G1764A;A1762T;G1896A 151;144;166 157;150;172 BCP;BCP;BCP;BCP;BCP;Precore;Precore;Precore;Precore;Precore 15;25;35;48;124;20;30;40;53;173 18;28;38;51;127;22;32;42;55;175 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. (A) HBV RT with LVDr substitutions, M204V+L180M, (B) HBV RT with LVDr + S202G. 2010 PloS one Figure HBV M204V;L180M;S202G 36;42;72 41;47;77 RT;RT 8;57 10;59 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. A) The relative location of the M250, Y203, M204V, and other resistance residues are shown with primer-template DNA and ETV-TP in the dNTP binding site. 2010 PloS one Figure HBV M204V 44 49 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. As indicated by the arrows (protein:green; DNA:gray; M250V:purple), the resulting conformational change in the protein to close the resultant hole repositions the RNA/DNA slightly over the NTP binding site. 2010 PloS one Figure HBV M250V 53 58 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. C) The smaller side chain of the M250V no longer packs against L66. 2010 PloS one Figure HBV M250V 33 38 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Comparison of strand-specific EC50 versus double stranded EC50 for wildtype polymerase (WT) or LVDr M204V+L180M HBV, or the LVDr substitutions with ETVr substitutions (+T184, +S202, +M250) as indicated. 2010 PloS one Figure HBV M204V;L180M 100;106 105;111 P 76 86 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. HBVs were tested independently 3 to 4 times, except the LVDr+M250V, which was tested twice. 2010 PloS one Figure HBV M250V 61 66 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The YMDD loop is shown with residues M204V+L180M and the H-bonding between residues T184, S202 and M204V are shown as dotted white lines. 2010 PloS one Figure HBV L180M;M204V;M204V 43;37;99 48;42;104 P 4 8 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. WT, wildtype nucleocapsids; LVDr, M204V+L180M substituted HBV nucleocapsids, LVDr+M250V, M204V+L180M+M250V substituted nucleocapsids; LVDr+T184G+S202I, M204V+L180M+T184G+S202I substituted nucleocapsids. 2010 PloS one Figure HBV M204V;L180M;M250V;M204V;L180M;M250V;T184G;S202I;M204V;L180M;T184G;S202I 34;40;82;89;95;101;139;145;152;158;164;170 39;45;87;94;100;106;144;150;157;163;169;175 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. A further mutation is located at position rtL180 M The HBV polymerase was amplified from patient material and cloned into TOPO vector, which was transformed into E. 2010 Virology journal Figure HBV L180M 44 50 P;RT 59;42 69;44 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In (c), (d), and (e), lanes 1-5 represent the expression of Flag-HBc proteins and beta-actin in Huh7 cells transfected with pCMV-Tag1, pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G) and pCMV-HBc (I97L), respectively. 2010 Virology journal Figure HBV L60V;S87G;I97L 160;177;197 164;181;201 C;C;C;C;C 65;140;155;172;192 68;143;158;175;195 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In the stably-transfected Huh7 cells, the expression of the WT and mutated (L60V, S87G and I97L) HBc proteins were detected by western blot using an anti-Flag antibody (e). 2010 Virology journal Figure HBV L60V;S87G;I97L 76;82;91 80;86;95 C 97 100 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. pU19-1.24HBV was co-transfected with Renilla luciferase vector into Huh7 cells stably expressing wild-type HBc protein, L60V, S87G or I97L mutated proteins, as well as into control cells stably transfected with empty vector. 2010 Virology journal Figure HBV L60V;S87G;I97L 120;126;134 124;130;138 C 107 110 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Consensus of each of the three single mutation patterns and wt were aligned with five known variants frequently associated with problems in diagnostic assays and/or escape to vaccine/HBIg therapy: T123N, M133I, M133T, M133V, and T143L, together with M54923 sequence (genotype B/adw) retrieved from GenBank as a reference. 2010 Virology journal Figure HBV T123N;M133I;M133T;M133V;T143L 197;204;211;218;229 202;209;216;223;234 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Tertiary structure prediction of M54923 (reference sequence), T123A, M133L, and T143M mutants. 2010 Virology journal Figure HBV T123A;M133L;T143M 62;69;80 67;74;85 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Three amino acid substitutions were identified in 7 HBV isolates in blood donors: Pattern 1, T123A, in one isolate; Pattern 2, M133L, in one isolate; Pattern 3, T143M, in five isolates. 2010 Virology journal Figure HBV T123A;M133L;T143M 93;127;161 98;132;166 21438026 Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival. Only the two amino acid differences resulting from the A1762T/G1764A base mutations which distinguish MutHBx from WtHBx are indicated. 2011 Molecular carcinogenesis Figure HBV G1764A;A1762T 62;55 68;61 X;X 105;116 108;119 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Binding of recombinant RFX1 to wild-type and G1613A mutant NRE. 2011 PloS one Figure HBV G1613A 45 51 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Electrophoretic mobility shift assay of wild-type and G1613A NRE oligos. 2011 PloS one Figure HBV G1613A 54 60 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The effect of G1613A mutation on the HBV DNA level. 2011 PloS one Figure HBV G1613A 14 20 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The effect of G1613A mutations on the levels of HBsAg and HBeAg. 2011 PloS one Figure HBV G1613A 14 20 C;S 58;48 63;53 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. (A) Rationale of the amplification created restriction enzyme method to assist the detection of a small percentage of the rtA181T mutant. 2011 BMC cancer Figure HBV A181T 124 129 RT 122 124 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Methods to detect rtA181T mutations and pre-S internal deletion mutations. 2011 BMC cancer Figure HBV A181T 20 25 PreS;RT 40;18 45;20 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The cumulative incidence of HCC was depicted according to the presence of the rtA181T mutation (A), use of rescue therapy (B), the presence of liver cirrhosis (C), and age > 50 years (D). 2011 BMC cancer Figure HBV A181T 80 85 RT 78 80 Hepatocellular carcinoma;Liver cirrhosis 28;143 31;158 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. (B) Constructed plasmid mutant-type (single mutation at nt 587 G to A) DNA and wild-type DNA were mixed. 2012 BMC research notes Figure HBV G587A 59 69 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. (C) Constructed plasmid mutant-type (single mutation at nt 587 G to A) DNA and wild-type DNA were mixed. 2012 BMC research notes Figure HBV G587A 59 69 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. (D) Constructed plasmid mutant-type (single mutation at nt 587 G to A) DNA and wild-type DNA were mixed. 2012 BMC research notes Figure HBV G587A 59 69 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 18 clones, six had a mutation at nt 587 from G to A. 2012 BMC research notes Figure HBV G587A 43 58 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 20 clones, 5 had a mutation at nt 587 from G to A. 2012 BMC research notes Figure HBV G587A 41 56 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. (A) The relative proportion of the G1896A pre-C mutant was determined in the serum of treatment-naive patients pre- and post-entecavir administration using quantitative real-time PCR. 2012 PloS one Figure HBV G1896A 35 41 Precore 42 47 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. (C) The relative proportion of the G1896A pre-C mutant was compared in 14 treatment-naive patients between pre- and post-entecavir administration. 2012 PloS one Figure HBV G1896A 35 41 Precore 42 47 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. *: p<0.05 (B) Semiquantitative PCR analysis was performed using primers specific to the wild-type (upper panel) or G1896A pre-C mutant (lower panel) pre- and post-entecavir administration. 2012 PloS one Figure HBV G1896A 115 121 Precore 122 127 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. The reduction in the relative proportion of the G1896A pre-C mutant clones after entecavir administration. 2012 PloS one Figure HBV G1896A 48 54 Precore 55 60 22672436 Detection of mixed populations of wild-type and YMDD hepatitis B variants by pyrosequencing in acutely and chronically infected patients. The direct sequencing method (A) detected the nucleotides (GTG) coding for the rtM204V variant, although the electropherogram indicated mixtures with small quantities of nucleotides A and T corresponding to the first and third nucleotide position of codon ATT (rt204I). 2012 BMC microbiology Figure HBV M204V 81 86 RT;RT 79;261 81;263 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. (A) Galbraith plot of the association between precore G1896A and HCC risk (The studies outside the range between -2 and 2 were seen as the outliers and the major source of heterogeneity); (B) Galbraith plot of the correlation between Pre-S2 deletion and HCC risk. 2012 PloS one Figure HBV G1896A 54 60 Precore;PreS2 46;234 53;240 Hepatocellular carcinoma;Hepatocellular carcinoma 65;254 68;257 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. (A) Pooled odds ratio for correlation of Precore G1896A with HCC (before adjustment for heterogeneity). 2012 PloS one Figure HBV G1896A 49 55 Precore 41 48 Hepatocellular carcinoma 61 64 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. (B) Pooled odds ratio for association between G1896A and HCC risk after adjustment for heterogeneity. 2012 PloS one Figure HBV G1896A 46 52 Hepatocellular carcinoma 57 60 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Forest plot for the correlation between Precore mutation G1896A and HCC risk. 2012 PloS one Figure HBV G1896A 57 63 Precore 40 47 Hepatocellular carcinoma 68 71 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Forest plot for the correlation between Precore mutation G1899A and HCC risk. 2012 PloS one Figure HBV G1899A 57 63 Precore 40 47 Hepatocellular carcinoma 68 71 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Galbraith plots for heterogeneity test of G1896A and Pre-S2 deletion. 2012 PloS one Figure HBV G1896A 42 48 PreS2 53 59 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. In contrast, the basal core promoter mutations A1762T and G1764A were detected more frequently in genotype C at 49% and 51% respectively, compared to only 22% and 18% in genotype B (p<0.0001). 2012 PloS one Figure HBV A1762T;G1764A 47;58 53;64 BCP 17 36 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. The mutation T1858C was identified only in genotype C viruses. 2012 PloS one Figure HBV T1858C 13 19 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. The precore stop mutation G1896A was identified in 35% (n = 82/236) of all samples and varied significantly by viral genotype, with a higher occurrence in genotype B (41%) compared to Genotype C (3%) (p<0.001). 2012 PloS one Figure HBV G1896A 26 32 Precore 4 11 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Four patterns (preC-/CP-, preC+/CP-, preC-/CP+, and preC+/CP+) were defined based on the presence (+) or absence (-) of pre-C mutation G1896A and CP A1762T/G1764A double mutation. 2012 PloS one Figure HBV G1764A;G1896A;A1762T 156;135;149 162;141;155 Core promoter;Core promoter;Core promoter;Core promoter;Core promoter;Precore;Precore;Precore;Precore;Precore 21;32;43;58;146;15;26;37;52;120 23;34;45;60;148;19;30;41;56;125 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Mice were injected hydrodynamically with 10mug pHBV4.1 (Wt) or pHBV rt A181T/sW172 (Mut) respectively, and were sacrificed at different time points. 2012 Virology journal Figure HBV A181T 71 76 RT;S 68;77 70;78 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Mice were injected with 10mug pHBV4.1 (Wt) or pHBV rtA181T/sW172* (Mut) respectively. 2012 Virology journal Figure HBV W172X;A181T 59;53 65;58 RT;S 51;59 53;60 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Confocal microscopy analysis of 1-48preS/S, G2A 1-48preS/S and G2S 1-48preS/S proteins. 2013 Virology journal Figure HBV G2S;G2A 63;44 66;47 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Electron microscopy analysis of immunogold-labelled G2S mutant of 1-48preS/S subviral particles after reaction with MAb MA18/7 recognizing preS1. 2013 Virology journal Figure HBV G2S 52 55 PreS1 139 144 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. Huh7 cells were infected at MOI 10 with rSFV encoding 1-48preS/S, G2A 1-48preS/S and 1-48preS/S0. 2013 Virology journal Figure HBV G2A 66 69 23442390 Posttranslational modifications and secretion efficiency of immunogenic hepatitis B virus L protein deletion variants. The filled triangle denotes the modified myristic acid attachment site, where Gly2 was replaced with Ala or Ser in L deletion variants G2A 1-48preS/S and G2S 1-48preS/S. 2013 Virology journal Figure HBV G2S;G2A 154;135 157;138 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Cumulative selection of 3TC resistant (rtM204V/I) strains over time in patients who ever received 3TC or FTC. 2013 Virology journal Figure HBV M204V;M204I 41;41 48;48 RT 39 41 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. *, p < 0.05, compared with sG145K HBsAg. 2013 Virology journal Figure HBV G145K 27 33 S;S 34;27 39;28 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. *, p < 0.05, compared with sG145R HBsAg. 2013 Virology journal Figure HBV G145R 27 33 S;S 34;27 39;28 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. *, p < 0.05, compared with sT118M HBsAg. 2013 Virology journal Figure HBV T118M 27 33 S;S 34;27 39;28 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. 1: wild type; 2: sT118M; 3: sT118M-rtM204I; 4: sT118M-rtM204V; 5: sG145K; 6: sG145K-rtM204I; 7: sG145K-rtM204V; 8: sG145R; 9: sG145R- rtM204I; 10: sG145R- rtM204V; 11: empty vector. 2013 Virology journal Figure HBV M204I;M204V;M204I;M204V;M204I;M204V;T118M;T118M;T118M;G145K;G145K;G145K;G145R;G145R;G145R 37;56;86;105;136;157;17;28;47;66;77;96;115;126;147 42;61;91;110;141;162;23;34;53;72;83;102;121;132;153 RT;RT;RT;RT;RT;RT;S;S;S;S;S;S;S;S;S 35;54;84;103;134;155;17;28;47;66;77;96;115;126;147 37;56;86;105;136;157;18;29;48;67;78;97;116;127;148 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. rtM204V (sW196S) mutation also reduced the recognition of sG145R HBsAg in ELISA kits WT and BN. 2013 Virology journal Figure HBV M204V;W196S;G145R 2;9;58 7;15;64 S;RT;S;S 65;0;9;58 70;2;10;59 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. rtM204V (sW196S) mutation did not cause antigenic variation of sG145K HBsAg. 2013 Virology journal Figure HBV M204V;W196S;G145K 2;9;63 7;15;69 S;RT;S;S 70;0;9;63 75;2;10;64 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. With the exception of ELISA kit KSB, which recognized sT118M-rtM204I (sT118M-sI195M) with reduced avidity, all of the kits had almost invariable slope or avidity to the sT118M mutant, sT118M-rtM204I (sT118M-sI195M), and sT118M-rtM204V (sT118M-sW196S) double mutant. 2013 Virology journal Figure HBV M204I;M204I;M204V;T118M;T118M;T118M;T118M;W196S;I195M;I195M;T118M;T118M;T118M 63;193;229;54;70;169;184;243;77;207;200;220;236 68;198;234;60;76;175;190;249;83;213;206;226;242 RT;RT;RT;S;S;S;S;S;S;S;S;S;S 61;191;227;54;70;77;169;184;200;207;220;236;243 63;193;229;55;71;78;170;185;201;208;221;237;244 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. With the rtM204I (sI195M) mutation in the backbone of sG145K, avidity was reduced significantly in four kits. 2013 Virology journal Figure HBV M204I;I195M;G145K 11;18;54 16;24;60 RT;S;S 9;18;54 11;19;55 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. With the rtM204I (sI195M) mutation in the backbone of sG145R, avidity was reduced significantly for all ELISA kits. 2013 Virology journal Figure HBV M204I;I195M;G145R 11;18;54 16;24;60 RT;S;S 9;18;54 11;19;55 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. After 48 hrs, incorporation of BrdU into the control, accumulation of mitotic L02 cells was significantly delayed in cells treated with LHBs and its mutations, especially N320K. 2013 Hepatitis monthly Figure HBV N320K 171 176 S 136 140 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. L02 cells were harvested after culturing for 24 hrs, then transfected with pCDNA3.1 (-), pCDNA3.1(-)-LHBs, pCDNA3.1(-)-N15S, pCDNA3.1(-)-N123S, pCDNA3.1(-)-N177S, and pCDNA3.1(-)-N320K respectively as described in Materials and Methods.After 48 hrs, proteins of cells were extracted and then run on an SDS-PAGE gel before being transferred for western blot. 2013 Hepatitis monthly Figure HBV N15S;N123S;N177S;N320K 119;137;156;179 123;142;161;184 S 101 105 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. L02 cells were harvested after culturing for 48 hrs, then transfected with pCDNA3.1 (-), pCDNA3.1 (-)-LHBs, pCDNA3.1(-)-N15S, pCDNA3.1(-)-N123S, pCDNA3.1(-)-N177S, and pCDNA3.1(-)-N320K respectively as described in Materials and Methods. 2013 Hepatitis monthly Figure HBV N15S;N123S;N177S;N320K 120;138;157;180 124;143;162;185 S 102 106 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. L02 cells were transfected with pCDNA3.1 (-), pCDNA3.1 (-)-LHBs, pCDNA3.1 (-)-N15S, pCDNA3.1 (-)-N123S, pCDNA3.1 (-)-N177S, and pCDNA3.1(-)-N320K respectively as described in Materials and Methods. 2013 Hepatitis monthly Figure HBV N15S;N123S;N177S;N320K 78;97;117;140 82;102;122;145 S 59 63 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. L02 cells were transfected with pCDNA3.1 (-), pCDNA3.1 (-)-LHBs, pCDNA3.1(-)-N15S, pCDNA3.1(-)-N123S, pCDNA3.1(-)-N177S, and pCDNA3.1(-)-N320K respectively as described in Materials and Methods. 2013 Hepatitis monthly Figure HBV N15S;N123S;N177S;N320K 77;95;114;137 81;100;119;142 S 59 63 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The results showed that LHBs and its mutations induced an increase in G1 phase and inhibition of S phase, especially N320K. 2013 Hepatitis monthly Figure HBV N320K 117 122 S 24 28 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. (B) Proposed secondary structure of the HBV epsilon signal with A1846T and C1913A/G mutations. 2013 Hepatitis monthly Figure HBV C1913G;A1846T;C1913A 75;64;75 83;70;83 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. A1846T comprised 65.5%, and 56.9% of ACLF-CHB and ACLF-LC patients. 2013 Hepatitis monthly Figure HBV A1846T 0 6 Chronic Hepatitis B;Liver cirrhosis 42;55 45;57 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. C1913A/G comprised 44.8%, and 50% of ACLF-CHB and ACLF-LC patients. 2013 Hepatitis monthly Figure HBV C1913G;C1913A 0;0 8;8 Chronic Hepatitis B;Liver cirrhosis 42;55 45;57 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Possible influences of A1846T and C1913A/G mutations on core protein expression. 2013 Hepatitis monthly Figure HBV C1913G;A1846T;C1913A 34;23;34 42;29;42 C 56 60 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. The C1913A/G mutation causes a substitution of the fifth amino acid in core protein from proline to threonine or alanine. 2013 Hepatitis monthly Figure HBV C1913G;C1913A 4;4 12;12 C 71 75 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Huh7 cells were transfected with pHBV1.3 (Figure 3 A), -rtQ267H (Figure 3 B), -rtM204V/Q267H (Figure 3 C), -rtL180M/M204V (Figure 3 D), -rtL180M/M204V/Q267H (Figure 3 E), and then treated with LMV at the indicated concentrations. 2013 Hepatitis monthly Figure HBV Q267H;M204V;Q267H;M204V;Q267H;M204V;L180M;L180M 87;116;151;145;58;81;110;139 92;121;156;150;63;86;115;144 RT;RT;RT;RT 56;79;108;137 58;81;110;139 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Huh7 cells were transfected with pHBV1.3, -rtQ267H, -rtM204V/Q267H, -rtL180M/M204V, -rtL180M/M204V/Q267H, and then treated with LMV at the indicated concentrations. 2013 Hepatitis monthly Figure HBV Q267H;M204V;Q267H;M204V;Q267H;M204V;L180M;L180M 61;77;99;93;45;55;71;87 66;82;104;98;50;60;76;92 RT;RT;RT;RT 43;53;69;85 45;55;71;87 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Follow-up the clinical course of three representative patients with HBV rtM204Q mutant during antiviral treatment. 2014 PloS one Figure HBV M204Q 74 79 RT 72 74 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. (B) Chromatograms of rtM204I (mutant). 2014 PloS one Figure HBV M204I 23 28 RT 21 23 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. Typical chromatograms of the cloning sequencing of HBV rtM204 and rtM204I. 2014 PloS one Figure HBV M204I 68 73 RT;RT 55;66 57;68 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The frequency of the G1896A precore mutation was higher compared to the BCP double mutations in our settings with majority of the strains harboring the C1858T mutation. 2014 PloS one Figure HBV G1896A;C1858T 21;152 27;158 BCP;Precore 72;28 75;35 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The major mutations in the MHC class I restricted (amino acids 18-27, 88-96, 130-140, 141-151) and MHC class II-restricted (amino acids 1-20, 50-69, 81-105, 117-131, 141-165) T-cell epitopes of core antigen includes the V27I and T12S respectively. 2014 PloS one Figure HBV V27I;T12S 220;229 224;233 C 194 198 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Among these participants, 47 (10.0%) harbored A799G and 48 (10.3%) harbored T1055A. 2014 PloS one Figure HBV A799G;T1055A 46;76 51;82 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Effects of the A799G and T1055A mutations on circulating HBV DNA levels in all participants. 2014 PloS one Figure HBV A799G;T1055A 15;25 20;31 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The effects of the mutations A799G and T1055A on circulating HBV DNA load were estimated using blood samples from a total of 468 participants (HCC patients or non-HCC controls). 2014 PloS one Figure HBV A799G;T1055A 29;39 34;45 Hepatocellular carcinoma;Hepatocellular carcinoma 143;163 146;166 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Described antiviral resistant mutations were highlighted and denoted at the top (e.g., L80V). 2014 PloS one Figure HBV L80V 87 91 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (A and B) Comparison of growth of WT- and W4P-LHB-expressing NIH3T3 cells (A) and Huh7 cells (B). 2015 Molecular cancer Figure HBV W4P 42 45 S 46 49 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (A and B) Serum levels of IL-6 (A) and TNF-alpha (B) measured from mice injected with NIH3T3, WT-LHB-NIH3T3 and W4P-LHB-NIH3T3 cells. 2015 Molecular cancer Figure HBV W4P 112 115 S;S 97;116 100;119 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (C) Comparison between male and female mice in terms of tumor size in nude mice injected with W4P cells. 2015 Molecular cancer Figure HBV W4P 94 97 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (C) Correlation between serum IL-6 levels and tumor volumes of W4P-LHB-NIH3T3-injected mice (10 male and 10 female mice) (r = 0.862, P < 0.001). 2015 Molecular cancer Figure HBV W4P 63 66 S 67 70 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (C) J774A.1 cells were treated with 10-mg lysates made from tumors expressing W4P LHB in the presence or absence of 20 nM estradiol. 2015 Molecular cancer Figure HBV W4P 78 81 S 82 85 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (D and E) Serum IL-6 (D) and TNF-alpha (E) was measured in 11 HCC patients with WT and 11 with W4P variant sequences. 2015 Molecular cancer Figure HBV W4P 95 98 Hepatocellular carcinoma 62 65 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. (D) Hematoxylin and eosin staining of the tumor mass of nude mice injected with W4P cells. 2015 Molecular cancer Figure HBV W4P 80 83 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Effect of estrogen on W4P-LHB-mediated IL-6 production and cell proliferation. 2015 Molecular cancer Figure HBV W4P 23 26 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Induction of IL-6 production by W4P LHB in a gender-dependent manner. 2015 Molecular cancer Figure HBV W4P 33 36 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. NIH3T3 cells and NIH3T3 cell lines expressing WT and W4P LHBs were subjected to a colony formation assay. 2015 Molecular cancer Figure HBV W4P 53 56 S 57 61 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Nude mice were injected with NIH3T3 (male, n = 10), WT-LHB-NIH3T3 (WT) (male, n = 10) and W4P-LHB-NIH3T3 [male (n = 10) and female (n = 10)] cells. 2015 Molecular cancer Figure HBV W4P 90 93 S;S 55;94 58;97 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. One week later, mice were injected with W4P-LHB-expressing cells subcutaneously together with 0.5 mg/kg beta-estradiol or PBS. 2015 Molecular cancer Figure HBV W4P 40 43 S 44 47 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Suppression of W4P-mediated tumorigenicity by estrogen. 2015 Molecular cancer Figure HBV W4P 16 19 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Transforming activity of W4P variant and gender disparity in tumorigenesis of W4P LHB expressing. 2015 Molecular cancer Figure HBV W4P;W4P 26;79 29;82 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. W4P variant LHB facilitates cell proliferation and cell cycle progression. 2015 Molecular cancer Figure HBV W4P 1 4 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. A) Deletion at ORF of Pre S1 region of the HBV genome in five patients Comparison was made with the reference sequence GQ924603 by alignment in Clustal Omega tool; B) W182 stop codon in the S gene region of HBV in two patients. 2014 Hepatitis monthly Figure HBV W182X 167 176 PreS1;S 22;190 28;191 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. children HBeAg positive patients containing A1762T/G1764A double mutation; B. 2015 PloS one Figure HBV G1764A;A1762T 51;44 57;50 C 9 14 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The association analysis between A1762T/G1764A double mutation and viral load, ALT level in different chronic HBV patients. 2015 PloS one Figure HBV G1764A;A1762T 40;33 46;39 Chronic Hepatitis B 102 113 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. (A) Atomic force microscope images of HBc-WT particle (left) and HBc-R154G particle (right). 2015 Journal of nanobiotechnology Figure HBV R154G 69 74 C;C 38;65 41;68 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. (B) Scanning electron microscope images of HBc-WT particle (left) and HBc-R154G particle (right). 2015 Journal of nanobiotechnology Figure HBV R154G 74 79 C;C 43;70 46;73 25890025 Mutation of arginine residues to avoid non-specific cellular uptakes for hepatitis B virus core particles. The average size of the HBc-R154G particle was 28.7 nm. 2015 Journal of nanobiotechnology Figure HBV R154G 28 33 C 24 27 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. A random-effects model was used for G1896A, A1762T/G1764A and G1764A, and a fixed-effects model was used for A1762T. 2015 Virology journal Figure HBV G1764A;G1896A;A1762T;G1764A;A1762T 51;36;44;62;109 57;42;50;68;115 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Funnel plot for A1762T, G1764A, A1762T/G1764A and G1896A. 2015 Virology journal Figure HBV G1764A;A1762T;G1764A;A1762T;G1896A 39;16;24;32;50 45;22;30;38;56 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Summary odds ratio (OR) of acute-on-chronic liver failure for A1762T, G1764A, A1762T/G1764A and G1896A mutations. 2015 Virology journal Figure HBV G1764A;A1762T;G1764A;A1762T;G1896A 85;62;70;78;96 91;68;76;84;102 Acute on chronic liver failure 27 57 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Test for heterogeneity: (G1896A) p = 0.002, I2 = 48.1 %; (A1762T/G1764A) p < 0.001, I2 = 80.7 %; (A1762T) p = 0.164, I2 = 25.7 %; (G1764A) p = 0.004, I2 = 56.4 %. 2015 Virology journal Figure HBV G1764A;G1896A;A1762T;A1762T;G1764A 65;25;58;98;131 71;31;64;104;137 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. A S202I mutation was also detected in one subjects (SH1), indicating the natural entecavir resistance. 2015 Hepatitis monthly Figure HBV S202I 2 7 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. M204I point mutation in YMDD motif, detected in 6 out 13 subjects, is pointed by black arrow. 2015 Hepatitis monthly Figure HBV M204I 0 5 P 24 28 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Effect of rtL269I and other substitutions on resistance to lamivudine (LMV). 2015 PloS one Figure HBV L269I 12 17 RT 10 12 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Effect of rtL269I substitution on the resistance to entecavir (ETV). 2015 PloS one Figure HBV L269I 12 17 RT 10 12 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Molecular modeling of rtL269I of HBV polymerase. 2015 PloS one Figure HBV L269I 24 29 P;RT 37;22 47;24 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. rtL269I substitution enhances the replication of both WT and drug-resistant hepatitis B virus (HBV). 2015 PloS one Figure HBV L269I 2 7 RT 0 2 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. Frequency (% of total reads) of HBV drug-resistant and immune escape (i.e., G145R) mutations detected in CD4+ and/or CD56+ immune cell subset by deep sequencing analysis in 2 HBV monoinfected cases (i.e., #3B and #8B) on tenofovir anti-HBV therapy. 2015 PloS one Figure HBV G145R 76 81 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. A: arrow indicates mutation in RT region in position Y135S. 2015 Jundishapur journal of microbiology Figure HBV Y135S 53 58 RT 31 33 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. B: arrows indicate mutations in the S region in positions T127P, P153L, and F170S. 2015 Jundishapur journal of microbiology Figure HBV T127P;P153L;F170S 58;65;76 63;70;81 S 36 37 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. (B) At baseline, the virus harbored an rtA181T substitution (1.4%), and other resistance mutations were present at low levels (<1%). 2016 Medicine Figure HBV A181T 41 46 RT 39 41 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. (B) At baseline, the virus only harbored an rtA181T substitution (1.2%) and had low fluctuations during the follow-up period. 2016 Medicine Figure HBV A181T 46 51 RT 44 46 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. (B) From 1 to 2 years, the resistant variants (rtL180 M, rtM204 V, rtS202G) began to rise to a high peak (84.60%, 79.56%, 76.88%), and double amino acid substitutions (rtL180M+rtM204 V) and triple substitutions (rtL180M+rtM204V+rtS202G) also began to rise. 2016 Medicine Figure HBV M204V;L180M;M204V;S202G;L180M;S202G;L180M;M204V 178;49;59;69;170;230;214;222 184;55;65;74;175;235;219;227 RT;RT;RT;RT;RT;RT;RT;RT 47;57;67;168;176;212;220;228 49;59;69;170;178;214;222;230 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. (B) Resistance mutations displayed low levels of fluctuation (<7%), and nonresistant variants (rtN248H/rtS223A) rose to 12.88%/13.1% by 2 years. 2016 Medicine Figure HBV N248H;S223A 97;105 102;110 RT;RT 95;103 97;105 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. A wave of resistant variants (rtM204 V [19.95%], rtL180 M [19.12%], and rtS202G [18.33%]) was detected at 1 year and then decreased to <1% by 2 years. 2016 Medicine Figure HBV M204V;L180M;S202G 32;51;74 38;57;79 RT;RT;RT 30;49;72 32;51;74 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Additionally, rtS256G substitutions were maintained at a high level (>55%).ETV = entecavir, DNA = di-ribonucleic acid, HBV = hepatitis B virus, RT = reverse transcriptase. 2016 Medicine Figure HBV S256G 16 21 RT;RT;RT 149;14;144 170;16;146 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. At baseline, this patient displayed rtM204I/V (3.5%), rtL180 M (2.1%), and rtS202G (3.4%) substitutions. 2016 Medicine Figure HBV M204I;M204V;L180M;S202G 38;38;56;77 45;45;62;82 RT;RT;RT 36;54;75 38;56;77 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Several other variants fluctuated at relatively high levels (ranging from 3.56% to 7.89%), including rtN248H, rtS223A, rtS256C, and rtI224 V mutations. 2016 Medicine Figure HBV N248H;S223A;S256C;I224V 103;112;121;134 108;117;126;140 RT;RT;RT;RT 101;110;119;132 103;112;121;134 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. The rtA181T substitution rose from 2.17% to 64.15% by 2 years and certain nonresistance mutations (rtN248A, rtI224 V, and rtS223A) increased significantly. 2016 Medicine Figure HBV N248A;S223A;A181T;I224V 101;124;6;110 106;129;11;116 RT;RT;RT;RT 4;99;108;122 6;101;110;124 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. Two variants (rtI187L/rtV191I) rose to a high level during the 4th year (84.43% /83.41%), and 2 other variants, namely, rtN248H and rtS256G, were maintained at a high level (>60%). 2016 Medicine Figure HBV I187L;V191I;N248H;S256G 16;24;122;134 21;29;127;139 RT;RT;RT;RT 14;22;120;132 16;24;122;134 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. BCP A1762T/G1764A dual mutations in HBV genotype B and C from chronic HBV infection patients, including HCC. 2016 Oncotarget Figure HBV G1764A;A1762T 11;4 17;10 BCP 0 3 Chronic HBV infection;Hepatocellular carcinoma 62;104 83;107 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Comparison of BCP A1762T/G1764A dual mutations grouped by HBeAg status from chronic HBV infection patients, including HCC. 2016 Oncotarget Figure HBV G1764A;A1762T 25;18 31;24 BCP;C 14;58 17;63 Chronic HBV infection;Hepatocellular carcinoma 76;118 97;121 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. HCC occurrence between BCP A1762T/G1764A dual mutation and non-BCP dual mutation patients with HBV genotype C and genotype B. 2016 Oncotarget Figure HBV G1764A;A1762T 34;27 40;33 BCP;BCP 23;63 26;66 Hepatocellular carcinoma 0 3 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (A) Representative image and quantification of hepatospheres in MIHA cells with HBx-Delta14 and HBx-Delta35 stably overexpressed, in the absence or presence of FXR inhibitor, Z-guggulsterone (Z-gugg; 25 muM). 2016 Oncotarget Figure HBV Delta35 100 107 X;X 80;96 83;99 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (B) Representative image and quantification of number of cells that migrated in MIHA cells with HBx-Delta14 and HBx-Delta35 stably overexpressed in the absence or presence of FXR inhibitor, Z-guggulsterone (Z-gugg; 25 muM). 2016 Oncotarget Figure HBV Delta35 116 123 X;X 96;112 99;115 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (B) Unique gene signatures of MIHA cells with or without expression of HBx-Delta14 and HBx-Delta35, as shown by hierarchical cluster analysis (fold change >= 1.5 and FDR <= 0.05). 2016 Oncotarget Figure HBV del 35 91 98 X;X 71;87 74;90 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (C) Cartoon summary of the role of C-terminal truncated HBx variants, in particular HBx-Delta14 and HBx-Delta35, in promoting cancer and stem cell-like features in vitro in HCC. 2016 Oncotarget Figure HBV del 35 104 111 X;X;X 56;84;100 59;87;103 Hepatocellular carcinoma 173 176 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (F) Flow cytometry dot plot analysis for CD133 expression in MIHA cells with HBx-Delta14 and HBx-Delta35 stably overexpressed. 2016 Oncotarget Figure HBV Delta35 97 104 X;X 77;93 80;96 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (G) Western blot analysis of MIHA with EV, HBx-Delta14 or HBx-Delta35 stably overexpressed for phosphorylated and total STAT3 expression. 2016 Oncotarget Figure HBV Delta35 62 69 X;X 43;58 46;61 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. (H) Relative expression of SOX2 in MIHA cells with or without HBx-Delta14 and HBx-Delta35 stably overexpressed. 2016 Oncotarget Figure HBV Delta35 82 89 X;X 62;78 65;81 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. HBx-Delta35 in MIHA cells. 2016 Oncotarget Figure HBV del 35 4 11 X 0 3 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. WT, wild-type; M1, sQ129N; M2, s131-133TSM NST; M3, s126-127 "RPCMNCTI" insertion; M4, sG145R; N, negative control. 2016 PloS one Figure HBV Q129N;G145R 19;87 25;93 S;S;S;S 19;31;52;87 20;32;53;88 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. WT, wild-type; M1, sQ129N; M2, s131-133TSM NST; M3, sI126V; M4, sG145R; M5, sI126V+sG145R; M6, s115-116 "INGTST" insertion; M7, s115-116 "INGTST" insertion+sG145R; M8, s122-123 "KSTGLCK" insertion+sQ129N; M9, s126-127 "RPCMNCTI" insertion; M10, nt 3014-3198 deletion; M11, nt 3046-3177 deletion; M12, preS2 initiation codon M I+s131+133TSM NST; M13, nt 2848-2862 deletion+preS2 initiation codon M I; M14, nt 3115-3123 deletion+sQ129N (* P < 0.05, mutant vs. 2016 PloS one Figure HBV Q129N;I126V;G145R;G145R;G145R;Q129N;Q129N;I126V 19;52;64;83;156;197;427;76 25;58;70;89;162;203;433;82 PreS2;PreS2;S;S;S;S;S;S;S;S;S;S;S;S;S;S 301;372;19;31;52;64;76;83;95;128;156;168;197;209;328;427 306;377;20;32;53;65;77;84;96;129;157;169;198;210;329;428 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. HBx A1762T/G1764A (TA) and T1753A/A1762T/G1764A/T1768A (Combo) mutant-stimulated migration and proliferation are partially blocked by Wnt antagonists. 2016 Cancer science Figure HBV G1764A;A1762T;T1768A;A1762T;G1764A;G1764A;T1753A;A1762T;G1764A;T1768A;A1762T;T1753A 11;5;48;34;41;12;28;35;42;49;4;27 17;11;54;40;47;18;34;41;48;55;10;33 X 0 3 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. HBx mutations (T1753V, A1762T, G1764A, and T1768A) activate the Wnt/beta-catenin pathway in hepatocellular carcinoma cells. 2016 Cancer science Figure HBV A1762T;G1764A;T1768A;T1753V;A1762T;G1764A;T1768A 24;32;44;15;23;31;43 30;38;50;21;29;37;49 X 0 3 Hepatocellular carcinoma 92 116 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. HBx mutations (T1753V, A1762T, G1764A, and T1768A) promote migration and proliferation of hepatoma cells. 2016 Cancer science Figure HBV A1762T;G1764A;T1768A;T1753V;A1762T;G1764A;T1768A 24;32;44;15;23;31;43 30;38;50;21;29;37;49 X 0 3 Hepatocellular carcinoma 90 98 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. HBx T1753A/A1762T/G1764A/T1768A (Combo) mutant upregulates beta-catenin in hepatocellular carcinoma (HCC) tissue. 2016 Cancer science Figure HBV T1768A;G1764A;A1762T;T1753A;A1762T;G1764A;T1768A;T1753A 25;18;11;5;12;19;26;4 31;24;17;11;18;25;32;10 X 0 3 Hepatocellular carcinoma;Hepatocellular carcinoma 75;101 99;104 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. A wave of resistance-associated variants was detected at year 3, when the frequency of the rtA181T substitution rose from 1.91% to 54.23%. 2016 Oncotarget Figure HBV A181T 93 98 RT 91 93 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient harbored the rtA181T (1.4%), rtN236T (1.8%), rtS202G (1%), and rtM204I/V (1%) substitutions, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Figure HBV A181T;N236T;M204I;M204V;S202G 41;57;91;91;73 46;62;98;98;78 RT;RT;RT;RT 39;55;71;89 41;57;73;91 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient harbored the rtA181T (4.7%), rtN236T (5.7%), rtL180M (12.5%), rtS202G (3.2%), and rtM204I/V (7%) substitutions. 2016 Oncotarget Figure HBV A181T;L180M;M204I;M204V;N236T;S202G 41;73;110;110;57;90 46;78;117;117;62;95 RT;RT;RT;RT;RT 39;55;71;88;108 41;57;73;90;110 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient harbored the rtA181T (8.7%), rtN236T (1.7%), rtL180M(10.5%), rtM204I/V (7.5%), and rtV173A/M (1.6%) substitutions, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Figure HBV A181T;N236T;L180M;M204I;M204V;V173A;V173M 41;57;73;89;89;111;111 46;62;78;96;96;118;118 RT;RT;RT;RT;RT 39;55;71;87;109 41;57;73;89;111 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. At baseline, this patient harbored the rtL180M (2.4%), rtM204I/V (3.4%), rtS202G (3.3%), rtA181V/T (4.7%), and rtN236T (6%) substitutions. 2016 Oncotarget Figure HBV M204I;M204V;A181V;A181T;L180M;S202G;N236T 57;57;91;91;41;75;113 64;64;98;98;46;80;118 RT;RT;RT;RT;RT 39;55;73;89;111 41;57;75;91;113 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. However, the frequencies of the rtS223A and rtN248H mutations declined in the first year with the addition of LdT and then increased significantly in the second year. 2016 Oncotarget Figure HBV S223A;N248H 34;46 39;51 RT;RT 32;44 34;46 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. However, the frequency of the rtS223A mutation increased significantly (ranging from 18.14% to 77.62%) with the addition of LdT. 2016 Oncotarget Figure HBV S223A 32 37 RT 30 32 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In contrast, the rtQ215R substitution increased to 10.89% in the second year with multi-drugs. 2016 Oncotarget Figure HBV Q215R 19 24 RT 17 19 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Meanwhile some certain non-resistance-related mutations of rtL145M (ranging from 76.77% to 7.30%) and rtF151Y (ranging from 72.61% to 7.15%) had decreased significantly in frequency with the addition of LdT. 2016 Oncotarget Figure HBV L145M;F151Y 61;104 66;109 RT;RT 59;102 61;104 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. Some non-resistance-associated mutations of rtD134N (ranging from 20.33% to 74.63%), rtL145M (ranging from 2.83% to 78.82%), rtF151Y (ranging from 2.92% to 75.51%) and rtS223A (ranging from 5.77% to 18.44%) increased significantly with ADV monotherapy, then declined with the addition of LdT. 2016 Oncotarget Figure HBV D134N;L145M;F151Y;S223A 46;87;127;170 51;92;132;175 RT;RT;RT;RT 44;85;125;168 46;87;127;170 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtA181T and rtN236T mutations increased during ADV monotherapy and declined when LdT was added, but the fluctuations were minor. 2016 Oncotarget Figure HBV A181T;N236T 25;37 30;42 RT;RT 23;35 25;37 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtA181V and rtN236T mutations in the HBV RT region were significantly elevated (up to 84.35% and 67.67%, respectively) after two years of ADV monotherapy and did not decreased after the addition of LdT. 2016 Oncotarget Figure HBV A181V;N236T 25;37 30;42 RT;RT;RT 23;35;64 25;37;66 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtI224V, rtS223A, rtD134E mutations slowly increased after 4 years of treatment. 2016 Oncotarget Figure HBV I224V;S223A;D134E 25;34;43 30;39;48 RT;RT;RT 23;32;41 25;34;43 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequencies of the rtL180M and rtM204V mutations fluctuated slightly in combination with LdT. 2016 Oncotarget Figure HBV L180M;M204V 25;37 30;42 RT;RT 23;35 25;37 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtA181T mutation was more than 10% after 4 years of treatment. 2016 Oncotarget Figure HBV A181T 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The frequency of the rtI224V mutation was always high (70~80%). 2016 Oncotarget Figure HBV I224V 23 28 RT 21 23 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. This patient harbored the rtA181T (1.2%), rtN236T (1.8%), rtS202G (1.1%), and rtM204I/V (1.1%) substitutions, and other resistance mutations were present at low levels (<1%) at baseline. 2016 Oncotarget Figure HBV A181T;N236T;M204I;M204V;S202G 28;44;80;80;60 33;49;87;87;65 RT;RT;RT;RT 26;42;58;78 28;44;60;80 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. This patient harbored the rtA181T (1.3%) and rtN236T (1.6%) substitutions at baseline, and other resistance mutations were present at low levels (<1%). 2016 Oncotarget Figure HBV A181T;N236T 28;47 33;52 RT;RT 26;45 28;47 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. This phenomenon usually appeared in non-resistance mutations of rtS223A (ranging from 79.67% to 4.41%) and rtN248H (ranging from 72.38% to 5.03%). 2016 Oncotarget Figure HBV S223A;N248H 66;109 71;114 RT;RT 64;107 66;109 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. A, RMSD and B, Rg Plots of the G145R Mutant and Wild-Type HBsAg. 2016 Hepatitis monthly Figure HBV G145R 31 36 S 58 63 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. A, Superposition of the wild-type HBsAg (blue) and the G145R mutant (gray). 2016 Hepatitis monthly Figure HBV G145R 55 60 S 34 39 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Analysis of HBsAg Antigenicity in the A, Wild-type and B, G145R Mutant Proteins. 2016 Hepatitis monthly Figure HBV G145R 58 63 S 12 17 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. ASA Plots of the G145R Mutant and Wild-Type HBsAg after 10-ns MD Simulations. 2016 Hepatitis monthly Figure HBV G145R 17 22 S 44 49 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. B, Representative positioning of the H-bond between the R145 and C147 mutation in the 3D structure of the G145R mutant HBsAg. 2016 Hepatitis monthly Figure HBV G145R 106 111 S 119 124 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Representation of the A, Wild and B, G145R Mutant HBsAg-MAb12 Interaction. 2016 Hepatitis monthly Figure HBV G145R 37 42 S 50 55 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. RMSF Plots of Wild- and G145R Mutant Types after 10-ns MD Simulations. 2016 Hepatitis monthly Figure HBV G145R 24 29 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The Effect of G145R Substitution on the Secondary Structure of the Wild-Type (Up) and G145R (Down) Mutations. 2016 Hepatitis monthly Figure HBV G145R;G145R 14;86 19;91 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Transmembrane Analysis of the A, Wild-Type and B, G145R Mutant HBsAg. 2016 Hepatitis monthly Figure HBV G145R 50 55 S 63 68 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. (A) Amino acid alignment of the wild-type HBsAgs (W1S, W3S and adr4 [X01587]) with other published sequences (adw [AF100308], adw [AY220698.1], ayr [AY38845.1] and ayw [DQ336692.1]). 2017 PloS one Figure HBV W1S;W3S 50;55 53;58 S 42 48 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. (B) The amino acid (aa) sequence alignment of the wild-type (W1S and W3S) and different mutants of HBsAg. 2017 PloS one Figure HBV W1S;W3S 61;69 64;72 S 99 104 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. All the mutants of W3S and wild-type HBsAgs (W1S and W3S) were expressed by transient transfection in HEK 293-T cells. 2017 PloS one Figure HBV W3S;W1S;W3S 19;45;53 22;48;56 S 37 43 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. All the wild-type HBsAgs (W1S, W3S and adr4) were expressed by transient transfection in HEK 293-T cells. 2017 PloS one Figure HBV W1S;W3S 26;31 29;34 S 18 24 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. HEK293-T cells were transfected with plasmid vectors expressing the wild-type HBsAgs (W1S, W3S and adr4). 2017 PloS one Figure HBV W1S;W3S 86;91 89;94 S 78 84 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Reactivity of HBsAg (W1S, W3S and adr4) with a commercial ELISA and an anti-tag Ab. 2017 PloS one Figure HBV W1S;W3S 21;26 24;29 S 14 19 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The amino acid residues identical to those of HBsAg (W1S) are indicated by dots. 2017 PloS one Figure HBV W1S 53 56 S 46 51 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The HEK 293-T cells were transfected with plasmid vectors expressing the wild-type and mutants of W3S and W1S HBsAg. 2017 PloS one Figure HBV W3S;W1S 98;106 101;109 S 110 115 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The OD values of HBsAg ELISA and anti-tag reactivity (except W1S N146G from the culture supernatant) were normalized by the ratios of densitometric intensity of Western blotting compared to W1S, except W1S Q129R/G145R from the supernatants, since this mutant exhibited a remarkable loss in secretion ability (Fig 4A). 2017 PloS one Figure HBV G145R;W1S;W1S;W1S;N146G;Q129R 212;61;190;202;65;206 217;64;193;205;70;211 S 17 22 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The OD values of HBsAg ELISA and the anti-tag reactivity were normalized by the ratios of densitometric intensity of the Western blotting compared to W1S (Fig 2A). 2017 PloS one Figure HBV W1S 150 153 S 17 22 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The reactivity of HBsAgs was presented as the percentage of the OD450-630 of samples compared to W1S in all cases (A, B, C and D). 2017 PloS one Figure HBV W1S 97 100 S 18 24 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. The reactivity of HBsAgs was presented as the percentage of the OD450-630 of samples compared to W1S. 2017 PloS one Figure HBV W1S 97 100 S 18 24 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The graph reports the intra-patient prevalence of sP203Q (white dots), sS210R (grey dots), sP203Q+sS210R (black dots) for each patient in the HCC group (N=13) A. 2017 Oncotarget Figure HBV P203Q;S210R;P203Q;S210R 50;71;91;98 56;77;97;104 S;S;S;S 50;71;91;98 51;72;92;99 Hepatocellular carcinoma 142 145 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The histogram reports HBsAg secretion factor for the wild-type virus and for mutants carrying P203Q, S210R and P203Q+S210R. 2017 Oncotarget Figure HBV P203Q;S210R;P203Q;S210R 94;101;111;117 99;106;116;122 S 22 27 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The histogram reports the prevalence of sP203Q, sS210R, and sP203Q+sS210R in 23 HBV-induced HCC patients and in 105 chronically HBV-infected patients (CHB patients) (used as reference group) 2017 Oncotarget Figure HBV P203Q;S210R 60;67 66;73 S;S;S;S 40;48;60;67 41;49;61;68 Hepatocellular carcinoma;Chronic Hepatitis B;HBV infections 92;151;128 95;154;140 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The histogram reports the prevalence of sP203Q, sS210R, and sP203Q+sS210R in 23 HBV-induced HCC patients and in 105 chronically HBV-infected patients (CHB patients) (used as reference group). 2017 Oncotarget Figure HBV P203Q;S210R;P203Q;S210R 40;48;60;67 46;54;66;73 S;S;S;S 40;48;60;67 41;49;61;68 Hepatocellular carcinoma;Chronic Hepatitis B;HBV infections 92;151;128 95;154;140 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Expression of hepatitis B virus DNA and antigens after transfection of Huh 7 cells with wild type hepatitis B virus genotype D clone (WT) and mutants with S gene mutations P120T (120T) and S143L (143L). 2017 World journal of hepatology Figure HBV P120T;S143L 172;189 177;194 S 155 156 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. (A) Odds ratios (OR) of hepatocellular carcinoma (HCC) for G1896A. 2017 Medicine Figure HBV G1896A 59 65 Hepatocellular carcinoma;Hepatocellular carcinoma 24;50 48;53 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. (B) OR of HCC for A1762T. 2017 Medicine Figure HBV A1762T 18 24 Hepatocellular carcinoma 10 13 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. (C) OR of HCC for G1764A. 2017 Medicine Figure HBV G1764A 18 24 Hepatocellular carcinoma 10 13 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. (D) OR of HCC for A1762T/G1764A double mutation. 2017 Medicine Figure HBV G1764A;A1762T 25;18 31;24 Hepatocellular carcinoma 10 13 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Galbraith plots for heterogeneity test of G1896A, A1762T, G1764A, and A1762T/G1764A double mutation. 2017 Medicine Figure HBV G1764A;G1896A;A1762T;G1764A;A1762T 77;42;50;58;70 83;48;56;64;76 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. (a) HBx mRNA levels in HBx (WT)-transgenic Tg and HBx (C1485T)-Tg mice. 2017 Scientific reports Figure HBV C1485T 55 61 X;X;X 4;23;50 7;26;53 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. (c) The number of tumors in each male mouse is represented as a circle in control non-Tg mice, as a square in HBx (WT) mice and as a triangle in HBx (C1485T) mice in the graph. 2017 Scientific reports Figure HBV C1485T 150 156 X;X 110;145 113;148 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Attenuation of NF-kappaB activation in the liver of C1485T-HBx transgenic mice. 2017 Scientific reports Figure HBV C1485T 52 58 X 59 62 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Enhanced proliferation and cell cycle progression in HBx C1485T-transgenic mice. 2017 Scientific reports Figure HBV C1485T 57 63 X 53 56 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Enhancement of GSK3beta and Wnt activation in the liver of C1485T-HBx transgenic mice. 2017 Scientific reports Figure HBV C1485T 59 65 X 66 69 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Frequencies of C1485T (a) and C1653T (b) mutations in non-LC and LC cases. 2017 Scientific reports Figure HBV C1485T;C1653T 15;30 21;36 Liver cirrhosis;Liver cirrhosis 65;58 67;60 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Frequencies of C1485T and C1653T mutation in non-LC and LC cases. 2017 Scientific reports Figure HBV C1485T;C1653T 15;26 21;32 Liver cirrhosis;Liver cirrhosis 56;49 58;51 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. HepG2 cells were transfected with expression vector of wild type HBx (dark gray), C1485T HBx (black), or an empty vector (white). 2017 Scientific reports Figure HBV C1485T 82 88 X;X 65;89 68;92 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Lane 1, 2; control non-Tg mice, lane 3, 4; HBx wild type transgenic mice, lane 5, 6; HBx C1485T transgenic mice. 2017 Scientific reports Figure HBV C1485T 89 95 X;X 43;85 46;88 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Liver were obtained from 6 weeks old male HBx-WT Tg mice and HBx-C1485T-Tg mice. 2017 Scientific reports Figure HBV C1485T 65 71 X;X 42;61 45;64 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Male control non-Tg mice, male HBx-WT Tg mice (Tg line 1), and male HBX-C1485T-Tg mice (Tg line 1) were treated with intraperitoneal injection of diethylnitrosamine (DEN, 100 mg/kg) and liver tissues were obtained 4 hours later. 2017 Scientific reports Figure HBV C1485T 72 78 X;X 31;68 34;71 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Male control non-Tg mice, male HBx-WT Tg mice (Tg line 1), and male HBX-C1485T-Tg mice (Tg line 1) were treated with intraperitoneal injection of diethylnitrosamine (DEN, 100 mg/kg). 2017 Scientific reports Figure HBV C1485T 72 78 X;X 31;68 34;71 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Male control non-Tg mice, male HBx-WT Tg mice, and male HBX-C1485T-Tg mice were treated with intraperitoneal injection of diethylnitrosamine (DEN, 25 mg/kg) and then the incidence of liver tumors was determined 8 months after the injection (n = 8-13). 2017 Scientific reports Figure HBV C1485T 60 66 X;X 31;56 34;59 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. a The incidence of A1762T/G1764A dual mutations was significantly higher in HBeAg negative hepatitis group than in both HBeAg positive (****p < 0.0001) and HBeAg negative ACLF-CHB groups (****p < 0.0001) and immune active group (*p < 0.05). 2017 Virology journal Figure HBV G1764A;A1762T 26;19 32;25 C;C;C 76;120;156 81;125;161 Chronic Hepatitis B;Hepatitis 176;91 179;100 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. b The incidence of G1896A mutation in HBV PC region was significantly more frequent in HBeAg negative hepatitis group than in both ACLF-CHB groups (****p < 0.0001) and immune active group (****p < 0.0001) 2017 Virology journal Figure HBV G1896A 19 25 C;Precore 87;42 92;44 Chronic Hepatitis B;Hepatitis 136;102 139;111 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. b The incidence of G1896A mutation in HBV PC region was significantly more frequent in HBeAg negative hepatitis group than in both ACLF-CHB groups (****p < 0.0001) and immune active group (****p < 0.0001). 2017 Virology journal Figure HBV G1896A 19 25 C;Precore 87;42 92;44 Chronic Hepatitis B;Hepatitis 136;102 139;111 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The median incidence of A1762T/G1764A dual mutations in HBV basal core promoter (BCP) region and G1896A mutation in HBV precore (PC) region among different groups (ACLF-CHB, immune active & HBeAg negative hepatitis CHB groups). 2017 Virology journal Figure HBV G1764A;A1762T;G1896A 31;24;97 37;30;103 BCP;BCP;C;Precore;Precore 60;81;190;129;120 79;84;195;131;127 Chronic Hepatitis B 169 172 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. *The translational or the Kozak sequence mutants include T1809G, C1810A/T, A1811C and T1812C. 2018 PloS one Figure HBV C1810T;T1809G;C1810A;A1811C;T1812C 65;57;65;75;86 73;63;73;81;92 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Prevalence comparison of the major BCP and PC mutations affecting HBeAg expression at the transcriptional (A1762T/G1764A), translational (nt 1809-1812), PC initiation (nt 1814-1816), stop codon G1896A (with C1858T) or post translational levels (G1862T) among study groups (Fig 2A) and HBeAg status (Fig 2B). 2018 PloS one Figure HBV G1764A;A1762T;G1896A;C1858T;G1862T 114;107;194;207;245 120;113;200;213;251 BCP;C;C;Precore;Precore 35;66;285;43;153 38;71;290;45;155 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. A: A plasmid map of pHY92 vector containing a copy of the 1.1x-unit length HBV genome under the control of a CMV promoter; B: The HBV full genome construct with a W4P missense mutation in the preS1 region; C: Screening of the constructed W4P TG mice by PCR targeting the preS1 region. 2018 World journal of gastroenterology Figure HBV W4P;W4P 163;238 166;241 PreS1;PreS1 192;271 197;276 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. A: Comparison of generated lipid droplets in the liver section by hematoxylin-eosin staining (x 200); B: Incidence of lipid droplets in W4P mutant mice (males: 24 mice; females: 18 mice) and non TG littermates (males: 17 mice; females: 15 mice) at 10 mo of age. 2018 World journal of gastroenterology Figure HBV W4P 136 139 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. A: Comparison of LHBs level in liver section by IHC analysis using anti-preS1 antibodies between W4P TG male and female mice (x 200); B: Comparison of HBsAg level in the liver and serum from W4P mutant mice (males: 24 mice; females: 18 mice) and nonTG littermates (males: 17 mice; females: 15 mice) at 10 mo of age (cP < 0.001 vs W4P male, one-way ANOVA). 2018 World journal of gastroenterology Figure HBV W4P;W4P;W4P 97;191;330 100;194;333 S;S;PreS1 151;17;72 156;21;77 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. A: In situ view of liver of W4P TG male mice and W4P TG female mice at 10 mo of age; B: Liver weight ratio against the total body weight (mg) in W4P mutant mice (males: 24 mice; females: 18 mice) and nonTG littermates (males: 17 mice; females: 15 mice) at 10 mo of age (aP < 0.05, bP < 0.01, and cP < 0.001 vs W4P male, one-way ANOVA. 2018 World journal of gastroenterology Figure HBV W4P;W4P;W4P;W4P 28;49;145;310 31;52;148;313 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Construction of the W4P TG mice expressing pHY92-1.1x the HBV full genome with the preS1 W4P mutation and the screening of the constructed W4P TG mice. 2018 World journal of gastroenterology Figure HBV W4P;W4P;W4P 20;89;139 23;92;142 PreS1 83 88 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Increased generation of lipid droplets in W4P male TG mice. 2018 World journal of gastroenterology Figure HBV W4P 42 45 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Increased hepatomegaly in the W4P male TG mice. 2018 World journal of gastroenterology Figure HBV W4P 30 33 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Increased secreted HBsAg level and liver LHBs in W4P male TG mice. 2018 World journal of gastroenterology Figure HBV W4P 49 52 S;S 19;41 24;45 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Secreted interleukin-6 levels in the W4P TG mice (males: 24 mice; females: 18 mice) and nonTG littermates (males: 17 mice; females: 15 mice) at 10 mo of age. 2018 World journal of gastroenterology Figure HBV W4P 37 40 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Serum alanine aminotransferase (A) and aspartate transaminase (B) levels in W4P TG mice (males: 24 mice; females: 18 mice) and nonTG littermates (males: 17 mice; females: 15 mice) at 10 mo of age. 2018 World journal of gastroenterology Figure HBV W4P 76 79 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. HBV rtA181T/sW172* mutant regulates key molecules expression involved in TGF-beta/Smad pathways. 2018 Virology journal Figure HBV W172X;A181T 12;6 18;11 RT;S 4;12 6;13 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The ratio of cell clones were less than 30% in L02-pHBV4.1-HBs(wt) (a) and L02-pHBV4.1-HBs(sW172L) (b), but well formed with a ratio of 60% in L02-pHBV4.1-HBs(sW172*) cell clones (c). 2018 Virology journal Figure HBV W172X;W172L 159;91 165;97 S;S;S;S;S 59;87;155;91;159 62;90;158;92;160 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. The tumor volume was significantly higher in nude mice with pHBV4.1-HBs(sW172*) or pcDNA3.1-HBs(sW172*) as compared to other groups. 2018 Virology journal Figure HBV W172X;W172X 72;96 78;102 S;S;S;S 68;92;72;96 71;95;73;97 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Though the ratio of cell clones were less than 20% in either L02-pcDNA3.1 (d), L02-pcDNA-HBs(wt) (e), L02-pcDNA-HBs(sW172L) (f) and L02-pcDNA-HBs(sW172*) (g), the ratio of cell clones was more in L02-pcDNA-HBs(sW172*) than in other three groups. 2018 Virology journal Figure HBV W172L;W172X;W172X 116;146;210 122;152;216 S;S;S;S;S;S;S 89;112;142;206;116;146;210 92;115;145;209;117;147;211 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Immune-associated escape mutations (sQ101K, sT114R, sP120S/T/A, sT123A/N, sT126N/S, sP127L, sA128V, sQ129R/N, sG130N/R, sT131I, sM133I/L/T, sY134L, sC138Y, sC139S, sT140S, sP142S, sD144A/E, sG145A/R, sN146S) were retrieved from literature and known to affect HBsAg recognition by antibodies [2, 13, 14, 39-47]. 2018 BMC infectious diseases Figure HBV Q101K;T114R;P120S;P120T;P120A;T123A;T123N;T126N;T126S;P127L;A128V;Q129R;Q129N;G130N;G130R;T131I;M133I;M133L;M133T;Y134L;C138Y;C139S;T140S;P142S;D144A;D144E;G145A;G145R;N146S 36;44;52;52;52;64;64;74;74;84;92;100;100;110;110;120;128;128;128;140;148;156;164;172;180;180;190;190;200 42;50;62;62;62;72;72;82;82;90;98;108;108;118;118;126;138;138;138;146;154;162;170;178;188;188;198;198;206 S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S;S 259;36;44;52;64;74;84;92;100;110;120;128;140;148;156;164;172;180;190;200 264;37;45;53;65;75;85;93;101;111;121;129;141;149;157;165;173;181;191;201 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. The NA-induced immune-escape mutations I195M, I196S, and E164D result from drug-resistance mutation M204 V, M204I, and V173 L (Torresi, 2002) 2018 BMC infectious diseases Figure HBV I195M;I196S;E164D;M204V;M204I;V173L 39;46;57;100;108;119 44;51;62;106;113;125 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. The NA-induced immune-escape mutations I195M, I196S, and E164D result from drug-resistance mutation M204 V, M204I, and V173 L (Torresi, 2002). 2018 BMC infectious diseases Figure HBV I195M;I196S;E164D;M204I 39;46;57;108 44;51;62;113 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. (D) Huh7 cells were transfected with empty vector, HBx-wt, HBx-S31A, or HBx-S31D mutant plasmid, and the transfection efficiency was determined with Western blotting using antiflag antibody. 2018 Cancer medicine Figure HBV S31A;S31D 63;76 67;80 X;X;X 51;59;72 54;62;75 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Sequencing chromatogram showing wild type in upper panel and G1896A mutation in lower. 2018 Saudi journal of biological sciences Figure HBV G1896A 61 67 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. (C) The reactivated viral clones in four cases (R4, R6, R7, and R12) of the non-HSCT group were variants with the M1I/V substitution at the PreS2 start codon, which resulted in the ablation of the middle S protein. 2018 Scientific reports Figure HBV M1I;M1V 114;114 119;119 S;PreS2 197;140 205;145 Hematopoietic stem cell transplantation 80 84 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. A case (R22) that acquired an immune escape mutation, sG145A, in the small S protein during the process of HBV reactivation. 2018 Scientific reports Figure HBV G145A 54 60 S;S 54;69 55;76 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. The frequency of sG145A variants in four serum samples at different time-points, analyzed by ultra-deep sequencing, is shown in the lower panel. 2018 Scientific reports Figure HBV G145A 17 23 S 17 18 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. (A) Analysis for 22 RT sequences containing rtL180M+A181C+M204V mutations from the 18 patients. 2019 Emerging microbes & infections Figure HBV L180M;A181C;M204V 46;52;58 51;57;63 RT;RT 20;44 22;46 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Phylogenetic tree analysis for HBV RT sequences from rtA181C-positive patients. 2019 Emerging microbes & infections Figure HBV A181C 55 60 RT;RT 35;53 37;55 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Two classical entecavir-resistance mutants (rtL180M+S202G+M204V, rtL180M+T184A+M204V) and one wild-type strain (WT2) from another entecavir-refractory patient were taken as references for the analysis (left part). 2019 Emerging microbes & infections Figure HBV L180M;L180M;S202G;M204V;M204V;T184A 46;67;52;58;79;73 51;72;57;63;84;78 RT;RT 44;65 46;67 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. (A) Huh-7 cells were cotransfected with the reporter construct along with vector, wild-type LHBs or sW182* mutant. 2019 PloS one Figure HBV W182X 100 106 S;S 92;100 96;101 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. (A) Huh-7 cells were cotransfected with vector, wild-type LHBs or sW182* mutant, and Flag-p53, Smad4-HA or 6xMyc-Smad3. 2019 PloS one Figure HBV W182X 66 72 S;S 58;66 62;67 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. (B) HepG2 and Huh-7 cells were transfected with control vector, 6xHis-tagged wild-type (full length) LHBs (WT) or sW182* mutant (MT) using different transfection reagents Lipofectamine LTX, R1, 2, 3). 2019 PloS one Figure HBV W182X 114 120 S;S 101;114 105;115 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. (E) Huh-7 cells were transfected with siRNA (a control (Scr) and two for Jab1 (#1 and 2)), followed by the expression constructs for sW182* mutant and Flag-p53 or Smad4-HA. 2019 PloS one Figure HBV W182X 133 139 S 133 134 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. A nonsense mutation at the codons for L95, W182 and L216 resulted in sL95*, sW182* and sL216*, respectively. 2019 PloS one Figure HBV L95X;W182X;L216X 69;76;87 74;82;93 S;S;S 69;76;87 70;77;88 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Effect of the LHBs sW182* mutant on downstream target genes of p53 and Smad4. 2019 PloS one Figure HBV W182X 19 25 S;S 14;19 18;20 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Expression of the LHBs sW182* truncation mutant in cultured liver cells. 2019 PloS one Figure HBV W182X 23 29 S;S 18;23 22;24 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Expression of the LHBs sW182* truncation mutant in hepatocytes in the living mouse liver. 2019 PloS one Figure HBV W182X 23 29 S;S 18;23 22;24 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Left panel, wild-type LHBs; right panel, sW182*. 2019 PloS one Figure HBV W182X 41 47 S;S 22;41 26;42 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Lower panel: Flag-tagged Jab1 and 6xHis-Myc-tagged wild-type LHBs or sW182* mutant were co-expressed in HK293T cells. 2019 PloS one Figure HBV W182X 69 75 S;S 61;69 65;70 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Physical interaction between Jab1 and the sW182* truncation mutant, but not wild-type LHBs. 2019 PloS one Figure HBV W182X 42 48 S;S 86;42 90;43 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Proteasome- and Jab1-dependent downregulation of tumor suppressors p53 and Smad4 by the LHBs sW182* mutant. 2019 PloS one Figure HBV W182X 93 99 S;S 88;93 92;94 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The precipitated sW182* protein is indicated by an arrowhead. 2019 PloS one Figure HBV W182X 17 23 S 17 18 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Upper panel: Flag-tagged wild-type LHBs or sW182* mutant expressed in HK293T cells was pulled down with GST-Jab1-beads. 2019 PloS one Figure HBV W182X 43 49 S;S 35;43 39;44 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. The bars above the 6272 graph show the percentage of codons with the HBsAg D144N mutation. 2019 Virology journal Figure HBV D144N 75 80 S 69 74 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. a A schematic diagram showing the structure of the pre-S1 promoter and the wild type (WT), G2765A (m5), and whole nucleotide mutation (m9) nucleotide sequences of the Sp1 region. 2019 Virology journal Figure HBV G2765A 91 97 S1 promoter;S1 promoter 51;167 66;170 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. A mutation in the pre-S1 promoter region Sp1 reduced transcription activity: (a-e) The levels of luciferase activity, mRNA expression, and protein expression of pre-S1 were evaluated using vectors containing the wild-type (WT), G2765A substitution (m5), and whole nucleotide mutation (m9) sequences. 2019 Virology journal Figure HBV G2765A 228 234 PreS1;S1 promoter;S1 promoter 161;18;41 167;33;44 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. c The G2765A substitution ratio and the HBV DNA viral load showed a negative correlation, and (d) the G2765A substitution ratio and the HBsAg level showed a weak negative correlation. 2019 Virology journal Figure HBV G2765A;G2765A 6;102 12;108 S 136 141 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. f-k The wild-type (WT) or G2765A (m5) 1.3-fold HBV genome vector was transfected into HepG2 cells. 2019 Virology journal Figure HBV G2765A 26 32 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. (A) The prevalence of mutations associated to M204I or V. 2019 Scientific reports Figure HBV M204I 46 51 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. The asterisk on the left of the mutation sites indicate significant differences in the mutations associated to M204I or V. 2019 Scientific reports Figure HBV M204I 111 116 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. (A) HepG2 cells seeded in the insert of trans-well were transfected with HBV WT and sC69* + pLMS, respectively. 2019 Frontiers in microbiology Figure HBV C69X 84 89 S 84 85 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. (A) Schematic workflow for detecting identifying ISGs expression during HBV and sC69* + pLMS infection with IFNbeta treatment. 2019 Frontiers in microbiology Figure HBV C69X 80 85 S 80 81 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. (A) Schematic workflow for detecting ISGs expression during HBV WT and sC69* + pLMS infection with poly (I:C) treatment in HepG2-NTCP cells. 2019 Frontiers in microbiology Figure HBV C69X 71 76 S 71 72 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. (A) The schematic illustration of HBV WT and sC69* + pLMS infection. 2019 Frontiers in microbiology Figure HBV C69X 45 50 S 45 46 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. (B) Immunofluorescent microscopy of HBcAg in the WT, sC69* and sC69* + pLMS infection, scale bars: 100 mum. 2019 Frontiers in microbiology Figure HBV C69X;C69X 53;63 58;68 C;S;S 36;53;63 41;54;64 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Briefly, we collected virions from HBV WT and sC69* + pLMS transfections that were used to, infect HepG2-NTCP cells with 10 mug/ml poly (I:C) during the infection and measured the viral and ISGs related marker 0.5, 1, 2, 4, and 6 days post-infection. 2019 Frontiers in microbiology Figure HBV C69X 46 51 S 46 47 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. HepG2 cells seeded in the insert of trans-well were transfected with HBV WT, sC69* and sC69* + pLMS, respectively. 2019 Frontiers in microbiology Figure HBV C69X;C69X 77;87 82;92 S;S 77;87 78;88 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The HepG2-NTCP cells were infected by viruses of WT or sC69* + pLMS and treated with 500 U/ml of IFNbeta during the infection. 2019 Frontiers in microbiology Figure HBV C69X 55 60 S 55 56 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* has no impact on IFNbeta induction of ISGs expression. 2019 Frontiers in microbiology Figure HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant attenuates the poly (I:C) inducing host immune response in HepG2-NTCP cells. 2019 Frontiers in microbiology Figure HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant inhibits host innate immune response compared to HBV WT in HepG2-NTCP cells. 2019 Frontiers in microbiology Figure HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant inhibits host innate immune response compared to HBV WT in trans-well system. 2019 Frontiers in microbiology Figure HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The truncated protein of sC69* attenuates the host innate immune response. 2019 Frontiers in microbiology Figure HBV C69X 25 30 S 25 26 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The viral infectivity affected by sC69* substitution could be rescued when co-existence with wild-type (WT) HBsAg. 2019 Frontiers in microbiology Figure HBV C69X 34 39 S;S 108;34 113;35 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We transfected HBV WT and sC69* + pLMS plasmid into HepG2 cells and washed the cells with PBS the next day. 2019 Frontiers in microbiology Figure HBV C69X 26 31 S 26 27 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. (b) Patients with high C1817T and A1838G variant frequency (based on 10% cutoff, see methods) had significantly lower HBV DNA levels. 2019 Scientific reports Figure HBV C1817T;A1838G 23;34 29;40 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Black box highlights HBeAg negative patients without detectable viral G1896A variant. 2019 Scientific reports Figure HBV G1896A 70 76 C 21 26 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Columns (patients, N = 1102) are ordered by HBeAg status and by G1896A frequency. 2019 Scientific reports Figure HBV G1896A 64 70 C 44 49 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. The green box highlights HBeAg positive patients with a high frequency of viral G1896A variant. 2019 Scientific reports Figure HBV G1896A 80 86 C 25 30 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. Second, IFN-I mediated enhanced expression of APOBEC3G and iNOS can lead to HBeAg negative infection and liver disease progression via frequent generation of preC mutations at 1896 (G to A). 2019 Frontiers in immunology Figure HBV G1896A 176 189 C;Precore 76;158 81;162 Liver disease 105 118 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. C1653T, T1753V, A1762T/G1764A exist in Enhancer II and the Basal Core Promoter. 2019 Scientific reports Figure HBV G1764A;C1653T;T1753V;A1762T 23;0;8;16 29;6;14;22 BCP;Enh II 59;39 78;50 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The rates of combination mutation at C1653T or T1753V and A1762T/G1764A were also raised significantly according to liver disease progression (among 3 groups P < 0.001; posthoc pairwise ASC vs CH P < 0.001, ASC vs LC/HCC P < 0.001, CH vs LC/HCC P < 0.001). 2019 Scientific reports Figure HBV G1764A;C1653T;T1753V;A1762T 65;37;47;58 71;43;53;64 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 116;217;241;214;238 129;220;244;216;240 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The rates of double mutation at A1762T/G1764A and combination mutation at C1653T and/or T1753V and A1762T/G1764A by liver disease status in 340 genotype C1 strains and Cambodian isolates. 2019 Scientific reports Figure HBV G1764A;G1764A;A1762T;C1653T;T1753V;A1762T 39;106;32;74;88;99 45;112;38;80;94;105 Liver disease 116 129 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The rates of double mutation at A1762T/G1764A were raised significantly according to liver disease progression (among 3 groups P < 0.001; posthoc pairwise ASC vs CH P < 0.001, ASC vs LC/HCC P < 0.001, CH vs LC/HCC P < 0.001). 2019 Scientific reports Figure HBV G1764A;A1762T 39;32 45;38 Liver disease;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 85;186;210;183;207 98;189;213;185;209 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. (a, b) CONTIN analysis of DLS studies reflected the growth of capsid from WT (a) and D2N/D4N (b) dimers with the addition of K. 2018 ACS omega Figure HBV D4N;D2N 89;85 92;88 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. (a) Effect of pH (charge) on assembly kinetics of WT and D2N/D4N proteins (Tris buffer covers pH 7.5-8.5; NaHCO3 buffer used at pH 9.6). 2018 ACS omega Figure HBV D4N;D2N 61;57 64;60 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. (a) Size exclusion chromatography (SEC) analysis of Cp1492 capsid assembly for 1.0 mg mL-1 WT and 1.0 mg mL-1 D2N/D4N protein solutions in low salt (0.2 M KCl) or high salt (0.7 M KCl) pH 7.5 buffer. 2018 ACS omega Figure HBV D4N;D2N 114;110 117;113 Capsid;C 59;52 65;54 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. (b) Final scattered intensity increment of WT and D2N/D4N capsid assemblies as a function of KCl concentration in pH 7.5 HEPES buffer after reaching equilibrium. 2018 ACS omega Figure HBV D4N;D2N 54;50 57;53 Capsid 58 64 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. A mutant ((b) D2N/D4N) was created by replacing the 2nd and 4th Asp with neutral Asn (shown as sticks) to reduce the overall charge density on a dimer. 2018 ACS omega Figure HBV D4N;D2N 18;14 21;17 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. TEM images of WT capsids (a) and D2N/D4N capsids (b) assembled at pH 7.5 with HEPES buffer containing 1.0 M KCl at room temperature. 2018 ACS omega Figure HBV D4N;D2N 37;33 40;36 Capsid;Capsid 17;41 24;48 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The assemblies in this plot were all prepared in Tris buffer; (d) the free energy per contact of the charge-matched WT and D2N/D4N capsids formation. 2018 ACS omega Figure HBV D4N;D2N 127;123 130;126 Capsid 131 138 31458664 Role of Protein Charge Density on Hepatitis B Virus Capsid Formation. The y-axis GammaG(Gamma) denotes the relative contribution to the total scattered intensity due to the particles with a given Rh; (c-e) time-resolved intensity increment of WT and D2N/D4N capsid formation with a single aliquot addition of K+ to reach 0.2 M (protein concentration 2.0 mg mL-1), 0.5 M (protein concentration 1.0 mg mL-1), and 0.7 M (protein concentration 1.0 mg mL-1) at pH 7.5. 2018 ACS omega Figure HBV D4N;D2N 184;180 187;183 Capsid 188 194 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (A) Extracellular HBV DNAs were prepared directly from equal volumes of mouse sera of WT and mutant I97L injections before Southern blot analysis. 2019 Journal of virology Figure HBV I97L 100 104 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (A) IFN-alpha receptor knockout (IFNAR-/-) mice were hydrodynamically injected with 30 mug of DNA of WT or mutant I97L HBV. 2019 Journal of virology Figure HBV I97L 114 118 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (A) Liver samples were collected at 3 days or 1 week after the hydrodynamic injection of 14 mug of HBV plasmid DNAs of WT or mutant I97L. 2019 Journal of virology Figure HBV I97L 132 136 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (B) The serum HBeAg titers in mice receiving WT or I97L DNAs were determined at the indicated time points with an enzyme immunoassay (see Materials and Methods). 2019 Journal of virology Figure HBV I97L 52 56 C 14 19 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (C) More rapid decay of viral DNA of mutant I97L in hepatocytes was observed by hydrodynamic delivery. 2019 Journal of virology Figure HBV I97L 44 48 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (E) Detection of only slightly reduced amounts of HBV core protein in the liver lysates of mutant I97L by Western blotting. 2019 Journal of virology Figure HBV I97L 98 102 C 54 58 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. (Upper right panel) A faster decline rate of mutant I97L SS DNA was observed in a time course experiment. 2019 Journal of virology Figure HBV I97L 52 56 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. **, the minor difference in the mobility of SS DNA between WT and I97L (lanes 1 and 2) is not reproducible, probably due to experimental variation in salt concentrations between these two particular samples. 2019 Journal of virology Figure HBV I97L 66 70 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Although the viral DNA levels were comparable between 10 mug of WT and 30 mug of I97L at 3 dpi (left panel), no viral DNA signal of I97L was detectable at 2 weeks postinjection (right panel). 2019 Journal of virology Figure HBV I97L;I97L 81;132 85;136 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. An immature secretion phenotype of HBc mutant I97L in tissue culture was recapitulated in this in vivo experimental setting. 2019 Journal of virology Figure HBV I97L 46 50 C 35 38 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. As described above, liver samples were collected for Southern and Northern blot analysis at 3 days or 2 weeks after the hydrodynamic injections of 10 mug of WT or 30 mug of mutant I97L HBV DNA. 2019 Journal of virology Figure HBV I97L 180 184 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. As highlighted by a red asterisk, fully mature full-length RC DNAs (lanes 2 and 4) in mutant I97L virions were significantly reduced. 2019 Journal of virology Figure HBV I97L 93 97 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. At different time points postinjection into NOD/SCID mice, intracellular core-associated HBV DNA in the liver (upper panel) and extracellular HBV DNA in the sera (lower panel) were compared between WT HBV and mutant I97L by Southern blotting. 2019 Journal of virology Figure HBV I97L 216 220 C 73 77 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. BALB/c mice were hydrodynamically injected with 30 mug of plasmid DNAs of a WT HBV (adr) or mutant I97L. 2019 Journal of virology Figure HBV I97L 99 103 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. BALB/c mice were hydrodynamically injected with four different HBV constructs (WT, I97L, P130T, and I97L/P130T). 2019 Journal of virology Figure HBV P130T;I97L;P130T;I97L 105;83;89;100 110;87;94;104 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Both intracellular and extracellular viral DNAs were compared among four different groups of BALB/c mice hydrodynamically injected with 30 mug of plasmid DNAs of WT, mutant I97L, mutant P130T, and double mutant I97L/P130T, respectively. 2019 Journal of virology Figure HBV P130T;I97L;P130T;I97L 216;173;186;211 221;177;191;215 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. HBc mutant I97L exhibited an immature secretion phenotype by in vivo hydrodynamic delivery. 2019 Journal of virology Figure HBV I97L 11 15 C 0 3 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. HBV core variants I97L and P130T exhibited abnormal behaviors in viral DNA synthesis and virion secretion. 2019 Journal of virology Figure HBV I97L;P130T 18;27 22;32 C 4 8 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In the bottom panel, poor persistence of I97L viral DNA was not rescued by P130T at 1 week postinjection (lane 6 versus lane 8). 2019 Journal of virology Figure HBV I97L;P130T 41;75 45;80 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In the middle panel, mutation I97L resulted in higher levels of extracellular virions at 3 dpi by native agarose gel and Western blot analysis with anti-core antibody. 2019 Journal of virology Figure HBV I97L 30 34 C 153 157 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Intracellular viral DNA of mutant P130T was also more persistent than WT and I97L mutants at 1 and 2 weeks postinjection. 2019 Journal of virology Figure HBV P130T;I97L 34;77 39;81 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L can synthesize full-length RC form by in vitro endogenous DNA polymerase reaction (EPR). 2019 Journal of virology Figure HBV I97L 7 11 P 74 84 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutant I97L replicates less efficiently than wild-type HBV in three different kinds of immunodeficient mice. 2019 Journal of virology Figure HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutation I97L appeared to be dominant over mutation P130T in vivo, since both the intracellular deficiency in RC DNA and poor persistence of mutant I97L were not significantly rescued by the mutation P130T. 2019 Journal of virology Figure HBV I97L;P130T;I97L;P130T 9;52;148;200 13;57;152;205 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Mutation P130T appeared to partially upshift the immature SS DNA of mutant I97L to the higher-MW RC form at 3 dpi (lane 2 versus lane 4). 2019 Journal of virology Figure HBV P130T;I97L 9;75 14;79 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Reduction in the persistence of intracellular HBV DNA level of mutant I97L in the mouse liver by hydrodynamic delivery. 2019 Journal of virology Figure HBV I97L 70 74 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The averaged total DNAs are calculated from two mice injected with WT HBV DNA and normalized to the averaged value from three mice injected with mutant I97L. 2019 Journal of virology Figure HBV I97L 152 156 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The characteristic hypermaturation phenotype of single mutant P130T was most pronounced at 1 week postinjection (red asterisk in the middle panel). 2019 Journal of virology Figure HBV P130T 62 67 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The full-length RC form was almost undetectable in mutant I97L. 2019 Journal of virology Figure HBV I97L 58 62 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The left panel postulates that an intracellular defect in genome maturation is the primary cause of the extracellular immature secretion of mutant I97L. 2019 Journal of virology Figure HBV I97L 147 151 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The overall viral DNA synthesis of mutant I97L is significantly reduced relative to WT HBV. 2019 Journal of virology Figure HBV I97L 42 46 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The red asterisk highlights the lessened abundance of fully mature full-length RC DNA associated with mutant I97L. 2019 Journal of virology Figure HBV I97L 109 113 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The right panel postulates that an overly efficient and less selective envelopment is the primary cause of the intracellular deficiency in the fully mature RC DNA in mutant I97L. 2019 Journal of virology Figure HBV I97L 173 177 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The SEAP activities in the sera indicated similar transfection efficiencies between WT and I97L in hydrodynamic delivery. 2019 Journal of virology Figure HBV I97L 91 95 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The viral DNA level of mutant I97L appeared to be much lower than those of WT HBV at day 3 or week 1 postinjection. 2019 Journal of virology Figure HBV I97L 30 34 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The viral DNA levels of mutant I97L, particularly the RC form, were greatly reduced in the liver at 3 dpi by Southern blotting. 2019 Journal of virology Figure HBV I97L 31 35 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Unlike the WT, mutant I97L displayed an excessive number of immature genomes. 2019 Journal of virology Figure HBV I97L 22 26 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. A: The decrease in hepatitis B virus (HBV) DNA was significantly less prominent in patients infected with naturally occurring rtM204I variants than in patients without pre-existing rtM204I variants at 3, 6, 9, 12, 15 mo of nucleos(t)ide analogues (all P < 0.05); B: There was no differences in HBV-DNA declines during tenofovir therapy between patients with and without naturally occurring rtM204I variants; C: The decrease in HBV DNA was significantly less prominent in patients infected with naturally occurring rtM204I variants than in patients without pre-existing rtM204I variants at 3, 6, 9, 12, 15 mo of entecavir (all P < 0.05); D: The decrease in HBV DNA was significantly less prominent in patients infected with naturally occurring rtM204I variants than in patients without pre-existing rtM204I variants at 3, 6, 9, 12, 15 mo of low genetic barriers (all P < 0.05). 2019 World journal of gastroenterology Figure HBV M204I;M204I;M204I;M204I;M204I;M204I;M204I 128;183;392;516;571;745;800 133;188;397;521;576;750;805 RT;RT;RT;RT;RT;RT;RT 126;181;390;514;569;743;798 128;183;392;516;571;745;800 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Confirmation of LNA real-time PCR identification results of hepatitis B virus rtM204I (YIDD) variant and rtM204 (YMDD) wild type by direct sequencing. 2019 World journal of gastroenterology Figure HBV M204I 80 85 RT;RT;P;P 78;105;87;113 80;107;91;117 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. LNA real-time PCR for identification of hepatitis B virus rtM204I (YIDD) variant and rtM204 (YMDD) wild type. 2019 World journal of gastroenterology Figure HBV M204I 60 65 RT;RT;P;P 58;85;67;93 60;87;71;97 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Primer and LNA-probe positions designed for the detection of hepatitis B virus rtM204I (YIDD) variant and rtM204 (YMDD) wild type. 2019 World journal of gastroenterology Figure HBV M204I 81 86 RT;RT;P;P 79;106;88;114 81;108;92;118 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The box represents the codon and amino acid sequences of the rtM204 (YMDD) wild type and rtM204I (YIDD) variant. 2019 World journal of gastroenterology Figure HBV M204I 91 96 RT;RT;P;P 61;89;98;69 63;91;102;73 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. A: In the forward read, the large peak indicates "C" (G145A) and the small peak indicates "G" (wild-type) in the forward read. 2019 BMC infectious diseases Figure HBV G145A 54 59 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. B: In the forward read, the large peak indicates "G" (wild-type) and the small peak indicates "G" (G145A) in the forward read. 2019 BMC infectious diseases Figure HBV G145A 99 104 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. (D-F) HepG2 cells were transfected with an HBV molecular clone (pUC19-C_JPNAT) and its site-directed mutant (T160A/S162A). 2020 Frontiers in cell and developmental biology Figure HBV S162A;T160A 115;109 120;114 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. (E) Pin1 interacts with HBc via its Thr160-Pro and Ser162-Pro motifs. 2020 Frontiers in cell and developmental biology Figure HBV T160P;S162P 36;51 46;61 C 24 27 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. (F) HepG2 cells were transfected with WT HBc or the T160A/S162A mutant followed by CHX assay as shown in (D). 2020 Frontiers in cell and developmental biology Figure HBV S162A;T160A 58;52 63;57 C 41 44 32083080 Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein. HepG2 cells were transfected with WT HBc or its site-directed (T160A/S162A) mutant for 48 h in the presence of protease inhibitors. 2020 Frontiers in cell and developmental biology Figure HBV S162A;T160A 69;63 74;68 C 37 40 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Percentage of LAMR rtM204I/V mutation in serum and liver biopsy samples of 5 EFFORT patients collected at week 104 and 2 ML18376 patients collected at baseline (A). 2021 Hepatology (Baltimore, Md.) Figure HBV M204I;M204V 21;21 28;28 RT 19 21 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. For the underlined pairs of mutations HBsAg release was significant also compared to the corresponding single mutation S204N (P<0.001) or Y206F (P=0.007, P=0.001 and <0.0001, respectively). 2020 Emerging microbes & infections Figure HBV S204N;Y206F 119;138 124;143 S 38 43 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Statistically significant differences were confirmed after correction for multiple comparison for all mutations with the exception of S210N. 2020 Emerging microbes & infections Figure HBV S210N 134 139 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. (A) A3G protein was detected by western blot with densitometry analysis 1-day post-transfection. 2020 Frontiers in microbiology Figure HBV A3G 4 7 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. HBeAg was decreased in mutant compared to wild-type and differences in HBV DNA (p = 0.0363) and HBV RNA (p = 0.0220) were noted between G1896A vs. 2020 Frontiers in microbiology Figure HBV G1896A 136 142 C 0 5 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. HepG2 cells were co-transfected with pcDNA-GFP +/- linearized wild-type (WT), G1896A or A1762T/G1764A (DMUT) HBV. 2020 Frontiers in microbiology Figure HBV G1764A;A1762T;G1896A 95;88;78 101;94;84 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Reduced A3G protein expression was found in mutants vs. 2020 Frontiers in microbiology Figure HBV A3G 8 11 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. In circles are mutations in the antigenic 'a' determinant (in yellow) and mutations (except K160N) in the other region of S that overlap with some viral polymerase mutations conferring resistance to nucleos(t)ide drugs. 2020 PloS one Figure HBV K160N 92 97 S;P;S 43;153;122 57;163;123 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. M1, sA159V; M2, rtM204I; M3, sA159V+rtM204I; M4, rtL180M+rtM204V; M5, sA159V+rtL180M+rtM204V; M6, rtL180M+rtT184L+rtM204V; M7,sA159V+rtL180M+rtT184L+rtM204V. 2020 World journal of gastroenterology Figure HBV M204I;M204I;L180M;M204V;L180M;M204V;L180M;T184L;M204V;L180M;T184L;M204V;A159V;A159V;A159V;A159V 18;38;51;59;79;87;100;108;116;135;143;151;4;29;70;126 23;43;56;64;84;92;105;113;121;140;148;156;10;35;76;132 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S 16;36;49;57;77;85;98;106;114;133;141;149;4;29;70;126 18;38;51;59;79;87;100;108;116;135;143;151;5;30;71;127 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. M1, sA159V; M2, rtM204I; M3, sA159V+rtM204I; M4, rtL180M+rtM204V; M5, sA159V+rtL180M+rtM204V; M6,sA159V+rtL180M+rtT184L+rtM204V; M7, rtL180M+rtT184L+rtM204V. 2020 World journal of gastroenterology Figure HBV M204I;M204I;L180M;M204V;L180M;M204V;L180M;T184L;M204V;L180M;T184L;M204V;A159V;A159V;A159V;A159V 18;38;51;59;79;87;106;114;122;135;143;151;4;29;70;97 23;43;56;64;84;92;111;119;127;140;148;156;10;35;76;103 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S 16;36;49;57;77;85;104;112;120;133;141;149;4;29;70;97 18;38;51;59;79;87;106;114;122;135;143;151;5;30;71;98 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. M1, sA159V; M2, rtM204I; M3, sA159V+rtM204I; M4, rtL180M+rtM204V; M5, sA159V+tL180M+rtM204V; M6, rtL180M+rtT184L+rtM204V; M7, sA159V+rtL180M+rtT184L+rtM204V. 2020 World journal of gastroenterology Figure HBV M204I;M204I;L180M;M204V;M204V;L180M;T184L;M204V;L180M;T184L;M204V;A159V;A159V;A159V;A159V 18;38;51;59;86;99;107;115;135;143;151;4;29;70;126 23;43;56;64;91;104;112;120;140;148;156;10;35;76;132 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;S;S;S;S 16;36;49;57;84;97;105;113;133;141;149;4;29;70;126 18;38;51;59;86;99;107;115;135;143;151;5;30;71;127 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Phylogenetic tree analysis of hepatitis B virus reverse transcriptase sequences from a patient with sA159V + resistance mutations. 2020 World journal of gastroenterology Figure HBV A159V 100 106 RT;S 48;100 69;101 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. (A) Bel-7404 cells were transfected with the plasmid p1.2DNA-WT, -M204V, -L229V, -M204V + L229V. 2020 Emerging microbes & infections Figure HBV M204V;L229V;M204V;L229V 66;74;82;90 71;79;87;95 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. (B) Bel-7404 cells were transfected with the plasmid p1.2DNA-WT, -M204V, -L229V, -M204V + L229V, and subsequently treated with antiviral drugs at the indicated concentrations. 2020 Emerging microbes & infections Figure HBV M204V;L229V;M204V;L229V 66;74;82;90 71;79;87;95 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. (C) Docking simulation of HBV RT with rtM204V mutation to ETV-TP. 2020 Emerging microbes & infections Figure HBV M204V 40 45 RT;RT 30;38 32;40 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. (D) Docking simulation of HBV RT with rtM204V + rtl229V mutation to ETV-TP. 2020 Emerging microbes & infections Figure HBV M204V 40 45 RT;RT;RT 30;38;48 32;40;50 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Small red arrows reflect the site of primary and secondary resistance mutations, from bottom to top: rtL180M, rtA181V/T/I, rtT184S/L, rtM204V/I, rtN236T/I. 2020 Emerging microbes & infections Figure HBV A181V;A181T;A181I;T184S;T184L;M204V;M204I;N236T;N236I;L180M 112;112;112;125;125;136;136;147;147;103 121;121;121;132;132;143;143;154;154;108 RT;RT;RT;RT;RT 101;110;123;134;145 103;112;125;136;147 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. The violin plot compares the frequency of the mutational pattern (A12S/P33S/P46S/T36G-D) between the clinical groups. 2021 Scientific reports Figure HBV P46S;P33S;T36G;A12S 76;71;81;66 80;75;85;70 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. T118X represents T118A/R/V; M133X represents M133I/L/T; Q129X represents Q129A/R; D144X represents D144A/E/G/N. 2021 Journal of viral hepatitis Figure HBV T118A;T118R;T118V;M133I;M133L;M133T;D144A;D144E;D144G;D144N;T118X;M133X;Q129X;Q129A;Q129R;D144X 17;17;17;45;45;45;99;99;99;99;0;28;56;73;73;82 26;26;26;54;54;54;110;110;110;110;5;33;61;80;80;87 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (A) Amount of HBV proteins and HBV DNA after transfection of HBV molecular clone plasmids with I97wt or I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 104 108 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (A) Southern blot analysis of HBV DNA species in fractions of iodixanol density gradients of HBV-I97wt and -I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 108 112 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (A) Transition of HBV DNA from the start to end of the observation period in patients with HBV-I97wt (left) or HBV-I97L (right). 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 115 119 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (B and C) Iodixanol density gradient analysis of cell culture-generated HBV-I97wt and HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 90 94 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (B) Efficiencies of cccDNA synthesis after infection with HBV-I97wt and -I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 73 77 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (B) Transition of HBsAg from the start to the end of the observation period in patients with HBV-I97wt (left) or HBV-I97L (right). 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 117 121 S 18 23 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (C) Infection of I97wt- and I97L-HBV/NL. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 28 32 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (C) Transcription of pgRNA after transfection of HBV molecular clone plasmids carrying I97wt and I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 97 101 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (C) Transition of ALT from the start to the end of the observation period in patients with HBV-I97wt (left) or HBV-I97L (right). 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 115 119 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (D and E) Iodixanol density gradient analysis of cell culture-generated HBV-I97wt and HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 90 94 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (D) Detection of core-associated DNA in I97wt and I97L HBV molecular clone plasmid-transfected HepG2 cells. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 50 54 C 17 21 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (E) Synthesis of cccDNA after transfection of HBV molecular clone plasmids with I97wt and I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 90 94 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (F) The points of the HBV life cycle affected by I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 49 53 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. (See previous page) Effects of I97L substitution on the HBV life cycle. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 31 35 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Culture medium of the HBV molecular clone with I97wt- or I97L-transfected cells was applied to iodixanol density gradient after adjusting amount of HBV DNA. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 57 61 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L substitution on HBV infection. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 11 15 HBV infections 32 45 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L substitution on HBV/NL infection. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 11 15 HBV infections 32 48 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Effects of I97L substitution on interaction between HBc and L-HBs. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 11 15 C;S 52;62 55;65 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Efficiencies of attachment and internalization of purified HBV-I97wt and -I97L viruses. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 74 78 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. I97wt- and I97L-HBV/NL were infected into G2/NT18-C cells at 20 GEq/cell. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 11 15 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. I97wt-HBV/NL (D) and I97L-HBV/NL (E) were analyzed by iodixanol density gradient after adjusting amount of HBsAg. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 21 25 S 107 112 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The amino acid substitution I97L was introduced into the HBV-dE plasmid. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 28 32 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The schemes of the HBV-I97wt (left) and HBV-I97L (right) life cycles are indicated. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 44 48 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Transition of HBV DNA, HBsAg, and ALT in patients with HBV-I97wt or -I97L. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L 69 73 S 23 28 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Two kinds of HBc-LgBit harboring I97wt (I97wt-HBc-LgBit) and I97L (I97L-HBc-LgBit) were generated. 2021 Cellular and molecular gastroenterology and hepatology Figure HBV I97L;I97L 61;67 65;71 C;C;C 13;46;72 16;49;75 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. A Polymerase mutants YIDD created corresponding changes in the overlapping envelope ORF:W196L and W196S. 2021 Journal of biomedical science Figure HBV W196L;W196S 88;98 93;103 S;P;P 75;2;21 83;12;25 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. B No apparent defect in virion secretion was detected in two polymerase YIDD mutants containing envelope mutations W196L and W196S, respectively. 2021 Journal of biomedical science Figure HBV W196L;W196S 115;125 120;130 S;P;P 96;61;72 104;71;76 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. HBV DNA signals of the complementation experiments were compared individually to the mutant M198P. 2021 Journal of biomedical science Figure HBV M198P 92 97 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Mutant W196L exhibited increased secretion of genome-containing virions. 2021 Journal of biomedical science Figure HBV W196L 7 12 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Only the small envelope protein can rescue the virion secretion defect of the proline substitution mutant M198P. 2021 Journal of biomedical science Figure HBV M198P 106 111 S 9 23 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Only the small envelope protein can successfully rescue the virion secretion defect of the small loop mutant M198P. 2021 Journal of biomedical science Figure HBV M198P 109 114 S 9 23 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Red asterisk * highlights the strongly reduced levels of HBc core protein signal of total virions in mutants CTP and M198P. 2021 Journal of biomedical science Figure HBV M198P 117 122 C;C 61;57 65;60 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Compared with pHBV1.3B, the fluorescence density of cells transfected with pHBV1.3B-E2G and pHBV1.3B-E2A was significantly higher (p < 0.0001), while pHBV1.3B-E2V and pHBV1.3B-E2D was significantly lower (p < 0.05) (A). 2021 Frontiers in microbiology Figure HBV E2G;E2A;E2V;E2D 84;101;159;176 87;104;162;179 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Compared with pHBV1.3C, the fluorescence density of cells transfected with pHBV1.3C-E2A was significantly higher (p < 0.001). 2021 Frontiers in microbiology Figure HBV E2A 84 87 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. No significant changing was found between pHBV1.3C-E2D and pHBV1.3C (B). 2021 Frontiers in microbiology Figure HBV E2D 51 54 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The positive fluorescent cells transfected with pHBV1.3C-E2G were too few to be included in the fluorescence intensity statistical analysis. 2021 Frontiers in microbiology Figure HBV E2G 57 60 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. The staining of cells transfected with pHBV1.3B-E2V/D and pHBV1.3C-E2D was similar to that of genotype-matched pHBV1.3B/C. 2021 Frontiers in microbiology Figure HBV E2V;E2D;E2D 48;48;67 53;53;70 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. (A) Effect of A1762T/G1764A+C1653T+T1674G on HCC occurrence. 2022 Frontiers in oncology Figure HBV G1764A;T1674G;A1762T;C1653T 21;35;14;28 27;41;20;34 Hepatocellular carcinoma 45 48 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. (B) Effect of A1762T/G1764A+T1674G+T1753C on HCC occurrence. 2022 Frontiers in oncology Figure HBV G1764A;T1674G;A1762T;T1753C 21;28;14;35 27;34;20;41 Hepatocellular carcinoma 45 48 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. (C) Effect of A1762T/G1764A+C1653T+T1753C on HCC occurrence. 2022 Frontiers in oncology Figure HBV G1764A;A1762T;C1653T;T1753C 21;14;28;35 27;20;34;41 Hepatocellular carcinoma 45 48 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. Changes at positions 1762-1764 have been described to be preferentially selected in patients infected with genotypes showing C instead of T at nt 1858. 2001 BMC microbiology Discussion HBV T1858C 125 150 11472634 Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers. The most common mutation was the G to A change at nt 1896 that creates a stop codon in the precore ORF. 2001 BMC microbiology Discussion HBV G1896A 33 57 Precore 91 98 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Besides these common mutations, a third lamivudine resistant, rare mutation, namely V519L, was detected in one clone derived from the sample collected in 1999 as well as in all HBV sequences derived from the sample collected in 2002. 2004 BMC infectious diseases Discussion HBV V519L 84 89 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Even so, the L526M mutation has been found alone in patients under lamivudine therapy. 2004 BMC infectious diseases Discussion HBV L526M 13 18 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Furthermore, the presence of L526M mutation in addition to mutation at position 550 seems to be associated with prolonged lamivudine treatment. 2004 BMC infectious diseases Discussion HBV L526M 29 34 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. Here, both L526M and M550V mutations were detected in all HBV sequences derived from the two blood samples collected during lamivudine treatment (1999 and 2002). 2004 BMC infectious diseases Discussion HBV L526M;M550V 11;21 16;26 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. However, another substitution, namely G473E, was observed that was associated to G119R substitution in the small S protein. 2004 BMC infectious diseases Discussion HBV G473E;G119R 38;81 43;86 S 107 114 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. It has been shown that this triple mutant has a reduced in vitro affinity to anti-HBs antibodies, similar to the hepatitis B vaccine escape mutant G145R. 2004 BMC infectious diseases Discussion HBV G145R 147 152 S 82 85 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. It is believed that the L526M mutation, when not accompanied with a mutation in the YMDD motif, does not confer lamivudine resistance. 2004 BMC infectious diseases Discussion HBV L526M 24 29 P 84 88 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. More rarely, HBV variant presenting M550S replacement may be selected during lamivudine treatment The M550V variant may be accompanied by a mutation (leucine to methionine) at position 526. 2004 BMC infectious diseases Discussion HBV M550S;M550V;L526M 36;102;149 41;107;188 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. The resistance occurs by replacement of a methionine residue at position 550 by either valine (M550V) or isoleucine (M550I). 2004 BMC infectious diseases Discussion HBV M550V;M550I 95;117 100;122 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. The triple mutation V519L, L526M, M550V causes the concomitant amino acid substitutions E164D and I195M in the small S protein. 2004 BMC infectious diseases Discussion HBV V519L;L526M;M550V;E164D;I195M 20;27;34;88;98 25;32;39;93;103 S 111 118 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. There is a general consensus that the lamivudine resistant single mutants in the YMDD motif (M550V/I) replicate substantially more slowly than the wild type. 2004 BMC infectious diseases Discussion HBV M550V;M550I 93;93 100;100 P 81 85 15339340 Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine. This result is in agreement with a recent study, showing that V519L mutation also enhances viral replication. 2004 BMC infectious diseases Discussion HBV V519L 62 67 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. Because of the emergence of the rtA181T mutation (which is closely located to codon 180), conferring resistance to lamivudine and closely related to rtA181V, we chose to treat this patient with tenofovir rather than with lamivudine. 2006 Comparative hepatology Discussion HBV A181V;A181T 151;34 156;39 RT;RT 32;149 34;151 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. In fact, the rtA181V mutation reduces the susceptibility to lamivudine 14 fold in vitro, while in vivo lamivudine has only a limited antiviral effect on that mutant strain. 2006 Comparative hepatology Discussion HBV A181V 15 20 RT 13 15 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. In this patient with the double rtN236T and rtA181T mutations, the antiviral response to tenofovir was excellent. 2006 Comparative hepatology Discussion HBV N236T;A181T 34;46 39;51 RT;RT 32;44 34;46 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. reported recently decreased in vitro susceptibility to both tenofovir and adefovir of two HBV resistant mutants (N236T adefovir and L180M + M204V + N236T lamivudine/adefovir resistant strains). 2006 Comparative hepatology Discussion HBV N236T;L180M;M204V;N236T;N236T;L180M;M204V;N236T 114;133;141;149;113;132;140;148 119;138;146;154;118;137;145;153 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. The patient developed both rtN236T and rtA181T mutations while under adefovir treatment for 2 years. 2006 Comparative hepatology Discussion HBV A181T;N236T 41;29 46;34 RT;RT 27;39 29;41 16405720 Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant. The rtN236T and rtA181V are well-described adefovir resistant mutations, whereas the rtA181T is very rare and has only been described in 1 out of 22 patients with adefovir resistance, after 4 years of treatment. 2006 Comparative hepatology Discussion HBV A181V;A181T;N236T 18;87;6 23;92;11 RT;RT;RT 4;16;85 6;18;87 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. In addition, mutation rtA181T is associated with the stop mutation sW172stop in the S gene. 2007 Virology journal Discussion HBV A181T;W172X 24;67 29;76 RT;S;S 22;67;84 24;68;85 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. The genotype prevalent in a population may determine the type of mutations prevalent in the infecting strains; for example, the immune-escape mutant G145R is closely associated with genotype D. 2007 Virology journal Discussion HBV G145R 149 154 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. The main mutations associated with LMV resistance are located at the RT gene in the 204 position (rtM204I/V), which is in the catalytic YMDD motif. 2007 Virology journal Discussion HBV M204I;M204V 100;100 107;107 RT;RT;P 69;98;136 71;100;140 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. The most relevant mutations seem to be the substitutions of amino acid G145R, K141E and T131I and insertion of 3 amino acids between residues 123 and 124, since they markedly affect the antigenic structure of HBsAg. 2007 Virology journal Discussion HBV G145R;K141E;T131I 71;78;88 76;83;93 S 209 214 17217533 Molecular analysis of hepatitis B virus "a" determinant in asymptomatic and symptomatic Mexican carriers. Thus for mutations associated with LMV resistance, the rtM204V change is associated with a I195M change in the S gene (sI195M), while the rtM204I change is associated with three possible changes in the S gene, sW196S, sW196L, or a stop codon. 2007 Virology journal Discussion HBV M204V;M204I;I195M;W196S;W196L;I195M 57;140;119;210;218;91 62;145;125;216;224;96 RT;RT;S;S;S;S;S 55;138;111;119;202;210;218 57;140;112;120;203;211;219 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. The deduced amino acid sequence of the S gene product also revealed three isolates bearing the determinant a substitution Y100C, which is associated with the HBsAg-negative/anti-HBc-positive phenotype in blood donors from Venezuela and has been found in an HBsAg-positive Brazilian patient. 2007 BMC microbiology Discussion HBV Y100C 122 127 C;S;S;S 178;158;257;39 181;163;262;40 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. The frequent lamivudine-resistance rtL180M-rtM204V double mutation was detected in two isolates (043-N and 209-CW), while a third isolate (043-N) displayed a rare rtV173L-rtL180M-rtM204V triple mutation (Table 2). 2007 BMC microbiology Discussion HBV L180M;M204V;L180M;M204V;V173L 37;45;173;181;165 42;50;178;186;170 RT;RT;RT;RT;RT 35;43;163;171;179 37;45;165;173;181 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. The T118V-A128V double mutation was found in three genotype D/ayw3 (subgenotype D2) isolates. 2007 BMC microbiology Discussion HBV T118V;A128V 4;10 9;15 18036224 Hepatitis B virus genotypes circulating in Brazil: molecular characterization of genotype F isolates. This triple mutant is known to exhibit reduced in vitro affinity for anti-HBs antibodies, similar to the hepatitis B vaccine escape mutant G145R. 2007 BMC microbiology Discussion HBV G145R 139 144 S 74 77 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. It has been shown that this triple mutant has a reduced in vitro affinity to anti-HBs antibodies, similar to what occurs with the hepatitis B vaccine escape mutant G145R. 2008 BMC microbiology Discussion HBV G145R 164 169 S 82 85 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. Single mutants in the YMDD motif (rtM204V/I) replicate substantially more slowly in vitro than the wild type. 2008 BMC microbiology Discussion HBV M204V;M204I 36;36 43;43 RT;P 34;22 36;26 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. The occurrence of mutations rtL180M and rtV173L has been associated with prolonged lamivudine treatment. 2008 BMC microbiology Discussion HBV L180M;V173L 30;42 35;47 RT;RT 28;40 30;42 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. The resistance occurs by replacement of a methionine residue at position rt204 by either valine (rtM204V) or isoleucine (rtM204I), accompanied or not by a substitution at position rt180 and more rarely by a substitution at position rt173. 2008 BMC microbiology Discussion HBV M204V;M204I 99;123 104;128 RT;RT;RT;RT;RT 73;97;121;180;232 75;99;123;182;234 18211717 Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil. The triple mutation rtV173L/rtL180M/rtM204V/I results in concomitant amino acid substitutions E164D and I195M in the small S protein. 2008 BMC microbiology Discussion HBV M204I;M204V;L180M;V173L;E164D;I195M 38;38;30;22;94;104 45;43;35;27;99;109 RT;RT;RT;S 20;28;36;117 22;30;38;124 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Also, severe clinical manifestations of chronic hepatitis in patients with abrupt elevation of serum ALT level (>200 U/L) are more frequently observed in those with the precore wild type than G1896A mutation. 2008 Journal of the National Cancer Institute Discussion HBV G1896A 192 198 Precore 169 176 Chronic Hepatitis B 40 57 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. As has been described by other studies (mostly from Asia), we also found that HBV genotype C infection was associated with a higher risk of HCC than HBV genotype B infection; in addition, we found that the BCP A1762T/G1764A mutant was associated with an increased risk of HCC compared with the double wild-type variant, whereas the precore G1896A mutation was associated with a decreased risk of HCC compared with the wild-type variant. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T;G1896A 217;210;340 223;216;346 BCP;Precore 206;332 209;339 HBV infections;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 78;140;272;396 102;143;275;399 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. However, in this study we demonstrated that both genotype C and BCP A1762T/G1764A mutation status are independent risk factors for the development of HCC. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 75;68 81;74 BCP 64 67 Hepatocellular carcinoma 150 153 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. In a multivariable Cox regression analysis, we found that the BCP A1762T/G1764A mutation was associated with an increased risk of HCC independent of viral load and other risk factors. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 73;66 79;72 BCP 62 65 Hepatocellular carcinoma 130 133 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. In conclusion, HBV genotype C and the BCP A1762T/G1764A mutant were independent risk factors for HCC, and the precore G1896A mutant was associated with a decreased risk of HCC. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T;G1896A 49;42;118 55;48;124 BCP;Precore 38;110 41;117 Hepatocellular carcinoma;Hepatocellular carcinoma 97;172 100;175 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. It has been proposed that the BCP A1762T/G1764A mutation may enhance HBV virulence by increasing host immune response, increasing viral replication, or altering the coding region for the X antigen. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 41;34 47;40 BCP;X 30;187 33;188 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Mutations in the BCP region, which overlaps the coding sequence for the X antigen of HBV, may result in amino acid changes K130M and V131I in the X antigen. 2008 Journal of the National Cancer Institute Discussion HBV K130M;V131I 123;133 128;138 BCP;X;X 17;72;146 20;73;147 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Our finding that the precore G1896A mutation was associated with a lower risk of HCC compared with wild-type virus appears to be at odds with several early case reports that found an association between the precore stop mutation and a marked increase in viral virulence and the development of fulminant hepatitis. 2008 Journal of the National Cancer Institute Discussion HBV G1896A 29 35 Precore;Precore 21;207 28;214 Hepatocellular carcinoma;Fulminant Hepatitis B 81;293 84;312 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Several mechanisms of hepatocarcinogenesis relating to the BCP A1762T/G1764A mutant have been hypothesized. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 70;63 76;69 BCP 59 62 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. The negative association between the precore G1896A mutant and HCC that we observed in this study after adjustment for sex, age, cigarette smoking status, alcohol consumption status, serum ALT level, and cirrhosis at study entry, as well as HBV genotype, viral load, and BCP mutant, suggested that the precore G1896A mutation was associated with a low risk of HCC. 2008 Journal of the National Cancer Institute Discussion HBV G1896A;G1896A 45;310 51;316 BCP;Precore;Precore 271;37;302 274;44;309 Hepatocellular carcinoma;Liver cirrhosis;Hepatocellular carcinoma 63;204;360 66;213;363 18695135 Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma. Therefore, other mechanisms of hepatocarcinogenesis, such as the alteration of transactivation capability of X antigen induced by amino acid changes related to the BCP A1762T/G1764A mutation, should be considered in future studies. 2008 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 175;168 181;174 BCP;X 164;109 167;110 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Furthermore, the C1653T and T1753V mutations occur almost invariably on the background of the A1762T, G1764A mutations. 2008 The American journal of gastroenterology Discussion HBV C1653T;T1753V;A1762T;G1764A 17;28;94;102 23;34;100;108 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. HBV A1762T, G1764A mutations are an etiological risk factor of HCC. 2008 The American journal of gastroenterology Discussion HBV A1762T;G1764A 4;12 10;18 Hepatocellular carcinoma 63 66 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Hepatitis B virus (HBV) A1762T, G1764A mutations are a valuable biomarker to identify males at extremely high risk of HCC. 2008 The American journal of gastroenterology Discussion HBV A1762T;G1764A 24;32 30;38 Hepatocellular carcinoma 118 121 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. In this study cohort, the C1653T and T1753V mutations were detected less frequently (from 20%-28.4%) than the A1762T, G1764A mutations and the differences between HCC cases and controls are not significant for either. 2008 The American journal of gastroenterology Discussion HBV C1653T;T1753V;A1762T;G1764A 26;37;110;118 32;43;116;124 Hepatocellular carcinoma 163 166 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Of note, 93.3% of male cases were infected with mutant HBV, suggesting that the A1762T, G1764A mutations are a valuable biomarker to identify a subset of male HBsAg carriers aged >30 at extremely high risk of hepatocellular carcinoma. 2008 The American journal of gastroenterology Discussion HBV A1762T;G1764A 80;88 86;94 S 159 164 Hepatocellular carcinoma 209 233 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Other studies have suggested that the core promoter mutations C1653T and T1753V also are associated with the occurrence of severe hepatitis B and development of HCC, although their prevalence is lower than that of the A1762T, G1764A mutations. 2008 The American journal of gastroenterology Discussion HBV C1653T;T1753V;A1762T;G1764A 62;73;218;226 68;79;224;232 Core promoter 38 51 Hepatocellular carcinoma 161 164 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. The number of males for surveillance for HCC can be narrowed down according to the presence of HBV A1762T, G1764A mutations. 2008 The American journal of gastroenterology Discussion HBV A1762T;G1764A 99;107 105;113 Hepatocellular carcinoma 41 44 18844615 HBV A1762T, G1764A mutations are a valuable biomarker for identifying a subset of male HBsAg carriers at extremely high risk of hepatocellular carcinoma: a prospective study. Therefore, we conclude that the A1762T, G1764A mutations are a valuable biomarker to identify those male HBsAg carriers who should be monitored regularly for signs of tumour. 2008 The American journal of gastroenterology Discussion HBV A1762T;G1764A 32;40 38;46 S 105 110 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. An alternative explanation is that Cp149-Y132A participates in assembly so poorly that it competitively inhibits nucleation but is incorporated during elongation. 2009 Biochemistry Discussion HBV Y132A 41 46 C 35 37 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Apparently even a small amount of Cp149-Y132A was sufficient to compromise capsid stability. 2009 Biochemistry Discussion HBV Y132A 40 45 Capsid;C 75;34 81;36 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. At higher NaCl, with stronger association energy, Cp149-Y132A is retained in capsids resulting in unstable capsids that dissociate in low NaCl SEC. 2009 Biochemistry Discussion HBV Y132A 56 61 Capsid;Capsid;C 77;107;50 84;114;52 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Based on structure, it is reasonable to posit that Cp149-Y132A has substantially weaker association energy. 2009 Biochemistry Discussion HBV Y132A 57 62 C 51 53 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Based on structure, we developed a point mutation within the HBV core protein, Cp149-Y132A, as a tool for examining the process of assembly inhibition. 2009 Biochemistry Discussion HBV Y132A 85 90 C;C 65;79 69;81 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Cp149-Y132A appears to be incapable of nucleating assembly. 2009 Biochemistry Discussion HBV Y132A 6 11 C 0 2 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Even in the full length core protein, where assembly is supported by interaction with nucleic acid, evidence suggests that the Y132A mutation prevents assembly in bacterial and in mammalian expression systems. 2009 Biochemistry Discussion HBV Y132A 127 132 C 24 28 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Evidence suggests that the Y132A mutation prevents assembly of full-length core protein (in bacterial and mammalian expression systems), even though the capsid is also stabilized by interaction with packaged nucleic acid. 2009 Biochemistry Discussion HBV Y132A 27 32 Capsid;C 153;75 159;79 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. However, the data suggest limiting models of the role of Cp149-Y132A. 2009 Biochemistry Discussion HBV Y132A 63 68 C 57 59 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. However, the effect of Y132A in Cp149 is unsubtle. 2009 Biochemistry Discussion HBV Y132A 23 28 C 32 34 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. In Figure 4 it is apparent that the rate of capsid formation is essentially unchanged by the presence of Cp149-Y132A, although yield is increased. 2009 Biochemistry Discussion HBV Y132A 111 116 Capsid;C 44;105 50;107 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. In high NaCl, Cp149-Y132A participates in assembly to generate fragile capsids, but does not poison assembly in a crystallographic sense by blocking further growth. 2009 Biochemistry Discussion HBV Y132A 20 25 Capsid;C 71;14 78;16 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. In low NaCl Cp149-Y132A does not stay included in capsids and thus mimics the effects of a protein with a tightly bound inhibitor that altogether prevents assembly. 2009 Biochemistry Discussion HBV Y132A 18 23 Capsid;C 50;12 57;14 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. In this scenario, the rate of nucleus formation is determined solely by the wildtype Cp149 and Cp149-Y132A participates only in "elongation" of intermediates, hence the greater yield of capsid. 2009 Biochemistry Discussion HBV Y132A 101 106 Capsid;C;C 186;85;95 192;87;97 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. It appears that only a limited amount of Y132A can be incorporated into capsids. 2009 Biochemistry Discussion HBV Y132A 41 46 Capsid 72 79 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. Two possible explanation arise for this result: (i) a patch of defective protein is too unstable to be retained, or (ii) Y132A promotes a quaternary structure change, weakening binding sites some distance from the defect, that limits association to the wildtype. 2009 Biochemistry Discussion HBV Y132A 121 126 19196007 A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly. We examined the effect of Cp149-Y132A on nucleation rate in a long-term kinetics experiment. 2009 Biochemistry Discussion HBV Y132A 32 37 C 26 28 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. However, in 5 other samples, UDPS detected cross-resistance mutations, including the ADV-resistance mutation rtN236T, the ETV-resistance mutations rtT184S and rtS202G, and the 3TC-ADV resistance mutations rtV173L, rtL180M, rtA181T, and rtM204V. 2009 The Journal of infectious diseases Discussion HBV M204V;N236T;T184S;S202G;V173L;L180M;A181T 238;111;149;161;207;216;225 243;116;154;166;212;221;230 RT;RT;RT;RT;RT;RT;RT 109;147;159;205;214;223;236 111;149;161;207;216;225;238 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Of 17 NRTI-naive patients, 2 had NRTI-resistance mutations detectable only by UDPS, including rtM204I at a level of 1.3% in one patient and rtA181T and rtM204I at levels of 1.0% in another patient. 2009 The Journal of infectious diseases Discussion HBV M204I;A181T;M204I 96;142;154 101;147;159 RT;RT;RT 94;140;152 96;142;154 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. The accessory 3TC-resistance mutation V173L was detected in 5 samples in which the primary 3TC-resistance mutations rtL180M and rtM204V/I were detected by direct PCR sequencing, a finding that does not influence HBV cross-resistance. 2009 The Journal of infectious diseases Discussion HBV M204V;M204I;L180M;V173L 130;130;118;38 137;137;123;43 RT;RT 116;128 118;130 19301976 Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients. Unrecognized G-to-A hypermutation may be responsible for over-estimation of the proportion of NRTI-resistance mutations caused by G-to-A changes (A181T, A194T, and M204I). 2009 The Journal of infectious diseases Discussion HBV A181T;A194T;M204I 146;153;164 151;158;169 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. The reason why patients harboring the G1896A precore mutation continued to express HBeAg was the co-existence of wild-type virus (the mutant was never detected as a pure population in any of our patients). 2009 Journal of medical virology Discussion HBV G1896A 38 44 C;Precore 83;45 88;52 19319958 Prevalence of basal core promoter and precore mutations in Chinese chronic hepatitis B patients and correlation with serum HBeAG titers. These HBeAg positive patients of genotype C infection also had a higher prevalence of the A1762T/G1764A BCP mutations but lower prevalence of the G1896A PC mutation, as have been reported by many other investigators. 2009 Journal of medical virology Discussion HBV G1764A;A1762T;G1896A 97;90;146 103;96;152 BCP;C;Precore 104;6;153 107;11;155 HBV infections 33 53 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. An F97L mutation causes the immature secretion phenotype, which could be overcome by a P130T mutation. 2009 Virology Discussion HBV F97L;P130T 3;87 7;92 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. In contrast, a P5T mutation impairs virion secretion when present alone and restores wild-type secretion phenotype when combined with the I97L mutation. 2009 Virology Discussion HBV P5T;I97L 15;138 18;142 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Moreover, together with the results of chimeric constructs they suggest that mutations present at the N-terminus of 2A core protein (A36T or G63V) reduce the stringency of virion secretion, whereas mutations present at the C-terminus of the 4B core protein (T147A, R151C, D153G, or Q179K) enhance genome maturity of secreted virions. 2009 Virology Discussion HBV A36T;G63V;T147A;R151C;D153G;Q179K 133;141;258;265;272;282 137;145;263;270;277;287 C;C 119;244 123;248 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Nevertheless, we have successfully used this approach to identify an G119E mutation in the envelope gene as responsible for impaired virion secretion of an HBV isolate, and also revealed ability of an M133T mutation in the envelope gene of clone 4B to overcome an I110M mutation, which would otherwise block virion secretion. 2009 Virology Discussion HBV G119E;M133T;I110M 69;201;264 74;206;269 S;S 91;223 99;231 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Remarkably, introduction of the C1766T/T1768A double mutation alone into a wild-type background reproduced a 15-fold increase in replication capacity. 2009 Virology Discussion HBV T1768A;C1766T 39;32 45;38 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The high replication capacity was mapped to nucleotides 1574-1986, where 7 core promoter mutations are present: G1751T, T1753A, G1757A, A1762T, G1764A, C1766T, and T1768A. 2009 Virology Discussion HBV G1751T;T1753A;G1757A;A1762T;G1764A;C1766T;T1768A 112;120;128;136;144;152;164 118;126;134;142;150;158;170 Core promoter 75 88 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. The most common core promoter mutations, A1762T/G1764A, had been found by other investigators to moderately increase genome replication. 2009 Virology Discussion HBV G1764A;A1762T 48;41 54;47 Core promoter 16 29 19327810 Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations. Thus, clone 4B contains a combination of T1753C, A1762T, G1764A, and C1766T mutations in the core promoter and replicated about 10-20 times more efficiently than clone 2A with a wild-type core promoter sequence. 2009 Virology Discussion HBV T1753C;A1762T;G1764A;C1766T 41;49;57;69 47;55;63;75 Core promoter;Core promoter 93;188 106;201 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A combined with other mutations within EnhII/BCP was more specific for HCC than A1762T/G1764A alone, indicating that the combined mutations increased the risk of HCC in an additive or synergistic fashion. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;G1764A;A1762T;A1762T 7;99;0;92 13;105;6;98 BCP;Enh II 57;51 60;56 Hepatocellular carcinoma;Hepatocellular carcinoma 83;174 86;177 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A increases viral replication; moreover, A1762T/G1764A + T1753V mutants show enhanced viral replication in cell culture, indicating that A1762T/G1764A alone or in combination with T1753V may be associated with high serum viral load in patients. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;G1764A;G1764A;A1762T;A1762T;T1753V;A1762T;T1753V 7;60;156;0;53;69;149;192 13;66;162;6;59;75;155;198 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A is frequently detected approximately 10 years before the diagnosis of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 7;0 13;6 Hepatocellular carcinoma 84 87 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. A1762T/G1764A was shown to be a valuable biomarker for identifying a subset of male HBsAg carriers who were at extremely high risk of HCC in a prospective study. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 7;0 13;6 S 84 89 Hepatocellular carcinoma 134 137 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Although the Precore mutation G1896A also affects HBeAg expression, it has no appreciable effect on the replication capacity of the virus in cell culture. 2009 Journal of the National Cancer Institute Discussion HBV G1896A 30 36 C;Precore 50;13 55;20 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. An important finding from this meta-analysis is that PreS mutations, C1653T, T1753V, and A1762T/G1764A are increasingly more prevalent as chronic HBV infection progresses from the asymptomatic HBsAg carrier state to liver cirrhosis or HCC, indicating that these mutations accumulate before the diagnosis of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 96;69;77;89 102;75;83;95 S;PreS 193;53 198;57 Chronic HBV infection;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma 138;216;235;307 159;231;238;310 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Because A1762T/G1764A was increasingly more prevalent as chronic HBV infection progressed from the asymptomatic HBsAg carrier state to liver cirrhosis or HCC, the predictive value of this mutation on HBV-induced HCC may be underestimated in the three cohort studies and the six nested case-control studies included in this meta-analysis because mutation data in the cohort and nested case-control studies are recorded at the beginning of cohort establishment. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 15;8 21;14 S 112 117 Chronic HBV infection;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma 57;135;154;212 78;150;157;215 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Because A1762T/G1764A was the most common mutation that was statistically significantly associated with a poor prognosis of HBV chronic infection (Figure 4), we compared the frequencies of A1762T/G1764A-based combined mutations between the patients with and without HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;G1764A;A1762T;A1762T 15;196;8;189 21;202;14;195 Chronic HBV infection;Hepatocellular carcinoma 124;266 145;269 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Because mutations at the EnhII/BCP/Precore region might decrease HBsAg expression, we investigated the summary odds ratios of HCC for C1653T, T1753V, G1896A, and A1762T/G1764A in groups that differed by HBeAg status. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;G1896A;A1762T 169;134;142;150;162 175;140;148;156;168 BCP;Enh II;C;S;Precore 31;25;203;65;35 34;30;208;70;42 Hepatocellular carcinoma 126 129 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1653T, T1753V, and A1762T/G1764A may alter the binding ability of these nuclear factors and may also lead to amino acid alterations of X protein, both of which could contribute to hepatocarcinogenesis. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 27;0;8;20 33;6;14;26 X 136 137 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. C1653T, T1753V, and A1762T/G1764A mutations in HBV C1 and/or C2 were statistically significantly associated with an increased risk of HCC (Table 3). 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 27;0;8;20 33;6;14;26 Hepatocellular carcinoma 134 137 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. G1896A and C1858T were not statistically significantly associated with HCC risk. 2009 Journal of the National Cancer Institute Discussion HBV G1896A;C1858T 0;11 6;17 Hepatocellular carcinoma 71 74 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. In conclusion, we found that PreS mutations, C1653T, T1753V, and A1762T/G1764A are associated with an increased risk of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 72;45;53;65 78;51;59;71 PreS 29 33 Hepatocellular carcinoma 120 123 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. It is biologically plausible that PreS mutations, C1653T, T1753V, and A1762T/G1764A could contribute to the risk of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 77;50;58;70 83;56;64;76 PreS 34 38 Hepatocellular carcinoma 116 119 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Moreover, HBV mutations, including A1762T/G1764A, accumulate with increasing age. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 42;35 48;41 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. On the basis of these data, we speculate that HBeAg and C1653T, T1753V, and A1762T/G1764A may play a synergistic role in hepatocarcinogenesis. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 83;56;64;76 89;62;70;82 C 46 51 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Other mutations that have been shown to be statistically significantly associated with the risk of HCC, such as those at T31C, T53C, G1613A, A1703G, G1719T, C1726A, and G1730C, were not included because few patients had these mutations. 2009 Journal of the National Cancer Institute Discussion HBV T31C;T53C;G1613A;A1703G;G1719T;C1726A;G1730C 121;127;133;141;149;157;169 125;131;139;147;155;163;175 Hepatocellular carcinoma 99 102 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Our finding that the summary odds ratios for T1753V and A1762T/G1764A were higher in the confounder-unmatched, low-quality studies than in the confounder-matched, high-quality studies suggests that potential confounders play an important role in evaluating HBV mutations and risk of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;T1753V;A1762T 63;45;56 69;51;62 Hepatocellular carcinoma 283 286 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The highest summary odds ratio for PreS mutations was found in the patients infected with genotype C, whereas the highest summary odds ratio for A1762T/G1764A mutations was found in those infected with genotype B. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 152;145 158;151 PreS 35 39 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The relative strength of the association between HCC risk and PreS mutations or A1762T/G1764A was higher than that between HCC risk and C1653T or T1753V. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T;C1653T;T1753V 87;80;136;146 93;86;142;152 PreS 62 66 Hepatocellular carcinoma;Hepatocellular carcinoma 49;123 52;126 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. The summary odds ratios for C1653T, T1753V, and A1762T/G1764A were higher in the HBeAg-positive group than in the HBeAg-negative group. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 55;28;36;48 61;34;42;54 C;C 81;114 86;119 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. These findings together with our combined mutation data suggest that A1762T/G1764A is an early event in hepatocarcinogenesis, whereas PreS mutations, C1653T, T1753V, and combined mutations are late events. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T;C1653T;T1753V 76;69;150;158 82;75;156;164 PreS 134 138 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. This meta-analysis shows that PreS mutations, C1653T, T1753V, and A1762T/G1764A are each associated with a statistically significantly increased risk of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 73;46;54;66 79;52;60;72 PreS 30 34 Hepatocellular carcinoma 153 156 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. Using the pooled crude odds ratios from the included studies, we found that PreS mutations were associated with 3.77-fold increased risk of HCC, C1653T with a 2.76-fold increased risk, T1753V with a 2.35-fold increased risk, and A1762T/G1764A with a 3.79-fold increased risk of HCC compared with HBV without mutations. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 236;145;185;229 242;151;191;235 PreS 76 80 Hepatocellular carcinoma;Hepatocellular carcinoma 140;278 143;281 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We found that A1762T/G1764A-based combined mutations were more frequent in patients with HCC than in those without HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;A1762T 21;14 27;20 Hepatocellular carcinoma;Hepatocellular carcinoma 89;115 92;118 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We found that PreS, C1653T, and C1653T + T1753V mutations and A1762T/G1764A-based combined mutations had high specificity for the prediction of HCC. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;C1653T;T1753V;A1762T 69;20;32;41;62 75;26;38;47;68 PreS 14 18 Hepatocellular carcinoma 144 147 19574418 Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis. We suggest that PreS mutations, C1653T, T1753V, and A1762T/G1764A, alone or in combination, could be used as potential markers to identify HBV-infected patients who should receive antiviral treatment. 2009 Journal of the National Cancer Institute Discussion HBV G1764A;C1653T;T1753V;A1762T 59;32;40;52 65;38;46;58 PreS 16 20 HBV infections 139 151 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. Another study also reported that K130M and V131I substitutions, which are corresponding to double mutation in BCP, from Indian inactive carrier were generally high (36.0%). 2009 Virology journal Discussion HBV K130M;V131I 33;43 38;48 BCP 110 113 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. Double mutation (A1762T/G1764A) was only found in 1.96% of HBV/B. 2009 Virology journal Discussion HBV G1764A;A1762T 24;17 30;23 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. In our previous study, we included 15 HBV-associated liver disease samples from Makassar, and found that the prevalence of T1753V and A1762T/G1764A mutations were 40.0% and 60.0%, respectively, suggesting that those mutations were associated with severity of liver disease. 2009 Virology journal Discussion HBV G1764A;T1753V;A1762T 141;123;134 147;129;140 Liver disease;Liver disease 53;259 66;272 19691824 Hepatitis B virus genotypes/subgenotypes in voluntary blood donors in Makassar, South Sulawesi, Indonesia. Since both T1753V and A1762T/G1764A mutations were less common in blood donors, the chance of developing severe liver disease might be relatively low in the blood donors in Makassar. 2009 Virology journal Discussion HBV G1764A;T1753V;A1762T 29;11;22 35;17;28 Liver disease 112 125 19748824 CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA. In our patients acquisition of similar mutations but with a more conservative effect in lowering viral replication, like Ser21Ala might considered as a cost to viral fitness that paid by HBV to permit survival by mitigating CTL response . 2009 Journal of clinical virology Discussion HBV S21A 121 129 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. As a result, both BCP triple mutational patterns were present significantly more so in HB-ACLF than in patients with CHB, irrespective of whether the G1896A PC mutation was there or not (Table 4). 2010 Journal of viral hepatitis Discussion HBV G1896A 150 156 BCP;Precore 18;157 21;159 Chronic Hepatitis B;Acute on chronic liver failure 117;87 120;94 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Further analysis indicated that the BCP mutations T1753V, A1762T and G1764A were more frequently detected in genotype C than in genotype B isolates, whereas the G1896A PC mutation was more frequently detected in genotype B than in genotype C ones (Table 2), confirming previous reports. 2010 Journal of viral hepatitis Discussion HBV T1753V;A1762T;G1764A;G1896A 50;58;69;161 56;64;75;167 BCP;Precore 36;168 39;170 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. It has been reported that combined A1762T/G1764A mutations with T1753V, C1766T and/or T1768A may enhance viral replication in vitro and are associated with ALF and advanced liver disease. 2010 Journal of viral hepatitis Discussion HBV G1764A;A1762T;T1753V;C1766T;T1768A 42;35;64;72;86 48;41;70;78;92 Liver disease;Liver disease 173;156 186;159 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. The A1762T/G1764A and G1896A well-recognized BCP/PC mutations were defined as basic BCP and PC mutations in our study. 2010 Journal of viral hepatitis Discussion HBV G1764A;A1762T;G1896A 11;4;22 17;10;28 BCP;BCP;Precore;Precore 45;84;49;92 48;87;51;94 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Therefore, we analyzed two triple BCP mutational patterns T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A) in patients infected with HBV genotype C, as T1753V was detected infrequently in genotype B and not at all in C1766T and T1768A. 2010 Journal of viral hepatitis Discussion HBV A1762T;G1764A;G1764A;C1766T;A1762T;T1768A;T1753V;C1766T;T1768A;T1753V 65;72;90;97;83;108;161;226;237;58 71;78;96;103;89;114;167;232;243;64 BCP 34 37 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. These data may suggest that emergence of the T1753V, C1766T and T1768A mutations was likely an additional driving factor for the development of HB-ACLF. 2010 Journal of viral hepatitis Discussion HBV T1753V;C1766T;T1768A 45;53;64 51;59;70 Acute on chronic liver failure 144 151 20070500 Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis. Thus, the G1896A mutants can sometimes be detected in HBeAg positive patients if they are present at higher levels. 2010 Journal of viral hepatitis Discussion HBV G1896A 10 16 C 54 59 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. A large percentage of the cases with rtA181T mutations developed sW172stop mutations. 2010 Journal of Korean medical science Discussion HBV A181T;W172X 39;65 44;74 RT;S 37;65 39;66 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Although sW172stop and sL173F mutations were detected in the polymerase mutation group, a reduction in HBsAg titer was not found. 2010 Journal of Korean medical science Discussion HBV L173F;W172X 23;9 29;18 S;P;S;S 103;61;9;23 108;71;10;24 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. An F46S mutation in the Pre-S2 region was detected only in patients with the ADV-resistant rtA181T/V mutation. 2010 Journal of Korean medical science Discussion HBV A181T;A181V;F46S 93;93;3 100;100;7 PreS2;RT 24;91 30;93 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. But it is difficult to conclude that it is caused by A184V mutation, because this difference was no longer significant when the analysis was done in pure Group P and patient's number was not enough. 2010 Journal of Korean medical science Discussion HBV A184V 53 58 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Drug resistant mutations to ADV have been reported mainly in the HBV polymerase domain D rtN236T or the domain B rtA181V/T. 2010 Journal of Korean medical science Discussion HBV N236T;A181V;A181T 91;115;115 96;122;122 P;RT;RT 69;89;113 79;91;115 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. However, the A184V mutation did not result in amino acid changes in the polymerase region. 2010 Journal of Korean medical science Discussion HBV A184V 13 18 P 72 82 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In addition, an ADV-resistant mutation at rtA181V results in a concomitant change at sL-173F. 2010 Journal of Korean medical science Discussion HBV A181V 44 49 RT 42 44 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In addition, V32A, I45T, and T49I mutations at Pre-S2 were detected in the HCC patients only. 2010 Journal of Korean medical science Discussion HBV V32A;I45T;T49I 13;19;29 17;23;33 PreS2 47 53 Hepatocellular carcinoma 75 78 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In cases with ADV treated LMV-resistant mutations, the rtA181T mutation was reported at the ADV treatment baseline with low HBV DNA titers. 2010 Journal of Korean medical science Discussion HBV A181T 57 62 RT 55 57 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In Group P, although statistically insignificant, Pre-S1 region nucleotide deletions at position '59', and mutations V60A and L74I were the primary changes detected. 2010 Journal of Korean medical science Discussion HBV V60A;L74I 117;126 121;130 PreS1 50 56 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. In our study, an I126T mutation was detected in 4 of 13 ADV mutants and one of nine control cases. 2010 Journal of Korean medical science Discussion HBV I126T 17 22 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. It is possible that these amino acid substitutions were caused by a remaining LMV-resistant mutation, though a rtM204I/V mutation was not detected in sequencing analysis. 2010 Journal of Korean medical science Discussion HBV M204I;M204V 113;113 120;120 RT 111 113 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. One case of a T131P mutation in Group C and one case of a T140S mutation in Group P were also detected. 2010 Journal of Korean medical science Discussion HBV T131P;T140S 14;58 19;63 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The LMV-resistant polymerase mutation, rtV173L (sE164D), has been reported to reduce the antigenicity of HBsAg. 2010 Journal of Korean medical science Discussion HBV V173L;E164D 41;48 46;54 S;P;RT;S 105;18;39;48 110;28;41;49 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The patients should be followed for a long period of time and the clinical impact of the rtA181T/V mutation should be evaluated. 2010 Journal of Korean medical science Discussion HBV A181T;A181V 91;91 98;98 RT 89 91 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The S gene mutation, A184V, was detected in the ADV-resistant rtA181T/V polymerase mutation group alone. 2010 Journal of Korean medical science Discussion HBV A181T;A181V;A184V 64;64;21 71;71;26 P;RT;S 72;62;4 82;64;5 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. The sA184V mutation was detected in the A181T/V polymerase mutation group alone. 2010 Journal of Korean medical science Discussion HBV A184V;A181T;A181V 4;40;40 10;47;47 P;S 48;4 58;5 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. There is one published report that the A184V mutation was related to reduced or negative HBsAg signal. 2010 Journal of Korean medical science Discussion HBV A184V 39 44 S 89 94 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Therefore, we selected LMV-resistant chronic hepatitis B patients who had developed ADV-resistant A181T/V mutations during ADV rescue therapy. 2010 Journal of Korean medical science Discussion HBV A181T;A181V 98;98 105;105 Chronic Hepatitis B 37 56 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. To determine the clinical significance of I126T, T131P, and T140S mutations, further studies are required. 2010 Journal of Korean medical science Discussion HBV I126T;T131P;T140S 42;49;60 47;54;65 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. We detected sW172stop and sL173F mutations in 10 of the 13 patients with ADV-resistant rtA181T/V polymerase mutations. 2010 Journal of Korean medical science Discussion HBV A181T;A181V;L173F;W172X 89;89;26;12 96;96;32;21 P;RT;S;S 97;87;12;26 107;89;13;27 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. When compared with patients who have not A184V mutation including Group C, ALT level alone was significantly lower in patients with A184V mutation. 2010 Journal of Korean medical science Discussion HBV A184V;A184V 41;132 46;137 20119580 Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations. Whereas a domain D rtN236T mutation does not overlap with the envelope gene, a mutation at rtA181T can result in a stop mutation in the envelope region of the S gene (sW172stop). 2010 Journal of Korean medical science Discussion HBV A181T;N236T;W172X 93;21;167 98;26;176 S;S;RT;RT;S;S 62;136;19;91;159;167 70;144;21;93;160;168 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. An additional unanswered issue is why ETVr substitutions leading to virologic breakthrough occur only in LVDr HBV with the M204V+L180M substitutions and not M204I HBV. 2010 PloS one Discussion HBV M204V;L180M;M204I 123;129;157 128;134;162 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. However, high level phenotypic resistance does not occur when ETVr substitutions are present with only the M204I LVDr substitution and does not result in virologic breakthrough. 2010 PloS one Discussion HBV M204I 107 112 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. I169T substitutions were found in both patients initially identified with ETVr and various I169 substitutions have been seen in twelve of our other ETVr patients. 2010 PloS one Discussion HBV I169T 0 5 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. In contrast, resistance to adefovir leading to virologic breakthrough can arise from either A181 V or T substitutions, or N236T. 2010 PloS one Discussion HBV A181V;N236T 92;122 98;127 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. In general, several residues at position 169 were observed, including I169 L, M, T and S. 2010 PloS one Discussion HBV I169L 70 76 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Indeed the variety of ETVr substitutions found in patients includes T184A, C, F, G, I, L, M or S, S202C, G or I, and M250 I, L or V. 2010 PloS one Discussion HBV T184A;S202C;M250I 68;98;117 73;103;123 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Modeling studies suggest that the N236T change may indirectly affect binding of the terminal gamma-phosphate of adefovir-diphosphate and changes at A181 of the alpha helix adjacent to the YMDD active site loop likely affect the position of the YMDD loop itself or the nucleotide in the +1 position through interactions of A181V or T with the M204 S-methyl moiety of the YMDD loop. 2010 PloS one Discussion HBV N236T;A181V;M204S 34;322;342 39;327;348 P;P;P 188;244;370 192;248;374 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Our current hypothesis is that interactions between residues at position 204 and those at 184, 202 or 250 are important for a functional HBV RT enzyme, or perhaps that the ETVr substitutions further decrease the replication capacity of the more impaired M204I virus to below levels required to survive. 2010 PloS one Discussion HBV M204I 254 259 RT 141 143 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. Substitutions T184G and S202G however are examples where the major changes appear to involve disruption of the stabilizing H-bonding network between T184 and S202. 2010 PloS one Discussion HBV T184G;S202G 14;24 19;29 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The larger T184L and S202I substitutions are examples that sterically affect the YMDD loop position. 2010 PloS one Discussion HBV T184L;S202I 11;21 16;26 P 81 85 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. The resistance pattern emerging from clinical studies of ETV suggest a more complex scenario; multiple changes in the HBV RT are required for clinically meaningful resistance, substitutions at T184, S202 or M250 in the HBV RT must be accompanied by LVDr substitutions M204V/I +- L180M. 2010 PloS one Discussion HBV M204V;M204I;L180M 268;268;279 275;275;284 RT;RT 122;223 124;225 20169198 Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir. We also have seen a very limited set of substitutions at T184 or M250 substitutions in viruses with the M204I LVDr change, and those that occur in both LVDr types show higher levels of resistance in the M204V+L180M background. 2010 PloS one Discussion HBV M204I;M204V;L180M 104;203;209 109;208;214 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. A well-documented immune escape mutant G145R in one clone, might occur naturally due to lack of proof-reading activity of rt domain and exist as quasi-species viral population. 2010 Virology journal Discussion HBV G145R 39 44 RT 122 124 20492719 A novel nucleotide insertion in S gene of hepatitis B virus in a chronic carrier. Some reported drug-resistant mutants, such as rtF166L and rtP177L, were found in clone18 and clone15, respectively, and rtD205N mutant(creating premature stop codon at aa196 in overlapping HBsAg) in clone13 led to change from YMDD motif to YMND motif. 2010 Virology journal Discussion HBV D205N;F166L;P177L 122;48;60 127;53;65 S;RT;RT;RT;P 189;46;58;120;226 194;48;60;122;230 20573234 Infection with hepatitis B virus carrying novel pre-S/S gene mutations in female siblings vaccinated at birth: two case reports. Notably, all three patients carried the sT126N mutation (Figure 2). 2010 Journal of medical case reports Discussion HBV T126N 40 46 S 40 41 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. In addition to the known rtM204V substitution, a novel virus variant with a methionine to lysine (YKDD) substitution was found. 2010 Virology journal Discussion HBV M204V 27 32 RT 25 27 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. Induction of isoleucine or valine in the YMDD motif results in a sterical hindrance, preventing lamivudine from appropriately configuring into the nucleotide binding site of the reverse transcriptase, and so the rtM204K substitution may also do. 2010 Virology journal Discussion HBV M204K 214 219 RT;RT;P 178;212;41 199;214;45 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. Quasispecies analyses revealed and proofed the presence of several mutations, including the rtM204V substitution, which is well known to be associated with the selection of lamivudine-resistance virus variants. 2010 Virology journal Discussion HBV M204V 94 99 RT 92 94 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. Resistance-associated mutations outside the YMDD motiv include amino acid exchanges at the reverse transcriptase codon L180 M (rtL180M) or the rtV207I codon. 2010 Virology journal Discussion HBV L180M;V207I;L180M 129;145;119 134;150;125 RT;RT;RT;P 91;127;143;44 112;129;145;48 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. The selection pressure caused by adefovir can lead to upraise of the mutations rtA181V and rtN236T or rtI233V. 2010 Virology journal Discussion HBV A181V;N236T;I233V 81;93;104 86;98;109 RT;RT;RT 79;91;102 81;93;104 20646332 Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case. The substitution of lysine to methionine at position rt180 is also connected and approved to contribute to lamivudine resistance and is known to augments the lamivudine resistant in conjunction with rtM204V. 2010 Virology journal Discussion HBV M204V 201 206 RT;RT 53;199 55;201 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. BCP A1762T and G1764A have a reported association with HCC in particular, and more severe clinical outcomes in general. 2010 Virology Discussion HBV A1762T;G1764A 4;15 10;21 BCP 0 3 Hepatocellular carcinoma 55 58 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. BCP A1762T and G1764A mutations were more common in patients with HBV genotype C mono-infection, as previously described in patients from Taiwan and China. 2010 Virology Discussion HBV A1762T;G1764A 4;15 10;21 BCP 0 3 HBV infections 66 95 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. BCP mutations A1762T and G1764A were more frequent in HBV genotype C mono-infection and the -1G frameshift was only observed in HBV genotype A co-infection. 2010 Virology Discussion HBV A1762T;G1764A 14;25 20;31 BCP 0 3 HBV infections;HBV infections 54;128 83;155 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. The majority of the PreS2 mutants identified in our study also encoded A1762T/G1764A basal core mutations. 2010 Virology Discussion HBV G1764A;A1762T 78;71 84;77 C;PreS2 91;20 95;25 20655563 HBV mutations in untreated HIV-HBV co-infection using genomic length sequencing. The presence of PreS2 deletions together with BCP A1762T/G1764A mutations have been reported in immunosuppressed genotype A HBV mono-infected patients with advanced liver disease. 2010 Virology Discussion HBV G1764A;A1762T 57;50 63;56 BCP;PreS2 46;16 49;21 Liver disease 165 178 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. A feature of those mutations, including T1753A/C, G1764A and A1762T, is their significance as risk factors in disease progression only shown by univariate analysis but not in the multivairate model when patient age was considered. 2010 BMC infectious diseases Discussion HBV T1753C;T1753A;G1764A;A1762T 40;40;50;61 48;48;56;67 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. As this is the first time proposing possible role of G1776A, further verification is needed in larger sample size. 2010 BMC infectious diseases Discussion HBV G1776A 53 59 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. In this study, we showed that G1776A is a new candidate mutation correlating to HBeAg negativity. 2010 BMC infectious diseases Discussion HBV G1776A 30 36 C 80 85 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Since nt1776 localizes at the binding site to transcription factor FXRalpha, which promotes the expression of e antigen, one possible mechanism for G1776A mutation is to interrupt normal transcription of preC region. 2010 BMC infectious diseases Discussion HBV G1776A 148 154 C;Precore 110;204 119;208 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. The effects of G1762A and A1764T in disease progression had attracted attentions especially in genotypes B and C, however our study suggests that the appearance of these mutations may just be a sign of long infection history and may not be very important in disease prognosis. 2010 BMC infectious diseases Discussion HBV G1762A;A1764T 15;26 21;32 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. The second type, such as G1896A, has high occurrence in ALD patients and is independent from infection history, suggesting mutants carrying this substitution may lead to worsening symptoms once they appear. 2010 BMC infectious diseases Discussion HBV G1896A 25 31 Liver disease 56 59 20846420 Prevalent HBV point mutations and mutation combinations at BCP/preC region and their association with liver disease progression. Thus far only G1896A, which leads a 2/3 truncated e antigen by a stop codon caused by mutation, was verified to be responsible for HBeAg negativity. 2010 BMC infectious diseases Discussion HBV G1896A 14 20 C;C 50;131 59;136 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Consistently, our data also showed that WT, L60V, S87G and I97L HBc protein downregulated the promoter activity of the MxA gene induced by IFN-alpha. 2010 Virology journal Discussion HBV L60V;S87G;I97L 44;50;59 48;54;63 C 64 67 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Different replicative characteristics and clinical significance of full-length HBV strains carrying core protein hot-spot mutations (L60V, S87G and I97L) has also been reported. 2010 Virology journal Discussion HBV L60V;S87G;I97L 133;139;148 137;143;152 C 100 104 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. From this study, we suppose that the mutated HBc proteins might down-regulate MxA gene transcription by inhibiting promoter activity induced by IFN-alpha in a similar way to that reported for WT HBc protein, but the special inhibitory role of I97L HBc on MxA transcription in Huh7 cells need to be further studied. 2010 Virology journal Discussion HBV I97L 243 247 C;C;C 45;195;248 48;198;251 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In our study, we showed that L60V and S87G HBc protein decreased the MxA mRNA level induced by IFN-alpha in Huh7 cells to a similar degree as WT. 2010 Virology journal Discussion HBV L60V;S87G 29;38 33;42 C 43 46 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. In particular, I97L HBc protein remarkably inhibited the MxA promoter activity compared to L60V, S87G or WT. 2010 Virology journal Discussion HBV I97L;L60V;S87G 15;91;97 19;95;101 C 20 23 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Moreover, compared with WT and the other two mutants (L60V, S87G), I97L HBc protein remarkably decreased the MxA mRNA level. 2010 Virology journal Discussion HBV L60V;S87G;I97L 54;60;67 58;64;71 C 72 75 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Our data showed that, in Huh7 cells stably expressing WT HBc protein or mutated proteins (L60V, S87G and I97L), IFN-alpha inhibited the extra- and intracellular levels of HBV DNA, and HBsAg secretion to a similar degree to that in the cells transfected with control plasmids. 2010 Virology journal Discussion HBV L60V;S87G;I97L 90;96;105 94;100;109 C;S 57;184 60;189 20959021 Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha. Our result demonstrated in vitro that the HBc hot-spot mutants also inhibited the mRNA level induced by IFN-alpha and I97L showed significantly more inhibitory effect than that of WT. 2010 Virology journal Discussion HBV I97L 118 122 C 42 45 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Comparison of variants T123A, M133L and T143M with the reference wild-type HBsAg showed different predicted tertiary structures with lesser degree of changes observed in the mainframe helices compared to the loops' structures (Figure 2). 2010 Virology journal Discussion HBV T123A;M133L;T143M 23;30;40 28;35;45 S 75 80 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. M133L mutant showed the least significant changes, probably because it is located in less-antigenic first loop, and also because both Met and Leu are non-polar residues with similar bulkiness of their side-chains. 2010 Virology journal Discussion HBV M133L 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Marked changes were also observed in T123N and T143L substitutions, which might be caused by both the shift from slightly small, polar Thr into either larger, more polar Asp or bulkier, non-polar Leu and the importance of their respective locations. 2010 Virology journal Discussion HBV T123N;T143L 37;47 42;52 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. Similarly, in T143M mutation, a major change from polar Thr into non-polar, significantly bulkier Met within the more antigenic second loop of the 'a' determinant occurred. 2010 Virology journal Discussion HBV T143M 14 19 S 148 162 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. T123A mutant, on the other hand, involved changes from a polar Thr into a non-polar and slightly smaller Ala. 2010 Virology journal Discussion HBV T123A 0 5 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. The degree of changes in antigenicity profile was highest in pattern T143M , followed closely by T123N and T143L, then lesser changes in M133I/T/V as well as T123A and M133L. 2010 Virology journal Discussion HBV M133I;M133T;M133V;T143M;T123N;T143L;T123A;M133L 137;137;137;69;97;107;158;168 146;146;146;74;102;112;163;173 21087462 Prediction of conformational changes by single mutation in the hepatitis B virus surface antigen (HBsAg) identified in HBsAg-negative blood donors. The trend in M133I/T/V can also be correlated with the differential amino acid properties, with similar changes between M133I and M133V that involve similarly-sized non polar Met, Ile, and Val; and slightly more significant antigenic alteration in M133T, in which there is a change from Met to polar Thr. 2010 Virology journal Discussion HBV M133I;M133T;M133V;M133I;M133V;M133T 13;13;13;120;130;248 22;22;22;125;135;253 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. A recent study based in Hong Kong has indeed suggested that M204V/I mutation is associated with the resistance of HBeAg-positive chronic HBV patients to lamivudine and adefovir dipivoxil combination treatment. 2010 Mediators of inflammation Discussion HBV M204V;M204I 60;60 67;67 C 114 119 Chronic Hepatitis B 129 140 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. Although these mutations were not reported in an earlier study of patients in China, we have detected HBV A181T/I mutations in one of our patients in the Chinese population. 2010 Mediators of inflammation Discussion HBV A181I;A181T 106;106 113;113 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. HBV A181T and N236T mutations have been reported in adefovir dipivoxil resistant patients in Taiwan and Singapore. 2010 Mediators of inflammation Discussion HBV A181T;N236T 4;14 9;19 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. HBV A181V/T and N236T mutations known to adefovir dipivoxil resistance in adefovir dipivoxil resistant patients. 2010 Mediators of inflammation Discussion HBV A181T;A181V;N236T 4;4;16 11;11;21 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. In the investigation of HBV mutations in adefovir dipivoxil resistance, we have identified HBV A181T/V mutations in one and M204V/I mutations in another of two patients that showed HBV DNA persistence through 104 weeks of adefovir dipivoxil treatment. 2010 Mediators of inflammation Discussion HBV A181T;A181V;M204V;M204I 95;95;124;124 102;102;131;131 21127728 Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil. The HBV L180M and M204V/I mutations are associated with lamivudine resistance and the concept that these mutations can be responsible for adefovir dipivoxil resistance is intriguing and remains to be confirmed in a sizable group of adefovir dipivoxil resistant patients. 2010 Mediators of inflammation Discussion HBV L180M;M204V;M204I 8;18;18 13;25;25 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. However, HBsAg levels produced in vitro by Y100C variant were slightly higher (about 1.5-fold) than the levels produced by wild-type strain. 2011 Hepatitis research and treatment Discussion HBV Y100C 43 48 S 9 14 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. In the case of Y100C variant, the replacement by a more polar amino acid at the end of TM2 segment (position 100) and the presence of a free sulfhydryl group in the amino acid C which increases its reactivity allowing the link to other molecules of C could have altered the conformation of HBsAg, affecting detection due to impaired recognition of epitopes and/or secretion due to defective insertion into the ER membrane and intracellular retention. 2011 Hepatitis research and treatment Discussion HBV Y100C 15 20 S 290 295 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. In the present study, we evaluated if Y100C substitution alone may influence the secretion pattern of HBsAg and/or may modify reactivity against commercial antibodies. 2011 Hepatitis research and treatment Discussion HBV Y100C 38 43 S 102 107 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Our findings indicated that Y100C mutation, which is potentially capable of altering protein conformation, reduce neither the production nor secretion of HBsAg. 2011 Hepatitis research and treatment Discussion HBV Y100C 28 33 S 154 159 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. The Y100C variation of the small S protein has been frequently detected in the absence of HBsAg and has been statistically associated with occult infection in studies conducted in Venezuela and in Brazil. 2011 Hepatitis research and treatment Discussion HBV Y100C 4 9 S;S 90;27 95;34 Occult Hepatitis B 139 155 21331286 Expression of Hepatitis B Virus Surface Antigen Containing Y100C Variant Frequently Detected in Occult HBV Infection. Viruses with G145R replacement have been almost invariably isolated as a major escape mutant after HBV vaccination. 2011 Hepatitis research and treatment Discussion HBV G145R 13 18 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Although in vitro phenotyping was not performed in this study, it has been shown that MDR strains with signature mutations to both LAM and ADV (rtM204V + A181V/N236T) have competent replicative capacity in the presence of LAM and ADV and obviously reduced susceptibility to each of the drugs in comparison with wild-type stains [51, 52]. 2011 Journal of viral hepatitis Discussion HBV N236T;M204V;A181V 160;146;154 165;151;159 RT 144 146 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Amongst these, rtL80I was reported to compensate for the loss of replication efficiency associated with the acquisition of LAM resistance, particularly in the case of rtM204I [45]. 2011 Journal of viral hepatitis Discussion HBV L80I;M204I 17;169 21;174 RT;RT 15;167 17;169 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. As rtL180M can compensate for the replication capacity of the YMDD mutant and higher viral replication may induce stronger immune responses, it is plausible that elevated ALT was associated with the fluctuating cycle of viral replication and hepatic inflammation. 2011 Journal of viral hepatitis Discussion HBV L180M 5 10 RT;P 3;62 5;66 Liver inflammation 242 262 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. By contrast, rtV84M and rtV214A were more likely to be concomitant mutations. 2011 Journal of viral hepatitis Discussion HBV V84M;V214A 15;26 19;31 RT;RT 13;24 15;26 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Consistent with this is the observation that rtL180M with rtM204I have been reported to decrease serum ALT normalization significantly after ADV therapy [44]. 2011 Journal of viral hepatitis Discussion HBV L180M;M204I 47;60 52;65 RT;RT 45;58 47;60 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Our results were consistent with this view as 85.2% of rtL80I concurred with rtM204I and rtM204I/V. 2011 Journal of viral hepatitis Discussion HBV L80I;M204I;M204V;M204I 57;79;91;91 61;84;98;98 RT;RT;RT 55;77;89 57;79;91 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The incidence of mutational patterns of rtM204I and rtM204V has been reported to be significantly different between genotype B and C HBV [43], but we did not observe any significant differences in this study. 2011 Journal of viral hepatitis Discussion HBV M204I;M204V 42;54 47;59 RT;RT 40;52 42;54 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtL80I occurred proportionally equally between the presence and absence of compensatory mutations rtL180M +- V173L, but it occurred more frequently in genotype C than in genotype B (7.6%vs 3.7%, P = 0.019). 2011 Journal of viral hepatitis Discussion HBV L80I;L180M;V173L 6;104;113 10;109;118 RT;RT 4;102 6;104 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtM204V was usually concomitant with rtL180M. 2011 Journal of viral hepatitis Discussion HBV L180M;M204V 43;6 48;11 RT;RT 4;41 6;43 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtQ215S, rtL217R and rtI233V had a lower incidence. 2011 Journal of viral hepatitis Discussion HBV I233V;Q215S;L217R 27;6;15 32;11;20 RT;RT;RT 4;13;25 6;15;27 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. The rtV84M, rtA181T and rtV214A were more common in LAM- and/or ADV-treated patients. 2011 Journal of viral hepatitis Discussion HBV V84M;A181T;V214A 6;14;26 10;19;31 RT;RT;RT 4;12;24 6;14;26 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. Therefore, LAM switching-to LdT is unsuitable once YMDD mutations occurred, as LdT is ineffective against both rtM204I and rtL180M + M204V mutants, though it remains effective against the single rtM204V mutation [6]. 2011 Journal of viral hepatitis Discussion HBV M204I;L180M;M204V;M204V 113;125;197;133 118;130;202;138 RT;RT;RT;P 111;123;195;51 113;125;197;55 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. To date, reports on clinical MDR HBV strains are restricted to double resistance against LAM and ADV [23, 46, 47, 48, 49, 50], if rtA181T/V cross-resistance alone and anti-HBs immunoglobulin resistance are excluded. 2011 Journal of viral hepatitis Discussion HBV A181T;A181V 132;132 139;139 S;RT 172;130 175;132 21392168 Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection. We found that the incidence of rtM204I concomitant with rtL180M was significantly higher in genotype C than in genotype B, and patients with rtM204I + L180M had a higher ALT level compared to those with rtM204I alone. 2011 Journal of viral hepatitis Discussion HBV L180M;M204I;M204I;M204I;L180M 58;33;143;205;151 63;38;148;210;156 RT;RT;RT;RT 31;56;141;203 33;58;143;205 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. In Korean adults, CP mutations (A1762T, G1654A) were found in 95.0% of ICP patients, in 67% of HBeAg negative carriers, and in 30.0% of ITP patients. 2011 Journal of Korean medical science Discussion HBV A1762T;G1654A 32;40 38;46 Core promoter;C 18;95 20;100 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. In the precore gene, the guanine-to-adenine mutation at nucleotide 1896 (G1896A) is the most prevalent. 2011 Journal of Korean medical science Discussion HBV G1896A 73 79 Precore 7 14 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. The common mutations of the CP genes are the adenine-to-thymine mutation at nucleotide 1762 (A1762T) and/or the guanine-to-adenine mutation at nucleotide 1764 (G1764A). 2011 Journal of Korean medical science Discussion HBV A1762T;G1764A 93;160 99;166 Core promoter 28 30 21468263 Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children. The precore mutation (G1896A) was less prevalent than CP mutations (i.e., 5% of ICP patients, 32.5% of HBeAg negative carriers, and 22.5% of ITP patients). 2011 Journal of Korean medical science Discussion HBV G1896A 22 28 Core promoter;C;Precore 54;103;4 56;108;11 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. In addition, chronic hepatitis B patients with C336/T336/C337 variants had a significant lower rate of severely elevated serum HBV DNA levels than those with the wild type A336/T337, which was in agreement with previous report that A336C/A336T/T337C variations caused the decreases in serum HBV DNA levels and HBV replication. 2011 Virology journal Discussion HBV A336T;T337C;A336C 238;244;232 243;249;237 Chronic Hepatitis B 13 32 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. In conclusion, A336C/A336T/T337C were naturally occurring polymorphisms in HBV core gene, and the presence of C336/T336/C337 variants was first demonstrated to be an independent factor associating with spontaneous HBeAg loss. 2011 Virology journal Discussion HBV A336T;T337C;A336C 21;27;15 26;32;20 C;C 79;214 83;219 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. In this cross-sectional study, 166 serum samples from chronic hepatitis B patients without any antiviral therapy were enrolled, and A336C/A336T/T337C variations and G1896A variation occurred in 24.1% (40/166) and 45.2% (75/166) serum samples, respectively. 2011 Virology journal Discussion HBV A336T;T337C;A336C;G1896A 138;144;132;165 143;149;137;171 Chronic Hepatitis B 54 73 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. One cross-sectional study from China found that among 223 HBV DNA-positive chronic patients, the G1896A variation was found in 47/128 HBeAg-negative patients and 5/95 HBeAg-positive patients. 2011 Virology journal Discussion HBV G1896A 97 103 C;C 134;167 139;172 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Statistical analysis showed A336C/A336T/T337C variations were closely associated with G1896A variation and more prone to occur in samples with A1896 variants, therefore, A336C/A336T/T337C were naturally occurring polymorphisms as well as G1896A. 2011 Virology journal Discussion HBV A336T;T337C;A336T;T337C;A336C;G1896A;A336C;G1896A 34;40;176;182;28;86;170;238 39;45;181;187;33;92;175;244 21569538 A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients. Therefore, A336C/A336T/T337C variations were proposed to be another major mechanism to explain spontaneous HBeAg loss in the natural history of chronic HBV infection as well as G1896A variation and genotype B. 2011 Virology journal Discussion HBV A336T;T337C;A336C;G1896A 17;23;11;177 22;28;16;183 C 107 112 Chronic HBV infection 144 165 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Compared with DNA sequencing, melting curve analysis has the advantage of distinguishing whether G1896A and G1899A are separate (single mutations) or in the same genome (double mutation). 2011 Journal of clinical virology Discussion HBV G1896A;G1899A 97;108 103;114 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Quantification of HBV G1896A mutant was reported previously using a TaqMan probe. 2011 Journal of clinical virology Discussion HBV G1896A 22 28 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. The probe matched with the G1896A sequence, being almost identical to our SPC2 probe except complementary to each other. 2011 Journal of clinical virology Discussion HBV G1896A 27 33 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. This could cause significant underestimation of the amount of G1896A. 2011 Journal of clinical virology Discussion HBV G1896A 62 68 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. This probe could be used to quantify the G1896A single mutation but not G1896A/G1899A because the amplification signals of the double mutation could not be separated from those of the WT DNA. 2011 Journal of clinical virology Discussion HBV G1899A;G1896A;G1896A 79;41;72 85;47;78 21665530 Quantification of complex precore mutations of hepatitis B virus by SimpleProbe real time PCR and dual melting analysis. Using this novel assay, we found that G1896A, previously reported to be associated with high virulence, replication advantage and HBeAg seronegativity, is present in 95% of HBeAg-positive patients. 2011 Journal of clinical virology Discussion HBV G1896A 38 44 C;C 130;173 135;178 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. Additional mutations able to restore replicative fitness to similar levels in the wild type such as rtV173L and rtP177S were not found. 2011 BMC infectious diseases Discussion HBV P177S;V173L 114;102 119;107 RT;RT 100;112 102;114 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. In presence of the rtL180M and rtM204V as well as entecavir-associated mutations, the susceptibility to entecavir decreased dramatically as seen by an increase in inhibitory concentration 50% (IC50) values from 280 to over 1500 fold. 2011 BMC infectious diseases Discussion HBV M204V;L180M 33;21 38;26 RT;RT 19;31 21;33 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. In spite of the fact that the A181T adefovir-resistance and the T184L entecavir-resistance mutations were present in the background, they were only minor components of the HBV quasispecies that emerged once tenofovir was added in two consecutive samples separated by a five-month interval. 2011 BMC infectious diseases Discussion HBV A181T;T184L 30;64 35;69 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. It was expected to find viral replication impairment when rtA181T mutation was detected under adefovir monotherapy, since this variant has a secretory defect and exerts a dominant negative effect on wild-type HBV virion secretion. 2011 BMC infectious diseases Discussion HBV A181T 60 65 RT 58 60 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The A194T mutation that appears to lead to an over ten-fold decrease in tenofovir sensitivity was not detected in the HBV quasispecies composition of those previous isolates during entecavir-tenofovir therapy. 2011 BMC infectious diseases Discussion HBV A194T 4 9 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The combination of the rtL180M+ rtM204V mutations harbored by our patient results in a replicative fitness of about 50% of that shown by the wild-type virus. 2011 BMC infectious diseases Discussion HBV L180M;M204V 25;34 30;39 RT;RT 23;32 25;34 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The role of the rtA200V and rtI253V mutations found during lamivudine therapy is not clear. 2011 BMC infectious diseases Discussion HBV A200V;I253V 18;30 23;35 RT;RT 16;28 18;30 21696601 Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations. The viral polymerase characterization in our patient at quasispecies level showed lamivudine-associated mutations rtL180M and rtM204V/I during adefovir, entecavir and entecavir-tenofovir therapies. 2011 BMC infectious diseases Discussion HBV M204V;M204I;L180M 128;128;116 135;135;121 P;RT;RT 10;114;126 20;116;128 21704589 Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. Our results in HepG2 and Huh7cells indicate that Combo mutant HBx I127N/K130M/V131/I/F132Y with changes corresponding to core promoter mutations T1753A/A1762T/G1764A/T1768A that are typically found in patients close to the time of diagnosis of HCC decreased p21 expression while TA double mutation or other single CP mutants had a more modest effect on p21 downregulation compared to control. 2011 Gastroenterology Discussion HBV I132Y;K130M;F132Y;G1764A;A1762T;T1768A;I127N;T1753A 83;72;85;159;152;166;66;145 90;77;90;165;158;172;71;151 Core promoter;Core promoter;X 121;314;62 134;316;65 Hepatocellular carcinoma 244 247 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. Among these mutants, the T361A nonsense mutation in the small S region, which resulted in a 69aa truncated HBsAg lacking the entire "a" determinant region (aa124-147), was first detected at the 2nd time point in one clone. 2011 Hepatitis research and treatment Discussion HBV T361A 25 30 S;S 107;56 112;63 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. In the meanwhile, new point mutations such as C339T and T770C were detected at the 3rd time point; the former occurred in the hydrophilic region of HBsAg and the latter was previously discovered in a HCC patient (Genbank number AY206393). 2011 Hepatitis research and treatment Discussion HBV C339T;T770C 46;56 51;61 S 148 153 Hepatocellular carcinoma 200 203 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. In the present study, all clones of the mother from three time points had double mutations of nucleotide A1762T/G1764A in basal core promoter (BCP), four of which were also coupled with G1896A. 2011 Hepatitis research and treatment Discussion HBV G1764A;A1762T;G1896A 112;105;186 118;111;192 BCP;BCP 122;143 141;146 21785721 Evolution of Hepatitis B Virus in a Chronic HBV-Infected Patient over 2 Years. Other mutations such as C934A, C2351T/A2353T, C2444T, A1762T/G1764A, and G1896A were scattered in the whole genomes. 2011 Hepatitis research and treatment Discussion HBV A2353T;G1764A;C934A;C2351T;C2444T;A1762T;G1896A 38;61;24;31;46;54;73 44;67;29;37;52;60;79 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. 1151-1684 in which our G1613A mutation is found. 2011 PloS one Discussion HBV G1613A 23 29 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. G1613A mutation was found in HCC patients, particularly associates to subgenotype Cs as we demonstrated in this study. 2011 PloS one Discussion HBV G1613A 0 6 Hepatocellular carcinoma 29 32 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. However, the functional consequences of G1613A mutation are not yet to be determined. 2011 PloS one Discussion HBV G1613A 40 46 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In our results, the phenotype of the G1613A mutation which includes the suppression of HBeAg secretion and the enhancement of viral DNA production may indicate a more aggressive disease stage of liver introduced by this mutation. 2011 PloS one Discussion HBV G1613A 37 43 C 87 92 Liver disease 167 185 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In summary, we demonstrated that the G1613A mutation, a hotspot mutation on NRE found in HCC patients suppresses the HBeAg secretion and enhances the viral load, which may possibly lead to a more active hepatitis and the risk to HCC. 2011 PloS one Discussion HBV G1613A 37 43 C 117 122 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatitis 89;229;203 92;232;212 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. In this report, we showed that the G1613A mutation is associated to a viral load of more than 6 log copies/ml in female carriers, indicating that there may be a link between this mutation and the HBV-related HCC development through the enhanced viral load. 2011 PloS one Discussion HBV G1613A 35 41 Hepatocellular carcinoma 208 211 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Intriguingly, the G1613A mutated NRE sequence share higher homology with the consensus RFX1 binding sequence than the wild-type sequence, indicating the higher affinity of the mutant NRE to the protein leads to the transactivation of the core promoter activity. 2011 PloS one Discussion HBV G1613A 18 24 Core promoter 238 251 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Moreover, we demonstrated that RFX1 plays a significant role on transactivating HBV core promoter activity with the G1613A mutation and suggested a possible molecular linkage between this mutation and the resulted phenotype of the virus. 2011 PloS one Discussion HBV G1613A 116 122 Core promoter 84 97 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Moreover, we found two main protein complexes that associated with NRE sequence of core promoter and showed differential binding affinity towards the wild-type and mutant NRE sequences, suggesting the possible role of the G1613A mutation on regulating core promoter activity, and hence modulating viral replication and protein secretion. 2011 PloS one Discussion HBV G1613A 222 228 Core promoter;Core promoter 83;252 96;265 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Moreover, we further investigated the functional consequences of the G1613A mutation in the context of 1.3x full-length replicative competent HBV genomes and provide a possible molecular mechanism of the G1613A mutation and resulted phenotype of the virus. 2011 PloS one Discussion HBV G1613A;G1613A 69;204 75;210 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Nevertheless, in our study, the G1613A mutation affects not only at promoter level but also possibly posttranscriptionally, suggesting the tightly regulated processes of HBV replication. 2011 PloS one Discussion HBV G1613A 32 38 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Our result also demonstrated that there was no correlation between the level of HBsAg and the G1613A mutation. 2011 PloS one Discussion HBV G1613A 94 100 S 80 85 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Our work demonstrated that the G1613A mutation leads to the suppression of HBeAg secretion. 2011 PloS one Discussion HBV G1613A 31 37 C 75 80 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Previously, we showed that the G1613A mutation in the HBV core promoter is a hotspot in HCC patients, which could be a potential biomarker for risk evaluation of HCC. 2011 PloS one Discussion HBV G1613A 31 37 Core promoter 58 71 Hepatocellular carcinoma;Hepatocellular carcinoma 88;162 91;165 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. The G1613A mutation within this region may possibly disrupts this secondary structure and hence, affect the function of PRE. 2011 PloS one Discussion HBV G1613A 4 10 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. We further identified a transactivator of the HBV enhancer I, RFX1, binds to the G1613A mutant with higher affinity than the wild-type sequence and possesses the trans-activating effect to enhance the core promoter activity in liver cells. 2011 PloS one Discussion HBV G1613A 81 87 Core promoter;Enh I 201;50 214;60 21814558 The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity. Whether the G1613A mutation affect the binding to these proteins deserves to be investigated in the future. 2011 PloS one Discussion HBV G1613A 12 18 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Additionally, owing to secretory defect and a dominant negative effect on wild-type HBV virion secretion, emergence of rtA181T/sW172* largely reduced the typical extent of virological breakthrough in serum, resulting in difficulty to recognize drug resistance. 2011 BMC cancer Discussion HBV W172X;A181T 127;121 133;126 RT;S 119;127 121;128 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Furthermore, because the reading frame of HBV polymerase overlaps with that of the S gene, some resistant mutations (such as rtA181T) in the polymerase gene coexist with S gene mutations, including stop codon mutations. 2011 BMC cancer Discussion HBV A181T 127 132 P;P;RT;S;S 46;141;125;83;170 56;151;127;84;171 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. In ADV add-on studies, it was found that rtA181T mutants could be either pre-existing in LAM-resistant patients or de novo-developed after ADV add-on therapy. 2011 BMC cancer Discussion HBV A181T 43 48 RT 41 43 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. In some patients with rtA181T mutants, a concomitant sW172* mutation was observed in the overlapping S reading frame, resulting in truncation of the pre-S/S proteins. 2011 BMC cancer Discussion HBV A181T;W172X 24;53 29;59 PreS;S;RT;S;S 149;155;22;53;101 154;156;24;54;102 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. In this study, a hypersensitive ACRES method was used to detect small percentages of the rtA181T mutants. 2011 BMC cancer Discussion HBV A181T 91 96 RT 89 91 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. Of the 10 rtA181T-positive patients, the mutants constituted < 5%, 10-30% and > 90% of the viral population in 6, 2, and 2 patients, respectively. 2011 BMC cancer Discussion HBV A181T 12 17 RT 10 12 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The de novo development of the cross-resistant mutant, rtA181T, was about 4% in a 4-year period of combination treatment with LAM plus ADV. 2011 BMC cancer Discussion HBV A181T 57 62 RT 55 57 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The most striking finding in this study was that pre-existing rtA181T mutant in LAM-resistant patients was independently associated with severe liver consequences, especially occurrence of HCC. 2011 BMC cancer Discussion HBV A181T 64 69 RT 62 64 Hepatocellular carcinoma 189 192 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The premature stop codon of the S gene in the rtA181T/sW172* mutant was located near the border of the transactivity-on-region and its transactivating activity was recently confirmed. 2011 BMC cancer Discussion HBV W172X;A181T 54;48 60;53 RT;S;S 46;32;54 48;33;55 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The present data indicated that in this special subgroup of patients, careful selection of antiviral agent and closely monitoring for viral mutants (including BCP and rtA181T mutations) are mandatory. 2011 BMC cancer Discussion HBV A181T 169 174 BCP;RT 159;167 162;169 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. The rtA181T mutant has been shown to confer ADV-resistant. 2011 BMC cancer Discussion HBV A181T 6 11 RT 4 6 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. This study demonstrated that age > 50 years, cirrhosis, BCP mutation, and the presence of the rtA181T mutation, prior to initiation of rescue therapy were significantly associated with severe liver consequences. 2011 BMC cancer Discussion HBV A181T 96 101 BCP;RT 56;94 59;96 Liver cirrhosis 45 54 21933446 Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B. We speculated that despite a small percentage of the mutants was detected in the serum, a larger percentage could exist in the liver, owing to the secretory defect of the sW172* mutant. 2011 BMC cancer Discussion HBV W172X 171 177 S 171 172 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. Other mutations and mixed combinations were also observed (rtM204I+rtV207M/L, rtM204I+rtV173L, rtM204I+rtS213T, rtM204V+rtL180M+rtV173L/M, rtM204V+rtL180M+rtV207M, rtM204I/V+rtL180M+rtS213T), but with the relatively small sample size in this study, it would be inappropriate to draw strong conclusions on the distributions of those genotypes in southern China. 2011 Medical science monitor Discussion HBV V207M;V207L;V173L;V173M;M204V;M204I;M204I;M204I;S213T;M204V;L180M;V173L;M204V;L180M;V207M;L180M;M204I;S213T 69;69;88;130;166;61;80;97;105;114;122;130;141;149;157;176;166;184 76;76;93;137;173;66;85;102;110;119;127;135;146;154;162;181;171;189 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 59;67;78;86;95;103;112;120;128;139;147;155;164;174;182 61;69;80;88;97;105;114;122;130;141;149;157;166;176;184 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. reported the incidence rate of rtA181V/T mutation in genotype C was significantly higher than that in genotype B. 2011 Medical science monitor Discussion HBV A181V;A181T 33;33 40;40 RT 31 33 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. The frequency of rt204 mutation in our study was 42.16% (78/185); 96.30% of the patients with rtM204V also had rtL180M, while 93.48% of the patients with rtM204I did not. 2011 Medical science monitor Discussion HBV M204I;M204V;L180M 156;96;113 161;101;118 RT;RT;RT;RT 17;94;111;154 19;96;113;156 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. The pattern of rtM204I alone was predominantly observed (36.26%), followed by rtM204V + rtL180M (23.08%). 2011 Medical science monitor Discussion HBV M204I;M204V;L180M 17;80;90 22;85;95 RT;RT;RT 15;78;88 17;80;90 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. The rtM204I alone mutation in genotype B (45.61%) was significantly more frequent than that in genotype C (20.59%) (chi2=5.77, P<0.05). 2011 Medical science monitor Discussion HBV M204I 6 11 RT 4 6 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. These findings agree with the hypothesis that the most frequent mutations are rtL180M and rtM204I/V. 2011 Medical science monitor Discussion HBV M204I;M204V;L180M 92;92;80 99;99;85 RT;RT 78;90 80;92 21959623 Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China. This verifies that the rtM204V mutations are always accompanied by rtL180M, while rtM204I mutations are not. 2011 Medical science monitor Discussion HBV M204V;L180M;M204I 25;69;84 30;74;89 RT;RT;RT 23;67;82 25;69;84 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A meta-analysis of 43 studies revealed that PreS mutation, C1653T, T1753V, and A1762T/G1764A were dominant in HCC. 2011 BMC cancer Discussion HBV G1764A;C1653T;T1753V;A1762T 86;59;67;79 92;65;73;85 PreS 44 48 Hepatocellular carcinoma 110 113 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. A recent study from China revealed that 1613 and 1653 mutations were included in mutations frequently detected in HCC patients; however, core region mutants A2189C and G2203W were independent risk factors for HCC. 2011 BMC cancer Discussion HBV A2189C;G2203W 157;168 163;174 C 137 141 Hepatocellular carcinoma;Hepatocellular carcinoma 114;209 117;212 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. All patients were infected with genotype C viruses, and the most common mutations were G1613A and C1653T. 2011 BMC cancer Discussion HBV G1613A;C1653T 87;98 93;104 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. An analysis of HCC development during the patient follow-up period revealed that the presence of G1613A and/or C1653T mutations was more prevalent in patients who developed HCC long afterward, as compared to the patients who never developed HCC. 2011 BMC cancer Discussion HBV G1613A;C1653T 97;111 103;117 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 15;173;241 18;176;244 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. found that G1613A and C1653T occurred in 38% and 40%, respectively, of 40 HCC patients. 2011 BMC cancer Discussion HBV G1613A;C1653T 11;22 17;28 Hepatocellular carcinoma 74 77 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. Our follow-up analysis revealed that the G1613A mutation was prevalent in patients who would later develop HCC. 2011 BMC cancer Discussion HBV G1613A 41 47 Hepatocellular carcinoma 107 110 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. reported that the combination of C1653T and/or V1753 mutations in addition to T1762/A1764 mutations was differentially associated with HCC in HBeAg-positive genotype C patients. 2011 BMC cancer Discussion HBV C1653T 33 39 C 142 147 Hepatocellular carcinoma 135 138 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The future emergence of HCC is correlated with only G1613A mutation, while the double mutation was associated with the presence of HCC. 2011 BMC cancer Discussion HBV G1613A 52 58 Hepatocellular carcinoma;Hepatocellular carcinoma 24;131 27;134 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The G1613A and C1653T mutations are both located in the core promoter region. 2011 BMC cancer Discussion HBV G1613A;C1653T 4;15 10;21 Core promoter 56 69 22014121 Hepatitis B virus core promoter mutations G1613A and C1653T are significantly associated with hepatocellular carcinoma in genotype C HBV-infected patients. The G1613A and C1653T mutations were not associated with sex or HBeAg-positive status. 2011 BMC cancer Discussion HBV G1613A;C1653T 4;15 10;21 C 64 69 22173170 Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion. This stable phase implies that the G1896A or A1762T/G1764A mutation per se may not confer replication advantage over the wild type virus as indicated by the earlier in vitro studies. 2012 Journal of hepatology Discussion HBV G1764A;G1896A;A1762T 52;35;45 58;41;51 22195774 Emergence of HBV resistance to lamivudine (3TC) in HIV/HBV co-infected patients in The Gambia, West Africa. Thus due to the potential association of the triple 3TC mutations (M204V+ L180M+ V173L+) with vaccine escape mutants, the continuous surveillance of resistance mutants is necessary in a country with a national HBV vaccination programme. 2011 BMC research notes Discussion HBV M204V;L180M;V173L 67;74;81 72;79;86 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Accordingly, in our previously published report, we found that rtQ215A/H/P/S substitutions could be detected as naturally occurring mutations in treatment-naive patients with CHB. 2011 Hepatitis monthly Discussion HBV Q215A;Q215H;Q215P;Q215S 66;66;66;66 77;77;77;77 RT 64 66 Chronic Hepatitis B 176 179 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. ADV drug resistance detected in this study was found to be associated with mutations at rtN236T and rtA181T/V. 2011 Hepatitis monthly Discussion HBV A181T;A181V;N236T 105;105;92 112;112;97 RT;RT 90;103 92;105 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Further, rtQ215S and rtV214A mutations were compensatory mutations arising from ADV treatment. 2011 Hepatitis monthly Discussion HBV Q215S;V214A 11;24 16;29 RT;RT 9;22 11;24 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Furthermore, rtQ215H/P/S substitutions occur as dominant compensatory mutations in treatment-naive hemodialysis patients infected with HBV genotype D (unpublished data). 2011 Hepatitis monthly Discussion HBV Q215H;Q215P;Q215S 15;15;15 24;24;24 RT 13 15 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. High levels of ETV resistance resulted from dual rtM250V and rtI169T mutations, and we detected another profile, the rtM204I/V + rtL180M + rtT184A/I/S or rtS202C triple mutation, as an ETV-resistant mutation in both NUC therapy strategies. 2011 Hepatitis monthly Discussion HBV M250V;M204I;M204V;T184A;T184I;T184S;S202C;I169T;L180M 57;128;128;150;150;150;165;70;140 62;135;135;159;159;159;170;75;145 RT;RT;RT;RT;RT;RT 55;68;126;138;148;163 57;70;128;140;150;165 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. However, while the rtN236T substitution does not significantly affect sensitivity to LAM, rtA181T/V and rtQ215S/rtV214A mutations confer partial cross-resistance to LAM. 2011 Hepatitis monthly Discussion HBV A181V;N236T;A181T;Q215S;V214A 95;22;95;109;117 102;27;102;114;122 RT;RT;RT;RT 20;93;107;115 22;95;109;117 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. In our study, the rtM204V mutation was detected as a single mutation in only 1 patient under monotherapy. 2011 Hepatitis monthly Discussion HBV M204V 22 27 RT 20 22 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. In the current study, we found 1 patient with dual ADV (rtN236T + rtQ215H) and LAM (rtM204V + rtL180M + rtV173L) resistance, detected in different serum samples from the same patient. 2011 Hepatitis monthly Discussion HBV N236T;Q215H;M204V;L180M;V173L 62;72;91;101;111 67;77;96;106;116 RT;RT;RT;RT;RT 60;70;89;99;109 62;72;91;101;111 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. In the current study, mutations at rtQ215S were only observed in the add-on therapy group in 12 patients (14%), while previous studies have described the rtQ215S mutation as a polymorphism that is detected in ~12% of patients treated with LAM. 2011 Hepatitis monthly Discussion HBV Q215S;Q215S 38;160 43;165 RT;RT 36;158 38;160 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. In this study, rtA181T mutations were detected in 6 patients who did not also carry the rtM204I/V mutation. 2011 Hepatitis monthly Discussion HBV A181T;M204I;M204V 17;91;91 22;98;98 RT;RT 15;89 17;91 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. In vitro studies have demonstrated that this mutation alone is insufficient to result in LAM resistance; however, this mutation augments both viral replication and LAM resistance in the context of rtM204I/V mutations. 2011 Hepatitis monthly Discussion HBV M204I;M204V 207;207 214;214 RT 205 207 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Mutant sG145R is the most frequently reported modification and is a known vaccine escape mutant . 2011 Hepatitis monthly Discussion HBV G145R 7 13 S 7 8 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Mutation at codon rtL80I/V may also be an alternative compensatory mutation to rtL180M in HBV genomes encoding the rtM204I mutation, and this mutation may act in a manner similar to rtQ215S. 2011 Hepatitis monthly Discussion HBV L80I;L80V;Q215S;L180M;M204I 20;20;187;82;118 26;26;192;87;123 RT;RT;RT;RT 18;80;116;185 20;82;118;187 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. Studies have shown that LAM-resistant HBV (harboring the rtV173L + rtL180M + rtM204V triple mutation) has significantly reduced anti-HBs binding capacity due to changes in the HBsAg. 2011 Hepatitis monthly Discussion HBV V173L;L180M;M204V 60;70;80 65;75;85 S;S;RT;RT;RT 134;177;58;68;78 137;182;60;70;80 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The results of this study demonstrated that add-on and switch therapy strategies using NUCs to treat CHB conferred similar major drug-resistance patterns at approximately the same frequency, with the exception of compensatory mutations such as rtQ215S. 2011 Hepatitis monthly Discussion HBV Q215S 254 259 RT 252 254 Chronic Hepatitis B 105 108 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The rtA181T HBV mutation is a major mutation pattern associated with LAM resistance, but selected for during ADV treatment and during the development of resistance to combination (ADV + LAM) therapy in the absence of mutations at rtM204I/V. 2011 Hepatitis monthly Discussion HBV A181T;M204I;M204V 6;238;238 11;245;245 RT;RT 4;236 6;238 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The rtL180M mutation was the most common compensatory mutation in our study. 2011 Hepatitis monthly Discussion HBV L180M 6 11 RT 4 6 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. The rtV173L HBV mutation occurs in 9% of LAM-resistant patients and serves to further increase the replication capacity of poorly replicating LAM-resistant HBV. 2011 Hepatitis monthly Discussion HBV V173L 6 11 RT 4 6 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. This mutation is usually not detected as a single mutation, but instead is usually found in combination with rtL180M. 2011 Hepatitis monthly Discussion HBV L180M 114 119 RT 112 114 22224083 Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies. We found similar results when analyzing our data manually and using the geno2pheno program, with the exception of 1 patient with ETV drug resistance (rtM204V + rtL180M + rtT184S). 2011 Hepatitis monthly Discussion HBV M204V;L180M;T184S 154;164;174 159;169;179 RT;RT;RT 152;162;172 154;164;174 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. After treatment with entecavir, the G145R mutant as well as the wild-type virus appeared again in the girl. 2012 BMC research notes Discussion HBV G145R 36 41 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. All of these mutants were reported in previous studies, but the pathogenicity of I/T126V, Q129L, T131P has not been confirmed. 2012 BMC research notes Discussion HBV T126V;I126V;Q129L;T131P 81;81;90;97 88;88;95;102 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Although the G145R mutant was mixed with the predominant wild-type virus and viral replication was influenced by pre-core and basal core promoter mutation, these findings suggest that infection with the G145R mutant does not always promise a good prognosis. 2012 BMC research notes Discussion HBV G145R;G145R 13;203 18;208 BCP;Precore 126;113 145;121 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Among these mutants, the I/T126S mutant was the most frequent (4/107 = 4.7%) in the group 2 of the present study. 2012 BMC research notes Discussion HBV T126S;I126S 25;25 32;32 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Compared with the previous study, the frequency of I/T126S of the present study is high. 2012 BMC research notes Discussion HBV T126S;I126S 51;51 58;58 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Direct sequencing showed that I/T126S, I/T126V, Q129L, T131P, M133T + T140I, and S136Y mutants were present as a predominant strain in 107 HBV carriers. 2012 BMC research notes Discussion HBV T126S;T126V;I126S;I126V;Q129L;T131P;M133T;T140I;S136Y 30;39;30;39;48;55;62;70;81 37;46;37;46;53;60;67;75;86 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. In the previous study targeting unselected Spanish carriers, the prevalence rate of the I/T126S mutant was 0.4% (1/272). 2012 BMC research notes Discussion HBV T126S;I126S 88;88 95;95 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. In this case, the number of the G145R mutant clones was 5 (25%) out of 20 clones. 2012 BMC research notes Discussion HBV G145R 32 37 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. In this study, however, the levels of serum transaminases had been elevated and the levels of HBV DNA had remained high for several years in the girl infected with the G145R mutant, which was detected by the mutant-specific real-time PCR. 2012 BMC research notes Discussion HBV G145R 168 173 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Moreover, the I/T126S mutant was detected in a child with the prophylactic failure in group 1. 2012 BMC research notes Discussion HBV T126S;I126S 14;14 21;21 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. Of the 18 the children with prophylactic failure in the present study, one had an a determinant mutant (I/T126S) as a predominant strain and one had an a determinant mutant (G145R) as a minor strain. 2012 BMC research notes Discussion HBV T126S;I126S;G145R 104;104;174 111;111;179 S;S 82;152 95;165 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The I/T126S mutant has been frequently observed in the studies from Japan, in 12% (5/42) and 13% (5/40) of adult HBV carriers. 2012 BMC research notes Discussion HBV T126S;I126S 4;4 11;11 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The levels of HBV DNA in the blood were not significantly lower in patients with the G145R mutant than in patients without the G145R mutant (data not shown). 2012 BMC research notes Discussion HBV G145R;G145R 85;127 90;132 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The present study showed that the mutant-specific real-time PCR identified a child in whom the G145R mutant and wild-type virus were mixed. 2012 BMC research notes Discussion HBV G145R 95 100 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The results of previous studies suggested that the G145R mutation reduced the ability of viral assembly and secretion. 2012 BMC research notes Discussion HBV G145R 51 56 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. The virulence of the G145R mutant is indeterminate. 2012 BMC research notes Discussion HBV G145R 21 26 22233650 Hepatitis B surface gene 145 mutant as a minor population in hepatitis B virus carriers. There is a possibility that the difference among HBV genotype could be associated with the frequency of the I/T126S mutant. 2012 BMC research notes Discussion HBV T126S;I126S 108;108 115;115 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. A new mutation pattern, rt181S + rtM204I, which arose under LAM treatment, conferring cross-resistance to ADV treatment, has recently been reported in a Turkish patient. 2010 Hepatitis monthly Discussion HBV M204I 35 40 RT;RT 24;33 26;35 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Actually,there has also been no significant relationship between primer drug resistance mutations (the YVDD variant and the rtN236T variant), and HBV DNA loads and ALT levels. 2010 Hepatitis monthly Discussion HBV N236T 126 131 RT;P 124;103 126;107 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. But, the rtN236T mutation responsible for primer ADV drug resistance (besides rtA181V/T) found by LIPAwas never detected in direct sequencing. 2010 Hepatitis monthly Discussion HBV A181V;A181T;N236T 80;80;11 87;87;16 RT;RT 9;78 11;80 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Detected rtM204I and rtA181V mutations in clones 2, 5 and 4, however, in the other serum sample clonally analyzed, was not consistent with the results of direct sequencing and LIPA assay (Table 1). 2010 Hepatitis monthly Discussion HBV A181V;M204I 23;11 28;16 RT;RT 9;21 11;23 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Hence, all of the methods applied in this study are sufficient to establish that the rtM204V + rtV173L + rtL180M mutations are in the same genome and predominate. 2010 Hepatitis monthly Discussion HBV M204V;V173L;L180M 87;97;107 92;102;112 RT;RT;RT 85;95;105 87;97;107 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. However, clonal analysis of the HBV variants revealed that the rtM204V + rtV173L + rtL180M mutations pattern was present in all clones in the sera sample of the 4th month of ETV + TDF therapy Table 2. 2010 Hepatitis monthly Discussion HBV M204V;V173L;L180M 65;75;85 70;80;90 RT;RT;RT 63;73;83 65;75;85 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. However, only the rtL180M mutation was detected by both methods. 2010 Hepatitis monthly Discussion HBV L180M 20 25 RT 18 20 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. In our study, applied LIPA assays showed wild types for the N236 and M204 amino acid positions, and this finding suggests that wild-type virus strains of rtN236T and rtM204V variants may still be reproducible in this patient's sera. 2010 Hepatitis monthly Discussion HBV N236T;M204V 156;168 161;173 RT;RT 154;166 156;168 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Interestingly, in addition to known primary and compensatory mutations, some previously undocumented mutations, such as R120K, H126R, S135Y, and H248N, were detected in 2 of the 5 clones of serum samples from the 11th month of ADV treatment, and in all clones of serum samples from the 4th month of ETV+TDF treatment. 2010 Hepatitis monthly Discussion HBV R120K;H126R;S135Y;H248N 120;127;134;145 125;132;139;150 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Most of the clones from the sera samples taken in the 11th month of ADV therapy revealed the presence of the rtL80V mutation in the clonal analysis of the HBV variants. 2010 Hepatitis monthly Discussion HBV L80V 111 115 RT 109 111 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. On the other hand, compensatory mutations such as rtV173L, rtQ215H, and rtL80I/V have been detected only by direct sequencing and LIPA, respectively. 2010 Hepatitis monthly Discussion HBV L80I;L80V;V173L;Q215H 74;74;52;61 80;80;57;66 RT;RT;RT 50;59;72 52;61;74 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Some compensatory mutations demonstrated in this study (rtL80I/V, rtV173L, rtL180M, rtQ215H) help to restore the replication efficiency of the mutant virus, but they tend to occur in the presence of antiviral selection pressure. 2010 Hepatitis monthly Discussion HBV L80I;L80V;V173L;L180M;Q215H 58;58;68;77;86 64;64;73;82;91 RT;RT;RT;RT 56;66;75;84 58;68;77;86 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. The resistance to LAM and ADV of an engineered laboratory mutant HBV strain harbouring the rtL180M + rtM204V+ rtN236T mutations pattern has been described in vitro, and it was suggested that non-optimal strategies based on the sequential use of NUCs might result in the emergence of selected multidrug-resistant strains. 2010 Hepatitis monthly Discussion HBV L180M;M204V;N236T 93;103;112 98;108;117 RT;RT;RT 91;101;110 93;103;112 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. The rtM204V mutation in our case was detected as a primer drug resistance to LAM in all applied direct sequencing assays and reconfirmed by LIPA findings. 2010 Hepatitis monthly Discussion HBV M204V 6 11 RT 4 6 22312387 Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient. Three primer drug resistance mutations in different domains of HBV viral polymerase, the rtA181V/T, rtL180M+ rtM204V mutations and the rtN236T mutation, were characterized in the same genome, which might explain the multidrug-resistance profile. 2010 Hepatitis monthly Discussion HBV A181V;A181T;L180M;M204V;N236T 91;91;102;111;137 98;98;107;116;142 P;RT;RT;RT;RT 73;89;100;109;135 83;91;102;111;137 22312396 Prevalence and clinical significance of hepatitis B Basal core promoter and precore gene mutations in southern Iranian patients. The other considerable point in our study was that all the patients had mutation from G to A at nucleotide 1896 (G1896A), and no other forms of mutations were observed in the PC region. 2010 Hepatitis monthly Discussion HBV G1896A;G1896A 113;86 119;111 Precore 175 177 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Besides of G145R, different aa substitutions within and outside of MHR were also found in the samples from HBV/B and HBV/C. 2012 Virology journal Discussion HBV G145R 11 16 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. G145R also has a direct impact on the diagnosis. 2012 Virology journal Discussion HBV G145R 0 5 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. Here, G145R could be identified in 5 samples, i.e., 531355, 546227, 563060, 506519, 525706. 2012 Virology journal Discussion HBV G145R 6 11 22500577 Hepatitis B surface antigen variants in voluntary blood donors in Nanjing, China. The well-known G145R was the major variation in the HBV isolates responsible for the occult HBV infections in Xiamen, China. 2012 Virology journal Discussion HBV G145R 15 20 HBV infections 92 106 22510694 Convergence and coevolution of hepatitis B virus drug resistance. For example, single HBV variants that carried the rtM204I substitution before therapy in Patients 6 and 9 were unsuccessful in establishing detectable intra-host HBV populations after treatment. 2012 Nature communications Discussion HBV M204I 52 57 RT 50 52 22510694 Convergence and coevolution of hepatitis B virus drug resistance. HBV resistance to lamivudine is considered to be primarily associated with point mutations, such as rtM204I/V and rtA181V/T (ref.). 2012 Nature communications Discussion HBV M204I;M204V;A181V;A181T 102;102;116;116 109;109;123;123 RT;RT 100;114 102;116 22510694 Convergence and coevolution of hepatitis B virus drug resistance. In Patient 9, the pre-treatment rtM204I-carrying variant belonged to genotype G but only recombinant A/G variants became established after treatment. 2012 Nature communications Discussion HBV M204I 34 39 RT 32 34 22510694 Convergence and coevolution of hepatitis B virus drug resistance. The data presented in this study indicate that, although essential, the mere presence of rtM204V/I is not sufficient for the development of the HBV lamivudine-resistance. 2012 Nature communications Discussion HBV M204V;M204I 91;91 98;98 RT 89 91 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. All but one patient (Liver #10) showing a predominance of A1762T and G1764A were infected with genotype C, while patient#10 was infected with genotype B. 2012 PloS one Discussion HBV A1762T;G1764A 58;69 64;75 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Based on these findings, early administration of NA might be an effective strategy for treating patients with active hepatitis infected predominantly with the G1896A pre-C mutant. 2012 PloS one Discussion HBV G1896A 159 165 Precore 166 171 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Because A1762T and G1764A are reported to be significantly more frequent in genotype C, the difference in the prevalence of A1762T and G1764A in our study might be a reflection of the viral HBV genotype rather than HBe serostatus. 2012 PloS one Discussion HBV A1762T;G1764A;A1762T;G1764A 8;19;124;135 14;25;130;141 C 215 218 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Consistent with our observation, previous studies utilizing conventional sequencing methods reported that the frequency of the G1896A pre-C mutant ranged from 12% to 85%. 2012 PloS one Discussion HBV G1896A 127 133 Precore 134 139 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Consistent with this hypothesis, several previous studies reported that NA is effective against acute or fulminant hepatitis caused by possible infection with the G1896A pre-C mutant. 2012 PloS one Discussion HBV G1896A 163 169 Precore 170 175 Fulminant Hepatitis B 105 124 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. In conclusion, we demonstrated that the majority of patients positive for anti-HBe and negative for HBeAg lacked the predominant infection of the G1896A pre-C mutant in the presence of NA treatment, suggesting that the G1896A pre-C mutant have increased sensitivity to NA therapy compared with wild-type HBV. 2012 PloS one Discussion HBV G1896A;G1896A 146;219 152;225 C;C;Precore;Precore 79;100;153;226 82;105;158;231 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. It is widely accepted that HBe seroconversion is highly associated with the emergence of G1896A pre-C and/or A1762T and G1764A core promoter mutant clones. 2012 PloS one Discussion HBV G1896A;A1762T;G1764A 89;109;120 95;115;126 Core promoter;C;Precore 127;27;96 140;30;101 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Moreover, entecavir administration significantly reduced the proportion of the G1896A pre-C mutant in the serum of the majority of patients irrespective of their HBeAg serostatus, while the G1896A pre-C mutant clones were detectable in a substantial proportion before treatment in all cases. 2012 PloS one Discussion HBV G1896A;G1896A 79;190 85;196 C;Precore;Precore 162;86;197 167;91;202 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. One thing to be noted is that the majority of the chronic-NA cases had extremely low levels of the G1896A pre-C mutant in their liver tissues, even though those cases were serologically positive for anti-HBe and negative for HBeAg. 2012 PloS one Discussion HBV G1896A 99 105 C;C;Precore 204;225;106 207;230;111 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. These findings suggest that the G1896A pre-C mutant have higher sensitivity to NA than the wild-type viruses. 2012 PloS one Discussion HBV G1896A 32 38 Precore 39 44 22523569 Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing. Unexpectedly, however, our results showed a diverse range of G1896A frequency (0-99.9%) in HBeAg-negative subjects and a high prevalence of core promoter mutations, irrespective of HBe serostatus. 2012 PloS one Discussion HBV G1896A 61 67 Core promoter;C;C 140;181;91 153;184;96 22592516 HIV and Hepatitis B coinfection among perinatally HIV-infected Thai adolescents. This is in line with a previous report that 3TC monotherapy is associated with a high risk of developing the M204V resistance mutation, at a rate of approximately 20-25% per year. 2012 The Pediatric infectious disease journal Discussion HBV M204V 109 114 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. During ETV, percentages of both rtA181T and rtV191I dramatically decreased, indicating sensitivity to this drug. 2012 PloS one Discussion HBV A181T;V191I 34;46 39;51 RT;RT 32;44 34;46 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. However, in contrast to this hypothesis, the sensitivity of the LMV-resistant signature to ETV did not change when the signature was combined with rtV207I in a previous phenotypic study. 2012 PloS one Discussion HBV V207I 149 154 RT 147 149 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In addition, due to the 250-bp-length limitation of the standard GS-FLX chemistry, the relevant NA-resistant substitutions, rtI233V and rtN236T linked to ADV treatment failure, and rtM250I/V linked to ETV failure, located outside the B and C HBV RT functional domains, were excluded from the fragment analyzed. 2012 PloS one Discussion HBV N236T;M250I;M250V;I233V 138;183;183;126 143;190;190;131 RT;RT;RT;RT 124;136;181;246 126;138;183;248 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In addition, the sS167L variant, associated with a silent RT substitution in rtL175 (CTC to CTT), showed a continuous percentage increase in the absence of treatment and during follow-up. 2012 PloS one Discussion HBV S167L 17 23 RT;RT;S 58;77;17 60;79;18 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In the case of the rtA200V substitution, although previously associated with resistance to LMV and LdT, in this longitudinal study it was only found significantly increased at ETV VBK, suggesting some "decreased sensitivity" to ETV. 2012 PloS one Discussion HBV A200V 21 26 RT 19 21 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In the longitudinal study of the patient sequentially treated with LMV, ADV, and ETV monotherapies, the blind SD-based algorithm ranked the 7 NA resistance-related aa substitutions previously detected by routine analysis (rtL180M, rtM204V, rtS202G, rtV207I, rtA181T, rtV173L and rtI169T) as the most variable, and 5 additional NA resistance substitutions (rtV191I, rtM204I, rtT184A, rtA181S and rtA200V) immediately after them. 2012 PloS one Discussion HBV A181T;I169T;V191I;A181S;A200V;L180M;M204V;S202G;V207I;V173L;M204I;T184A 260;281;358;385;397;224;233;242;251;269;367;376 265;286;363;390;402;229;238;247;256;274;372;381 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 222;231;240;249;258;267;279;356;365;374;383;395 224;233;242;251;260;269;281;358;367;376;385;397 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In this particular case, percentages of rtV191I increased during LMV and ADV, mainly in combination with the major variant rtA181T, suggesting a compensatory role of rtV191I to restore its replicative fitness. 2012 PloS one Discussion HBV V191I;A181T;V191I 42;125;168 47;130;173 RT;RT;RT 40;123;166 42;125;168 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In this particular case, the frequency of the LMV resistance signature (rtL180M-M204V) alone showed a considerable increase at ETV VBK relative to its frequency after LMV, as also occurred with the more complex variant rtV173L-L180M-M204V. 2012 PloS one Discussion HBV L180M;V173L;M204V;L180M;M204V 74;221;80;227;233 79;226;85;232;238 RT;RT 72;219 74;221 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In this sense, the increase in percentages of NA-resistant rtV191I in the absence of treatment concurs with its reported link to humoral immune response escape by an association with the surface stop codon sW182*, recently related to liver disease progression. 2012 PloS one Discussion HBV V191I;W182X 61;206 66;212 RT;S;S 59;206;187 61;207;194 Liver disease 234 247 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. In this sense, the rtA181T variant, which strongly increased from pre-treatment to LMV and slightly decreased during ADV therapy, appeared to be more resistant to LMV than to ADV, in agreement with its previous phenotypic characterization. 2012 PloS one Discussion HBV A181T 21 26 RT 19 21 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Moreover, rtA181S is linked to the sW172C substitution in the minimal recognized sequence of the surface epitope TH-s156/s175; hence, it is likely to provide immune escape. 2012 PloS one Discussion HBV A181S;W172C 12;35 17;41 RT;S;S;S;S 10;35;116;121;97 12;36;117;122;104 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Moreover, the only variant found in proportions above 0.1% was the well-known immune escape substitution sG145R, which modifies the antigenicity of the "a determinant", while viral particles remain infective. 2012 PloS one Discussion HBV G145R 105 111 S;S 153;105 166;106 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The envelope stop codon variant sW172*, which is related to the major NA-resistant variant rtA181T, became the most highly represented following LMV and ADV treatments, yielding a major viral population that is defective in secretion of viral particles, as reported by Warner et al. 2012 PloS one Discussion HBV A181T;W172X 93;32 98;38 S;RT;S 4;91;32 12;93;33 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The substitution patterns were particularly complex at ETV VBK, with rtL180M-S202G-M204V-V207I being the main combination. 2012 PloS one Discussion HBV L180M;S202G;M204V;V207I 71;77;83;89 76;82;88;94 RT 69 71 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. The variation in percentages of rtA181S followed a pattern similar to that of rtA181T, but with a less intense effect (moderately increased after LMV VBK, maintained during ADV, and undetectable after ETV treatment), therefore, position rt181 had a major role in resistance to multiple NAs in the longitudinally followed patient. 2012 PloS one Discussion HBV A181S;A181T 34;80 39;85 RT;RT;RT 32;78;237 34;80;239 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. This strongly suggests that secretion of genomes harboring the sW172* substitution would be enabled by trans-complementation with a functional S protein from other HBV genomes occurring in the same quasispecies, as previously suggested. 2012 PloS one Discussion HBV W172X 63 69 S;S 63;143 64;144 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. This variant was mainly selected in combination with rtM204V, a fact that strongly suggests a compensatory role to restore the replicative efficiency of complex HBV variants carrying rtM204V, likely to compromise the success of ETV. 2012 PloS one Discussion HBV M204V;M204V 55;185 60;190 RT;RT 53;183 55;185 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. UDPS analysis showed that aa changes known to be associated with NA resistance above this detection limit (rtA181T, rtV191I, rtA194T and rtM204I) were present in low percentages (ranging from 0.07 to 0.59) in the baseline HBV quasispecies, probably representing a background due to the natural dynamics of the viral quasispecies. 2012 PloS one Discussion HBV A181T;V191I;A194T;M204I 109;118;127;139 114;123;132;144 RT;RT;RT;RT 107;116;125;137 109;118;127;139 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Unexpectedly, the rtV207I variant, which to date has only been associated with low sensitivity to LMV and resistance to famciclovir, was present in the most prevalent combined variants at ETV VBK (81% of sequences) and was also significantly increased at LMV VBK. 2012 PloS one Discussion HBV V207I 20 25 RT 18 20 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. Using this approach, we found that in our MDR patient, with the single exception of rtA181T, all these substitutions were mainly found in combinations in all the samples studied. 2012 PloS one Discussion HBV A181T 86 91 RT 84 86 22666402 Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome. With this approach, the sensitivity to different NAs of the less common resistant variants (rtV191I, rtA181S, and rtA200V) found among the most variable ones can also be studied. 2012 PloS one Discussion HBV V191I;A181S;A200V 94;103;116 99;108;121 RT;RT;RT 92;101;114 94;103;116 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Besides, G1899A also locates at Precore region of HBV genome and associated with a 3.14-fold increased risk of HCC compared with HBV patients without G1899A. 2012 PloS one Discussion HBV G1899A;G1899A 9;150 15;156 Precore 32 39 Hepatocellular carcinoma 111 114 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Besides, G1899A, Pre-S1 deletion, Pre-S2 deletion as well as other common mutations like BCP double mutation A1762T/G1764A, T1753V and C1653T, all of them correlate with HCC risk. 2012 PloS one Discussion HBV G1764A;G1899A;A1762T;T1753V;C1653T 116;9;109;124;135 122;15;115;130;141 BCP;PreS1;PreS2 89;17;34 92;23;40 Hepatocellular carcinoma 170 173 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Despite these limitations, our study indicates that Precore mutation G1896A is significantly associated with the increased risk of HCC and the progression of liver disease, especially among Asians. 2012 PloS one Discussion HBV G1896A 69 75 Precore 52 59 Hepatocellular carcinoma;Liver disease 131;158 134;171 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For C1653T and T1753V, significant correlations with HCC are still observed in the two mutations. 2012 PloS one Discussion HBV C1653T;T1753V 4;15 10;21 Hepatocellular carcinoma 53 56 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For the mechanisms that underlie the interaction between G1899A and the onset of HCC still remain elusive. 2012 PloS one Discussion HBV G1899A 57 63 Hepatocellular carcinoma 81 84 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. For the other common mutations, BCP double mutation A1762T/G1764A is generally accepted that it independently correlates with the risk of HCC and the progression of liver diseases, which is consistent with our results. 2012 PloS one Discussion HBV G1764A;A1762T 59;52 65;58 BCP 32 35 Hepatocellular carcinoma;Liver disease 138;165 141;179 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. From our subgroup analysis, we may conclude that HBV genotype C patients with certain mutations like BCP double mutation, C1653T and T1753V would be exposed to a much higher risk of HCC. 2012 PloS one Discussion HBV C1653T;T1753V 122;133 128;139 BCP 101 104 Hepatocellular carcinoma 182 185 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. In our study, when pooling data from 43 studies including 3097 cases and 5530 controls, statistically significant association was determined between G1896A (OR = 1.46; p = 0.002) and the increased risk of HCC, which was totally different from Yin's conclusion whose summary OR was 1.15 (95%CI = 0.83-1.60), pooling data from 24 studies. 2012 PloS one Discussion HBV G1896A 149 155 Hepatocellular carcinoma 205 208 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. It was once reported that G1896A correlated with severe forms of liver diseases. 2012 PloS one Discussion HBV G1896A 26 32 Liver disease 65 79 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Mutation G1896A locates at nt.1896 in the precore region leading to a G-to-A shift, which could induce a stop codon and subsequently suppress the expression of HBeAg. 2012 PloS one Discussion HBV G1896A 9 15 C;Precore 160;42 165;49 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Our study showed that Precore mutation G1896A and G1899A, Pre-S1 deletion, Pre-S2 deletion and other common mutations mentioned above were all independently associated with an increased risk of HCC as well as the progression of liver diseases. 2012 PloS one Discussion HBV G1896A;G1899A 39;50 45;56 Precore;PreS1;PreS2 22;58;75 29;64;81 Hepatocellular carcinoma;Liver disease 194;228 197;242 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Precore G1896A was still associated with the progressive diseases contributing to a 1.85-fold increased risk suffering from a more severe disease status. 2012 PloS one Discussion HBV G1896A 8 14 Precore 0 7 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. So far, this study is the first to report that significant correlation exists between G1899A and the increased risk of HCC based on a powerful meta-analysis, which might be a potential biomarker for foreseeing the occurrence of HCC. 2012 PloS one Discussion HBV G1899A 86 92 Hepatocellular carcinoma;Hepatocellular carcinoma 119;228 122;231 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. They may act as G1896A does but still merit further exploration. 2012 PloS one Discussion HBV G1896A 16 22 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Thus large-number, well-designed case-control studies are entailed in elucidating the relationship between G1896A and HCC risk. 2012 PloS one Discussion HBV G1896A 107 113 Hepatocellular carcinoma 118 121 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. We found a 5.46-fold increased risk of HCC and LC in BCP double mutation, 2.77-fold in T1753V and 2.59-fold in C1653T. 2012 PloS one Discussion HBV T1753V;C1653T 87;111 93;117 BCP 53 56 Hepatocellular carcinoma;Liver cirrhosis 39;47 42;49 22675557 Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis. Yin and his colleagues who did the former meta-analysis also reported a significant association between G1896A and HCC with an OR = 5.10 in genotype B and 3.60 in genotype C patients in their recent research. 2012 PloS one Discussion HBV G1896A 104 110 Hepatocellular carcinoma 115 118 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Although the numbers were too low to reach statistical significance, we also identified a difference in the G1896A and A1762T/G1764A mutations at the subgenotype level, which has also been previously reported. 2012 PloS one Discussion HBV G1764A;G1896A;A1762T 126;108;119 132;114;125 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Analysis of the preS region demonstrated that a total of 5% of specimens had preS deletions (primarily identified in high risk individuals), 5.5% contained amino acid mutations in the start codon of the preS2 and 5.3% had an F22L mutation in the preS2, all of which have been significantly associated with the development of HCC. 2012 PloS one Discussion HBV F22L 225 229 PreS;PreS;PreS2;PreS2 16;77;203;246 20;81;208;251 Hepatocellular carcinoma 325 328 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Genetic mutations and deletions in the pre-S and basal core promoter regions of the HBV genome including T1753V, A1762T, G1764A, and C1766T have been associated with more severe liver disease and the development of HCC. 2012 PloS one Discussion HBV T1753V;A1762T;G1764A;C1766T 105;113;121;133 111;119;127;139 BCP;PreS 49;39 68;44 Liver disease;Hepatocellular carcinoma 178;215 191;218 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. Of particular note, 2.2% of sequences analysed contained the major vaccine escape mutation G145A as a dominant or as a mixed population. 2012 PloS one Discussion HBV G145A 91 96 22720022 A multicentre molecular analysis of hepatitis B and blood-borne virus coinfections in Viet Nam. We identified the precore stop mutation G1896A in 35% (n = 82/236) of all samples, and this varied significantly with viral genotype, with a higher incidence in genotype B compared to genotype C, which is in agreement with previous studies. 2012 PloS one Discussion HBV G1896A 40 46 Precore 18 25 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. A large percentage of the cases with rtA181T mutations developed SW172stop mutations. 2012 PloS one Discussion HBV A181T;W172X 39;65 44;74 RT 37 39 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. As previously reported, the P120T/S substitution may cause problems with diagnostic assays, and may also cause vaccine escape and poor response to HBIG therapy. 2012 PloS one Discussion HBV P120T;P120S 28;28 35;35 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. Drug resistant mutations to ADV have been reported mainly in the HBV polymerase domain D rtN236T or the domain B rtA181V/T, whereas a domain D rtN236T mutation does not overlap with the envelope gene, a mutation at rtA181T can result in a stop mutation in the envelope region of the S gene (SW172stop). 2012 PloS one Discussion HBV N236T;A181V;A181T;A181T;N236T;W172X 91;115;115;217;145;291 96;122;122;222;150;300 S;S;P;RT;RT;RT;RT;S 186;260;69;89;113;143;215;283 194;268;79;91;115;145;217;284 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. However, the A184V mutation did not result in amino acid changes in the polymerase region. 2012 PloS one Discussion HBV A184V 13 18 P 72 82 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. In addition, an ADV-resistant mutation at rtA181V results in a concomitant change at SL- 173F. 2012 PloS one Discussion HBV A181V 44 49 RT 42 44 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. In cases with ADV treated LMV-resistant mutations, the rtA181T mutation was reported at the ADV treatment baseline with low HBV DNA titers. 2012 PloS one Discussion HBV A181T 57 62 RT 55 57 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. In contrast, analysis of sera or plasma from Japanese subjects with AC, CH, LC and HCC infected with HBV genotype C showed that the percentage of T1753V mutation increased with progression of liver disease [Takahashi et al., 1999]. 2012 PloS one Discussion HBV T1753V 146 152 Hepatocellular carcinoma;Liver disease;Chronic Hepatitis B;Liver cirrhosis 83;192;72;76 86;205;74;78 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. In this study, the P120T/S was the most important substitution. 2012 PloS one Discussion HBV P120T;P120S 19;19 26;26 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. It is also reported that T1753V mutation was higher in HCC (53.2%) compared with LC (18.8%) and CH (9.8%). 2012 PloS one Discussion HBV T1753V 25 31 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 55;96;81 58;98;83 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. The P120T/S was detected in 7.8% of chronic hepatitis and 11.2% in patients with cirrhosis. 2012 PloS one Discussion HBV P120T;P120S 4;4 11;11 Chronic Hepatitis B;Liver cirrhosis 36;81 53;90 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. The S gene mutation, A184V, was detected in the ADV resistant rtA181T/V chronic hepatitis. 2012 PloS one Discussion HBV A181T;A181V;A184V 64;64;21 71;71;26 RT;S 62;4 64;5 Chronic Hepatitis B 72 89 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. The T1762/A1764 and T1753V mutations in BCP could be one of the indicators for progression of liver disease in India. 2012 PloS one Discussion HBV T1753V 20 26 BCP 40 43 Liver disease 94 107 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. There is one published report that the A184V mutation was related to reduced or negative HBsAg signal. 2012 PloS one Discussion HBV A184V 39 44 S 89 94 22720023 Hepatitis B virus gene mutations in liver diseases: a report from New Delhi. We detected sW172stop (6.4%) and sL173F (4.2%) mutations in LC patients with ADV-resistant rtA181T/V polymerase mutations. 2012 PloS one Discussion HBV A181T;A181V;W172X;L173F 93;93;12;33 100;100;21;39 P;RT;S;S 101;91;12;33 111;93;13;34 Liver cirrhosis 60 62 22860080 Long-term hepatitis B virus (HBV) response to lamivudine-containing highly active antiretroviral therapy in HIV-HBV co-infected patients in Thailand. Over the 5 years of follow-up, 6 of 7 patients presenting HBV breakthrough had the rtM204I (due to the ntG741A uncommon mutation) or M204V mutations associated with 3TC resistance along with rtL180M and/or rtV173L. 2012 PloS one Discussion HBV L180M;V173L;M204I;G741A;M204V 193;208;85;104;133 198;213;90;110;138 RT;RT;RT 83;191;206 85;193;208 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. And rtD134E/G/N/S mutation could also generate the sI126N/V mutation in the S gene of HBV. 2012 Liver international Discussion HBV D134E;D134G;D134N;D134S;I126N;I126V 6;6;6;6;51;51 17;17;17;17;59;59 RT;S;S 4;51;76 6;52;77 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. And the rtS106C and rtD134E/G/N/S mutations may be associated with necro-inflammation, immune response and cirrhosis development in these treatment naive patients. 2012 Liver international Discussion HBV D134E;D134G;D134N;D134S;S106C 22;22;22;22;10 33;33;33;33;15 RT;RT 8;20 10;22 Necrotic inflammation;Liver cirrhosis 67;107 85;116 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. Due to the overlapping structure of HBV genomes, the most of RT-HBsAg concomitant mutations were found centered in the A-B interdomain, corresponding to the overlapping 'a' determinant with a cluster of affirmed immune-escape mutations, such as s126A/N/S, sT131N and sG145R. 2012 Liver international Discussion HBV T131N;G145R 256;267 262;273 S;S;RT;S;S;S 170;64;61;245;256;267 184;69;63;246;257;268 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. It was interesting that we observed rtS106C and rtD134E/G/N/S mutations were more frequently detected in the CHB and cirrhotic patients when compared to those in the HCC patients. 2012 Liver international Discussion HBV D134E;D134G;D134N;D134S;S106C 50;50;50;50;38 61;61;61;61;43 RT;RT 36;48 38;50 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 109;166;117 112;169;126 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. The immune response towards active necro-inflammation seen in patients with CHB or cirrhosis may also induce the rtS106C and rtD134E/G/N/S mutations. 2012 Liver international Discussion HBV D134E;D134G;D134N;D134S;S106C 127;127;127;127;115 138;138;138;138;120 RT;RT 113;125 115;127 Chronic Hepatitis B;Liver cirrhosis;Necrotic inflammation 76;83;35 79;92;53 22882650 Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients. The rtS106C and rtD134E/G/N/S mutations may be an induced consequence from the overacting immune response towards severe necro-inflammation seen during different disease stages of CHB. 2012 Liver international Discussion HBV D134E;D134G;D134N;D134S;S106C 18;18;18;18;6 29;29;29;29;11 RT;RT 4;16 6;18 Necrotic inflammation;Chronic Hepatitis B 121;180 139;183 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. All these results led us to speculate that persistent HBV replication after HBeAg seroconversion occurs independently of G1896A, with no pathogenic role of this mutation in the subsequent course of liver disease. 2012 PloS one Discussion HBV G1896A 121 127 C 76 81 Liver disease 198 211 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Also C1766T and T1768A were mostly found alone among ACH patients and mostly accompanied by C1653T, T1753V and A1762T/G1764A in AdLD patients. 2012 PloS one Discussion HBV G1764A;C1766T;T1768A;C1653T;T1753V;A1762T 118;5;16;92;100;111 124;11;22;98;106;117 Chronic active Hepatitis;Aggressive Hepatitis and advanced liver disease 53;128 56;132 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Another important observation is that in ICs harboring C1653T, T1753V and A1762T/G1764A, these mutations were not found in combination. 2012 PloS one Discussion HBV G1764A;C1653T;T1753V;A1762T 81;55;63;74 87;61;69;80 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. As it has been previously reported that A1762T/G1764A appears earlier than G1896A during the course of HBV infection, we suggest that the carriage of G1896A mutation in the absence of A1762T/G1764A double mutation, is beneficial for maintaining an inactive disease status. 2012 PloS one Discussion HBV G1764A;G1764A;A1762T;G1896A;G1896A;A1762T 47;191;40;75;150;184 53;197;46;81;156;190 HBV infections 103 116 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Because cytoplasmic localization of HBcAg is closely related to active necroinflammation of hepatocytes, these data may partly explain the association between the emergence of A1762T/G1764A double mutation and liver damage. 2012 PloS one Discussion HBV G1764A;A1762T 183;176 189;182 C 36 41 Liver disease 210 222 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Besides A1762T/G1764A double mutation, other mutations in the CP, including T1753V, C1653T and C1766T/T1768A, appear to be implicated in disease severity in Moroccan HBV carriers as reflected by their higher frequencies among patients with AdLD compared to IC and ACH patients. 2012 PloS one Discussion HBV G1764A;T1768A;A1762T;T1753V;C1653T;C1766T 15;102;8;76;84;95 21;108;14;82;90;101 Core promoter 62 64 Aggressive Hepatitis and advanced liver disease;Chronic active Hepatitis 240;264 244;267 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. C1653T mutation changes the box-alpha binding site for C/EBP and related factors into a perfect palindromic sequence, which could enhance the activity of the core promoter and HBV replication. 2012 PloS one Discussion HBV C1653T 0 6 Core promoter 158 171 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. For the double mutation C1766T/T1768A, it has been described as an independent factor predictive of cirrhosis in HBeAg-negative patients and associated with a higher replication phenotype by increasing the encapsidation of pg-mRNA. 2012 PloS one Discussion HBV T1768A;C1766T 31;24 37;30 C 113 118 Liver cirrhosis 100 109 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Functional studies demonstrated that A1762T/G1764A was associated with the upregulation of viral replication by creating a hepatocyte nuclear factor-1 (HNF-1) binding site or by reducing pre-C expression and concomitantly increasing pg-mRNA level, which result in increased HBV virulence. 2012 PloS one Discussion HBV G1764A;A1762T 44;37 50;43 Precore 187 192 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. However, because of the very low number of cases with A1762T/G1764A alone, it could be difficult to establish the effect of combined CP mutations on HBV replication. 2012 PloS one Discussion HBV G1764A;A1762T 61;54 67;60 Core promoter 133 135 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In addition, a recent in vitro study revealed that A1762T/G1764A double mutation was associated with more cytoplasmic localization of intracellular hepatitis B core antigen (HBcAg) than wild-type strain. 2012 PloS one Discussion HBV G1764A;A1762T 58;51 64;57 C;C 160;174 164;179 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In addition, A1762T mutation introduced a translation initiation site ATG at the C-terminal region of HBx protein. 2012 PloS one Discussion HBV A1762T 13 19 X 102 105 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In addition, this mutation changes the aa 94 (H94Y) in the HBx protein, which affect the transactivation effects of this protein. 2012 PloS one Discussion HBV H94Y 46 50 X 59 62 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In agreement with these data, we found that patients carrying A1762T/G1764A double mutation have significantly higher HBV-DNA levels compared to those with wild-type virus. 2012 PloS one Discussion HBV G1764A;A1762T 69;62 75;68 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In conclusion, our results showed that the pre-C G1896A mutation is the major cause of HBeAg negativity in Moroccan chronic HBV carriers, with probably a beneficial role in the course of liver disease. 2012 PloS one Discussion HBV G1896A 49 55 C;Precore 87;43 92;48 Liver disease;Chronic Hepatitis B 187;116 200;127 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In contrast to genotype D strains, a higher frequency of the CP A1762T/G1764A double mutation was detected in genotype A2 strains. 2012 PloS one Discussion HBV G1764A;A1762T 71;64 77;70 Core promoter 61 63 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In contrast, we found that the prevalence of A1762T/G1764A double mutation increased significantly with disease progression from IC to AdLD state, implicating this mutation in disease severity. 2012 PloS one Discussion HBV G1764A;A1762T 52;45 58;51 Aggressive Hepatitis and advanced liver disease 135 139 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the present study, 93.2% of genotype D strains had pre-C stop codon G1896A mutation, whereas only four genotype A2 strains had this mutation. 2012 PloS one Discussion HBV G1896A 71 77 Precore 54 59 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the present work, multivariate analysis showed that G1896A mutation was associated to a lower risk of AdLD compared to the wild-type virus. 2012 PloS one Discussion HBV G1896A 55 61 Aggressive Hepatitis and advanced liver disease 105 109 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In the present work, no difference was observed in the viral load between patients with and without C1653T, in agreement with some in vitro studies. 2012 PloS one Discussion HBV C1653T 100 106 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In variance with this suggestion, we observed that the presence of A1762T/G1764A occurred more frequently in ACH and AdLD cases and was associated with higher HBV-DNA levels irrespective of pre-C 1896 status. 2012 PloS one Discussion HBV G1764A;A1762T 74;67 80;73 Precore 190 195 Aggressive Hepatitis and advanced liver disease;Chronic active Hepatitis 117;109 121;112 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. In vitro studies have demonstrated a gradual enhancement of HBV replication when mutations at positions 1753, 1766 and 1768 are added to A1762T/G1764A double mutation. 2012 PloS one Discussion HBV G1764A;A1762T 144;137 150;143 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Interestingly, it has been reported that the CP mutations accumulate in a certain order: A1762T/G1764A emerge first, being detectable approximately 10 years before the diagnosis of HCC followed by C1653T and finally, T1753V, C1766T or T1768A mutations. 2012 PloS one Discussion HBV G1764A;A1762T;C1653T;T1753V;C1766T;T1768A 96;89;197;217;225;235 102;95;203;223;231;241 Core promoter 45 47 Hepatocellular carcinoma 181 184 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Interestingly, we found that HBV sequences with G1896A alone were significantly more prevalent among IC than patients with ACH and AdLD. 2012 PloS one Discussion HBV G1896A 48 54 Chronic active Hepatitis;Aggressive Hepatitis and advanced liver disease 123;131 126;135 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Moreover, comparable frequencies of G1896A have been reported among HBeAg-negative carriers in Turkey (85%) and Algeria (80%). 2012 PloS one Discussion HBV G1896A 36 42 C 68 73 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Moreover, T1768A result in aa changes at HBx codon 132 (F132Y), that have been showed to play a synergetic role with K130M and V131I introduced by A1762T/G1764A for leading to carcinogenesis. 2012 PloS one Discussion HBV G1764A;T1768A;F132Y;K130M;V131I;A1762T 154;10;56;117;127;147 160;16;61;122;132;153 X 41 44 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. No significant difference was found in the HBV-DNA level between our patients with and without G1896A, suggesting that G1896A had no effect on HBV replication and supporting previous in vivo and in vitro studies, but contradicted others reporting that G1896A mutation may enhance HBV replication by increasing the encapsidation signal stability. 2012 PloS one Discussion HBV G1896A;G1896A;G1896A 95;119;252 101;125;258 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Of the six mutations pathologically implicated, C1653T, T1753V, A1762T, G1764A, C1766T and T1768A, a combination of three or more mutations was more likely associated with ACH and AdLD stages. 2012 PloS one Discussion HBV C1653T;T1753V;A1762T;G1764A;C1766T;T1768A 48;56;64;72;80;91 54;62;70;78;86;97 Chronic active Hepatitis;Aggressive Hepatitis and advanced liver disease 172;180 175;184 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Our current results support these findings and suggest that C1766T/T1768A associated with high HBV-DNA levels may induce severe liver injury and increase the risk of AdLD. 2012 PloS one Discussion HBV T1768A;C1766T 67;60 73;66 Aggressive Hepatitis and advanced liver disease 166 170 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Our result was supported by the findings of previous studies reporting a significant link between G1896A mutation and inactive HBV carrier state. 2012 PloS one Discussion HBV G1896A 98 104 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Previously, it has been suggested that the impact of A1762T/G1764A on viral replication may be modulated by G1896A. 2012 PloS one Discussion HBV G1764A;A1762T;G1896A 60;53;108 66;59;114 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Regarding the biological aspects, it was suggested that T1753V lead to the enhancement of transactivation and antiproliferation activity of HBx protein by altering HBx aa 127 (I127T/N/S) and enhancement of virus replication leading to persistent infection and higher frequency of HBV-DNA integration events into the human genome. 2012 PloS one Discussion HBV I127T;I127N;I127S;T1753V 176;176;176;56 185;185;185;62 X;X 140;164 143;167 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Similarly, another study reported that hepatic inflammation occurred more frequently in patients with the wild type than those with G1896A mutation. 2012 PloS one Discussion HBV G1896A 132 138 Liver inflammation 39 59 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The A1762T/G1764A double mutation changes two codons in HBx protein (K130M and V131I). 2012 PloS one Discussion HBV G1764A;A1762T;K130M;V131I 11;4;69;79 17;10;74;84 X 56 59 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The A1762T/G1764A double mutation might be used as a biomarker for the prediction of future disease activity and might be helpful in the identification of patients that should be regularly followed for HBV-DNA level and criteria of AdLD or require therapeutic intervention. 2012 PloS one Discussion HBV G1764A;A1762T 11;4 17;10 Aggressive Hepatitis and advanced liver disease 232 236 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The analysis of nucleotide sequences of the pre-C and CP regions showed that the pre-C stop codon G1896A mutation was the major cause of HBeAg negativity, detected in 83.9% of patients. 2012 PloS one Discussion HBV G1896A 98 104 Core promoter;C;Precore;Precore 54;137;44;81 56;142;49;86 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The basis of the relation between G1896A mutation and HBV genotypes is due to the base pairing of the stem loop structure of the encapsidation signal (epsilon), essential for viral replication. 2012 PloS one Discussion HBV G1896A 34 40 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The biological mechanisms that explain the association of C1653T, T1753V, C1766T and T1768A mutations with the pathogenesis of HBV infection are less well defined. 2012 PloS one Discussion HBV C1653T;T1753V;C1766T;T1768A 58;66;74;85 64;72;80;91 HBV infections 127 140 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The clinic-pathologic importance of the common G1896A and A1762T/G1764A mutations in the course of HBV infection has been extensively studied. 2012 PloS one Discussion HBV G1764A;G1896A;A1762T 65;47;58 71;53;64 HBV infections 99 112 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The co-existence of A1762T/G1764A and G1896A mutations was observed in 22% of our patients. 2012 PloS one Discussion HBV G1764A;A1762T;G1896A 27;20;38 33;26;44 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The CP A1762T/G1764A double mutation that diminishes HBeAg production was found in 29.5% of patients. 2012 PloS one Discussion HBV G1764A;A1762T 14;7 20;13 Core promoter;C 4;53 6;58 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The mechanism by which A1762T/G1764A increased HBV related pathogenesis is not fully understood. 2012 PloS one Discussion HBV G1764A;A1762T 30;23 36;29 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The nt 1896 is located opposite to nt 1858 in the stem loop, therefore, G1896A is restricted to genotypes that have T at nt 1858 (non-A genotypes), since its stabilizes the encapsidation signal, and occurred rarely in genotypes that have C at nt 1858 (genotype A), which is line with our findings. 2012 PloS one Discussion HBV G1896A 72 78 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The persistence of HBV replication and the severity of liver damage are attributed to A1762T/G1764A double mutation and associated mutations C1653T, T1753V and C1766T/T1768A in the CP. 2012 PloS one Discussion HBV G1764A;T1768A;A1762T;C1653T;T1753V;C1766T 93;167;86;141;149;160 99;173;92;147;155;166 Core promoter 181 183 Liver disease 55 67 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The reason that may account for the higher prevalence of A1762T/G1764A double mutation in these countries compared to Morocco is unclear. 2012 PloS one Discussion HBV G1764A;A1762T 64;57 70;63 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The role of the changes induced by A1762T/G1764A mutation on HBx protein is another important issue to consider in future studies. 2012 PloS one Discussion HBV G1764A;A1762T 42;35 48;41 X 61 64 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. The T1753V mutation had earlier been associated with HCC development among Mongolian patients with genotype D. 2012 PloS one Discussion HBV T1753V 4 10 Hepatocellular carcinoma 53 56 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Therefore, A1762T/G1764A may serve as a useful biomarker for progressive liver damage. 2012 PloS one Discussion HBV G1764A;A1762T 18;11 24;17 Liver disease 73 85 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. This finding was supported by the results of a previous study suggesting that the double mutation A1762T/G1764A would be associated with the loss of HBeAg in HBV/A2 carriers. 2012 PloS one Discussion HBV G1764A;A1762T 105;98 111;104 C 149 154 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. This result seems to be in line with two recent studies reporting a negative association between G1896A mutation and HCC. 2012 PloS one Discussion HBV G1896A 97 103 Hepatocellular carcinoma 117 120 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. This result was consistent with previous data showing that G1896A mutation was the strongest factor of HBeAg clearance in HBV/D-infected individuals. 2012 PloS one Discussion HBV G1896A 59 65 C 103 108 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. Using multivariate analysis, we found that A1762T/G1764A mutation was an independent risk factor for AdLD development, which is agreement with several studies. 2012 PloS one Discussion HBV G1764A;A1762T 50;43 56;49 Aggressive Hepatitis and advanced liver disease 101 105 22905181 Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression. We can also explained the ACH and AdLD cases found in G1896A-associated disease by the fact that G1896A has been acquired after the liver damage established by A1762T/G1764A. 2012 PloS one Discussion HBV G1764A;G1896A;G1896A;A1762T 167;54;97;160 173;60;103;166 Aggressive Hepatitis and advanced liver disease;Liver disease;Chronic active Hepatitis 34;132;26 38;144;29 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Although G145A had not been identified in vivo, it was detectable with all kits tested; thus, a false-negative HBsAg result in vivo seems unlikely. 2012 Journal of viral hepatitis Discussion HBV G145A 9 14 S 111 116 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Although the K122R mutation results in a serotype change from 'd' to 'y', both K122R and M103I may have minor effects with respect to protein folding, antigenicity, detection by anti-HBs, and protein expression, due to their location within the antigenic determinant region of HBsAg. 2012 Journal of viral hepatitis Discussion HBV K122R;K122R;M103I 13;79;89 18;84;94 S;S 183;277 186;282 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Although the lack of detectable HBsAg could represent a diagnostic error, HBsAg synthesis was consistently detectable for G145A with the commercial ELISA kit utilized even at low levels. 2012 Journal of viral hepatitis Discussion HBV G145A 122 127 S;S 32;74 37;79 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Finally, in the third study, the I110M, G119E, and R169P mutations were each capable of impairing virion secretion. 2012 Journal of viral hepatitis Discussion HBV I110M;G119E;R169P 33;40;51 38;45;56 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. First, the specific mutations assessed in this study - M103I, K122R, and G145A - had not been included in previous functional analyses of HBsAg expression during O-HBV infection and, therefore, extend the small body of previously available research that utilized in vitro models to evaluate specific instances of undetectable HBsAg in vivo. 2012 Journal of viral hepatitis Discussion HBV M103I;K122R;G145A 55;62;73 60;67;78 S;S 138;326 143;331 HBV-HIV coinfections 162 177 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. For example, one polymerase mutation (terminal protein mutation T165P) or several amino acid mutations throughout the genome have resulted in defective replication or overall decreases in HBsAg and HBV DNA levels. 2012 Journal of viral hepatitis Discussion HBV T165P 64 69 S;P 188;17 193;27 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. For one wild-type construct, the small amount of HBsAg produced with the G145A mutation, alone or in combination, was retained within hepatocytes, as indicated by higher intracellular HBsAg ratios in Table 3. 2012 Journal of viral hepatitis Discussion HBV G145A 73 78 S;S 49;184 54;189 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In addition, one study compared several commercial ELISA kits to assess detection of amino acid changes at position 145, including G145A. 2012 Journal of viral hepatitis Discussion HBV G145A 131 136 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In summary, the S gene mutations M103I, K122R, and G145A were evaluated for their impact on HBsAg synthesis given that a lack of detectable HBsAg in the serum is a hallmark of O-HBV infection. 2012 Journal of viral hepatitis Discussion HBV M103I;K122R;G145A 33;40;51 38;45;56 S;S;S 92;140;16 97;145;17 HBV-HIV coinfections 176 191 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In the second study, HBsAg expression was decreased by 40% with the P142A mutation and by 60% with the D144V mutation; however, when both mutations were included, HBsAg expression was decreased by only 20%. 2012 Journal of viral hepatitis Discussion HBV P142A;D144V 68;103 73;108 S;S 21;163 26;168 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. In this study, extracellular levels of HBsAg were slightly above detectable levels at times with the G145A mutation, indicating that the HBsAg secreted from infected hepatocytes would likely be below the limit of detection for commercial assays once diluted in the blood. 2012 Journal of viral hepatitis Discussion HBV G145A 101 106 S;S 39;137 44;142 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Interestingly, the G145A mutation, also results in a W153C mutation in the reverse transcriptase region of the HBV polymerase. 2012 Journal of viral hepatitis Discussion HBV G145A;W153C 19;53 24;58 P;RT 115;75 125;96 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Of the three mutations characterized, G145A contributes the most to decreased HBsAg synthesis in vitro. 2012 Journal of viral hepatitis Discussion HBV G145A 38 43 S 78 83 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. One study evaluated the Y100C mutation. 2012 Journal of viral hepatitis Discussion HBV Y100C 24 29 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Previous mutations at this position, although not W153C, have been shown to decrease HBV replication. 2012 Journal of viral hepatitis Discussion HBV W153C 50 55 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The G145A mutation, alone and in combination, resulted in significantly decreased extracellular and intracellular HBsAg expression. 2012 Journal of viral hepatitis Discussion HBV G145A 4 9 S 114 119 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The G145R mutation has been described as an immune escape mutant, as well as a potential contributor to lamivudine resistance; therefore, G145A may also represent a potential vaccine escape mutant. 2012 Journal of viral hepatitis Discussion HBV G145R;G145A 4;138 9;143 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The G145R mutation has consistently resulted in decreased HBsAg levels and increased replication in lamivudine resistant mutants, especially among those with additional polymerase mutations, such as L180M and M204V. 2012 Journal of viral hepatitis Discussion HBV G145R;L180M;M204V 4;199;209 9;204;214 S;P 58;169 63;179 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. The M103I or K122R mutations alone did not significantly affect HBsAg expression, although it is interesting to note that when these two mutations were combined, HBsAg expression was decreased. 2012 Journal of viral hepatitis Discussion HBV M103I;K122R 4;13 9;18 S;S 64;162 69;167 22967103 Mutations associated with occult hepatitis B virus infection result in decreased surface antigen expression in vitro. Thus, we examined the effects of three previously identified O-HBV mutations in the S region - M103I, K122R, and G145A - on HBsAg expression. 2012 Journal of viral hepatitis Discussion HBV M103I;K122R;G145A 95;102;113 100;107;118 S;S 124;84 129;85 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Although, with the exception of sS174N, there was no significant difference between the frequency of the mutations in the S region from HBsAg+ve and HBsAg-ve participants, there were a number of mutations that could account for the inability to detect HBsAg. 2012 PloS one Discussion HBV S174N 32 38 S;S;S;S;S 136;149;252;32;122 141;154;257;33;123 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. Even though the participants in the present study had not initiated ART, ten percent, 3 of 29 isolates sequenced, had drug resistance mutations rtV173L, rtL180M+rtM204V and rtV214A, respectively. 2012 PloS one Discussion HBV V214A;V173L;L180M;M204V 175;146;155;163 180;151;160;168 RT;RT;RT;RT 144;153;161;173 146;155;163;175 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. HBV with V168A occurred more frequently in participants with higher viral loads. 2012 PloS one Discussion HBV V168A 9 14 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. In South Africa, rtM204I has been detected in therapy-naive HBV/HIV co-infected individuals and rtM204V in treated HBV mono-infected participants. 2012 PloS one Discussion HBV M204I;M204V 19;98 24;103 RT;RT 17;96 19;98 HBV-HIV coinfections 64 79 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. ps2Q10R is in the major pre-S2 antigenic region known to carry numerous B cell, T-helper cell and cytotoxic T-lymphocyte epitopes and may therefore reduce the binding ability of the antibodies to the epitope and interfere with their neutralising effect. 2012 PloS one Discussion HBV Q10R 3 7 PreS2;PreS2 24;0 30;3 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. sP120T and sQ129R/H fall within the 'a' determinant and would therefore affect its antigenic ability and infectivity. 2012 PloS one Discussion HBV P120T;Q129R;Q129H 0;11;11 6;19;19 S;S;S 37;0;11 51;1;12 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. sP120T, which also leads to an rt128N mutation in the polymerase, has been detected in participants with severe hepatitis following lamivudine (LAM) and HBIg treatment and can partially restore the replicative capacity of LAM-resistant HBV in vitro . 2012 PloS one Discussion HBV P120T 0 6 P;RT;S 54;31;0 64;33;1 Hepatitis 112 121 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. sQ164A, has been shown to reduce the antigenicity of HDV particles and sE164D, with the concomitant rtV173L, a lamivudine escape mutant, has reduced affinity for anti-HBs antibodies in vitro, similar to that of the classical G145R. 2012 PloS one Discussion HBV V173L;Q164A;E164D;G145R 102;0;71;225 107;6;77;230 S;RT;S;S 167;100;0;71 170;102;1;72 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. sY100C has previously been detected in subgenotype A1 isolated from occult hepatitis participants and has been associated with HBsAg-negativity in blood donors. 2012 PloS one Discussion HBV Y100C 0 6 S;S 127;0 132;1 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The 1762T/1764A mutations have been closely related to progression of chronic liver disease and together with T1753C, found in five Shongwe HBV isolates, have been described as markers for HCC. 2012 PloS one Discussion HBV T1753C 110 116 Hepatocellular carcinoma 189 192 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The G1862T mutation occurred in HBV from HBsAg-ve participants but not in HBV from HBsAg+ve participants (p<0.05). 2012 PloS one Discussion HBV G1862T 4 10 S;S 41;83 46;88 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The HBeAg negativity found in 44/49 Shongwe participants (89,7%) could be accounted for by the following HBV mutations: the basic core promoter mutations A1762T/G1764A, which can down-regulate transcription of precore mRNA; the Kozak sequence mutants that affect HBeAg translation; precore start codon mutations that abolish HBeAg expression, the G1862T mutation,which interferes with post-translational modification of the HBeAg-precursor, and the classical G1896A stop codon mutation with C1858T. 2012 PloS one Discussion HBV G1764A;A1762T;G1862T;G1896A;C1858T 161;154;347;459;491 167;160;353;465;497 BCP;C;C;C;C;Precore;Precore 124;4;263;325;424;210;282 143;9;268;330;429;217;289 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. The reactivation markers V168A occurred together with S174N, which was only found in isolates from HBsAg-ve but not HBsAg+ve participants. 2012 PloS one Discussion HBV V168A;S174N 25;54 30;59 S;S 99;116 104;121 23029487 Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa. These included ps1F25L, ps1I48V, ps1V88L/A in the pre-S1 region, ps2M1I, ps2Q10R, ps2R48K/T, ps2A53V in the pre-S2 and sY100C, sP120T/A, sQ129R/H, sE164D and sS174N in the S region (figure 3). 2012 PloS one Discussion HBV V88L;V88A;R48K;R48T;F25L;I48V;M1I;Q10R;A53V;Y100C;P120T;P120A;Q129R;Q129H;E164D;S174N 36;36;86;86;18;27;68;76;96;119;127;127;137;137;147;158 42;42;91;91;22;31;71;80;100;125;135;135;145;145;153;164 PreS1;PreS2;PreS1;PreS1;PreS1;PreS2;PreS2;PreS2;PreS2;S;S;S;S;S;S 50;108;15;24;33;65;73;82;93;119;127;137;147;158;172 56;114;18;27;36;68;76;85;96;120;128;138;148;159;173 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. C-I97F/L, most frequently found in HCC-related mutations, is well known as the most frequently encountered HBcAg mutation, as mentioned in several studies. 2012 PloS one Discussion HBV I97L;I97F 2;2 8;8 C;C 0;107 1;112 Hepatocellular carcinoma 35 38 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. However, no variant of those five related to the HBeAg-negative serostatus was significantly related to HCC, although preC-W28* tended to be linked to HCC (p = 0.093). 2012 PloS one Discussion HBV W28X 123 127 C;Precore 49;118 54;122 Hepatocellular carcinoma;Hepatocellular carcinoma 104;151 107;154 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. In particular, to the best of our knowledge, two types of mutations (C-D32N/H, and C-E43K) related to the HBeAg positive serostatus have not been introduced to date in HBV variants. 2012 PloS one Discussion HBV D32H;D32N;E43K 71;71;85 77;77;89 C;C;C 69;83;106 70;84;111 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Of seven mutations affecting HBeAg serostatus observed in this study, it is noteworthy that five (C-D32N/H, C-E43K, C-P50A/H/Y, C-A131G/N/P and C-S181H/P) in the C region may have been first introduced in relation to the HBeAg serostatus. 2012 PloS one Discussion HBV P50A;A131G;D32H;P50H;P50Y;A131N;A131P;D32N;E43K;S181H;S181P 118;130;100;118;118;130;130;100;110;146;146 126;139;106;126;126;139;139;106;114;153;153 C;C;C;C;C;C;C;C 98;108;116;128;144;162;29;221 99;109;117;129;145;163;34;226 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. Of the five mutations in the C region positively related to HCC found in this study, the following three types, C-P5H/L/T, C-E83D, and C-I97F/L were introduced by other studies. 2012 PloS one Discussion HBV P5H;P5L;P5T;I97L;E83D;I97F 114;114;114;137;125;137 121;121;121;143;129;143 C;C;C;C 29;112;123;135 30;113;124;136 Hepatocellular carcinoma 60 63 23071796 Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma. To the best of our knowledge, the remaining two types (C-L100I and C-Q182K/*) may have been introduced for the first time in this study. 2012 PloS one Discussion HBV L100I;Q182K 57;69 62;76 C;C 55;67 56;68 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. In summary, none of common genomic changes in HBV (A1762T/G1764A in BCP, G1896A in precore, C1653T and T1753V in X gene, and pre-S2 deletion) was associated with clinical outcome of patients with HBV-associated HCC after curative surgical resection. 2013 Annals of surgical oncology Discussion HBV G1764A;A1762T;G1896A;C1653T;T1753V 58;51;73;92;103 64;57;79;98;109 BCP;Precore;PreS2;X 68;83;125;113 71;90;131;114 Hepatocellular carcinoma 211 214 23104706 Effects of genomic changes in hepatitis B virus on postoperative recurrence and survival in patients with hepatocellular carcinoma. The mutations at BCP A1762T/G1764A, precore G1896A, X gene C1653T, and X gene T1753V, as well as pre-S2 deletion in HBV were not significantly associated with the prognosis of HBV-associated HCC treated with curative surgical resection. 2013 Annals of surgical oncology Discussion HBV G1764A;A1762T;G1896A;C1653T;T1753V 28;21;44;59;78 34;27;50;65;84 BCP;Precore;PreS2;X;X 17;36;97;52;71 20;43;103;53;72 Hepatocellular carcinoma 191 194 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. As compared to wild type HBV strain, the transcription and replication levels of the HBV rtA181T/sW172* mutant strain in vivo delayed in reaching the peak level and lasted significantly longer, and the mutation also was demonstrated HBsAg and HBcAg continued retention in liver. 2012 Virology journal Discussion HBV W172X;A181T 97;91 103;96 C;S;RT;S 243;233;89;97 248;238;91;98 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Because the sW172* mutation of HBsAg gene is not inside the 'a' determinant, currently commercially antibody for truncated HBsAg is effective. 2012 Virology journal Discussion HBV W172X 12 18 S;S;S;S 61;31;123;12 75;36;128;13 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Clinically rtA181T is a common resistance mutation to ADV. 2012 Virology journal Discussion HBV A181T 13 18 RT 11 13 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Compared with the wild mice, the level of HBV DNA in mutant mice serum decreased significantly, and these finds were consistent with the conditions of patients who had the HBV rtA181T/sW172* mutation. 2012 Virology journal Discussion HBV W172X;A181T 184;178 190;183 RT;S 176;184 178;185 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Firstly, we found that serum HBsAg level of the rtA181T/sW172* mutant was very low (OD<0.4) from day 1 to day 15 after in vivo transfection (Figure 1A), and that the serum HBV DNA level of the mutant was lower than that of wild type (Figure 1C). 2012 Virology journal Discussion HBV W172X;A181T 56;50 62;55 S;RT;S 29;48;56 34;50;57 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. If the patient carries the variation and we failed to change drug in time, the disease would deteriorate, once rtA181T/sW172* become the dominant strains. 2012 Virology journal Discussion HBV W172X;A181T 119;113 125;118 RT;S 111;119 113;120 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. In conclusion, our results indicated that the rtA181T/sW172* mutation might impair serum HBsAg secretion and reduce serum HBV DNA level. 2012 Virology journal Discussion HBV W172X;A181T 54;48 60;53 S;RT;S 89;46;54 94;48;55 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. Many studies showed that treatment of CHB patients with LAM, ADV, or LdT could result in the emergence of the HBV rtA181T mutant . 2012 Virology journal Discussion HBV A181T 116 121 RT 114 116 Chronic Hepatitis B 38 41 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. So in this study, the antiviral effect to HBV rtA181T/sW172* is ETV>ADV>LAM>LdT. 2012 Virology journal Discussion HBV W172X;A181T 54;48 60;53 RT;S 46;54 48;55 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. The rtA181T/sW172* mutation thus leads to defects in the assembly and secretion of HBsAg and virion, which results in decreased levels of serum HBsAg and HBV DNA. 2012 Virology journal Discussion HBV W172X;A181T 12;6 18;11 S;S;RT;S 83;144;4;12 88;149;6;13 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. This makes us to focus on the HBV rtA181T/sW172* mutation. 2012 Virology journal Discussion HBV W172X;A181T 42;36 48;41 RT;S 34;42 36;43 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. This may be explained by the fact that the rtA181T/sW172* mutation causing the production of truncated HBsAg, which cannot be secreted into the serum. 2012 Virology journal Discussion HBV W172X;A181T 51;45 57;50 S;RT;S 103;43;51 108;45;52 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. This mutation is therefore also called HBV rtA181T/sW172*, which may affect the biological characteristics and pathogenesis of HBV . 2012 Virology journal Discussion HBV W172X;A181T 51;45 57;50 RT;S 43;51 45;52 23171829 Biological characteristics of the rtA181T/sW172* mutant strain of Hepatitis B virus in animal model. We have constructed the rtA181T/sW172* mutant strain of HBV and investigated its biological characteristics in vivo with our HBV replication mouse model. 2012 Virology journal Discussion HBV W172X;A181T 32;26 38;31 RT;S 24;32 26;33 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. A1762T/G1764A mutations in CHB and LC patients were up to 41.25% (66/160) and 57.33% (86/150), respectively, which suggested it were an early event in HCC development in patients with chronic HBV infection. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 7;0 13;6 Hepatocellular carcinoma;Chronic HBV infection;Chronic Hepatitis B;Liver cirrhosis 151;184;27;35 154;205;30;37 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV A1762T/G1764A mutations were first identified by Okamato and Sato et al. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 11;4 17;10 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. HBV BCP region overlaps partially with HBx coding sequence, so A1762T/G1764A mutations result in coding changes at codons 130 and 131 in the HBX protein changing lysine to methionine and valine to isoleucine, respectively, which affect the transactivation capability of HBX protein. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 70;63 76;69 BCP;X;X;X 4;39;141;270 7;42;144;273 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. In conclusion, HBV subgenotype C2 infection and A1762T/G1764A mutations are both risk factors of LC and HCC with cirrhosis development in CHB patients in Southeast China, which may be useful biomarkers alone or in combination for predicting these diseases, but all no helpful for predicting HCC development in LC patients. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 55;48 61;54 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 104;113;138;291;97;310 107;122;141;294;99;312 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Meanwhile, we speculated that HCC development in patients with chronic HBV subgenotype C2 infection was related to A1762T/G1764A mutations which contributed to cirrhosis in Chinese. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 122;115 128;121 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B 30;160;63 33;169;74 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. So far, the mechanisms of HBV genotype C infection and A1762T/G1764A mutations developing to advanced liver disease are still vague. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 62;55 68;61 HBV infections;Liver disease 26;102 50;115 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. Some reports suggested that HBV genotype C infection and A1762T/G1764A mutations were not related to LC and HCC. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 64;57 70;63 HBV infections;Hepatocellular carcinoma;Liver cirrhosis 28;108;101 52;111;103 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. The results showed subgenotype C2 infection and A1762T/G1764A mutations were not related to tumor stage, vascular invasion or lymph node metastasis and tumor size, but were both significant difference in distribution frequencies between HCC with cirrhosis and without cirrhosis(P=0.016 for subgenotype C2; P=0.009 for the mutations; respectively). 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 55;48 61;54 Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 237;246;268 240;255;277 23304671 HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China. We found the frequencies of both subgenotype C2 and A1762T/G1764A mutations were higher in LC or HCC group than in CHB group, but the differences of both variants did not be found between LC and HCC groups. 2012 Iranian journal of public health Discussion HBV G1764A;A1762T 59;52 65;58 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 97;115;195;91;188 100;118;198;93;190 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. A previous meta-analysis study, evaluating 43 studies with a total of 11582 HBV-infected participants, found that the frequency of C1653T, T1753V, and TA mutations increased successively from asymptomatic carrier to cirrhosis, and were independent factors associated with HCC. 2013 Virology journal Discussion HBV C1653T;T1753V 131;139 137;145 Liver cirrhosis;Hepatocellular carcinoma;HBV infections 216;272;76 225;275;88 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. Furthermore, the study mentioned that pre-S mutations C1653T, T1753V, and A1762T/G1764A accumulated during the progression of chronic HBV infection from the asymptomatic carrier state to HCC (Ptrend<0.001 for each mutation). 2013 Virology journal Discussion HBV G1764A;C1653T;T1753V;A1762T 81;54;62;74 87;60;68;80 PreS 38 43 Chronic HBV infection;Hepatocellular carcinoma 126;187 147;190 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. In Padang population, the data demonstrated significantly higher prevalence of pre-S mutant, T1753V, and A1762T/G1764A in the Minangkabau compared to the non-Minangkabau ethnic group. 2013 Virology journal Discussion HBV G1764A;T1753V;A1762T 112;93;105 118;99;111 PreS 79 84 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The A1762T/G1764A mutation is more commonly found in patients with genotype C than those with genotype B. 2013 Virology journal Discussion HBV G1764A;A1762T 11;4 17;10 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The C1653T mutation in HBV subgenotype C2 and T1753V and A1762T/G1764A in HBV subgenotypes C1 and C2 were statistically significantly associated with an increased risk of HCC. 2013 Virology journal Discussion HBV G1764A;C1653T;T1753V;A1762T 64;4;46;57 70;10;52;63 Hepatocellular carcinoma 171 174 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The prevalence of pre-S, A1762T/G1764A, and T1753V mutations were higher among HBV carriers of Minangkabau ethnicity. 2013 Virology journal Discussion HBV G1764A;A1762T;T1753V 32;25;44 38;31;50 PreS 18 23 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. The prevalence of the A1762T/G1764A mutation was significantly higher in the Minangkabau compared to the Javanese ethnic group. 2013 Virology journal Discussion HBV G1764A;A1762T 29;22 35;28 23336976 High prevalence of hepatitis B virus genotype C/C1 in the Minangkabau ethnic group in Indonesia. This result demonstrated the high prevalence of the A1762T/G1764A mutation in HBV/C regardless of the stage of infection. 2013 Virology journal Discussion HBV G1764A;A1762T 59;52 65;58 23346148 Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence. It was established that a change from G to A at position 1896 increases the stability of stem-loop structure of the pre-genome encapsidation sequence, if a T is present at the opposite nt 1858 position. 2012 Hepatitis monthly Discussion HBV G1896A;G1896T;G1896A 38;38;38 192;192;61 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. According to previous studies, the HBV genomic mutations affecting HCC occurrence include the BCP double mutation, the precore G1896A, the C1653T and T1753V in the HBx region and pre-S deletions. 2013 Journal of viral hepatitis Discussion HBV G1896A;C1653T;T1753V 127;139;150 133;145;156 BCP;X;Precore;PreS 94;164;119;179 97;167;126;184 Hepatocellular carcinoma 67 70 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Also, in the present study, the BCP double mutation, A1762T/G1764A, tended to occur more frequently in the HCC group compared with the CHB group although it was not statistically significant. 2013 Journal of viral hepatitis Discussion HBV G1764A;A1762T 60;53 66;59 BCP 32 35 Hepatocellular carcinoma;Chronic Hepatitis B 107;135 110;138 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Also, the C1653T and G1896A PC mutations are both independent risk factors for the development of HCC. 2013 Journal of viral hepatitis Discussion HBV C1653T;G1896A 10;21 16;27 Precore 28 30 Hepatocellular carcinoma 98 101 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Hence, the C1653T could influence HBeAg production and viral replication through BCP activity. 2013 Journal of viral hepatitis Discussion HBV C1653T 11 17 BCP;C 81;34 84;39 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. However, the present study showed that the G1896A and C1653T were independent risk factors for HCC. 2013 Journal of viral hepatitis Discussion HBV G1896A;C1653T 43;54 49;60 Hepatocellular carcinoma 95 98 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. In conclusion, the BCP A1762T/G1764A double mutation may act in synergy with the C1653T mutation to increase the risk of HCC in patients with genotype C2 HBV infection. 2013 Journal of viral hepatitis Discussion HBV G1764A;A1762T;C1653T 30;23;81 36;29;87 BCP 19 22 Hepatocellular carcinoma 121 124 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. In the HBx region, the presence of the C1653T mutation was significantly associated with the development of HCC in earlier studies. 2013 Journal of viral hepatitis Discussion HBV C1653T 39 45 X 7 10 Hepatocellular carcinoma 108 111 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. In view of this synergistic effect, our study results showed that the combined BCP A1762T/G1764A and C1653T mutations occurred more frequently in the HCC than in the CHB group and suggest that the C1653T in addition to the BCP double mutation may be a promoter of HCC development in patients with chronic HBV infection. 2013 Journal of viral hepatitis Discussion HBV G1764A;A1762T;C1653T;C1653T 90;83;101;197 96;89;107;203 BCP;BCP 79;223 82;226 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma;Chronic HBV infection 150;166;264;297 153;169;267;318 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Moreover, the synergistic effect of A1762T/G1764A and C1653T on HCC occurrence was also demonstrated in this study. 2013 Journal of viral hepatitis Discussion HBV G1764A;A1762T;C1653T 43;36;54 49;42;60 Hepatocellular carcinoma 64 67 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. Our study did not show an association between the BCP A1762T/G1764A, T1753V or pre-S deletion and HCC development. 2013 Journal of viral hepatitis Discussion HBV G1764A;A1762T;T1753V 61;54;69 67;60;75 BCP;PreS 50;79 53;84 Hepatocellular carcinoma 98 101 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The C1653T mutation converts the box alpha binding site for CCAAT/enhancer-binding protein EBP and related factors into the perfect palindromic sequence 1648-TCTTATATAAGA, which might enhance binding affinity and enhancer II/core promoter activity. 2013 Journal of viral hepatitis Discussion HBV C1653T 4 10 Core promoter;Enh II 225;213 238;224 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. The G1896A mutation creates a stop codon that prevents translation of the PC protein and abolishes the production of HBeAg. 2013 Journal of viral hepatitis Discussion HBV G1896A 4 10 C;Precore 117;74 122;76 23383661 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in genotype c2 hepatitis B virus on development of hepatocellular carcinoma. This result would support the previous finding that the G1896A mutation plays a significant role in the progression of the chronic HBV infection to HCC. 2013 Journal of viral hepatitis Discussion HBV G1896A 56 62 Chronic HBV infection;Hepatocellular carcinoma 123;148 144;151 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Both 1862/1896 mutations reduced expression of HBeAg but the difference is that G1862T reduced virus replication; however, G1896A did not. 2013 The open virology journal Discussion HBV G1862T;G1896A 80;123 86;129 C 47 52 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Conversely, they presented enhancement of the same protein for G1899A. 2013 The open virology journal Discussion HBV G1899A 63 69 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. For example, T3098C in the preS1 region and T53C were associated with HCC but further investigation is essential. 2013 The open virology journal Discussion HBV T3098C;T53C 13;44 19;48 PreS1 27 32 Hepatocellular carcinoma 70 73 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1862T mutation should motivate researchers due to its vague effect by its own or by association with other mutations and because there are quite a few research on G1862T. 2013 The open virology journal Discussion HBV G1862T;G1862T 0;164 6;170 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1862T showed no effects on HBeAg expression. 2013 The open virology journal Discussion HBV G1862T 0 6 C 28 33 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. G1899A mutation has an interesting effect on the pair of 1855 position. 2013 The open virology journal Discussion HBV G1899A 0 6 23400390 Effects of hepatitis B virus mutations on its replication and liver disease severity. Interestingly, association of 1899 mutation with G1862A greatly enhanced the replication. 2013 The open virology journal Discussion HBV G1862A 49 55 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. In addition, Y126H was more frequent among treatment non responders infected with HBV/D (68.75%, 11/16) than among treatment naive patients infected with HBV/D (35%, 7/20; Table 2), although not statistically significant (p=0.2). 2013 Virology journal Discussion HBV Y126H 13 18 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. In conclusion, in our study classical antiviral resistance mutations (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-rtM204V/I-rtN236T-rtM250V) were not detected both in naive patients and NA therapy non responders infected with any of the three HBV genotypes present. 2013 Virology journal Discussion HBV L80I;L80V;I169T;V173L;L180M;A181T;A181V;A181S;T184A;T184S;T184G;T184C;A194T;S202C;S202G;S202I;M204V;M204I;N236T;M250V 72;72;81;89;97;105;105;105;117;117;117;117;131;139;139;139;151;151;161;169 78;78;86;94;102;114;114;114;128;128;128;128;136;148;148;148;158;158;166;174 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 70;79;87;95;103;115;129;137;149;159;167 72;81;89;97;105;117;131;139;151;161;169 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. In the present study, no established primary mutations related to antiviral drugs (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-rtM204V/I-rtN236T-rtM250V) were detected neither among the therapy naive patients nor among the non-responders to NA therapy. 2013 Virology journal Discussion HBV L80I;L80V;I169T;V173L;L180M;A181T;A181V;A181S;T184A;T184S;T184G;T184C;A194T;S202C;S202G;S202I;M204V;M204I;N236T;M250V 85;85;94;102;110;118;118;118;130;130;130;130;144;152;152;152;164;164;174;182 91;91;99;107;115;127;127;127;141;141;141;141;149;161;161;161;171;171;179;187 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 83;92;100;108;116;128;142;150;162;172;180 85;94;102;110;118;130;144;152;164;174;182 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Our study showed that rtI91L was favored in HBV/C and HBV/D. 2013 Virology journal Discussion HBV I91L 24 28 RT 22 24 23409946 Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population. Whereas, in patients infected with HBV/C or HBV/A, Y126H is common among both naive and treated patients. 2013 Virology journal Discussion HBV Y126H 51 56 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. In summary, the allele-specific quantitative PCR described here, which uses a combination of locked nucleic acid primers and a minor groove binder probe, is a highly sensitive, specific, rapid, and inexpensive method for directly measuring minor viral quasispecies of the triple combination mutation rtV173L+rtL180M+rtM204V within one HBV genome. 2013 Journal of virological methods Discussion HBV V173L;L180M;M204V 302;310;318 307;315;323 RT;RT;RT 300;308;316 302;310;318 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. locked nucleic acids (LNAs) and minor groove binders (MGBs), was utilized to increase the specificity of detection of the triple mutation rtV173L+rtL180M+rtM204V in HBV polymerase without reducing the sensitivity. 2013 Journal of virological methods Discussion HBV V173L;L180M;M204V 140;148;156 145;153;161 P;RT;RT;RT 169;138;146;154 179;140;148;156 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. Therefore, this approach works best for the detection of multiple mutations in close proximity, as is the case for the combination rtV173L+rtL180M+rtM204V in HBV. 2013 Journal of virological methods Discussion HBV V173L;L180M;M204V 133;141;149 138;146;154 RT;RT;RT 131;139;147 133;141;149 23454647 Combination of allele-specific detection techniques to quantify minority resistance variants in hepatitis B infection: a novel approach. When the three mutations rtV173L+rtL180M+rtM204V are present simultaneously, there is an associated vaccine epitope immune escape phenotype due to associated changes in the overlapping envelope reading frame. 2013 Journal of virological methods Discussion HBV V173L;L180M;M204V 27;35;43 32;40;48 S;RT;RT;RT 185;25;33;41 193;27;35;43 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. Pre-existing ADV-resistance mutations such as rtN236T, prior to starting ADV mono-therapy or ADV add-on treatment may adversely affect its antiviral efficacy. 2013 Iranian journal of microbiology Discussion HBV N236T 48 53 RT 46 48 23467016 Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran. The results of alignment of protein coding sequences indicated the rtN236T mutation was observed in two (6.6%) patients, while 28 others had neither rtN236T, nor rtA181V/T mutation. 2013 Iranian journal of microbiology Discussion HBV A181V;A181T;N236T;N236T 164;164;69;151 171;171;74;156 RT;RT;RT 67;149;162 69;151;164 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Adefovir resistance mutations were exceptionally detected (rtA181T-change in 2.2%) and no change was observed for rtN236. 2013 Virology journal Discussion HBV A181T 61 66 RT;RT 59;114 61;116 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Among the 15 genotype G infected patients, all but two were HBeAg-positive, which is surprising as genotype G naturally carries the G1896A stop-codon mutation that prevents HBeAg translation from the pre-C start codon . 2013 Virology journal Discussion HBV G1896A 132 138 C;C;Precore 60;173;200 65;178;205 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. Even if one considers that the rtA181T-strains have a slight decreased sensitivity to TDF, it is reassuring to observe a very low prevalence of ADV-resistance, leaving the opportunity to treat these patients with TDF . 2013 Virology journal Discussion HBV A181T 33 38 RT 31 33 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. The distribution of 3TC-resistance mutations was very similar to what was previously reported even though rtL180M (29.1%) was found more often than rtM204V/I (26%) . 2013 Virology journal Discussion HBV L180M;M204V;M204I 108;150;150 113;157;157 RT;RT 106;148 108;150 23497042 Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study. The rtA181T or -V change is rarely selected by 3TC treatment and one can not exclude that this was not the case for these patients . 2013 Virology journal Discussion HBV A181T 6 11 RT 4 6 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. In a multivariate regression equation, pri-miR-34b/c rs4938723 variant genotypes in dominant genetic model was significantly associated with an increased risk of HCC; however, its interaction with C1730G, a HBV mutation inversely associated with HCC risk, was significantly associated with a reduced risk of HCC (Table 4). 2013 PloS one Discussion HBV C1730G 197 203 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 162;246;308 165;249;311 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. In the HBV-infected subjects with the data of HBV mutations, however, pri-miR-34b/c rs4938723 CC genotype was significantly associated with increased frequencies of HCC-related HBV mutation T1674C/G (Table 3). 2013 PloS one Discussion HBV T1674C;T1674G 190;190 198;198 Hepatocellular carcinoma;HBV infections 165;7 168;19 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. miR-34b/c might be involved in immune selection of T1674C/G and this immune selection might be independent of exacerbation during chronic HBV infection. 2013 PloS one Discussion HBV T1674C;T1674G 51;51 59;59 Chronic HBV infection 130 151 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. Pre-miR-196a2 rs11614913 TC genotype was significantly associated with increased frequencies of HCC-related HBV mutation G1896A (Table 3), furthermore, the interaction of this genotype with G1896A significantly increased HCC risk (Table 4); whereas the interaction of this genotype with A3120G/T, a strong HCC-related HBV mutation, significantly reduced the risk of HCC (Table 5). 2013 PloS one Discussion HBV A3120T;G1896A;G1896A;A3120G 287;121;190;287 295;127;196;295 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 96;221;306;366 99;224;309;369 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. rs4938723 CC genotype and rs11614913 TC genotype might predispose the host to immune selection of T1674C/G, and G1896A, respectively. 2013 PloS one Discussion HBV T1674G;T1674C;G1896A 98;98;112 106;106;118 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. The effect of pre-miR-196a2 rs11614913 on HCC risk might be neutralized in the patients with both of G1896A and A3120G/T. 2013 PloS one Discussion HBV A3120T;G1896A;A3120G 112;101;112 120;107;120 Hepatocellular carcinoma 42 45 23516510 Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk. Thus, pre-miR-196a2 rs11614913 TC genotype has a synergistic effect with G1896A and an antagonistic effect with A3120G/T on HCC risk. 2013 PloS one Discussion HBV A3120T;G1896A;A3120G 112;73;112 120;79;120 Hepatocellular carcinoma 124 127 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Adefovir resistance has been associated with a primary mutation in the D domain at rtN236T and rtA181T/Vin the B domain. 2013 Hepatitis monthly Discussion HBV A181T;N236T 97;85 102;90 RT;RT 83;95 85;97 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. For this specific mutation, the rtL180M is the main compensatory change. 2013 Hepatitis monthly Discussion HBV L180M 34 39 RT 32 34 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. In addition, a number of other mutations have been detected in our study and were clustered into three distinct regions of the RT: the D and A domains (rtP237H, rtN238T/D, rtV84M, and rtS85A) and the C-D interdomain (rtS213T/N, rtV214A, and rtQ215S). 2013 Hepatitis monthly Discussion HBV N238T;N238D;V84M;S85A;S213T;S213N;P237H;V214A;Q215S 163;163;174;186;219;219;154;230;243 170;170;178;190;226;226;159;235;248 RT;RT;RT;RT;RT;RT;RT;RT 127;152;161;172;184;217;228;241 129;154;163;174;186;219;230;243 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. In this study we found that L180M 3.37%, M204I 2.76%, and M204V 1.23% were more common than had been reported previously in Iran. 2013 Hepatitis monthly Discussion HBV L180M;M204I;M204V 28;41;58 33;46;63 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. M204I/V and M204V/I/L180M are related to entecavir resistance. 2013 Hepatitis monthly Discussion HBV L180M;M204I;M204V;M204V;M204I 20;0;0;12;12 25;7;7;19;19 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Other compensatory mutations include the rtV173L and rtL80I changes. 2013 Hepatitis monthly Discussion HBV L80I;V173L 55;43 59;48 RT;RT 41;53 43;55 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Preliminary evidence indicates that the primary lamivudine-resistance mutation rtM204V/I seems to be a prerequisite for the development of entecavir and telbivudine resistance. 2013 Hepatitis monthly Discussion HBV M204I;M204V 81;81 88;88 RT 79 81 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. Recently, the GLOBE-Trial demonstrated that in vitro telbivudine resistance is conferred by either rtM204I or rtM204V+rtL180M and L80I/M204I but not by the rtM204V mutation alone, while in vivo telbivudine resistance is almost exclusively due to the presence of M204I. 2013 Hepatitis monthly Discussion HBV M204I;M204I;L180M;M204V;M204V;L80I;M204I 135;101;120;112;158;130;262 140;106;125;117;163;134;267 RT;RT;RT;RT 99;110;118;156 101;112;120;158 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. The most commonly described mutations are the substitution of valine or isoleucine for methionine at residue 204 (rtM204I/V). 2013 Hepatitis monthly Discussion HBV M204I;M204V;M204I 116;116;72 123;123;112 RT 114 116 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. The results showed that viral mutations related to lamivudine, adefovir ,telbivudine, and entecavir resistance were discovered in patients who had never been treated with these drugs, with various mutation frequencies ranging between 1.23% (for M204V) and 7.06% (for L91I). 2013 Hepatitis monthly Discussion HBV M204V;L91I 245;267 250;271 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. The rtA181T change has been reported to occur in the absence of rtM204I/V and is considered a primary resistance mutation. 2013 Hepatitis monthly Discussion HBV A181T;M204I;M204V 6;66;66 11;73;73 RT;RT 4;64 6;66 23596461 Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients. These secondary mutations have also been detected in the absence of rtN236T (both alone and in combination) in patients who have either not responded to or have had a virological breakthrough during adefovir treatment. 2013 Hepatitis monthly Discussion HBV N236T 70 75 RT 68 70 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. A1762T and G1764A double mutations can reduce HBeAg synthesis by inhibiting the transcription of the precore mRNA. 2013 Hepatitis monthly Discussion HBV A1762T;G1764A 0;11 6;17 C;Precore 46;101 51;108 23599717 Correlation between viral load of HBV in chronic hepatitis B patients and precore and Basal core promoter mutations. The G1896A mutation in the precore region has been found in patients with HBeAg negative chronic hepatitis B. 2013 Hepatitis monthly Discussion HBV G1896A 4 10 C;Precore 74;27 79;34 Chronic Hepatitis B 89 108 23679074 Late HBsAg seroreversion of mutated hepatitis B virus after bone marrow transplantation. Interestingly, in both cases HBsIE double mutations were also identified (D144G/G145E and P142L/G145R). 2013 BMC infectious diseases Discussion HBV G145E;G145R;D144G;P142L 80;96;74;90 85;101;79;95 23679074 Late HBsAg seroreversion of mutated hepatitis B virus after bone marrow transplantation. The D144E mutation may have been acquired during replication under immune selective pressure. 2013 BMC infectious diseases Discussion HBV D144E 4 9 23679074 Late HBsAg seroreversion of mutated hepatitis B virus after bone marrow transplantation. The presence of an uncommon double mutation (D144E/G145R) in HBsAg may indicate HBV reinfection from PBMCs because the mutation G145R appears to occur more often in PBMCs. 2013 BMC infectious diseases Discussion HBV G145R;D144E;G145R 51;45;128 56;50;133 S 61 66 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. As expected, while rtL180M and rtM204V/I variants were present as a single mutation prior to LAM treatment, the rtL180M+rtM204V/I combination mutations became predominant at 6 months and at VB. 2013 Gut and liver Discussion HBV M204V;M204I;L180M;M204V;M204I;L180M 122;122;21;33;33;114 129;129;26;40;40;119 RT;RT;RT;RT 19;31;112;120 21;33;114;122 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. For instance, a change at sI195M, sW196L associated with rtM204V/I was detected in one and two of 100 colonies in patient 1 and 5, respectively. 2013 Gut and liver Discussion HBV M204V;M204I;I195M;W196L 59;59;26;34 66;66;32;40 RT;S;S 57;26;34 59;27;35 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In addition to classical ADV resistance mutations such as rtN236S or rtA181T, a few other related-variants including rtV84I/S, rtL84S, and rtQ215H were identified before VB in patient 1, 3, 4, and 6. 2013 Gut and liver Discussion HBV N236S;V84I;V84S;L84S;A181T;Q215H 60;119;119;129;71;141 65;125;125;133;76;146 RT;RT;RT;RT;RT 58;69;117;127;139 60;71;119;129;141 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In another large-scale study, three out of 255 (1.2%) treatment-naive patients had the rtM250L/V mutation typical of ETV resistance. 2013 Gut and liver Discussion HBV M250L;M250V 89;89 96;96 RT 87 89 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. In our sequencing data, rtI169L mutation was present in 8%, 1%, and 1% of 100 colonies in patient 1, 3, and 4, as well as rtA181V/T ADV resistance mutations in patient 1 and 4. 2013 Gut and liver Discussion HBV A181V;A181T;I169L 124;124;26 131;131;31 RT;RT 24;122 26;124 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Interestingly, the rtV173A/L mutation that had been described in previous reports was detected at baseline, but not thereafter in patient 1, 4, and 6. 2013 Gut and liver Discussion HBV V173A;V173L 21;21 28;28 RT 19 21 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. LAM compensatory mutations, rtL80V/I and/or rtV173L, were seen in patient 1, 2, 4, and 6. 2013 Gut and liver Discussion HBV L80V;L80I;V173L 30;30;46 36;36;51 RT;RT 28;44 30;46 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Pre-existing LAM-resistance mutation, rtM204V/I, was found in 3% (3/100) of clones in patient 5, whereas rtL180M mutation was detected in 1% (1/100) of clones in patient 1 and 2. 2013 Gut and liver Discussion HBV M204V;M204I;L180M 40;40;107 47;47;112 RT;RT 38;105 40;107 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Regarding HBV quasispecies associated with ADV resistance, the rtV84I/S, rt N236H, rtA181T, and rtQ215H mutations, were detected at baseline and at 6 months of LAM therapy in patient 1, 3, 4, and 6. 2013 Gut and liver Discussion HBV V84I;V84S;Q215H;A181T;N236H 65;65;98;85;76 71;71;103;90;81 RT;RT;RT;RT 63;73;83;96 65;75;85;98 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The finding that more diverse HBV quasispecies was identified in LAM-failure patients than in LAM-responding patients and that the frequency of pre-existing M204V/I substitution was not different between two groups suggests that degree of overall viral quasispecies rather than M204V/I substitition might predict response to LAM. 2013 Gut and liver Discussion HBV M204V;M204I;M204V;M204I 157;157;278;278 164;164;285;285 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The importance of pre-existing ETV resistant HBV variants was highlighted in a previous study, in which three out of 111 (2.7%) patients had substitutions in the HBV polymerase gene corresponding to variants associated with ETV resistance (rtS202S/I) prior to LAM treatment. 2013 Gut and liver Discussion HBV S202S;S202I 242;242 249;249 P;RT 166;240 176;242 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The LAM resistance quasispecies (rtM204V+-rt180M) emerged as early as 48 weeks, and ETV resistant quasispecies (rtM204+-rtL180M plus S202G) were found after 112 weeks. 2013 Gut and liver Discussion HBV M204V;L180M;S202G 35;122;133 40;127;138 RT;RT;RT;RT 33;42;112;120 35;44;114;122 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. The mutation at sF161H, which is located adjacent to the region that was defined as the "a" determinant, in association with rtI169L mutation was observed in patient 1, 3, and 4. 2013 Gut and liver Discussion HBV I169L;F161H 127;16 132;22 RT;S 125;16 127;17 23710315 Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B. Unlike the previous study, rtI169S/L and/or rtS202G mutations were detected in the absence of LAM resistance variants at pretreatment, even though those variants disappeared during LAM therapy until VB. 2013 Gut and liver Discussion HBV I169S;I169L;S202G 29;29;46 36;36;51 RT;RT 27;44 29;46 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. Clevudine resistance is associated with rtM204I mutation in the HBV polymerase gene. 2013 Hepatitis monthly Discussion HBV M204I 42 47 P;RT 68;40 78;42 23805155 Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients. Resistant mutations were rtM204I and/or rtM204V and/or rtL180M; these are well-known antiviral resistant mutations in HBV DNA against lamivudine and telbivudine. 2013 Hepatitis monthly Discussion HBV M204V;M204I;L180M 42;27;57 47;32;62 RT;RT;RT 25;40;55 27;42;57 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. Despite these inconvenient findings, it was found that the patients with occult HBVCI had a higher bilirubin level and a higher prevalence of precore stop codon G1896A mutation. 2013 PloS one Discussion HBV G1896A 161 167 Precore 142 149 HBV-HCV coinfections 80 85 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. Furthermore, precore G1896A mutation usually developed in patients suffering from repeated hepatitis flares during a long course of HBV infection. 2013 PloS one Discussion HBV G1896A 21 27 Precore 13 20 HBV infections;Hepatitis 132;91 145;100 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. However, development of the precore G1896A mutation prevents the production of HBeAg, which provides a possible means to evade immune clearance and contributes to the persistence of occult HBVCI. 2013 PloS one Discussion HBV G1896A 36 42 C;Precore 79;28 84;35 HBV-HCV coinfections 189 194 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. Reports regarding association between precore G1896A mutant and development of HBV-associated HCC were very conflicting so far. 2013 PloS one Discussion HBV G1896A 46 52 Precore 38 45 Hepatocellular carcinoma 94 97 23805180 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. Whether a higher prevalence of the precore G1896A mutant in occult HBVCI patients had any effect on the increased risk of HCC recurrence remained to be determined. 2013 PloS one Discussion HBV G1896A 43 49 Precore 35 42 Hepatocellular carcinoma;HBV-HCV coinfections 122;67 125;72 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Interestingly, three genotype E isolates had the sM133T mutation, which could possibly compromise antibody neutralization and may represent potential vaccine escape mutants. 2013 BMC infectious diseases Discussion HBV M133T 49 55 S 49 50 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Other mutations including transcriptional A1762T/G1764A and translation initiation mutations were responsible of HBeAg-negativity in a number of patients. 2013 BMC infectious diseases Discussion HBV G1764A;A1762T 49;42 55;48 C 113 118 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. Six genotype E and three genotype D isolates had preS2F22L, which is a risk factor for HCC. 2013 BMC infectious diseases Discussion HBV F22L 54 58 PreS2 49 54 Hepatocellular carcinoma 87 90 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. The majority of the HBeAg-negativity was as a result of the classical G1896A, which abolishes HBeAg expression and occurs in genotype D or E but not A because the encapsidation signal secondary structure precludes this mutation in genotype A. 2013 BMC infectious diseases Discussion HBV G1896A 70 76 C;C 20;94 25;99 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. The reverse transcriptase mutations rtA194T, rtV207M, rtS213T, rtV214A and rtS215Q detected in the present study are neither primary resistance mutations, nor have they ever been seen in overt resistance during therapy. 2013 BMC infectious diseases Discussion HBV V214A;A194T;V207M;S213T;S215Q 65;38;47;56;77 70;43;52;61;82 RT;RT;RT;RT;RT;RT 4;36;45;54;63;75 25;38;47;56;65;77 23865777 Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan. When mutations rtA194T, rtV207M rtS213T rtV214A and rtQ215S were tested in our sensitive and reliable in vitro resistance test system, the mutants showed no resistance to lamivudine (LMV), entecavir (ETV), adenofovir (ADF) and tenofovir (TDF). 2013 BMC infectious diseases Discussion HBV Q215S;A194T;V207M;S213T;V214A 54;17;26;34;42 59;22;31;39;47 RT;RT;RT;RT;RT 15;24;32;40;52 17;26;34;42;54 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Each combined mutation containing A1762T and/or G1764A occurred in the early stage of advanced liver disease, which means that the A1762T and/or G1764A mutation may stimulate the occurrence of the other mutations in the enhII/BCP/precore regions. 2013 Brazilian journal of medical and biological research Discussion HBV A1762T;G1764A;A1762T;G1764A 34;48;131;145 40;54;137;151 BCP;Enh II;Precore 226;220;230 229;225;237 Liver disease 95 108 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. In addition, the C1653T, T1753C, A1762T, and G1764A mutations lead to H94Y, I127T, K130M, and V131I amino acid substitutions in HBx. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;T1753C;A1762T;G1764A;H94Y;I127T;K130M;V131I 17;25;33;45;70;76;83;94 23;31;39;51;74;81;88;99 X 128 131 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Multivariate analysis revealed that HBV subgenotype C2 infection and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) contributed to the development of LC from CHB, and that B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) contributed to the development of HCC from LC. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;T1753C;A1762T;G1764A;C1810T;A1846T;G1862T;G1896A 102;110;118;130;227;235;243;255 108;116;124;136;233;241;249;261 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 180;297;172;306 183;300;174;308 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Our results showed that HBV subgenotype C2 and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) were independent risk factors for LC when CHB was the control and that B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) were independent risk factors for HCC when LC was the control. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;T1753C;A1762T;G1764A;C1810T;A1846T;G1862T;G1896A 80;88;96;108;220;228;236;248 86;94;102;114;226;234;242;254 Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Liver cirrhosis 290;150;158;299 293;152;161;301 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Seven of 13 mutation patterns (C1653T, G1719T, G1730C, T1753C, A1762T, G1764A, and G1799C) in the CP region were associated with C2 infection, and 4 mutation patterns (C1810T, A1846T, G1862T, and G1896A) close to the precore region were associated with B2 infection. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;G1719T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A 31;39;47;55;63;71;83;168;176;184;196 37;45;53;61;69;77;89;174;182;190;202 Core promoter;Precore 98;217 100;224 HBV infections;HBV infections 129;253 141;265 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Ten mutation patterns (C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, and G1896A) were associated with HCC compared with CHB (P<0.05), and 4 mutation patterns (C1810T, A1846T, G1862T, and G1896A) located close to the precore region were associated with HCC compared with LC (P<0.05). 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C;C1810T;A1846T;G1862T;G1896A;C1810T;A1846T;G1862T;G1896A 23;31;39;47;55;63;71;79;87;99;185;193;201;213 29;37;45;53;61;69;77;85;93;105;191;199;207;219 Precore 242 249 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 128;146;278;296 131;149;281;298 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The A1762T and G1764A mutations are associated with diminished HBeAg production at the transcriptional level, enhanced host immune response, and viral replication. 2013 Brazilian journal of medical and biological research Discussion HBV A1762T;G1764A 4;15 10;21 C 63 68 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The C1653T mutation occurs at the center of the immunodominant antigenic domain and may be involved in inflammatory processes. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T 4 10 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The C1653T, T1753C, A1762T, and G1764A mutations may play critical roles in persistent viral infections and inflammatory processes, and therefore may be responsible for severe liver fibrosis. 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;T1753C;A1762T;G1764A 4;12;20;32 10;18;26;38 Liver fibrosis 176 190 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The C1810T and G1862T mutations affect the expression of HBeAg at the translational and post-translational levels, respectively. 2013 Brazilian journal of medical and biological research Discussion HBV C1810T;G1862T 4;15 10;21 C 57 62 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The C1810T, A1846T, G1862T, and G1896A mutations most likely result in crude expression of HBeAg and accumulation of the HBeAg precursor in the endoplasmic reticulum/Golgi apparatus of the cell. 2013 Brazilian journal of medical and biological research Discussion HBV C1810T;A1846T;G1862T;G1896A 4;12;20;32 10;18;26;38 C;C 91;121 96;126 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The G1896A mutation produces a stop codon for HBeAg expression, while the role of the A1846T mutation in the regulation of HBeAg expression requires further study. 2013 Brazilian journal of medical and biological research Discussion HBV G1896A;A1846T 4;86 10;92 C;C 46;123 51;128 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. The T1753C mutation enhances viral replication, leading to persistent infection. 2013 Brazilian journal of medical and biological research Discussion HBV T1753C 4 10 23903686 Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively. Univariate analyses showed that 6 mutation patterns (C1653T, G1730C, T1753C, A1762T, G1764A, and G1799C) located in the CP region were associated with LC compared with CHB (P<0.05). 2013 Brazilian journal of medical and biological research Discussion HBV C1653T;G1730C;T1753C;A1762T;G1764A;G1799C 53;61;69;77;85;97 59;67;75;83;91;103 Core promoter 120 122 Chronic Hepatitis B;Liver cirrhosis 168;151 171;153 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. Although primary drug resistance changes in the RT domains studied were completely absent, secondary drug resistance changes in domains C (rtV207L) and D (rtN238T) were identified in one (6%) and five (31%) samples, respectively, which were higher than previous reports, although the study group was small (n = 16) . 2013 Memorias do Instituto Oswaldo Cruz Discussion HBV V207L;N238T 141;157 146;162 RT;RT;RT 48;139;155 50;141;157 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. Mutation analysis in the Enh II region found the G1613A mutation in two subjects; although both samples were HBeAg-positive, in vitro studies have linked this mutation with HBeAg suppression in CHB. 2013 Memorias do Instituto Oswaldo Cruz Discussion HBV G1613A 49 55 Enh II;C;C 25;109;173 31;114;178 Chronic Hepatitis B 194 197 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. The mutation pair A1762T/G1764A was found in three samples, with one sample concurrently showing the BCP mutation G1896A; this group of mutations abolished the secretion of HBeAg in this specimen, as evidenced by a negative result in the immunoassay used. 2013 Memorias do Instituto Oswaldo Cruz Discussion HBV G1764A;A1762T;G1896A 25;18;114 31;24;120 BCP;C 101;173 104;178 23903967 Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City. The substitution Q129H was observed in one sample; this residue has been reported as capable of reducing serological detection in some diagnostic assays. 2013 Memorias do Instituto Oswaldo Cruz Discussion HBV Q129H 17 22 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. A G1862T nucleotide mutation, which was identified in two study sequences (4070 and 4312) has also been reported to negatively affect HBeAg expression at post-translational level, however, both these participants were HBeAg-positive. 2013 Journal of medical virology Discussion HBV G1862T 2 8 C;C 134;218 139;223 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. G1899A found in participant 3319 has been reported in patients with fulminant hepatitis failure and has also been found in high frequency in hepatocellular carcinoma (HCC), liver cirrhosis, and chronic hepatitis. 2013 Journal of medical virology Discussion HBV G1899A 0 6 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Chronic Hepatitis B;Fulminant Hepatitis B 141;167;173;194;68 165;170;188;211;87 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. However, preC start codon mutations noted in this study have also been reported in published data from South Africa (A1814C/T, T1815C/A), and in patients from Cameroon who were infected with HBV genotype A3 (A1814C and A1814T). 2013 Journal of medical virology Discussion HBV A1814T;T1815A;A1814C;T1815C;A1814C;A1814T 117;127;117;127;208;219 125;135;125;135;214;225 Precore 9 13 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. I97L and A131P amino acid mutations have been associated with failure to express HBeAg; both these mutations have also been found in this study in patients who did not express HBeAg (3812, 3464, 3734, and 3319). 2013 Journal of medical virology Discussion HBV I97L;A131P 0;9 4;14 C;C 81;176 86;181 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. Most published data state that HBeAg-negative chronic hepatitis B due to preC mutations is common in non-A genotypes only, and that mutations that often lead to reduced production of HBeAg in genotype A are confined to the core promoter region (A1762T and G1764A). 2013 Journal of medical virology Discussion HBV A1762T;G1764A 245;256 251;262 Core promoter;C;C;Precore 223;31;183;73 236;36;188;77 Chronic Hepatitis B 46 65 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. Only N199 and 3274 sequences had a Kozak sequence mutation (T1812C), which is also known to interfere with HBeAg expression. 2013 Journal of medical virology Discussion HBV T1812C 60 66 C 107 112 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. P5H/L and I97L amino acid mutations in genotype C of HBV (all of which were noticed in this study) were recently found to be associated with HCC, and I97L was found at a higher frequency (16%) among study participants. 2013 Journal of medical virology Discussion HBV P5H;P5L;I97L;I97L 0;0;10;150 5;5;14;154 Hepatocellular carcinoma 141 144 23925707 Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV. The finding that 24% (6) of the study participants had preC start codon mutations (A1814C/T and G1816T) suggests that mutations that lead to failure of HBeAg production are common in subgenotype A1. 2013 Journal of medical virology Discussion HBV A1814C;A1814T;G1816T 83;83;96 91;91;102 C;Precore 152;55 157;59 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. Among OBI adults and overt infection patients in these regions, few had the common HBsAg mutant G145R. 2013 PloS one Discussion HBV G145R 96 101 S 83 88 Occult Hepatitis B 6 9 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. G145R is the most common escape mutation in the surface protein. 2013 PloS one Discussion HBV G145R 0 5 S 48 55 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. identified the OBI-associated mutations Y100S, T116N, R122P, S143L and S167L from a large-sample, blood-donor study. 2013 PloS one Discussion HBV Y100S;T116N;R122P;S143L;S167L 40;47;54;61;71 45;52;59;66;76 Occult Hepatitis B 15 18 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. In Iran, 10 of 14 OBI isolates from children (71%) contained the G145R mutation. 2013 PloS one Discussion HBV G145R 65 70 Occult Hepatitis B 18 21 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. In this study, 4 OBI infants with C/D genotype had S143L mutation, and their HBsAg-negative occult state may be attributed to the escape mutation. 2013 PloS one Discussion HBV S143L 51 56 S 77 82 Occult Hepatitis B 17 20 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. No G145R mutations were found in OBI isolates from children in the present study or a previous study in Taiwan. 2013 PloS one Discussion HBV G145R 3 8 Occult Hepatitis B 33 36 23951004 Occult hepatitis B virus infection in anti-HBs-positive infants born to HBsAg-positive mothers in China. Other common escape mutations, including G145R, D144A, P142S, Q129H, I/T126N/A and M133L, were not found in our OBI isolates. 2013 PloS one Discussion HBV I126N;I126A;T126N;T126A;G145R;D144A;P142S;Q129H;M133L 69;69;69;69;41;48;55;62;83 78;78;78;78;46;53;60;67;88 Occult Hepatitis B 112 115 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. Compared with rtM204I (sI195M), the YMDD mutation rtM204V (sW196S) appeared to have minimal influence on the immune-escaped HBsAg mutants. 2013 Virology journal Discussion HBV M204I;M204V;I195M;W196S 16;52;23;59 21;57;29;65 S;RT;RT;S;S;P 124;14;50;23;59;36 129;16;52;24;60;40 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. In the current study no changes to the antigenicity of sT118M HBsAg was observed when the drug-resistant mutants rtM204I (sI195M) or rtM204V (sW196S) were present on the sT118M backbone. 2013 Virology journal Discussion HBV M204I;M204V;T118M;I195M;W196S;T118M 115;135;55;122;142;170 120;140;61;128;148;176 S;RT;RT;S;S;S;S 62;113;133;55;122;142;170 67;115;135;56;123;143;171 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. rtM204I (sI195M) significantly reduced the antigenicity of immune-escaped HBsAg, especially for the most common mutants sG145K and sG145R HBsAg. 2013 Virology journal Discussion HBV M204I;I195M;G145K;G145R 2;9;120;131 7;15;126;137 S;S;RT;S;S;S 74;138;0;9;120;131 79;143;2;10;121;132 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The immune escape mutant sT118M HBsAg can decrease the antigenicity of HBsAg considerably . 2013 Virology journal Discussion HBV T118M 25 31 S;S;S 32;71;25 37;76;26 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. The presence of rtM204I (sI195M) on the sG145R HBsAg mutant backbone, also resulted in a loss in avidity of ELISA kits or the antigenicity of HBsAg. 2013 Virology journal Discussion HBV M204I;I195M;G145R 18;25;40 23;31;46 S;S;RT;S;S 47;142;16;25;40 52;147;18;26;41 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. This was demonstrated with the mutation sW196S in HBsAg, which was associated with reduced binding to anti-HBs antibody, and corresponding to rtM204I in polymerase and conferring resistance to lamivudine . 2013 Virology journal Discussion HBV M204I;W196S 144;40 149;46 S;S;P;RT;S 107;50;153;142;40 110;55;163;144;41 24053482 Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants. YMDD mutations, particularly rtM204I (sI195M), reduced the antigenicity of sG145K HBsAg significantly, causing the great drop in the slope of an antibody titration curve in four of the five ELISA kits. 2013 Virology journal Discussion HBV M204I;I195M;G145K 31;38;75 36;44;81 S;RT;S;S;P 82;29;38;75;0 87;31;39;76;4 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Although preliminary data using ADV belonging to acyclic phosphonates on LAM-resistance patients seem promising, a shared pathway (rtA181T/V) of both L-nucleosides and acyclic phosphonates could be selected, which would affect both LAM and ADV sensitivity. 2013 Virology journal Discussion HBV A181T;A181V 133;133 140;140 RT 131 133 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. In present study, HBV rtA181T/V mutation was observed in 19.3% (22/114) of patients with LAM/LdT-based therapy and 23.9% (11/46) of patients with ADV-based therapy, and our results suggested that rtA181T/V antiviral resistance mutation has become a relatively common phenomenon in Chinese patients. 2013 Virology journal Discussion HBV A181T;A181V;A181T;A181V 24;24;198;198 31;31;205;205 RT;RT 22;196 24;198 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. In this cohort, three classic evolutionary pathways of L-nucleoside pathway against LAM, LdT or ETV (rtM204 I/V), the acyclic phosphonate pathway (rtN236T) against ADV and the shared pathway against both LAM and ADV (rtA181T T/V) were all involved, and our findings were also supported by recent studies. 2013 Virology journal Discussion HBV M204I;M204V;A181T;N236T 103;103;219;149 111;111;224;154 RT;RT;RT 101;147;217 103;149;219 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. In this study, majority of patients had resistance that was associated with the L-nucleoside pathway [rtM204I (or V or I/V)], which could potentially lead to resistance to LAM, ETV and LdT treatment in LAM-experienced patients. 2013 Virology journal Discussion HBV M204I 104 109 RT 102 104 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. It has reported that rtA194T mutation was associated with tenofovir (TDF), and it could be selected by long-term application of ADV. 2013 Virology journal Discussion HBV A194T 23 28 RT 21 23 24160943 Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B. Thus, we also thought that HBV rtA194T might be not a common mutation induced by ADV and TDF would be used as a rescue medication for ADV treatment failure. 2013 Virology journal Discussion HBV A194T 33 38 RT 31 33 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. Although we were not able to correlate the genotypes with the mutations detected, probably because of the small number samples analyzed, we found the mutation sF183C in an individual infected with genotype F, which corroborates with other studies that found that this mutation is a natural polymorphism for genotype F and H. 2013 Virology journal Discussion HBV F183C 159 165 S 159 160 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. However, among chronically infected and treated Brazilian individuals, the rate of LAM resistance (rtM204V + rtL180M) ranges from 16% to 41%. 2013 Virology journal Discussion HBV M204V;L180M 101;111 106;116 RT;RT 99;109 101;111 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. In fact, a chimpanzee study performed by Kamili et al., reported a successful infection by HBV mutants harboring the mutations rtM204V + rtL180M, which corroborates our finding that these variants can be infectious and stable. 2013 Virology journal Discussion HBV M204V;L180M 129;139 134;144 RT;RT 127;137 129;139 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. sY100C has been reported in cases of occult hepatitis, however Mello et al. 2013 Virology journal Discussion HBV Y100C 0 6 S 0 1 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. The primary mutation rtM204V reduces susceptibility to LAM and decreases viral fitness, which is restored by compensatory mutations. 2013 Virology journal Discussion HBV M204V 23 28 RT 21 23 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. Then, it is conceivable that we were able to detect the rtM204V variant because it was associated with the compensatory mutation at position rt180 (rtL180M), which may recover its fitness and stability in vivo. 2013 Virology journal Discussion HBV M204V;L180M 58;150 63;155 RT;RT;RT 56;141;148 58;143;150 24165277 Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil. We found the transmitted mutation rtM204V (2.94%) with the compensatory mutation rtL180M in a blood donor sample. 2013 Virology journal Discussion HBV M204V;L180M 36;83 41;88 RT;RT 34;81 36;83 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. Furthermore, increasing TLR2 is associated with serum ALT concentration in G1896A precore mutant patients. 2013 Advances in virology Discussion HBV G1896A 75 81 Precore 82 89 24187552 The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation. In conclusion, our data show that the concentration of serum TLR2 was significantly higher in HBeAg negative patients with G1896A mutation which in turn was associated with higher serum ALT in this group. 2013 Advances in virology Discussion HBV G1896A 123 129 C 94 99 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. A recent paper demonstrated that the G1757A substitution is associated with protection against advanced liver disease (P = 0.001). 2013 PloS one Discussion HBV G1757A 37 43 Liver disease 104 117 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. Concerning the HBV heterogeneity in the PC region, the most frequently reported mutation is G1896A, which pairs with a T in nucleotide 1858. 2013 PloS one Discussion HBV G1896A 92 98 Precore 40 42 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In Guinea, a similar G1896A mutation prevalence (21%) was described in blood donors infected with HBV/E. 2013 PloS one Discussion HBV G1896A 21 27 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In our population, the majority of PC sequences (98%) harbored the C1858T mutation. 2013 PloS one Discussion HBV C1858T 67 73 Precore 35 37 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. In our study, it was surprising to note the low prevalence of the G1896A mutation (21.4%) with the high percentage of the C1858T mutation (99.1%) detected in HBV/E, whereas these two point mutations are usually associated. 2013 PloS one Discussion HBV G1896A;C1858T 66;122 72;128 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. Our results confirm those of previous reports indicating a G1896A mutation prevalence in African pregnant women inferior to 50%. 2013 PloS one Discussion HBV G1896A 59 65 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. The low frequency of the PC mutation could be explained by the high prevalence of the G1757A mutation in our population. 2013 PloS one Discussion HBV G1757A 86 92 Precore 25 27 24265811 High endemicity and low molecular diversity of hepatitis B virus infections in pregnant women in a rural district of North Cameroon. The low prevalence of the PC/BCP mutants in conjunction with the high percentage of the G1757A mutation might influence the clinical characteristics of HBV/E. 2013 PloS one Discussion HBV G1757A 88 94 BCP;Precore 29;26 32;28 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. As shown in Figure 3B, incorporation of BrdU into the control, accumulation of mitotic L02 cells was delayed by LHBs and its mutations, especially in N320K. 2013 Hepatitis monthly Discussion HBV N320K 150 155 S 112 116 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. But the interaction between N320K and EDEM may block the ERAD pathway and its secretion (Figure 5). 2013 Hepatitis monthly Discussion HBV N320K 28 33 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. In conclusion, the N320K may be the key sites N-linked glycosylation modification of LHBs. 2013 Hepatitis monthly Discussion HBV N320K 19 24 S 85 89 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. LHBs and its mutations induced an increase in G1 phase and inhibition of S phase, especially in N320K (Figure 3A). 2013 Hepatitis monthly Discussion HBV N320K 96 101 S 0 4 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. Our results confirmed that LHBs and its four mutated proteins contained p62-derived UBA domain, especially in N15S, N123S and N320K mutations. 2013 Hepatitis monthly Discussion HBV N15S;N123S;N320K 110;116;126 114;121;131 S 27 31 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. Our results demonstrated that the modification of N-glycosylation of LHBs was related to ER stress, especially in N-glycosylation sites N177S and N320K. 2013 Hepatitis monthly Discussion HBV N177S;N320K 136;146 141;151 S 69 73 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. PNGase F converted especially gp42 to the nonglycosylated p39 form of the N320K mutation LHBs. 2013 Hepatitis monthly Discussion HBV N320K 74 79 S 89 93 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The markers of ER stress, GADD34 and GRp78 expression were significantly upregulated by LHBs and its mutations, especially N320K (Figure 1A). 2013 Hepatitis monthly Discussion HBV N320K 123 128 S 88 92 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S and N123S mutations of LHBs contained fucosylated modification sites by Lectin array. 2013 Hepatitis monthly Discussion HBV N15S;N123S 4;13 8;18 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N15S, N123S, N177S and N320K LHBs mutation proteins interacted with EDEM protein in L02 cells, especially in N177S, but not LHBs (Figure 1C). 2013 Hepatitis monthly Discussion HBV N15S;N123S;N177S;N320K;N177S 4;10;17;27;113 8;15;22;32;118 S;S 33;128 37;132 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The N320K LHBs mutation proteins could induce overexpression of cyclin E (Figure 5). 2013 Hepatitis monthly Discussion HBV N320K 4 9 S 10 14 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The research showed that the N15S, N123S and N177S mutated LHBs proteins could induce overexpression of cyclinA in L02 cells. 2013 Hepatitis monthly Discussion HBV N15S;N123S;N177S 29;35;45 33;40;50 S 59 63 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. The secretion of LHBs or its mutations were blocked, especially in N320K. 2013 Hepatitis monthly Discussion HBV N320K 67 72 S 17 21 24282423 The N-Glycosylation Modification of LHBs (Large Surface Proteins of HBV) Effects on Endoplasmic Reticulum Stress, Cell Proliferation and its Secretion. We found that the N15S, N123S and N177S mutated LHBs proteins could induce overexpression of EDEM in L02 cells (Figure 1B). 2013 Hepatitis monthly Discussion HBV N15S;N123S;N177S 18;24;34 22;29;39 S 48 52 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. A1846T or C1913A/G mutation in both genotypes B and C was associated with ACLF from CHB. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 10;0;10 18;6;18 Acute on chronic liver failure;Chronic Hepatitis B 74;84 78;87 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Furthermore, multivariate analysis demonstrated that A1846T and A/G1913 were independent factors for ACLF, with odds ratios of 2.86 and 5.93, respectively. 2013 Hepatitis monthly Discussion HBV A1846T 53 59 Acute on chronic liver failure 101 105 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Genotype C with A1846T or C1913A/G mutation was associated with ACLF development from LC. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 26;16;26 34;22;34 Acute on chronic liver failure;Liver cirrhosis 64;86 68;88 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In comparison with CHB patients, the HBV isolates in LC patients had higher frequencies of the mutations in BCP/PC region, which included A1762T/G1764T, T1753V, and/or G1896A. 2013 Hepatitis monthly Discussion HBV G1764T;A1762T;T1753V;G1896A 145;138;153;168 151;144;159;174 BCP;Precore 108;112 111;114 Chronic Hepatitis B;Liver cirrhosis 19;53 22;55 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. In conclusion, HBV precore mutation of A1846T and the fifth amino acid substitution in the core protein due to C1913A/G were found more frequently in ACLF patients than in their respective CHB or LC patients. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 111;39;111 119;45;119 C;Precore 91;19 95;26 Chronic Hepatitis B;Acute on chronic liver failure;Liver cirrhosis 189;150;196 192;154;198 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Our results showed that the epsilon signal with A1846T mutation had lower value of minimum free energy, suggesting a higher stability than wild type HBV (Figure 3C). 2013 Hepatitis monthly Discussion HBV A1846T 48 54 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Positions of A1846T and C1913A/G mutations compared to HBV wild type were shown in Figure 3A. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 24;13;24 32;19;32 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Previous studies showed that the A1846T was found in patients with fulminant hepatitis and ACLF . 2013 Hepatitis monthly Discussion HBV A1846T 33 39 Fulminant Hepatitis B;Acute on chronic liver failure 67;91 86;95 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. The C1913A/G mutation causes a substitution of the fifth amino acid of the core protein from proline to threonine or alanine (Figure 3A, B). 2013 Hepatitis monthly Discussion HBV C1913G;C1913A 4;4 12;12 C 75 79 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. These results support our hypothesis that those previous reported BCP/PC mutations (T1753V, A1762T, G1764T, G1896A, and G1899A) might be associated with liver cirrhosis, but not ACLF development. 2013 Hepatitis monthly Discussion HBV T1753V;A1762T;G1764T;G1896A;G1899A 84;92;100;108;120 90;98;106;114;126 BCP;Precore 66;70 69;72 Liver cirrhosis;Acute on chronic liver failure 153;178 168;182 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. This observation is different from previous studies in which the mutations of T1753V, A1762T, G1764T, G1896A, and G1899A were found to be more prevalent in ACLF patients. 2013 Hepatitis monthly Discussion HBV T1753V;A1762T;G1764T;G1896A;G1899A 78;86;94;102;114 84;92;100;108;120 Acute on chronic liver failure 156 160 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. Thus, HBV of A1846T and A/G1913 mutation may promote ACLF development through either enhancing HBV replication or core protein expression. 2013 Hepatitis monthly Discussion HBV A1846T 13 19 C 114 118 Acute on chronic liver failure 53 57 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. We showed that the HBV precore mutation of A1846T and core mutation of C1913A/G (substitution at the fifth amino acid: proline to threonine or alanine) were associated with HBV-related ACLF development. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 71;43;71 79;49;79 C;Precore 54;23 58;30 Acute on chronic liver failure 185 189 24282424 Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases. When ACLF patients were categorized into ACLF-CHB and ACLF-LC based on their underlying liver diseases, a significantly higher prevalence of the A1846T, and C1913A/G mutations were observed compared to respective CHB or LC patients. 2013 Hepatitis monthly Discussion HBV C1913G;A1846T;C1913A 157;145;157 165;151;165 Chronic Hepatitis B;Liver disease;Chronic Hepatitis B;Acute on chronic liver failure;Liver cirrhosis;Liver cirrhosis 46;88;213;5;220;59 49;102;216;9;222;61 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. A recent study from South India reported the presence of rtS106C mutation among the chronic HBV carriers. 2013 TheScientificWorldJournal Discussion HBV S106C 59 64 RT 57 59 Chronic Hepatitis B 84 95 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. In the BCP region mutations such as 1752C, only 1753C, 1753C + 1762T/1764A (triple mutation), and 1762T/1764A (double mutation) are noteworthy, and in HBVrt region, rtS106C mutation was found among the OBI isolates. 2013 TheScientificWorldJournal Discussion HBV S106C 167 172 BCP;RT 7;165 10;167 Occult Hepatitis B 202 205 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Interestingly, in one isolate, a quasispecies clone showed R160K substitution that resulted in serotype conversion, and thus, a unique mixed serotype pattern of infection was documented. 2013 TheScientificWorldJournal Discussion HBV R160K 59 64 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Mutations related to diagnostic failure (such as M133T/I, F134N, and S143L) including vaccine escape mutations such as D144A and G145R could not be found. 2013 TheScientificWorldJournal Discussion HBV M133T;M133I;F134N;S143L;D144A;G145R 49;49;58;69;119;129 56;56;63;74;124;134 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Notably, T125M substitution was exclusive among the HBV/D3 isolates (data not shown). 2013 TheScientificWorldJournal Discussion HBV T125M 9 14 24302857 Characterization of the occult hepatitis B virus variants circulating among the blood donors from eastern India. Similar association of this T125M substitution with HBV/D3 strains was documented in previous studies. 2013 TheScientificWorldJournal Discussion HBV T125M 28 33 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Altogether, most of HBx point mutants retained the ability to upregulate HIF-1alpha, and especially the dual mutations K130M/V131I enhanced this function. 2014 British journal of cancer Discussion HBV V131I;K130M 125;119 130;124 X 20 23 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Dual mutations K130M/V131I have also been demonstrated to associate with an increased risk of HCC independent for viral loading and other risk factor. 2014 British journal of cancer Discussion HBV V131I;K130M 21;15 26;20 Hepatocellular carcinoma 94 97 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Here, we revealed that the dual mutations K130M/V131I can enhance the function of HBx in upregulating HIF-1alpha. 2014 British journal of cancer Discussion HBV V131I;K130M 48;42 53;47 X 82 85 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Indeed, HBx mutants with dual mutations K130M/V131I have been shown to possess the increased capability of binding to p53 compared with the wild-type HBx. 2014 British journal of cancer Discussion HBV V131I;K130M 46;40 51;45 X;X 8;150 11;153 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. The dual point mutations K130M/V131I in this region result in enhanced functionality of HBx, whereas mutations of C-terminal truncation or deletion may weaken the function of HBx in upregulating HIF-1alpha. 2014 British journal of cancer Discussion HBV V131I;K130M 31;25 36;30 X;X 88;175 91;178 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. The underlying mechanisms accounted for the difference of the function between dual mutations K130M/V131I and other mutations may be dependent on their secondary structures and the target molecules. 2014 British journal of cancer Discussion HBV V131I;K130M 100;94 105;99 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. Whether the dual mutations K130M/V131I exert more potent activity in the upregulation of HIF-1alpha than other mutations is due to its greater ability to bind to HIF-1alpha would be an important issue for further investigations. 2014 British journal of cancer Discussion HBV V131I;K130M 33;27 38;32 24346287 HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma. With the dual mutations K130M/V131I, HBx would gain more potent secondary structures to interact with HIF-1alpha, and thus increase the expression and the transcriptional activity of HIF-1alpha. 2014 British journal of cancer Discussion HBV V131I;K130M 30;24 35;29 X 37 40 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Although the emergence of rtQ267H may be more serious for CHB patients with LMVr/LdTr, fortunately ADV, ETV and TDF showed comparative antiviral activity against LMVr/LdTr HBV mutants and WT HBV in vitro. 2013 Hepatitis monthly Discussion HBV Q267H 28 33 RT 26 28 Chronic Hepatitis B 58 61 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Due to selection advantage under high selection pressure of LMV or LdT, HBV virions with rtM204V/I, especially together with rtL180M and/or rtL80I and/or rtV173L at the same time, would be selected as dominant strains. 2013 Hepatitis monthly Discussion HBV M204V;M204I;L180M;L80I;V173L 91;91;127;142;156 98;98;132;146;161 RT;RT;RT;RT 89;125;140;154 91;127;142;156 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Hydrodynamically injected mice HBV model was used widely in our previous research to analyze the drug-resistant phenotype of HBV; we would explore the susceptibility of WT/LMVr HBV carrying rtQ267H to NAs with replication-competent pAAV-HBV1.3. 2013 Hepatitis monthly Discussion HBV Q267H 192 197 RT 190 192 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. In further research, we plan to bring rtQ267H to the model of HBV-RT to study the association between LMV/LdT and rtQ267H. 2013 Hepatitis monthly Discussion HBV Q267H;Q267H 40;116 45;121 RT;RT;RT 38;66;114 40;68;116 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. In our study, besides these three mutations, another adaptive mutation rtQ267H was found, not only restored the HBV replication, but also exacerbated LMVr and LdTr. 2013 Hepatitis monthly Discussion HBV Q267H 73 78 RT 71 73 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. In the following step, rtQ267H was introduced into WT or MT replication-competent plasmid to demonstrate that it was not only responsible for enhancing HBV replication, but also aggravating LMV resistance degree of known LMV-resistant mutants in vitro, such as rtL180M/M204V. 2013 Hepatitis monthly Discussion HBV M204V;L180M;Q267H 269;263;25 274;268;30 RT;RT 23;261 25;263 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtM204V/I significantly changes the three-dimensional structure of HBV-RT, thus it would be difficult for LMV and LdT to enter the catalytic pocket or separate from the catalytic pocket when this mutation take place. 2013 Hepatitis monthly Discussion HBV M204V;M204I 15;15 22;22 RT;RT 13;84 15;86 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitution rtQ267H of hepatitis B virus leads to slight resistance to LMV and LdT, enhances HBV replication, aggravates existing LMV-resistance, and is likely to be another adaptive mutation of LMV, except rtL180M and rtV173L. 2013 Hepatitis monthly Discussion HBV Q267H;L180M;V173L 15;210;222 20;215;227 RT;RT;RT 13;208;220 15;210;222 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Substitutions rtL180M /rtL80I/rtV173L which can restore the impaired HBV replication ability, are called adaptive mutations of HBV to LMV. 2013 Hepatitis monthly Discussion HBV L80I;L180M;V173L 25;16;32 29;21;37 RT;RT;RT 14;23;30 16;25;32 24348637 Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance. Through sequence analysis of the samples from patients' serum, a series of mutations were found, except for existing reported LMVr mutations only rtQ267H was newly found closely related to LMV usage in all patients. 2013 Hepatitis monthly Discussion HBV Q267H 148 153 RT 146 148 24379746 Naturally occurring hepatitis B virus B-cell and T-cell epitope mutants in hepatitis B vaccinated children. We did not find the most important and best-documented G145R mutation, but we found a G145A mutation and other substitutions (T126I, N131T, and T143S) within the "a" determinant. 2013 TheScientificWorldJournal Discussion HBV G145R;G145A;T126I;N131T;T143S 55;86;126;133;144 60;91;131;138;149 24444423 Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies. F134V mutation was supposed to be a vaccine induced escape mutant and L175S mutation was found in patients with HBsAg-anti-HBs coexistence. 2014 Virology journal Discussion HBV F134V;L175S 0;70 5;75 S;S 123;112 126;117 24444423 Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies. M133I and D144E mutation were reported to cause a reduced HBsAg affinity to anti-HBs. 2014 Virology journal Discussion HBV M133I;D144E 0;10 5;15 S;S 81;58 84;63 24444423 Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies. Most of the other aa substitution in the HBsAg found during the flare-up phase described here have been reported before and in combination with the K122R mutation, possibly causing HBV escape from anti-HBs. 2014 Virology journal Discussion HBV K122R 148 153 S;S 202;41 205;46 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Adefovir resistance was caused by N236T and /or A181V amino acid substitution, whereas entecavir resistance resulted from HBV reverse transcriptase substitutions at positions T184, S202, or M250L which emerge in the presence of lamivudine resistance substitutions M204I/V and L180M. 2014 Hepatitis monthly Discussion HBV N236T;A181V;M250L;M204I;M204V;L180M 34;48;190;264;264;276 39;53;195;271;271;281 RT 126 147 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. All three patients with liver cirrhosis contained HBV mutant L180M in combination with M204I. 2014 Hepatitis monthly Discussion HBV L180M;M204I 61;87 66;92 Liver cirrhosis 24 39 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Emtricitabine resistance was often accompanied with lamuvudine resistance because of L180M, V173L, and M204I mutations. 2014 Hepatitis monthly Discussion HBV L180M;V173L;M204I 85;92;103 90;97;108 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Lamivudine resistance mutants were reported to harbor M240V/I in the YMDD motif of the polymerase gene. 2014 Hepatitis monthly Discussion HBV M240V;M240I 54;54 61;61 P;P 87;69 97;73 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Resistance to telbivudine has been associated with M204I mutation. 2014 Hepatitis monthly Discussion HBV M204I 51 56 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Similarly, three out of five patients contained both M204I and L180M/V. 2014 Hepatitis monthly Discussion HBV M204I;L180M;L180V 53;63;63 58;70;70 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. Some study reported that in most cases, the M204V/I mutation was not present alone but linked with a leucine to methionine exchange at position 180 (L180M). 2014 Hepatitis monthly Discussion HBV M204V;M204I;L180M;L180M 44;44;149;101 51;51;154;147 24497877 Drug-resistance associated mutations in polymerase (p) gene of hepatitis B virus isolated from malaysian HBV carriers. The mutations found in the four patients were L180M/V, M204I, A181T, and V173L.Among these, L180M/V and M204I were frequently observed. 2014 Hepatitis monthly Discussion HBV L180M;L180V;M204I;A181T;V173L;L180M;L180V;M204I 46;46;55;62;73;92;92;104 53;53;60;67;78;99;99;109 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. A previous study reported the emergence of rtM204Q with rtA181T in a TDF-treated ADV-resistant patient. 2014 PloS one Discussion HBV A181T;M204Q 58;45 63;50 RT;RT 43;56 45;58 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Accordingly, rtM204Q was detected in seven LAM-refractory patients and the emergence of the mutation was closely linked with virologic breakthrough in clinical course for all of the seven patients and biochemical breakthrough in two of them. 2014 PloS one Discussion HBV M204Q 15 20 RT 13 15 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. but it had higher natural replication capacity compared with rtM204I (of 89.9% vs. 2014 PloS one Discussion HBV M204I 63 68 RT 61 63 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. By contrast, rtM204Q mutation requires two or three nucleotide changes (from ATG to CAG or CAA), which increases genetic barrier of the mutation and could be one reason for its low incidence in clinic. 2014 PloS one Discussion HBV M204Q 15 20 RT 13 15 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. For the position of rt204 in the HBV RT region, rtM204V and rtM204I are well-known primary LAM- and/or LdT-resistant mutation, and rtM204S was also reported to be induced by LAM treatment and conferred LAM resistance. 2014 PloS one Discussion HBV M204S;M204V;M204I 133;50;62 138;55;67 RT;RT;RT;RT;RT 20;37;48;60;131 22;39;50;62;133 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. However, the clinical incidence and association of rtM204Q mutation with LAM resistance remained unclear. 2014 PloS one Discussion HBV M204Q 53 58 RT 51 53 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. In addition, after rescue therapy with ADV or ADV plus LAM, proportion of rtM204Q mutant obviously declined and wild-type strain obviously increased simultaneously with the decrease of viral load as shown in patient 1. 2014 PloS one Discussion HBV M204Q 76 81 RT 74 76 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. In conclusion, our data showed that rtM204Q confers a significant decreased susceptibility to LAM with relatively competent replication capacity and associates with virologic breakthrough during LAM treatment. 2014 PloS one Discussion HBV M204Q 38 43 RT 36 38 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. In this study, we reported a novel LAM-resistance-associated mutation rtM204Q after screening of a large number of patients with chronic HBV infection. 2014 PloS one Discussion HBV M204Q 72 77 RT 70 72 Chronic HBV infection 129 150 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Moreover, a recent analysis of Bayesian networks that connect rtM204I/V to many sites of HBV proteins confirmed that LAM resistance was a complex trait encoded by the entire HBV genome rather than by a single mutation. 2014 PloS one Discussion HBV M204V;M204I 64;64 71;71 RT 62 64 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Phenotypic analysis of drug resistance showed that the rtM204Q mutation significantly reduced LAM susceptibility of the mutant virus. 2014 PloS one Discussion HBV M204Q 57 62 RT 55 57 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Phenotypic analysis showed that rtM204Q mutant was less resistance to LAM compared with rtM204I mutant (of 76-fold vs. 2014 PloS one Discussion HBV M204I;M204Q 90;34 95;39 RT;RT 32;88 34;90 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. rtM204Q mutant was proved being predominant in three representative patients' samples by clonal sequencing at the time of virologic breakthrough. 2014 PloS one Discussion HBV M204Q 2 7 RT 0 2 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Switching-to or adding-on of ADV could serve as a rescue therapy for rtM204Q related LAM refractory patients. 2014 PloS one Discussion HBV M204Q 71 76 RT 69 71 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The evidence together suggested rtM204Q as a main contributor for the drug resistance of the LAM-refractory patients. 2014 PloS one Discussion HBV M204Q 34 39 RT 32 34 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The position 184 in RT domain of human immunodeficiency virus shared similar profile of resistance pattern to LAM, such that rtM184I appears early in therapy, and rtM184V replaces rtM184I later, the outgrowth of rtM184V was a balance between mutation and selection. 2014 PloS one Discussion HBV M184I;M184V;M184I;M184V 127;165;182;214 132;170;187;219 RT;RT;RT;RT;RT 20;125;163;180;212 22;127;165;182;214 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtA181T has been related with LAM exposure and it induces a stop codon (sW172stop) in the overlapping hepatitis B surface protein. 2014 PloS one Discussion HBV A181T;W172X 6;76 11;85 RT;S;S 4;76;118 6;77;125 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtA181T mutant was simultaneously detected with rtM204Q in patient 1, patient 4 and patient 6; and rtA181V mutant was simultaneously detected with rtM204Q in patient 4 and patient 6. 2014 PloS one Discussion HBV A181T;A181V;M204Q;M204Q 6;105;54;153 11;110;59;158 RT;RT;RT;RT 4;52;103;151 6;54;105;153 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtA181V as a primary mutation of ADV resistance could also be induced by LAM though it was not a primary mutation of LAM. 2014 PloS one Discussion HBV A181V 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204I and rtM204V were the mostly detected mutations and were found in 25.5% of the patient population and rtM204Q was only found in 0.1% of the patient population. 2014 PloS one Discussion HBV M204I;M204V;M204Q 6;18;115 11;23;120 RT;RT;RT 4;16;113 6;18;115 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204I mutation only requires one nucleotide change, i.e., from ATG to ATT, ATA, or ATC. 2014 PloS one Discussion HBV M204I 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204K mutation was reported to be found in a LAM unsuccessfully-treated patient. 2014 PloS one Discussion HBV M204K 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204Q mutant remained susceptible to ETV, ADV, and TDF in phenotypic analysis. 2014 PloS one Discussion HBV M204Q 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. The rtM204V usually requires one nucleotide change, i.e., from ATG to GTG, and infrequently requires two nucleotide change, i.e., from ATG to GTT/GTC/GTA. 2014 PloS one Discussion HBV M204V 6 11 RT 4 6 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Therefore, rtM204Q might be a novel LAM-resistance-associated mutation. 2014 PloS one Discussion HBV M204Q 13 18 RT 11 13 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. This could be associated with rtA181V mutant in the patients. 2014 PloS one Discussion HBV A181V 32 37 RT 30 32 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. This may account for that rtM204Q had competence over rtM204I mutant and wild-type strains in a few of cases. 2014 PloS one Discussion HBV M204Q;M204I 28;56 33;61 RT;RT 26;54 28;56 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. This suggested that rtM204Q mutation, like rtM204I and rtM204V mutations, was specific to LAM resistance. 2014 PloS one Discussion HBV M204Q;M204I;M204V 22;45;57 27;50;62 RT;RT;RT 20;43;55 22;45;57 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. We also found the emergence of rtM204Q in one case refractory to LAM. 2014 PloS one Discussion HBV M204Q 33 38 RT 31 33 24586482 rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus. Whether these factors affect development of rtM204Q mutation needs further study. 2014 PloS one Discussion HBV M204Q 46 51 RT 44 46 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. also reported that sW182* mutation was associated with progression of liver disease in genotype C HBV patients. 2014 PloS one Discussion HBV W182X 19 25 S 19 20 Liver disease 70 83 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Among the 11 HBV S gene truncation mutants we have identified (sL15*, sL21*, sS61*, sC69*, sL95*, sW156*, sW163*, sW172*, sW182*, sW196*, and sL216*) in HBV-related HCCs, all except one (sL95*) were belonged to genotype C of HBV, which is also quite interesting, since genotype C has been found to be one risk factor for development of HBV-related HCC in Taiwan. 2014 PloS one Discussion HBV L15X;L21X;S61X;C69X;L95X;W156X;W163X;W172X;W182X;W196X;L216X;L95X 63;70;77;84;91;98;106;114;122;130;142;187 68;75;82;89;96;104;112;120;128;136;148;192 S;S;S;S;S;S;S;S;S;S;S;S;S 17;63;70;77;84;91;98;106;114;122;130;142;187 18;64;71;78;85;92;99;107;115;123;131;143;188 Hepatocellular carcinoma;Hepatocellular carcinoma 165;348 169;351 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Among them, sW182* was found in 2 tumors with one identified in the noncancerous parts, too. 2014 PloS one Discussion HBV W182X 12 18 S 12 13 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. As such, it is difficult to identify the phenotypic characteristics of HCCs specific to the sW182* mutation. 2014 PloS one Discussion HBV W182X 92 98 S 92 93 Hepatocellular carcinoma 71 75 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Clinical analysis by comparing the tumor characteristics in HCC patients with and without sW182* mutation showed no difference (data not shown), since these tumors should all have gone though highly complex processes in the cancer development by the time of resections. 2014 PloS one Discussion HBV W182X 90 96 S 90 91 Hepatocellular carcinoma 60 63 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Furthermore, we discovered that 3 tumor tissues with sW182* had multiple S nonsense mutations (Table S1), which might result in an additive effect to enhance their transformation ability. 2014 PloS one Discussion HBV W182X 53 59 S;S 53;73 54;74 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. In addition, they also found similar results in the HuH-7 and HEK 293 stable clone cells with sW182* mutation. 2014 PloS one Discussion HBV W182X 94 100 S 94 95 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. In our study, the incidence of sW182* was quite low (6/50, 12%) in HCC cancerous tissue samples, while the incidence was rather high in the study by Lee, et al. 2014 PloS one Discussion HBV W182X 31 37 S 31 32 Hepatocellular carcinoma 67 70 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. In this study, two of the 6 HCC patients harbored the sW182* mutation.in their tumor tissues also had the same mutation in the non tumor parts, suggesting this mutation occurred before the HCC development. 2014 PloS one Discussion HBV W182X 54 60 S 54 55 Hepatocellular carcinoma;Hepatocellular carcinoma 28;189 31;192 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. On the other hand, three nonsense mutations of S gene were found in the cancerous part (sL95*, sW182* and sL216*). 2014 PloS one Discussion HBV L95X;W182X;L216X 88;95;106 93;101;112 S;S;S;S 47;88;95;106 48;89;96;107 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. The other two S truncation mutants, sL95* and sL216*, also found to had transformation activities, though weaker than sW182*. 2014 PloS one Discussion HBV L95X;L216X;W182X 36;46;118 41;52;124 S;S;S;S 14;36;46;118 15;37;47;119 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. The results demonstrated that the cell growth, cell cycle progression and cell transforming abilities were all significantly increased in the sW182* expressing stable clone, when compared with mock and wild type clones, which was quite similar to our results. 2014 PloS one Discussion HBV W182X 142 148 S 142 143 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. The study results demonstrated the potent oncogenic activity of the sW182* mutant, especially the xenograft study and in vivo migration assay (Figure S4 and S5). 2014 PloS one Discussion HBV W182X 68 74 S 68 69 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. They also have performed functional study of sW182* mutation, including cell growth, cell cycle regulation, and cell transforming ability by using NIH3T3 cell line. 2014 PloS one Discussion HBV W182X 45 51 S 45 46 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. They found a significantly higher incidence of sW182* mutation in HBV patients with cirrhosis or HCC (37.8%), when compared with chronic hepatitis or carriers (17.2%). 2014 PloS one Discussion HBV W182X 47 53 S 47 48 Liver cirrhosis;Hepatocellular carcinoma;Chronic Hepatitis B 84;97;129 93;100;146 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. Together with the 3 nonsense mutations in our previous report (sL21*, sW156*, sW172*), we already found 6 different HBV S nonsense mutations with transformation activities. 2014 PloS one Discussion HBV L21X;W156X;W172X 63;70;78 68;76;84 S;S;S;S 63;70;78;120 64;71;79;121 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. was the incidence of sW812* mutation. 2014 PloS one Discussion HBV W812X 21 27 S 21 22 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. We also have performed HBV S gene sequencing in the serum sample of 64 genotype C HBV-related HCC patients, and the incidence of sW182* (4/64, 6.25%) was lower than from HCC cancerous tissue (preliminary unpublished data). 2014 PloS one Discussion HBV W182X 129 135 S;S 27;129 28;130 Hepatocellular carcinoma;Hepatocellular carcinoma 94;170 97;173 24587012 Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma. When we performed whole HBV genome sequencing on the 25 gender and age-matched HBcAg(-) HCCs, additional nonsense mutations of S gene were found in the cancerous part, and sW182* was recurrently found in the tumor tissue (6 of the 50 HCCs). 2014 PloS one Discussion HBV W182X 172 178 C;S;S 79;127;172 84;128;173 Hepatocellular carcinoma;Hepatocellular carcinoma 88;234 92;238 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. But the polymorphisms in HBV strains required the use of degenerated primer pairs according to a similar successful primer design described in Ntziora's research with respect to quantitative detection of the M204V hepatitis B virus minor variants. 2014 PloS one Discussion HBV M204V 208 213 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. In this study, we developed a new assay for the detection of the variant rtM204I with high-sensitivity. 2014 PloS one Discussion HBV M204I 75 80 RT 73 75 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. It is known that rtM204I is one of the most important and common resistance mutation sites, which can not only cause the selection of LMV and LdT resistance, but also lead to ETV resistance. 2014 PloS one Discussion HBV M204I 19 24 RT 17 19 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. successfully developed an allele-specific quantitative PCR with combination of locked nucleic acid primers and a minor groove binder probe for the quantitative determination of minor viral quasispecies of the triple combination mutation rtV173L+rtL180M+rtM204V within one HBV genome. 2014 PloS one Discussion HBV V173L;L180M;M204V 239;247;255 244;252;260 RT;RT;RT 237;245;253 239;247;255 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. Therefore, establishing a simple, rapid, reliable and highly sensitive assay to detect the rtM204I mutant as early as possible is of great clinical significance. 2014 PloS one Discussion HBV M204I 93 98 RT 91 93 24587198 Establishment of real time allele specific locked nucleic acid quantitative PCR for detection of HBV YIDD (ATT) mutation and evaluation of its application. Thirdly, the limitation is that validation data was restricted to rtM204I. 2014 PloS one Discussion HBV M204I 68 73 RT 66 68 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. A previous study also demonstrated that G1862T mutation was appreciably related to HBV/A1 rather than HBV/A2. 2014 PloS one Discussion HBV G1862T 40 46 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. A recent study showed that HBV/C related P5H, I97F/L and L100I mutations were significantly associated with HCC. 2014 PloS one Discussion HBV P5H;I97F;I97L;L100I 41;46;46;57 44;52;52;62 Hepatocellular carcinoma 108 111 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Additional mutation outside the MHL region was also observed including the E164G mutation, which was earlier reported by another study on chronic HBV carriers. 2014 PloS one Discussion HBV E164G 75 80 Chronic Hepatitis B 138 149 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Additionally, the F141L mutation in the PreS region was not found in any of the HIV/HBV co-infected individuals, although this mutation was found to be significant among the liver cirrhosis patients compared to the chronic HBV cases with HBV mono-infection. 2014 PloS one Discussion HBV F141L 18 23 PreS 40 44 Liver cirrhosis;HBV infections;HBV-HIV coinfections;Chronic Hepatitis B 174;238;80;215 189;256;99;226 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. As per previous reports from India, the presence of G1896A might lead to inactivation of liver diseases. 2014 PloS one Discussion HBV G1896A 52 58 Liver disease 89 103 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Finally, this study for the first time also reports the presence of the -1 G frameshift deletion and the W182* mutations among the Indian population but with a lower frequency. 2014 PloS one Discussion HBV W182X 105 110 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Furthermore, the frequency of the A1762T/G1764A mutations was comparatively lower than its frequency among HBV mono-infected cases from this part of the country with majority of the HBV/C strains being associated with this mutation. 2014 PloS one Discussion HBV G1764A;A1762T 41;34 47;40 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. However, the prevalence of G1896A was markedly high among the HBeAg negative HIV/HBV co-infected patients and therefore, needs further follow-up to assess whether this mutation is associated with any severe clinical implications in this cohort. 2014 PloS one Discussion HBV G1896A 27 33 C 62 67 HBV-HIV coinfections 77 96 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. However, the prevalence of the A1762T/G1764A mutations were relatively lower in case of the HIV/HBV co-infected patients, as our previous study on HBV mono-infection from eastern India showed that about 61% of the subjects harbored this double mutation. 2014 PloS one Discussion HBV G1764A;A1762T 38;31 44;37 HBV infections;HBV-HIV coinfections 147;92 165;111 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. In the present study, 50% of the subjects infected with HBV/C harbored the A1762T/G1764A mutations, thus increasing the chances of advanced liver disease among the HIV/HBV co-infected cohort. 2014 PloS one Discussion HBV G1764A;A1762T 82;75 88;81 Liver disease;HBV-HIV coinfections 140;164 153;183 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Interestingly, in contrast to our earlier reports which showed that 18-24% of the HBeAg negative HBV mono-infected patients harbored the G1896A mutation, the prevalence of G1896A precore mutation was considerably high (61.5%) among the HBeAg negative HIV/HBV co-infected subjects from eastern India. 2014 PloS one Discussion HBV G1896A;G1896A 137;172 143;178 C;C;Precore 82;236;179 87;241;186 HBV-HIV coinfections 251 270 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Moreover, all the HBV/A isolates of this present study were associated with the G1862T, irrespective of HBeAg status. 2014 PloS one Discussion HBV G1862T 80 86 C 104 109 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Notably, it was seen that all the isolates which harbored the PreS1/S2 deletion were accompanied by the BCP A1762T/G1764A double mutations. 2014 PloS one Discussion HBV G1764A;A1762T 115;108 121;114 BCP;PreS1;PreS2 104;62;62 107;67;68 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. On the other hand, the clinical relevance of G1896A mutation is ambiguous, with some reporting its association with severe forms of chronic liver disease while other studies suggest no such relevant association. 2014 PloS one Discussion HBV G1896A 45 51 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. On the other hand, the prevalence of both BCP double mutation and G1896A were considerably low among the HBeAg positive HIV/HBV co-infected patients which was in accordance with our previous reports. 2014 PloS one Discussion HBV G1896A 66 72 BCP;C 42;105 45;110 HBV-HIV coinfections 120 139 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Our findings also revealed that the A1762T/G1764A mutations were more common among HIV/HBV co-infected subjects who were infected with HBV/A or HBV/C whereas the G1896A precore mutation was more associated with HBV/D which was in concordance with earlier studies on HBV mono-infection from this part of India. 2014 PloS one Discussion HBV G1764A;A1762T;G1896A 43;36;162 49;42;168 Precore 169 176 HBV infections;HBV-HIV coinfections 266;83 284;102 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Several amino acid substitutions within the major hydrophilic loop were observed in our study population which included Y100D, Q101R/H, M103V/I, T125M, A128V, M133L, D144E and G145S. 2014 PloS one Discussion HBV Y100D;Q101R;Q101H;M103V;M103I;T125M;A128V;M133L;D144E;G145S 120;127;127;136;136;145;152;159;166;176 125;134;134;143;143;150;157;164;171;181 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Several clinically significant HBV mutations were observed in our settings including the BCP double mutations, PreS deletions and the G1896A precore mutation, which was predominant among the HBeAg negative HIV/HBV co-infected patients who were treatment naive. 2014 PloS one Discussion HBV G1896A 134 140 BCP;C;Precore;PreS 89;191;141;111 92;196;148;115 HBV-HIV coinfections 206 225 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The complete analysis of the BCP and the precore/core region in this study showed that 13.6% of the isolates harbored the BCP double mutation whereas about 22% of them had the G1896A precore mutation. 2014 PloS one Discussion HBV G1896A 176 182 BCP;BCP;C;Precore;Precore 29;122;49;41;183 32;125;53;48;190 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The G1862T mutation is known for affecting the expression of HBeAg at the post-translational level. 2014 PloS one Discussion HBV G1862T 4 10 C 61 66 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The major mutations include the T12S, V27I and T67N which were predominant among the HBV/C strains. 2014 PloS one Discussion HBV T12S;V27I;T67N 32;38;47 36;42;51 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The presence of T118V and A128V were found significantly in HBV/D2, which concurs with our previous study and hence are considered as signature residues of this subgenotype. 2014 PloS one Discussion HBV T118V;A128V 16;26 21;31 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. The W182* mutation had been previously reported to have severe clinical implications. 2014 PloS one Discussion HBV W182X 4 9 24587360 Molecular characterization of HBV strains circulating among the treatment-naive HIV/HBV co-infected patients of eastern India. Therefore, since we found that the frequency of G1896A mutation was noticeably high among the HBeAg negative HIV/HBV co-infected individuals, further studies are needed to monitor the clinical outcome of these patients in future and examine whether G1896A has any clinical significance in this cohort. 2014 PloS one Discussion HBV G1896A;G1896A 48;249 54;255 C 94 99 HBV-HIV coinfections 109 128 24632784 Analysis of complete nucleotide sequences of Angolan hepatitis B virus isolates reveals the existence of a separate lineage within genotype E. Here, substitutions (notably R34K in the pre-S1- and R16K and R18K in the pre-S2 region) were noted which were only present in samples with concurrent HBsAg and anti-HBs and may be responsible for this phenotype. 2014 PloS one Discussion HBV R34K;R16K;R18K 29;53;62 33;57;66 S;S;PreS1;PreS2 166;151;41;74 169;156;47;80 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. All the 5 patients with Anti HBc positive (Occult Hepatitis) profile were found to contain mutations in this region (P127T). 2014 PloS one Discussion HBV P127T 117 122 C 29 32 Occult Hepatitis B 43 59 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Entecavir associated drug resistant mutations I169N, A181G, S202I reported earlier were observed in 4 cases. 2014 PloS one Discussion HBV I169N;A181G;S202I 46;53;60 51;58;65 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. However, quarter of HBeAg negative isolates has genotype A (A1762T and G1764A) HBV infection (Basal Core Promoter mutation) 2014 PloS one Discussion HBV A1762T;G1764A 60;71 66;77 BCP;C 94;20 113;25 HBV infections 79 92 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. However, quarter of HBeAg negative isolates has genotype A (A1762T and G1764A) HBV infection (Basal Core Promoter mutation). 2014 PloS one Discussion HBV A1762T;G1764A 60;71 66;77 BCP;C 94;20 113;25 HBV infections 79 92 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. In our study we have observed K130M, T36A and G50R to be significantly associated with HCC (Table 9). 2014 PloS one Discussion HBV K130M;T36A;G50R 30;37;46 35;41;50 Hepatocellular carcinoma 87 90 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. In the present study more than half of HBV isolates were HBeAg negative and often associated with Genotype D (G1896A) HBV infection (pre-core mutation). 2014 PloS one Discussion HBV G1896A 110 116 C;Precore 57;133 62;141 HBV infections 118 131 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. K130M and V131I are translated due to basal core promoter mutations Adenine to Threonine at nucleotide position 1762 (A1762T) and Guanosine to Adenine at nucleotide position 1764 (G1764A). 2014 PloS one Discussion HBV K130M;V131I;A1762T;G1764A 0;10;118;180 5;15;124;186 BCP 38 57 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. L80* which was reported to be associated with lamivudine resistance and enhanced viral replication in vitro was observed in 17 cases. 2014 PloS one Discussion HBV L80X 0 4 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. rtN236T a primary mutation in the D domain, rtA181T/V at the B domain and rtQ215S at the C-D inter-domain have been associated with Adefovir and Lamivudine resistance were also observed in 8 cases. 2014 PloS one Discussion HBV N236T;A181T;A181V;Q215S 2;46;46;76 7;53;53;81 RT;RT;RT 0;44;74 2;46;76 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Similarly, several studies have reported association of D7A, M129L, V163I and I253V with HBV genotype A.Both observations were in concordance with our results. 2014 PloS one Discussion HBV D7A;M129L;V163I;I253V 56;61;68;78 59;66;73;83 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. The following mutations in RT region of polymerase gene A21S, Y54H, F122L, Y135S, were reported to be associated with HBV genotype D in previous studies. 2014 PloS one Discussion HBV A21S;Y54H;F122L;Y135S 56;62;68;75 60;66;73;80 P;RT 40;27 50;29 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. The mutations in core region(T49S and E64N) were also present in the amino-terminal domain of the core protein, which is required for the assembly and the stability of the nucleocapsid. 2014 PloS one Discussion HBV T49S;E64N 29;38 33;42 C;C 17;98 21;102 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. The mutations in the polymerase region (D45L, T70x and S74X) were present in the amino- terminal domain of DNA polymerase that serves as a primer for Reverse Transcriptase (RT). 2014 PloS one Discussion HBV D45L;S74X 40;55 44;59 P;P;RT;RT 21;111;150;173 31;121;171;175 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. The presence of a cytosine at position 1858 precludes the G-to-A mutation at nt 1896, since this would destabilize the stem-loop structure of the RNA encapsidation signal. 2014 PloS one Discussion HBV G1896A 58 84 24637457 Mutation profiling of the hepatitis B virus strains circulating in North Indian population. Therefore, in HBV genotype A, the G1896A mutation usually arises together with a C1858T nucleotide exchange. 2014 PloS one Discussion HBV G1896A;C1858T 34;81 40;87 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. A799G and T1055A are missense mutations that cause rtI224V and rtM309K aa substitutions, respectively, in RT. 2014 PloS one Discussion HBV M309K;I224V;A799G;T1055A 65;53;0;10 70;58;5;16 RT;RT;RT 51;63;106 53;65;108 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. After the full-length HBV sequence information from all of the cases in this study is obtained, we will definitely perform the linkage disequilibrium analysis between A987G, as well as the other 2 identified RT mutations, and well-known HCC-related mutations. 2014 PloS one Discussion HBV A987G 167 172 RT 208 210 Hepatocellular carcinoma 237 240 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Another possibility to explain the rationality of A987G is that this mutation may be in linkage disequilibrium with other well-defined HCC-related mutations such as pre-S deletion, the BCP/EnhII region mutations C1653T, T1753A/G, C1762T, and T1764A, and the precore mutations G1896A, G1899A. 2014 PloS one Discussion HBV T1753G;A987G;C1653T;T1753A;C1762T;T1764A;G1896A;G1899A 220;50;212;220;230;242;276;284 228;55;218;228;236;248;282;290 BCP;Enh II;Precore;PreS 185;189;258;165 188;194;265;170 Hepatocellular carcinoma 135 138 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. However the mechanism underling the association of rtM309K and HCC is not clear. 2014 PloS one Discussion HBV M309K 53 58 RT 51 53 Hepatocellular carcinoma 63 66 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. In this case, rtM309K aa substitution is likely to affect the precise conformation of the two alpha-helices and their interactions with the DNA template-primer, consequently impairing polymerase activity. 2014 PloS one Discussion HBV M309K 16 21 P;RT 184;14 194;16 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. In this study, we characterized spontaneous mutations in the HBV RT region and report, for the first time that the A799G, A987G, and T1055A mutations are independent risk factors for HCC. 2014 PloS one Discussion HBV A799G;A987G;T1055A 115;122;133 120;127;139 RT 65 67 Hepatocellular carcinoma 183 186 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. In vitro and in vivo experiments using a 1.3x genome-length HBV construct containing rtM309K are needed to explore its biological impact on viral replication. 2014 PloS one Discussion HBV M309K 87 92 RT 85 87 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Interestingly, we also observed a significantly lower level of HBV DNA in the patients infected with rtM309K mutant in our study, providing further evidence from patients to support the important role of rt304-311 in viral replication. 2014 PloS one Discussion HBV M309K 103 108 RT;RT 101;204 103;206 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. It is thus speculated that the mutation A987G might modulate the function of Enhancer I, and subsequently promote the transcription of HBx protein, which plays a role in the carcinogenesis of HCC. 2014 PloS one Discussion HBV A987G 40 45 Enh I;X 77;135 87;138 Hepatocellular carcinoma 192 195 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Our study revealed that the A799G and T1055A mutations have a significantly and consistently higher frequency in HCC patients than in non-HCC patients in both of the two validation sets. 2014 PloS one Discussion HBV A799G;T1055A 28;38 33;44 Hepatocellular carcinoma;Hepatocellular carcinoma 113;138 116;141 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. The multivariate analysis of the combined datasets showed that the presence of the A799G, A987G, and T1055A mutations was an independent risk factor for HCC development. 2014 PloS one Discussion HBV A799G;A987G;T1055A 83;90;101 88;95;107 Hepatocellular carcinoma 153 156 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. Unlike the mutations A799G and T1055A, A987G does not cause an amino acid change in HBV polymerase. 2014 PloS one Discussion HBV A799G;T1055A;A987G 21;31;39 26;37;44 P 88 98 24788140 Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma. We found that the mutations A799G, A987G, and T1055A were detectable in >75% patients (3 of 4 patients for A799G, 2 of 2 patients for A987G, and 4 of 5 patients for T1055A) 4-5 years before the clinical diagnosis of HCC (Table S3 in File S1). 2014 PloS one Discussion HBV A799G;A987G;T1055A;A799G;A987G;T1055A 28;35;46;107;134;165 33;40;52;112;139;171 Hepatocellular carcinoma 216 219 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. In our study, as expected, the rtM204I/V and rtL180M mutations related to lamivudine resistance were the most frequent, followed by the rtA181V/T mutation associated with adefovir resistance. 2014 Annals of laboratory medicine Discussion HBV M204I;M204V;A181V;A181T;L180M 33;33;138;138;47 40;40;145;145;52 RT;RT;RT 31;45;136 33;47;138 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. In our study, rtM204V was always accompanied by rtL180M. 2014 Annals of laboratory medicine Discussion HBV M204V;L180M 16;50 21;55 RT;RT 14;48 16;50 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. reported that rtM204I mutation alone had lower replication competency than rtL180M/rtM204V, but clinically there was no difference in ALT, HBV DNA levels, and HBeAg positivity, similar to our data. 2014 Annals of laboratory medicine Discussion HBV M204I;M204V;L180M 16;85;77 21;90;82 C;RT;RT;RT 159;14;75;83 164;16;77;85 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. The cases with the rtM204I mutation had higher HBeAg positive rates than the cases with rtM204V/rtL180M; however, this difference was statistically insignificant. 2014 Annals of laboratory medicine Discussion HBV L180M;M204I;M204V 98;21;90 103;26;95 C;RT;RT;RT 47;19;88;96 52;21;90;98 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. The rtM204I mutation occurs alone followed by rtL180M mutation to increase viral replication. 2014 Annals of laboratory medicine Discussion HBV M204I;L180M 6;48 11;53 RT;RT 4;46 6;48 24790911 Analysis of reverse transcriptase gene mutations in the hepatitis B virus at a university hospital in Korea. The rtM204V/rtL180M mutations are associated with much lower resistance to lamivudine than rtM204I alone. 2014 Annals of laboratory medicine Discussion HBV M204V;L180M;M204I 6;14;93 11;19;98 RT;RT;RT 4;12;91 6;14;93 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Besides other previously described resistance mutations, the best-described drug resistance mutations are the LAM resistance mutations rtL180M and rtM204V/I and the adefovir resistance mutations rtA181V/T and rtN236T. 2014 PloS one Discussion HBV M204V;M204I;A181V;A181T;L180M;N236T 149;149;197;197;137;211 156;156;204;204;142;216 RT;RT;RT;RT 135;147;195;209 137;149;197;211 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. However, in this domain (loop 2) the most prominent vaccine escape mutations sG145R and sD144E/A were not found in the patient collective. 2014 PloS one Discussion HBV G145R;D144E;D144A 77;88;88 83;96;96 S;S 77;88 78;89 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Of the 170 HBV isolates analyzed, 148 (87.06%) showed wild-type sequences and only 22 (12.94%) revealed mutations in the HBsAg gene and of these two isolates (1.1%) showed the described vaccine escape mutation sP120T. 2014 PloS one Discussion HBV P120T 210 216 S;S 121;210 126;211 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Of these, the well-characterized sP120T mutation could be detected in 2/170 HBV-infected patients. 2014 PloS one Discussion HBV P120T 33 39 S 33 34 HBV infections 76 88 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. One patient was determined to have the suspected adefovir-resistant mutation (rtS85A). 2014 PloS one Discussion HBV S85A 80 84 RT 78 80 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Other antiviral therapy resistance mutations, such as rtA181V/T or rtN236T, were not detected. 2014 PloS one Discussion HBV A181V;A181T;N236T 56;56;69 63;63;74 RT;RT 54;67 56;69 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. Other vaccine escape mutations, especially the G145R and D144E/A mutation, could not been detected. 2014 PloS one Discussion HBV D144E;D144A;G145R 57;57;47 64;64;52 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. The best-described and stable vaccine escape mutations are the sG145R, sD144E/A, and sP120T mutations. 2014 PloS one Discussion HBV G145R;D144E;D144A;P120T 63;71;71;85 69;79;79;91 S;S;S 63;71;85 64;72;86 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. The identified sT/S143L/M mutations of the HBsAg gene, mapped to loop 2 of the "a" determinant, and were thought to be associated with vaccination allowing ongoing replication of HBV. 2014 PloS one Discussion HBV T143L;T143M;S143L;S143M 16;16;16;16 25;25;25;25 S;S 43;15 48;16 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. The LAM mutations rtM204V/I are mapped to the catalytic center of the viral RT domain, the YMDD motif. 2014 PloS one Discussion HBV M204V;M204I 20;20 27;27 RT;RT;P 18;76;91 20;78;95 24835494 Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman. We found the sP120T, sT126S, sM133T, and sT/S143L/M mutations in the HBsAg-positive patients while these mutations have been previously described as possible vaccine escape mutations (reviewed in:). 2014 PloS one Discussion HBV T143L;T143M;S143L;S143M;P120T;T126S;M133T 42;42;42;42;13;21;29 51;51;51;51;19;27;35 S;S;S;S;S 69;13;21;29;41 74;14;22;30;42 24849936 Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China. We also observed that control subjects showed a significant higher frequency of the synonymous substitution of T53C in pre-S2 region than case patients. 2014 PloS one Discussion HBV T53C 111 115 PreS2 119 125 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. Although [V173L] mutations are associated with exposure to lamivudine, it has also been found in ART naive patients previously. 2014 PloS one Discussion HBV V173L 10 15 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. However, only one patient with possibly lamivudine induced resistance [L180M,M204V] mutation was found suggesting that the majority of patients had low HBV DNA levels when ART was commenced. 2014 PloS one Discussion HBV M204V;L180M 77;71 82;76 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. The [V173L] mutation has also been described in a study from the nearby country Gambia. 2014 PloS one Discussion HBV V173L 5 10 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. The [V214A] and the [N238D] mutations may be considered as secondary resistance mutations against adefovir conferring very low-level resistance in vitro , however the clinical relevance of these HBV polymerase mutations in ART naive patients still needs to be elucidated. 2014 PloS one Discussion HBV V214A;N238D 5;21 10;26 P 199 209 24915064 Hepatitis B and Delta virus are prevalent but often subclinical co-infections among HIV infected patients in Guinea-Bissau, West Africa: a cross-sectional study. Tripple [M204V, L180M, V173L] mutation has been associated with vaccine escape mutants. 2014 PloS one Discussion HBV M204V;L180M;V173L 9;16;23 14;21;28 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Amino acid substitutions of rtL180M, rtS202G, and rtM204V have emerged in cases in which serum HBV DNA increased during TDF and ETV therapy. 2014 Drug design, development and therapy Discussion HBV L180M;S202G;M204V 30;39;52 35;44;57 RT;RT;RT 28;37;50 30;39;52 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. For these 45 patients, which included ten with virologic breakthrough, both line probe assay and direct sequencing revealed no new amino acid substitutions, including substitutions that could be associated with reduced TDF susceptibility (rtA181V/T, rtN236T, or rtA194T). 2014 Drug design, development and therapy Discussion HBV A181V;A181T;N236T;A194T 241;241;252;264 248;248;257;269 RT;RT;RT 239;250;262 241;252;264 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. In our case, virologic breakthrough occurred at month 31 of TDF and ETV therapy, and the ETV-resistant strain (L180M + S202G + M204V) of our case was not identical with that in the in vitro drug susceptibility study above. 2014 Drug design, development and therapy Discussion HBV L180M;S202G;M204V 111;119;127 116;124;132 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. In vitro drug susceptibility showed that TDF displayed one- to twofold resistance to ETV-resistant viral strains (N123D + H124Y + L180M + S202G + M204V + Y257H, I163V + L164M + L180M + S202G + M204V + C256S, and H124Y + L180M + S202G + M204V + Y257H). 2014 Drug design, development and therapy Discussion HBV N123D;H124Y;L180M;S202G;M204V;Y257H;I163V;L164M;L180M;S202G;M204V;C256S;H124Y;L180M;S202G;M204V;Y257H 114;122;130;138;146;154;161;169;177;185;193;201;212;220;228;236;244 119;127;135;143;151;159;166;174;182;190;198;206;217;225;233;241;249 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. It has been shown that rtA181V + rtN236T double mutants are resistant to TDF in vitro, but clinical data suggest that patients with rtA181 or rtN236T remain susceptible to TDF. 2014 Drug design, development and therapy Discussion HBV A181V;N236T;N236T 25;35;144 30;40;149 RT;RT;RT;RT 23;33;132;142 25;35;134;144 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Moreover, Karatayli et al reported that HBV DNA, in seven of eight patients with ETV resistance mutations (T184F/A/L/I, S202G, and M250V), became undetectable with TDF and LAM after 6 months of treatment. 2014 Drug design, development and therapy Discussion HBV T184F;T184A;T184L;T184I;S202G;M250V 107;107;107;107;120;131 118;118;118;118;125;136 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. Moreover, these amino acid substitutions changed from rtL180M, rtT184M, and rtM204V to rtL180M, rtS202G, and rtM204V. 2014 Drug design, development and therapy Discussion HBV L180M;T184M;M204V;L180M;S202G;M204V 56;65;78;89;98;111 61;70;83;94;103;116 RT;RT;RT;RT;RT;RT 54;63;76;87;96;109 56;65;78;89;98;111 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. The substitution rtA194T (plus rtL180M + rtM204V) has been associated with TDF resistance, albeit that a second report failed to confirm this. 2014 Drug design, development and therapy Discussion HBV A194T;L180M;M204V 19;33;43 24;38;48 RT;RT;RT 17;31;41 19;33;43 25061278 Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir. The substitution rtP177G and rtF249A reduced susceptibility to TDF in an in vitro study, but no clinical findings have yet been reported. 2014 Drug design, development and therapy Discussion HBV P177G;F249A 19;31 24;36 RT;RT 17;29 19;31 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. Furthermore, rtL180M mutations were newly emerged in four patients as minor population at 48 weeks of LAM-ADV combination therapy but they were restored as baseline mutation profile at 96 weeks. 2015 Gut and liver Discussion HBV L180M 15 20 RT 13 15 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. In the present study, baseline rtL180M was not associated with cumulative virological response. 2015 Gut and liver Discussion HBV L180M 33 38 RT 31 33 25287170 Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B. The rtL180M could compensate for the impact of a mutation in the YMDD motif on viral replication in vitro. 2015 Gut and liver Discussion HBV L180M 6 11 RT;P 4;65 6;69 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. A mixture of D144G/D144A or combined D144E / G145R mutations were detected after hepatitis B immune globulin treatment. 2014 Clinical and molecular hepatology Discussion HBV D144A;D144G;D144E;G145R 19;13;37;45 24;18;42;50 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Functional analysis through transfection experiments in HepG2 cells suggest that some of the mutations found in our patients do impair HBsAg antigenicity (C139R, D144E) or block its secretion (Y225del). 2014 Clinical and molecular hepatology Discussion HBV C139R;D144E;Y225del 155;162;193 160;167;200 S 135 140 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. In a previous report, a combination of amino acid changes in the surface protein, including G145R, was found to cause secretion defect of HBsAg. 2014 Clinical and molecular hepatology Discussion HBV G145R 92 97 S;S 138;65 143;72 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. In this regard, we previously found several point mutations in the MHR region and W172stop corresponding to the multidrug-resistant rtA181T mutation in polymerase impair the secretion of both virions and HBsAg. 2014 Clinical and molecular hepatology Discussion HBV A181T;W172X 134;82 139;90 S;P;RT 204;152;132 209;162;134 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. Therefore, the C139R mutation observed in patient 22 may destroy the major antigenic determinant thus reducing affinity to anti-HBs. 2014 Clinical and molecular hepatology Discussion HBV C139R 15 20 S 128 131 25320728 Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers. This mutant surface gene shares with clone 21 the D144E mutation. 2014 Clinical and molecular hepatology Discussion HBV D144E 50 55 S 12 19 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. 116-127) of HBx are frequently altered in HBV-genotype C and B, but no significant sequence heterogeneity was noted in the epitopes of HBV-genotype D, except three mutations I127T (T1753C), K130M (A1762T) and V131I (G1764A), though H94Y (T1653C) was present with high frequencies in both LC and HCC (Table 3) as observed in previous study. 2014 PloS one Discussion HBV I127T;T1753C;K130M;A1762T;V131I;G1764A;H94Y;T1653C 174;181;190;197;209;216;232;238 179;187;195;203;214;222;236;244 X 12 15 Hepatocellular carcinoma;Liver cirrhosis 295;288 298;290 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. According to the previous studies in HBV genotype B, genotype C and few studies with genotype D, BCP_A1762T/G1764A, precore_G1896A, EnhII_C1653T, BCP_T1753V mutations and pre S2 deletions are frequently associated risk factors of HCC. 2014 PloS one Discussion HBV G1764A;A1762T;G1896A;C1653T;T1753V 108;100;123;137;149 114;107;130;144;156 BCP;BCP;Enh II;PreS2;Precore 97;146;132;171;116 100;149;137;177;123 Hepatocellular carcinoma 230 233 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Again, in consistence with the previous report in HBV genotype C, this mutation in combination with BCP_A1762T/G1764A showed significant association with HBeAg positive HCC development (Figure 1). 2014 PloS one Discussion HBV G1764A;A1762T 111;103 117;110 BCP;C 100;154 103;159 Hepatocellular carcinoma 169 172 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Another precore mutation, T1858C, which makes a pair with G1896A to stabilize the viral encapsidation signal and enhance viral replication, was observed significantly associated with more aggressive course of liver diseases in HBeAg negative HCC (Figure 1) similar to previous study. 2014 PloS one Discussion HBV T1858C;G1896A 26;58 32;64 C;Precore 227;8 232;15 Liver disease;Hepatocellular carcinoma 209;242 223;245 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. But the clinical relevance of the high prevalence of A1053G and T1050G/A mutation in HBV-genotype D and its association with HCC is not clear (Table 3). 2014 PloS one Discussion HBV T1050A;A1053G;T1050G 64;53;64 72;59;72 Hepatocellular carcinoma 125 128 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. But the compensatory mutation of codon 97 at codon 130, P130Q was found as independent risk factor for HCC in HBeAg negative patients. 2014 PloS one Discussion HBV P130Q 56 61 C 110 115 Hepatocellular carcinoma 103 106 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Few new combination of mutations in the enhancer-I region were also noted in LC and HCC such as T1029C/A1032G (>30%), T1059A/A1105C (>25%), and C1249T/T1250C (>15%) indicating their importance in LC and HCC development (data not shown) but not found significant in this study. 2014 PloS one Discussion HBV T1250C;A1032G;A1105C;C1249T;T1029C;T1059A 151;103;125;144;96;118 157;109;131;150;102;124 Enh I 40 50 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 84;203;77;196 87;206;79;198 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. From our multivariate analysis it is obvious that the two core mutations, T147C and P130Q could be potential predictor of HCC in high-risk HBeAg positive and negative CHB patients respectively (Table 4). 2014 PloS one Discussion HBV T147C;P130Q 74;84 79;89 C;C 58;139 62;144 Hepatocellular carcinoma;Chronic Hepatitis B 122;167 125;170 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. In a previous study from India BCP_T1753C mutation was reported as risk factor for LC rather than HCC which was similar to our analysis from frequency distribution (Table 3) but univariate analysis further identified this mutation as risk factor for HCC in HBeAg positive patients. 2014 PloS one Discussion HBV T1753C 34 41 BCP;C 31;257 34;262 Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 98;250;83 101;253;85 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. In addition, T147C with classical BCP mutation A1762T/G1764A was noted significantly high in HCC than non-HCC and hence these mutations in combination could predict the progression of liver diseases more precisely. 2014 PloS one Discussion HBV G1764A;T147C;A1762T 54;13;47 60;18;53 BCP 34 37 Hepatocellular carcinoma;Liver disease;Hepatocellular carcinoma 93;184;106 96;198;109 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Interestingly, the most frequently observed naturally occurring core protein mutation found in CHB and also in HCC patients I97L or F97L which is associated with "immature virion secretion" was completely absent in Indian patients with HBV-genotype D while among the "low secretion core variants" such as P5T/A/S, a new variant P5R was noted with high frequency in HBV-genotype D related HCC in previous Indian study. 2014 PloS one Discussion HBV P5T;P5A;P5S;P5R;I97L;F97L 305;305;305;328;124;132 312;312;312;331;128;136 C;C 64;282 68;286 Chronic Hepatitis B;Hepatocellular carcinoma;Hepatocellular carcinoma 95;111;388 98;114;391 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Koschel et al showed that deletion at codon 12 is defective in virion secretion while other two mutations S35T, T67N might be able to evade the host immune response for their persistence at low levels. 2014 PloS one Discussion HBV S35T;T67N;del aa12 106;112;26 110;116;46 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Mutation T147C was not documented as HCC risk factor previously with respect to any genotype. 2014 PloS one Discussion HBV T147C 9 14 Hepatocellular carcinoma 37 40 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. One point mutation L213I observed in the overlapping surface and polymerase gene (F221Y/A222T) in combination with classical BCP mutations A1762T/G1764A showed association with HCC in HBeAg positive patient (Figure 1). 2014 PloS one Discussion HBV A222T;G1764A;L213I;F221Y;A1762T 88;146;19;82;139 93;152;24;87;145 BCP;C;P;S 125;184;65;53 128;189;75;60 Hepatocellular carcinoma 177 180 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Our study had also found a significant association of BCP_A1762T/G1764A mutation to the liver disease progression from nLF to HCC (Table 3). 2014 PloS one Discussion HBV G1764A;A1762T 65;57 71;64 BCP 54 57 Liver disease;Hepatocellular carcinoma 88;126 101;129 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Previously, the G1053A mutation at the p53 factor like binding site was shown to enhance the expression of HBx and it was correlated well with the high replication efficiency of the HBV-genotype C virus. 2014 PloS one Discussion HBV G1053A 16 22 X 107 110 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. Recently it has been found that this combination of mutations exhibited an enhanced viral replication phenotype like BCP_A1762T/G1764A alone but its exact role in hepatocarcinogenesis is unclear. 2014 PloS one Discussion HBV G1764A;A1762T 128;120 134;127 BCP 117 120 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The clinical significance of G1896A mutation is ambiguous. 2014 PloS one Discussion HBV G1896A 29 35 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The frequency of BCP_C1653T mutation in the enhancer-II region was increasing with disease severity (Table 3) but it did not correlate well with LC or HCC, which was previously documented as an independent risk factor for HCC with HBV-genotype C suggesting its genotype specific role in HCC development. 2014 PloS one Discussion HBV C1653T 20 27 BCP;Enh II 17;44 20;55 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Liver cirrhosis 151;222;287;145 154;225;290;147 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. The S98T mutation found in the overlapping T and B cell epitope region of pre S1, which is the binding site of heat shock protein 70 (HSP70) (aa74-118) might be an independent predictor for HCC in HBeAg negative patient (Table 4). 2014 PloS one Discussion HBV S98T 4 8 C;PreS1 197;74 202;80 Hepatocellular carcinoma 190 193 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. These mutations might not affect HBsAg but could alter polymerase activity as another mutation in this region, T1055A has been reported to affect the conformation of two helices and impair HBV DNA-primer interaction. 2014 PloS one Discussion HBV T1055A 111 117 S;P 33;55 38;65 25333524 Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma. While three mutations in Th epitopes (T12S, S35T, T67N), T147C in CTL epitope and two mutations I116L, P130Q in B cell epitopes showed significant association with disease severity (Table 3). 2014 PloS one Discussion HBV T12S;S35T;T67N;T147C;I116L;P130Q 38;44;50;57;96;103 42;48;54;62;101;108 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. In a biological model, transfection of HBV genotype A clones in HepG2 cells revealed that the C149R mutation severely impaired HBV secretion in vitro. 2014 PloS one Discussion HBV C149R 94 99 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. Mutations in the MHR (Q101H, C149R, L158G and G159R) were identified in three patients (one of which did not have any hepatitis B serological markers). 2014 PloS one Discussion HBV Q101H;C149R;L158G;G159R 22;29;36;46 27;34;41;51 25462190 Epidemiology, risk factors and genotypes of HBV in HIV-infected patients in the northeast region of Colombia: high prevalence of occult hepatitis B and F3 subgenotype dominance. The mutation G159R has been observed in Iran among HBsAg-positive individuals with genotype D whereas mutation Q101H was found in an OBI patient in India. 2014 PloS one Discussion HBV G159R;Q101H 13;111 18;116 S 51 56 Occult Hepatitis B 133 136 25471066 Occult hepatitis B virus infection among blood donors in Colombia. In the present study was also described a mutation at position 141 (sK141N). 2014 Virology journal Discussion HBV K141N 68 74 S 68 69 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Lai et al, demonstrated that mutations sL173F, sI195M, and sY200H also related to these mutations rtA181V, rtM204V, and rtV208A, all of them associated to interferon resistance. 2014 Virology journal Discussion HBV V208A;A181V;M204V;L173F;I195M;Y200H 122;100;109;39;47;59 127;105;114;45;53;65 RT;RT;RT;S;S;S 98;107;120;39;47;59 100;109;122;40;48;60 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Moreover, the change of Leucine to Methionine has been described in association with other mutations in the YMDD polymerase domain, in particular with the substitutions rtM204V and rtM204I, related to interferon resistance and polymerase protein dysfunction. 2014 Virology journal Discussion HBV M204V;M204I 171;183 176;188 P;P;RT;RT;P 113;227;169;181;108 123;237;171;183;112 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Six amino acid substitutions rtL108P, rtR110G, rtL180M, rtR192C, rtT150S and rtI187V were detected in the sequence of 4/6 OBI cases, three of them were present in sample 001. 2014 Virology journal Discussion HBV I187V;L108P;R110G;L180M;R192C;T150S 79;31;40;49;58;67 84;36;45;54;63;72 RT;RT;RT;RT;RT;RT 29;38;47;56;65;77 31;40;49;58;67;79 Occult Hepatitis B 122 125 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Some of these mutations, including K141E, impaired the secretion of virions and subviral particles and reduced the reactivity of antibodies anti-HBs used in immunoassays. 2014 Virology journal Discussion HBV K141E 35 40 S 145 148 25471066 Occult hepatitis B virus infection among blood donors in Colombia. The rtL180M substitution has already been reported in the literature. 2014 Virology journal Discussion HBV L180M 6 11 RT 4 6 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Thirteen MHR mutations (G119R, P120T, C124R, C124Y, I126S, Q129R, S136P, C139R, T140I, K141E, D144A, G145A, and G145R) were detected and functionally characterized in vitro and in vivo. 2014 Virology journal Discussion HBV G119R;P120T;C124R;C124Y;I126S;Q129R;S136P;C139R;T140I;K141E;D144A;G145A;G145R 24;31;38;45;52;59;66;73;80;87;94;101;112 29;36;43;50;57;64;71;78;85;92;99;106;117 25471066 Occult hepatitis B virus infection among blood donors in Colombia. This is first report of the mutations rtL108P, rtR110G, rtR192C, rtT150S and rtI187V. 2014 Virology journal Discussion HBV I187V;L108P;R110G;R192C;T150S 79;40;49;58;67 84;45;54;63;72 RT;RT;RT;RT;RT 38;47;56;65;77 40;49;58;67;79 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Three non-synonymous mutations were detected in OBI cases; Mutations in the S region T1387C, T1640C, and A1512T and the amino acid substitutions sY100H, sV184A, and sK141N, respectively. 2014 Virology journal Discussion HBV Y100H;V184A;K141N;T1387C;T1640C;A1512T 145;153;165;85;93;105 151;159;171;91;99;111 S;S;S;S 76;145;153;165 77;146;154;166 Occult Hepatitis B 48 51 25471066 Occult hepatitis B virus infection among blood donors in Colombia. Two of these mutations (sV184A and sY100H) were found outside of the HBsAg Major Hydrophilic Region (MHR) and therefore outside of the "a" determinant (Figure 3). 2014 Virology journal Discussion HBV V184A;Y100H 24;35 30;41 S;S;S 69;24;35 74;25;36 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. In Asia and the Pacific Ocean, BCP A1762T and G1764A mutations were more common. 2014 Hepatitis monthly Discussion HBV A1762T;G1764A 35;46 41;52 BCP 31 34 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. In chronic B hepatitis patients with negative HBeAg was described in the PC region the mutation G1896A. 2014 Hepatitis monthly Discussion HBV G1896A 96 102 C;Precore 46;73 51;75 Chronic Hepatitis B 3 22 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. In summary, genotype D was the main genotype detected in Romanian patients with chronic HBV and is associated with BCP A1762T/G1764A mutation, followed by the PC G1896A mutation and high HBV DNA load, suggesting an association between BCP mutations, high viral DNA load and hepatocarcinogenesis, consistent with previous reports. 2014 Hepatitis monthly Discussion HBV G1764A;A1762T;G1896A 126;119;162 132;125;168 BCP;BCP;Precore 115;235;159 118;238;161 Chronic Hepatitis B 80 91 25477976 Hepatitis B virus core promoter mutations in patients with chronic hepatitis B and hepatocellular carcinoma in bucharest, romania. The most frequent core promoter mutation is the double A1762T and G1764A nucleotide exchange, which results in a substantial decrease in HBeAg expression but enhanced viral genome replication. 2014 Hepatitis monthly Discussion HBV A1762T;G1764A 55;66 61;72 Core promoter;C 18;137 31;142 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Evidence for this selection may be the amino acid exchanges I110L and Y206L; each occurred twice in Palestinian patients and was caused each time by different nucleotide substitution events. 2014 PloS one Discussion HBV I110L;Y206L 60;70 65;75 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. In the second report, authors propose that antibodies produced due to vaccination may not be effective in neutralizing HBV mutants including the L209V in genotype E. 2014 PloS one Discussion HBV L209V 145 150 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. It is probably that an unrecognized antibody response of the patients against their own HBsAg had exerted some selective pressure in favor of classical escape mutants and mutations to an amino acid associated with another genotype like Y134F and S143T. 2014 PloS one Discussion HBV Y134F;S143T 236;246 241;251 S 88 93 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. None of the six non-synonymous mutations found in the only Palestinian D3 sample was attributed to critical functional impact on viral activity (Table 3), in contrast, L209V, the only mutation found in the S gene of all three Palestinian A2 samples was reported in transplant recipients, who received HBIG and in vaccinated individuals. 2014 PloS one Discussion HBV L209V 168 173 S 206 207 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Table 1 shows that the mutations found upstream-I86F, I92T, and I110L-and those found downstream-T189I, Y200F, S204R, Y206L, S207N, S210R, L213I, and L213F-were recorded in different studies but were not associated with critical functions (Table 1). 2014 PloS one Discussion HBV I86F;I92T;I110L;T189I;Y200F;S204R;Y206L;S207N;S210R;L213I;L213F 48;54;64;97;104;111;118;125;132;139;150 52;58;69;102;109;116;123;130;137;144;155 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. The amino acid exchange Y134F found in two patients correlated either with the HBsAg genotype A/adw2 or genotype D/ayw2. 2014 PloS one Discussion HBV Y134F 24 29 S 79 84 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. The other four mutations found in the a determinant-T126S, P127S, D144E, and G145R-are known escape mutants and were detected in five Palestinian D1 samples accounting for 12.5% of the total 40 samples. 2014 PloS one Discussion HBV T126S;P127S;D144E;G145R 52;59;66;77 57;64;71;82 S 38 51 25503289 Subgenotypes and mutations in the s and polymerase genes of hepatitis B virus carriers in the West Bank, palestine. Two of these samples presented with the escape mutations D144E and G145R simultaneously, while the other three samples presented with one single escape mutation each; G145R, T126S, or P127S. 2014 PloS one Discussion HBV D144E;G145R;G145R;T126S;P127S 57;67;167;174;184 62;72;172;179;189 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Expression of W4P LHB resulted in downregulation of the p53 pathway. 2015 Molecular cancer Discussion HBV W4P 14 17 S 18 21 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. However, in our careful inspection of the literature, we did not find any notable mutations, except for W4P, related to liver disease severity. 2015 Molecular cancer Discussion HBV W4P 104 107 Liver disease 120 133 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. In an effort to determine HBV mutation types that contribute to gender disparity in HCC, we recently discovered the W4P/R mutation, which is found only in men, using a molecular epidemiological approach. 2015 Molecular cancer Discussion HBV W4P;W4R 116;116 121;121 Hepatocellular carcinoma 84 87 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. In our study, we showed that estrogen suppressed production of IL-6 and subsequently reduced W4P-induced tumor growth in male mice, which suggests that a high level of estrogen in female mice suppresses tumorigenesis by W4P variant HBV through regulating IL-6 signaling. 2015 Molecular cancer Discussion HBV W4P;W4P 93;220 96;223 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. In this study, we demonstrated that the expression of LHBs enhanced cell proliferation and W4P LHB exerted a stronger effect. 2015 Molecular cancer Discussion HBV W4P 91 94 S;S 95;54 98;58 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. It is likely that W4P LHB impairs the cell-cycle checkpoint at the G1/S phase by inhibiting the p53-p21 axis, which in turn may contribute to HCC by the accumulation of mutations due to the maintenance of genome stability. 2015 Molecular cancer Discussion HBV W4P 18 21 S 22 25 Hepatocellular carcinoma 142 145 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. It should be noted that W4P LHB upregulates expression of cyclin A in hepatocytes, because it is overexpressed in HCC tissue. 2015 Molecular cancer Discussion HBV W4P 24 27 S 28 31 Hepatocellular carcinoma 114 117 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Moreover, HCC patients with W4P variant displayed a higher IL-6 serum level than HCC patients with WT. 2015 Molecular cancer Discussion HBV W4P 28 31 Hepatocellular carcinoma;Hepatocellular carcinoma 10;81 13;84 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Our in vivo data also showed that the gender disparity in W4P-LHB-induced tumorigenicity was closely related to the difference in IL-6 production between the genders. 2015 Molecular cancer Discussion HBV W4P 58 61 S 62 65 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Our in vivo mouse data clearly proved that W4P LHB, but not WT LHB, had higher potential for tumor formation in male than in female mice, suggesting mutations in LHB, such as W4P, occurring in a later stage of chronic hepatitis B, could contribute to the gender disparity in HCC generation. 2015 Molecular cancer Discussion HBV W4P;W4P 43;175 46;178 S;S;S 47;63;162 50;66;165 Chronic Hepatitis B;Hepatocellular carcinoma 210;275 229;278 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Sequence comparison between W4P LHB and WT LHB showed that there were seven variations including W4P. 2015 Molecular cancer Discussion HBV W4P;W4P 28;97 31;100 S;S 32;43 35;46 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Similar patterns were observed in W4P-LHB-expressing Huh7 HCC cell lines. 2015 Molecular cancer Discussion HBV W4P 34 37 S 38 41 Hepatocellular carcinoma 58 61 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Taken together, our in vitro data suggest that mutation in the LHB region, such as W4P, during the natural course of chronic hepatitis B, may contribute to HCC generation. 2015 Molecular cancer Discussion HBV W4P 83 86 S 63 66 Chronic Hepatitis B;Hepatocellular carcinoma 117;156 136;159 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The enhanced colony-forming capability of W4P LHB provides further support for the potential role of the W4P mutation in HBV-related hepatocarcinogenesis. 2015 Molecular cancer Discussion HBV W4P;W4P 42;105 45;108 S 46 49 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. The NIH3T3 cell line constitutively expressing W4P LHB induced preferential tumor formation in male nude mice over females, as well as having oncogenic potential at a high level, with 95% tumor generation incidence within 4 weeks. 2015 Molecular cancer Discussion HBV W4P 47 50 S 51 54 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. This strongly supports the previous epidemiological finding showing a higher prevalence of W4P mutation in patients with severe forms of liver disease than in those with milder forms of liver disease. 2015 Molecular cancer Discussion HBV W4P 91 94 Liver disease;Liver disease 137;186 150;199 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Thus, a likely explanation of the preponderance of tumor generation in male mice observed in our W4P-injected mouse model is that female hormonal factors play a suppressive role in W4P-induced tumorigenicity by inhibiting IL-6 production. 2015 Molecular cancer Discussion HBV W4P;W4P 97;181 100;184 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. Thus, although the acquisition of W4P mutation is likely to affect mostly the tumorigenic nature of variant LHB, the synergistic or additive effect of other variations cannot be excluded. 2015 Molecular cancer Discussion HBV W4P 34 37 S 108 111 25645622 Male-specific hepatitis B virus large surface protein variant W4P potentiates tumorigenicity and induces gender disparity. We selected W4P LHB and WT LHB from an HCC patient and a carrier with or without W4P mutation, respectively. 2015 Molecular cancer Discussion HBV W4P;W4P 12;81 15;84 S;S 16;27 19;30 Hepatocellular carcinoma 39 42 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Association of HBV genotypes and occurrence of W182* mutant is not clearly known. 2014 Hepatitis monthly Discussion HBV W182X 47 52 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. In conclusion, genomic analysis of the of HBV S gene isolated from Malaysian HBV carriers revealed the occurrence of two important variants,pre-S1 deletion and W182* mutant. 2014 Hepatitis monthly Discussion HBV W182X 160 165 PreS1;S 140;46 146;47 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. Other studies have also reported that the presence of W182* mutation in patients with Hepatitis Bcaused progressive forms of the disease (HCC and liver disease).Hepatitis B virus can evolve by mutations in the major hydrophilic region (MHR) of the HBsAg which allows its escape from host immune responses. 2014 Hepatitis monthly Discussion HBV W182X 54 59 S 248 253 Hepatocellular carcinoma;Liver disease 138;146 141;159 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The current study findings revealed that both patients with this mutation were infected with HBV genotype C suggesting the probable association of genotype C and presence of W182* mutant. 2014 Hepatitis monthly Discussion HBV W182X 174 179 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The MHR region contains residues 99-169 of HBsAg and T/I126S, Q129H, G130N, S143L, D144A, G145A, and G145R were among the commonly reported mutations. 2014 Hepatitis monthly Discussion HBV I126S;T126S;Q129H;G130N;S143L;D144A;G145A;G145R 53;53;62;69;76;83;90;101 60;60;67;74;81;88;95;106 S 43 48 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The occurrence of another mutation W182* was identified in the present study in two HBV patients. 2014 Hepatitis monthly Discussion HBV W182X 35 40 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. The W182* mutant was present in HBV genotype C and patients who showed progression to HCC. 2014 Hepatitis monthly Discussion HBV W182X 4 9 Hepatocellular carcinoma 86 89 25737728 S gene mutants occurrence among hepatitis B carriers in malaysia. This crucial finding suggests that W182* could serve as a molecular marker to predict HCC. 2014 Hepatitis monthly Discussion HBV W182X 35 40 Hepatocellular carcinoma 86 89 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. A previous study reported that T1858C mutations are often found in combination with A1775G. 2015 Hepatitis monthly Discussion HBV T1858C;A1775G 31;84 37;90 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. In addition, other combined mutation types such as C1856T/T1858C/G1721A and G1721A/G1757A/A1775G/T1858C were also exclusively detected in children with genotype C infection, while the clinical characteristics of these combined mutation-containing patients showed no statistical difference compared to those without combined mutations. 2015 Hepatitis monthly Discussion HBV T1858C;G1721A;T1858C;A1775G;G1757A;C1856T;G1721A 58;65;97;90;83;51;76 64;71;103;96;89;57;82 HBV infections 152 172 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. In our results, we showed that 16 of 17 T1858C mutation-containing sequences were in T1858C/A1775G/G1721A triple mutations. 2015 Hepatitis monthly Discussion HBV A1775G;G1721A;T1858C;T1858C 92;99;40;85 98;105;46;91 25741368 Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C. Statistical analysis demonstrated that the presence of a combined triple-mutation type, G1721A/A1775G/T1858C, was correlated with younger ages, genotype C strains, and a higher DNA load. 2015 Hepatitis monthly Discussion HBV T1858C;A1775G;G1721A 102;95;88 108;101;94 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. In contrast to these findings, cross-sectional studies of HBV viral level and liver disease severity have generally suggested associations with A1762T/G1764A double mutation, although these studies were mostly conducted among participants with other HBV genotypes. 2015 Hepatitis monthly Discussion HBV G1764A;A1762T 151;144 157;150 Liver disease 78 91 25788956 Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran. Some studies indicated that the A1762T/G1764A mutation typically appears earlier than G1896A during the course of HBV infection. 2015 Hepatitis monthly Discussion HBV G1764A;A1762T;G1896A 39;32;86 45;38;92 HBV infections 114 127 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. A1846T mutation is silent at the amino acid level, and previous studies have observed that this mutation is associated with the progression of age-dependent disease (liver cirrhosis and hepatocellular carcinoma) as well as severe liver disease (fulminant hepatitis and acute-on-chronic liver failure, ACLF); however, the relationship between this mutation and HBeAg seroconversionneeds further experimental validation. 2015 PloS one Discussion HBV A1846T 0 6 C 360 365 Liver cirrhosis;Hepatocellular carcinoma;Liver disease;Fulminant Hepatitis B;Acute on chronic liver failure;Acute on chronic liver failure 166;186;230;245;301;269 181;210;243;264;305;299 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Although the G1899A mutation only changes the glycine at codon 29 into aspartic acid and is always accompanied by the G1896A mutation, a previous study revealed that approximately 50% of the HBeAg negative variants contained this combined mutation. 2015 PloS one Discussion HBV G1899A;G1896A;G29D 13;118;46 19;124;84 C 191 196 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. An A1762T/G1764A double mutation in the BCP/precore region would reduce the levels of HBeAg by inhibiting precore mRNA expression, leading to the transition from the immune tolerance to the immune reactive phase, followed by lower DNA viral loads and elevated ALT levels. 2015 PloS one Discussion HBV G1764A;A1762T 10;3 16;9 BCP;C;Precore;Precore 40;86;44;106 43;91;51;113 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Deletions in core regions instead of the G1896A and A1762T/G1764A double mutation were observed in early seroconversion processes in a longitudinal study of infants (our own unpublished data), which also supports the idea that HBeAg seroconversion does not solely rely on BCP/precore mutations. 2015 PloS one Discussion HBV G1764A;G1896A;A1762T 59;41;52 65;47;58 BCP;C;C;Precore 272;13;227;276 275;17;232;283 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. In our study, the nt A1846T mutation ratio in HBeAg-negative child and adult patients was also significantly higher than in HBeAg-positive child and adult patients(17.8% vs 0.6%,P<0.01, 37.5% vs 6.8%, P<0.01 for children and adults, respectively), providing a clue that A1846T is closely associated with HBeAg seroconversion. 2015 PloS one Discussion HBV A1846T;A1846T 21;270 27;276 C;C;C 46;124;304 51;129;309 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. In these six HBeAg seroconversion statistics-related sites, G1896A and the A1762T/G1764A double mutation had obviously higher mutation ratios in HBeAg-negative patients, which is in accordance with previous studies. 2015 PloS one Discussion HBV G1764A;G1896A;A1762T 82;60;75 88;66;81 C;C 13;145 18;150 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Interestingly, the frequency of the A1752G mutation was significantly higher in HBeAg-positive child patients(42.6% vs 27.8%, P<0.05)but was negatively correlated with HBeAg seroconversion. 2015 PloS one Discussion HBV A1752G 36 42 C;C 80;168 85;173 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. It is worth noting that the mutation ratio of G1896A is obviously lower in HBeAg-negative child(41.1%) than in HBeAg-negative adult patients(91.7%)(P<0.001). 2015 PloS one Discussion HBV G1896A 46 52 C;C 75;111 80;116 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. One variation is a G-to-A mutation at nt1896, which creates a premature stop codon and then abolishes the synthesis of HBeAg. 2015 PloS one Discussion HBV G1896A 19 44 C 119 124 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. Similar features were also observed for other sites located in the BCP/precore regions(G1899A and A1846T, P<0.05)(Table 2). 2015 PloS one Discussion HBV G1899A;A1846T 87;98 93;104 BCP;Precore 67;71 70;78 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The other is a two-nucleotide substitution, T1762A and G1764A, and transfection studies have shown that the T1762A and G1764A double mutation decreases the level of pre-C mRNA by 50% to 70%, leading to reduced HBeAg synthesis. 2015 PloS one Discussion HBV T1762A;G1764A;T1762A;G1764A 44;55;108;119 50;61;114;125 C;Precore 210;165 215;170 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The reasons for the lower viral loads with A1762T/G1764A double mutations in HBeAg-positive patients were more likely related to the decreased HBeAg synthesis and alterations in the complex delicate balance between the virus and the host immune system, but the alterations cannot simply be attributed to reduced viral replication mediated by the double mutation. 2015 PloS one Discussion HBV G1764A;A1762T 50;43 56;49 C;C 77;143 82;148 25822176 Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients. The relationship between the A1762T/G1764A double mutation and the level of viral DNA replication level is unclear, and studies that employed the transfection of human hepatoma cell lines with clinical HBV viral samples may not truly reflect the true in vivo status. 2015 PloS one Discussion HBV G1764A;A1762T 36;29 42;35 Hepatocellular carcinoma 168 176 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. Furthermore, despite the fact that all subgenotypes D have T1858, only subgenotypes D1 and D7 have a tendency to mutate G1896A. 2015 PloS one Discussion HBV G1896A 120 126 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. Given the fact that pC region overlaps the encapsidation signal, which is essential for efficient replication, those genotypes with T1858 would tend to mutate G1896A in order to increase stability of the stem loop in the encapsidation signal structure. 2015 PloS one Discussion HBV G1896A 159 165 Precore 20 22 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In summary, those genotypes carrying 1858C seem to prevent G1896A mutation; however, T1858 polymorphism seems to be necessary but not sufficient to promote G1896A substitution. 2015 PloS one Discussion HBV G1896A;G1896A 59;156 65;162 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. In vitro studies have shown that mutation A1762T/G1764A does not abrogate HBeAg expression but decreases its levels, while concomitantly increasing viral replication. 2015 PloS one Discussion HBV G1764A;A1762T 49;42 55;48 C 74 79 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. On the other hand, the high prevalence of mutations other than G1896A in the preCore region in subgenotype A2 indicates that during virus-host interaction, the virus explores different molecular alternatives to regulate HBeAg expression. 2015 PloS one Discussion HBV G1896A 63 69 C;Precore 220;77 225;84 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. Since subgenotypes F1b and F4 carry T1858, it would be expected that G1896A mutation would predominate in both subgenotypes; however, this was only observed in subgenotype F4. 2015 PloS one Discussion HBV G1896A 69 75 25822666 Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina. The difference in the mutation pattern among genotypes was initially described in the 90s after the identification of genotypes A to D, when it was observed that the occurrence of G1896A was restricted to HBV genotypes with T at nucleotide 1858. 2015 PloS one Discussion HBV G1896A 180 186 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. A higher rate (95.3%) of the G1896A mutation was also reported in the HBeAg-negative group. 2015 Jundishapur journal of microbiology Discussion HBV G1896A 29 35 C 70 75 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. In agreement with our results, a study from Brazil showed that the G1896A PC mutation occurred in 36% of Brazilian patients with CHB, of which 58.6% were HBeAg-negative. 2015 Jundishapur journal of microbiology Discussion HBV G1896A 67 73 C;Precore 154;74 159;76 Chronic Hepatitis B 129 132 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. The clinical relevance of the G1896A PC mutation in chronic hepatitis B (CHB) is still poorly understood. 2015 Jundishapur journal of microbiology Discussion HBV G1896A 30 36 Precore 37 39 Chronic Hepatitis B;Chronic Hepatitis B 52;73 71;76 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. The G1896A mutation in the PC region has been found to be the most common mutation in chronic HBeAg-negative patients. 2015 Jundishapur journal of microbiology Discussion HBV G1896A 4 10 C;Precore 94;27 99;29 25825644 Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients. This study indicates that the rate of G1896A mutation at the PC region among HBeAg-negative patients in the Golestan province of Iran was similar to the average rate of other parts of Iran. 2015 Jundishapur journal of microbiology Discussion HBV G1896A 38 44 C;Precore 77;61 82;63 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Also it was found that the frequencies of T216C, G1896A, G1913A/G, and A2159G/C were >45% in the patients with ACLF, the combinative mutations at these sites could be utilized to diagnose clinically and to discriminate the HBV-infected patients with advanced disease. 2015 PloS one Discussion HBV G1913G;T216C;G1896A;G1913A;A2159G;A2159C 57;42;49;57;71;71 65;47;55;65;79;79 Acute on chronic liver failure;Liver disease;HBV infections 111;250;223 115;266;235 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Also T216C is a missense mutation, which can cause the amino acid changes of HBsAg codon 21. 2015 PloS one Discussion HBV T216C 5 10 S 77 82 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Although the symptoms of early ACLF are similar to the symptoms of CHB-S, the prognosis of ACLF was much poorer than that of CHB-S, so A2159G/C and A2189T/C may be very important, which could serve as markers to distinguish ACLF from CHB-S in the subjects with genotype B. 2015 PloS one Discussion HBV A2159C;A2159G;A2189T;A2189C 135;135;148;148 143;143;156;156 Acute on chronic liver failure;Acute on chronic liver failure;Acute on chronic liver failure;Chronic Hepatitis B;Chronic Hepatitis B;Chronic Hepatitis B 31;91;224;234;67;125 35;95;228;237;70;128 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. As compared with the non-ACLF group, the AOR of T216C and A2189T/C mutation in ACLF cases with genotype B significantly increased, but AOR of T216C and A2189T/C mutation in ACLF cases with genotype C did not elevate significantly. 2015 PloS one Discussion HBV A2189C;A2189C;T216C;A2189T;T216C;A2189T 58;152;48;58;142;152 66;160;53;66;147;160 Acute on chronic liver failure;Acute on chronic liver failure 79;173 83;177 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. However, the results of stepwise multivariate regression analysis in our study exhibited that AOR values of T216C and A2159G/C mutations in ACLF cases were 2.60 (1.39-4.85) and 2.76 (1.56-4.87) that significantly enhanced as compared with non-ACLF cases. 2015 PloS one Discussion HBV A2159C;T216C;A2159G 118;108;118 126;113;126 Acute on chronic liver failure 140 144 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Multivariate regression analysis showed that T216C, G1896A, C1913A/G and A2159G/C mutations were independent risk factors for ACLF cases. 2015 PloS one Discussion HBV C1913G;A2159C;T216C;G1896A;C1913A;A2159G 60;73;45;52;60;73 68;81;50;58;68;81 Acute on chronic liver failure 126 130 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Of the HBV mutations at nt.216, nt.1896, nt.1913 and nt.2159 sites independently associated with ACLF, only G1896A has been studied extensively and it can abolish HBeAg expression at the translational level. 2015 PloS one Discussion HBV G1896A 108 114 C 163 168 Acute on chronic liver failure 97 101 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Of these seven mutations, A1846T/G, G1896A and C1913A/G were studied extensively, whereas T216C, G285A, A2159G, and A2189C were novel ACLF-related mutations identified in this study. 2015 PloS one Discussion HBV C1913G;A2159G;A1846T;A1846G;G1896A;C1913A;T216C;G285A;A2189C 47;104;26;26;36;47;90;97;116 55;110;34;34;42;55;95;102;122 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. So far the mutations at T216C and A2159G/C sites as independent risk factors for ACLF have not been reported. 2015 PloS one Discussion HBV A2159C;T216C;A2159G 34;24;34 42;29;42 Acute on chronic liver failure 81 85 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Some previous studies also indicated that G1896A and C1913A/G mutations were in close relationship with ACLF. 2015 PloS one Discussion HBV G1896A;C1913A;C1913G 42;53;53 48;61;61 Acute on chronic liver failure 104 108 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. T216C, G1896A, C1913A/G and A2159G/C were factors independently associated with ACLF. 2015 PloS one Discussion HBV A2159C;T216C;G1896A;C1913A;C1913G;A2159G 28;0;7;15;15;28 36;5;13;23;23;36 Acute on chronic liver failure 80 84 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. The C1913A/G mutation causes a substitution of the fifth amino acid (proline changes to threonine or alanine) in core protein, which may alter function of HBcAg. 2015 PloS one Discussion HBV C1913G;C1913A 4;4 12;12 C;C 113;155 117;160 25849554 New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing. Thus, according to the results of our investigation, the old HBV patients with genotype B virus and mutations at T216C, G1896A, C1913A/G and A2159G/C sites may be prone to ACLF development. 2015 PloS one Discussion HBV T216C;G1896A;C1913A;C1913G;A2159G;A2159C 113;120;128;128;141;141 118;126;136;136;149;149 Acute on chronic liver failure 172 176 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. It is reasonable to speculate that rs1234220 variant genotypes increase HCC risk, possibly via facilitating the generation of A1652G, C1673T, and C1730G, the three HCC-risk HBV mutations in genotype B HBV-infected subjects. 2015 Chinese medical journal Discussion HBV A1652G;C1673T;C1730G 126;134;146 132;140;152 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 72;164;201 75;167;213 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. The effect of rs1234220 variant genotypes on HCC risk is only observed in genotype B HBV-infected subjects, possibly via facilitating the immune selection of A1652G, C1673T, and C1730G, the three HCC-risk mutations in genotype B HBV-infected subjects. 2015 Chinese medical journal Discussion HBV A1652G;C1673T;C1730G 158;166;178 164;172;184 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections;HBV infections 45;196;85;229 48;199;97;241 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. The interactions of rs2299939 polymorphism with A3054T mutation or rs1234213 polymorphism with C3116T mutation significantly increased the risk of HCC in male HBV-infected subjects; whereas the interaction of rs2299939 polymorphism with C3116T mutation significantly decreased the risk of HCC [Table 6]. 2015 Chinese medical journal Discussion HBV A3054T;C3116T;C3116T 48;95;237 54;101;243 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 147;289;159 150;292;171 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. The interactions of rs2299939 polymorphism with A3054T mutation or rs1234213 polymorphism with C3116T mutation significantly increased the risk of HCC in male HBV-infected subjects; whereas the interaction of rs2299939 polymorphism with C3116T mutation significantly decreased the risk of HCC. 2015 Chinese medical journal Discussion HBV A3054T;C3116T;C3116T 48;95;237 54;101;243 Hepatocellular carcinoma;Hepatocellular carcinoma;HBV infections 147;289;159 150;292;171 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. Thus, the effects of important HCC-related HBV mutations such as A3054T and C3116T on HCC susceptibility can be moderated by host genetic susceptibility such as PTEN polymorphisms. 2015 Chinese medical journal Discussion HBV A3054T;C3116T 65;76 71;82 Hepatocellular carcinoma;Hepatocellular carcinoma 31;86 34;89 25881591 Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma. We also found that rs1234220 variant genotype was significantly associated with increased frequencies of HBV mutations A1652G, C1673T, and C1730G in genotype B HBV-infected subjects. 2015 Chinese medical journal Discussion HBV A1652G;C1673T;C1730G 119;127;139 125;133;145 HBV infections 160 172 25942596 The characteristic changes in hepatitis B virus x region for hepatocellular carcinoma: a comprehensive analysis based on global data. Sixteen nucleotide differences between the two groups were found and seven of them (A1383C, R1479Y, C1485T, C1631T, C1653T, G1719T, and T1800C) were further identified to be critical for genotype C HBV-related HCC, also observed in AA analyses in parallel as for the nonsynonymous mutations. 2015 PloS one Discussion HBV A1383C;R1479Y;C1485T;C1631T;C1653T;G1719T;T1800C 84;92;100;108;116;124;136 90;98;106;114;122;130;142 Hepatocellular carcinoma 210 213 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. In addition, no LAM-resistant rtM204I/V or ETV-resistant variants were selected during 27-36 months of combination therapy. 2015 International journal of medical sciences Discussion HBV M204I;M204V 32;32 39;39 RT 30 32 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. In contrast, in the present study, we observed that replication of the ADV-resistant variants, rtA181V and/or rtN236T, were fully inhibited after 21-24 months of ADV-ETV combination therapy. 2015 International journal of medical sciences Discussion HBV A181V;N236T 97;112 102;117 RT;RT 95;110 97;112 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. It should be noted that during ADV-ETV combination rescue therapy, although the replication of ADV-resistant variants, rtA181V and/or rtN236T, was fully inhibited and no LAM-resistant rtM204I/V or ETV-resistant variants were selected after 27-36 months of combination rescue therapy, HBV DNA reduction was delayed even with potent ADV-ETV combination therapy. 2015 International journal of medical sciences Discussion HBV A181V;M204I;M204V;N236T 121;186;186;136 126;193;193;141 RT;RT;RT 119;134;184 121;136;186 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. This is mainly attributed to the ADV mutation, rtA181V/T, which is responsible for cross-resistance to LAM and ADV. 2015 International journal of medical sciences Discussion HBV A181V;A181T 49;49 56;56 RT 47 49 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. This study demonstrated that replication of the ADV-resistant variants, rtA181V and rtN236T, was fully inhibited by ADV-ETV combination rescue therapy. 2015 International journal of medical sciences Discussion HBV A181V;N236T 74;86 79;91 RT;RT 72;84 74;86 26005376 Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy. Whether ADV-resistant variants will re-emerge and LAM-resistant rtM204I/V or ETV-resistant variants (rtT184, rtS202, or rtM250) will be selected in these patients warrants further investigation. 2015 International journal of medical sciences Discussion HBV M204I;M204V 66;66 73;73 RT;RT;RT;RT 64;101;109;120 66;103;111;122 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. Further studies are warranted to determine whether rtD263E mutation is associated with partial resistance to TDF, an anti-HBV molecule with the highest resistance barrier. 2015 Hepatitis monthly Discussion HBV D263E 53 58 RT 51 53 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. In addition, two mutations of rtL91I and rtN238H/T/S presented in 10% of baseline sequences from patients, were not detected in these patients after the treatment with TDF. 2015 Hepatitis monthly Discussion HBV L91I;N238H;N238T;N238S 32;43;43;43 36;52;52;52 RT;RT 30;41 32;43 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. In the present study, a new amino acid substitution (rtD263E) was observed to develop in 60% of patients with viremia on TDF therapy. 2015 Hepatitis monthly Discussion HBV D263E 55 60 RT 53 55 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. The other three non-classical mutations, including rtC256G, rtN53S/T and rtY54N observed in 6%, 4% and 8% of patients with viremia, respectively, were detected significantly lower than pretreatment time. 2015 Hepatitis monthly Discussion HBV N53S;N53T;Y54N;C256G 62;62;75;53 68;68;79;58 RT;RT;RT 51;60;73 53;62;75 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. The rtD263E is located after an E domain at RT-area and in the C-term part of the palm domain with 65.5% conserved amino acids that do not overlap with HBsAg region. 2015 Hepatitis monthly Discussion HBV D263E 6 11 S;RT;RT 152;4;44 157;6;46 26045705 Efficacy of tenofovir disoproxil fumarate therapy in nucleoside-analogue naive Iranian patients treated for chronic hepatitis B. We also identified one new amino acid substitution as rtD263E in the HBV RT. 2015 Hepatitis monthly Discussion HBV D263E 56 61 RT;RT 54;73 56;75 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. A combination of A1762T/G1764A and G1896A showed a higher specificity than A1762T/G1764A double mutations (Table 4), suggesting that mutations that accumulate at different sites have synergistic effects in promoting the risk of HBV-ACLF. 2015 Virology journal Discussion HBV G1764A;G1764A;A1762T;G1896A;A1762T 24;82;17;35;75 30;88;23;41;81 Acute on chronic liver failure 228 236 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. In G1896A patients, the concentration of serum toll-like receptor 2 (TLR2) reached a significantly higher level than in HBV-infected patients lacking G1896A. 2015 Virology journal Discussion HBV G1896A;G1896A 3;150 9;156 HBV infections 120 132 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Most mutations remained significantly associated with ACLF development in age and sex-matched groups and the association with G1896A was still significant after matching age, sex, HBV genotype and HBV DNA load. 2015 Virology journal Discussion HBV G1896A 126 132 Acute on chronic liver failure 54 58 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Our meta-analysis showed that T1753V, A1762T, G1764A, A1762T/G1764A, C1766T, T1768A, A1846T, G1896A, G1899A and G1896A/A1762T/G1764A were all related to increasing the risk of HBV-ACLF by a factor of 1.919, 2.685, 2.901, 2.376, 1.849, 2.199, 3.163, 2.181, 3.525 and 1.575, respectively. 2015 Virology journal Discussion HBV G1764A;A1762T;G1764A;T1753V;A1762T;G1764A;A1762T;C1766T;T1768A;A1846T;G1896A;G1899A;G1896A 61;119;126;30;38;46;54;69;77;85;93;101;112 67;125;132;36;44;52;60;75;83;91;99;107;118 Acute on chronic liver failure 176 184 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. Third, the data was insufficient to allow analysis of mutations such as G1896A/G1899A, G1896A/G1899A/A1762T/G1764A and C1913V that were implicated in ACLF development in some studies. 2015 Virology journal Discussion HBV G1899A;G1899A;G1764A;A1762T;G1896A;G1896A;C1913V 79;94;108;101;72;87;119 85;100;114;107;78;93;125 Acute on chronic liver failure 150 154 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. TLR2 is a potential connection between G1896A and HBeAg-negative status. 2015 Virology journal Discussion HBV G1896A 39 45 C 50 55 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. We discovered that HBV BCP/PC variations such as T1753V, A1762T, G1764A, A1762T/G1764A, C1766T, T1768A, A1846T, G1896A, G1899A and G1896A/A1762T/G1764A, and HBeAg-negative status correlated with an increased risk of HBV-ACLF. 2015 Virology journal Discussion HBV G1764A;A1762T;G1764A;T1753V;A1762T;G1764A;A1762T;C1766T;T1768A;A1846T;G1896A;G1899A;G1896A 80;138;145;49;57;65;73;88;96;104;112;120;131 86;144;151;55;63;71;79;94;102;110;118;126;137 BCP;C;Precore 23;157;27 26;162;29 Acute on chronic liver failure 216 224 26063382 Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis. When exploring the potential value of HBV variation in predicting HBV-ACLF, we found that T1753V, G1764A, C1766T, T1768A, G1899A and G1896A/A1762T/G1764A triple mutations were useful in predicting ACLF. 2015 Virology journal Discussion HBV G1764A;A1762T;T1753V;G1764A;C1766T;T1768A;G1899A;G1896A 147;140;90;98;106;114;122;133 153;146;96;104;112;120;128;139 Acute on chronic liver failure;Acute on chronic liver failure 197;66 201;74 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. As expected, both CAdA and CdG proved to significantly reduce the production of both HBVWT and HBVETV-RL180M/S202G/M204V in cell-based assays and productively HBV-infected hu-liver-chimeric-uPA+/+/SCID+/+ mice. 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 109;115 114;120 HBV infections 159 171 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. Considering that the multiple antiviral mechanisms involved represent a unique feature of the 4'-modified NRTIs, we hypothesized that CAdA and CdG would also act as efficient HBV DNA chain terminators through the mechanism(s) mentioned above, which should differ from the mechanism(s) through which ETV exerts its activity against HBV and that CAdA and CdG would also be active against HBVETV-RL180M/S202G/M204V. 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 400;406 405;411 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. However, it should be noted that the potential efficacy against HBVETV-RL180M/S202G/M204V of CAdA and CdG in the clinical settings is to be determined only in carefully managed clinical trials. 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 78;84 83;89 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. In conclusion, the data presented in this study suggest that CAdA and CdG represent promising candidates as novel therapeutics for HBVETV-RL180M/S202G/M204V infection and that further structural optimization of 4'-modified nucleosides should help develop more novel NRTIs that have unique and better antiviral profiles against HBV. 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 145;151 150;156 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. In the mouse model, the difference in the viremia reduction magnitude between HBVWT and HBVETV-RL180M/S202G/M204V was 30-fold (-2.9 vs -1.4 log10 copies/ml) for CAdA treatment and 30-fold (-2.7 vs -1.2 log10 copies/ml) for CdG treatment. 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 102;108 107;113 26122273 4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus. The IC50 value difference in the HBV signal reduction in the Southern blot between HBVWT and HBVETV-RL180M/S202G/M204V was 9.7-fold for CAdA treatment and 4.3-fold for CdG treatment (Table 2). 2015 Hepatology (Baltimore, Md.) Discussion HBV S202G;M204V 107;113 112;118 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. The results of mutations were similar to those of the previous studies reporting that the most common mutation affects the highly conserved YMDD motif, resulting in a methionine to valine or isoleucine substitution at codon 204 (M204V/I) and between them, M204I mutant is significantly more resistant to LAM than the M204V mutant. 2015 Hepatitis monthly Discussion HBV M204V;M204I;M204I;M204V 229;229;256;317 236;236;261;322 P 140 144 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. The sequential analyses of the current study genes also revealed the natural presence of ENC resistance mutation (S202I), not previously reported in Iran. 2015 Hepatitis monthly Discussion HBV S202I 114 119 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. The study found M204I as the dominant mutation in all LAM resistant patients. 2015 Hepatitis monthly Discussion HBV M204I 16 21 26300928 YMDD Motif Mutation Profile Among Patients Receiving Liver Transplant Due to Hepatitis B Virus Infection With Long Term Lamivudine/Immunoglobulin Therapy. These findings, consistent with previous studies, demonstrated that the most common mutation affects the highly conserved motif in the catalytic domain of the HBV P gene is M204I. 2015 Hepatitis monthly Discussion HBV M204I 173 178 P 163 164 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Although the rtL269I mutation alone could increase the replication capacity (Fig 2D), the rtL269I mutant was susceptible to LMV and ETV, and the mutation did not affect the extent of LMV or ETV resistance (Figs 3B and 4B). 2015 PloS one Discussion HBV L269I;L269I 15;92 20;97 RT;RT 13;90 15;92 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Approximately 2-, 3-, 4-, and 7-fold higher replication capacity was observed when the rtL269I mutation was introduced to WT, rtM204I, rtV173L+M204I, and rtM129L+V173L+M204I+H337N mutants, respectively (Fig 2D). 2015 PloS one Discussion HBV L269I;M204I;V173L;M129L;M204I;M204I;V173L;H337N 89;128;137;156;143;168;162;174 94;133;142;161;148;173;167;179 RT;RT;RT;RT 87;126;135;154 89;128;137;156 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Here, it must be noted that the antiviral resistance and reduced polymerase activity conferred by the rtM204I mutant HBV polymerase could be explained by a deformed catalytic site; the bulky side chain of rtM204I protrudes into the active site to form a steric gate, which restricts the binding of the ligand. 2015 PloS one Discussion HBV M204I;M204I 104;207 109;212 P;P;RT;RT 65;121;102;205 75;131;104;207 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. However, among the 16 patients in whom the YMDD mutation was detectable during antiviral treatment, 7 (43.8%) displayed the rtL269I substitution along with rtM204I/V mutation (Table 1). 2015 PloS one Discussion HBV M204I;M204V;L269I 158;158;126 165;165;131 RT;RT;P 124;156;43 126;158;47 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. However, whether the rtL269I substitution can emerge in the milieu of YMDD mutation alone remains to be determined. 2015 PloS one Discussion HBV L269I 23 28 RT;P 21;70 23;74 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In addition, we suggest that the rtL269I substitution emerges as part of complex mutations to maximize viral fitness (Table 2). 2015 PloS one Discussion HBV L269I 35 40 RT 33 35 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In our molecular modeling strategy, the rtL269I substitution may induce the conformational changes of the template strand, which could enhance replication in the WT and YMDD mutants. 2015 PloS one Discussion HBV L269I 42 47 RT;P 40;169 42;173 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. In this study, we discovered that the rtL269I substitution is associated with efficient replication in the multi-drug resistant HBV, and thus represents a novel compensatory mutation for the YMDD mutants. 2015 PloS one Discussion HBV L269I 40 45 RT;P 38;191 40;195 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. It must also be noted that most of the patients (95.5%, 21 out of 22) treated with LMV or CLV monotherapy (primary treatment) did not express the rtL269I substitution before therapy (Table 1). 2015 PloS one Discussion HBV L269I 148 153 RT 146 148 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. It will be interesting to further investigate the effect of rtL269I substitution in other HBV genotypes. 2015 PloS one Discussion HBV L269I 62 67 RT 60 62 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Our results suggested that sequence information on the rtL269I substitution would be helpful for the development of treatment regimens for patients demonstrating a sub-optimal response or treatment failure during antiviral therapy. 2015 PloS one Discussion HBV L269I 57 62 RT 55 57 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. rtM204I/V in the YMDD motif is the primary mutation conferring resistance against LMV, CLV, and ETV. 2015 PloS one Discussion HBV M204I;M204V 2;2 9;9 RT;P 0;17 2;21 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Similarly, in the presence of antivirals the rtL269I substitution had the maximal effect on replication of the rtM129L+V173L+M204I+H337N mutant (Figs 3C and 4C). 2015 PloS one Discussion HBV L269I;M129L;M204I;V173L;H337N 47;113;125;119;131 52;118;130;124;136 RT;RT 45;111 47;113 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The compensatory mutations discovered thus far in the YMDD mutants include rtL180M, L80I/V, V173L, S117F, and L229F/V. 2015 PloS one Discussion HBV L180M;L80I;L80V;V173L;S117F;L229F;L229V 77;84;84;92;99;110;110 82;90;90;97;104;117;117 RT;P 75;54 77;58 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. The rtM129L+V173L+M204I+H337N mutant showed about 20% of replication level of the WT virus without therapy, whereas the rtM129L+V173L+M204I+L269I+H337N mutant showed 230% replication level (Fig 2C). 2015 PloS one Discussion HBV M129L;M129L;M204I;V173L;H337N;L269I;M204I;V173L;H337N 6;122;18;12;24;140;134;128;146 11;127;23;17;29;145;139;133;151 RT;RT 4;120 6;122 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Therefore, the restoration of the volume of the substrate-binding site by template strand repositioning resulting from rtL269I substitution might be a mechanism counteracting the rtM204I mutation. 2015 PloS one Discussion HBV L269I;M204I 121;181 126;186 RT;RT 119;179 121;181 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. Therefore, we do not know whether the effect of rtL269I substitution is genotype-specific. 2015 PloS one Discussion HBV L269I 50 55 RT 48 50 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. These clinical data suggested that rtM204I/V+L269I was selected during antiviral therapy to confer viral fitness. 2015 PloS one Discussion HBV M204I;M204V;L269I 37;37;45 44;44;50 RT 35 37 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. These data suggested that other mutations cooperate with the rtL269I mutation to achieve maximal viral fitness. 2015 PloS one Discussion HBV L269I 63 68 RT 61 63 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. These two limitations necessitate further studies for the elucidation of the possible association between rtL269I mutation and other types of drug-resistant mutations. 2015 PloS one Discussion HBV L269I 108 113 RT 106 108 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. We further investigated the mode of action of rtL269I using molecular modeling, and also validated the clinical relevance of this mutation in patients within the "difficult-to-treat" category. 2015 PloS one Discussion HBV L269I 48 53 RT 46 48 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. We have previously identified a multi-drug resistant HBV mutant containing the quintuple mutation (rtM129L+V173L+M204I+L269I+H337N), which exhibited robust replication and strong cross-resistance to LMV, CLV, and ETV. 2015 PloS one Discussion HBV M129L;L269I;V173L;M204I;H337N 101;119;107;113;125 106;124;112;118;130 RT 99 101 26322642 Substitution at rt269 in Hepatitis B Virus Polymerase Is a Compensatory Mutation Associated with Multi-Drug Resistance. When combined with other drug resistant mutations, the effect of rtL269I on the replication ability was found to be backbone-dependent. 2015 PloS one Discussion HBV L269I 67 72 RT 65 67 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. In Case #3B, the classic vaccine escape mutant (i.e., G145R) was also detected in both the CD4+ T cell and the CD56+ T cell subset, albeit in greater frequency in the estimated error rate based on the NGS-sequenced plasmid clone of the CD56+ samples (S1 Table), thus the data requires confirmation in further studies. 2015 PloS one Discussion HBV G145R 54 59 26390290 Detection of Hepatitis B Virus (HBV) Genomes and HBV Drug Resistant Variants by Deep Sequencing Analysis of HBV Genomes in Immune Cell Subsets of HBV Mono-Infected and/or Human Immunodeficiency Virus Type-1 (HIV-1) and HBV Co-Infected Individuals. Other studies have also described detection of the classic vaccine escape mutant (i.e., G145R) in the PBMC compartment that was linked to vertical and intrafamilial horizontal occult (i.e., low-level) HBV transmission. 2015 PloS one Discussion HBV G145R 88 93 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Recent in vitro studies found that Q129R significantly impaired virion and/or S protein secretion in HuH7 cells and in mice is associated with lower reactivity in HBsAg assays. 2015 Virology journal Discussion HBV Q129R 35 40 S;S 163;78 168;79 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. Significant predominance of amino acid substitutions T125M and Q129R was observed in HBsAg isolated from occult hepatitis B cases. 2015 Virology journal Discussion HBV T125M;Q129R 53;63 58;68 S 85 90 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. T125M was detected in 11.9 % of cases with occult HBV genotype D, while none of the patients with occult HBV genotype A harbored this mutant strain. 2015 Virology journal Discussion HBV T125M 0 5 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. The T125M substitution represents a non-conservative amino acid change which may affect the conformation of the HBsAg a determinant region and thus the binding of HBsAg-specific antibody. 2015 Virology journal Discussion HBV T125M 4 9 S;S;S 118;112;163 131;117;168 26420301 Hepatitis B surface gene variants isolated from blood donors with overt and occult HBV infection in north eastern Egypt. While T125M and Q129R were the predominant HBsAg variants in these occult HBV cases, P120T and S143L were more frequent in HBsAg + blood donors. 2015 Virology journal Discussion HBV T125M;Q129R;P120T;S143L 6;16;85;95 11;21;90;100 S;S 43;123 48;128 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. The remaining two also have detection escape mutations (T131N and M133L). 2015 PloS one Discussion HBV T131N;M133L 56;66 61;71 26457811 Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection. The T118K, T123N and N145A substitutions in the MHR have been reported to lead to failure of detection [- ]. 2015 PloS one Discussion HBV T118K;T123N;N145A 4;11;21 9;16;26 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. And they found rs2856718 variant genotypes significantly decreased HCC risk and the variant genotypes of rs2856718 were significantly associated with an increased frequency of HBV A1726C mutation in genotype C. 2015 Scientific reports Discussion HBV A1726C 180 186 Hepatocellular carcinoma 67 70 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. Finally, they found the interaction of rs1053004 with T1674C/G significantly increased the HCC risk. 2015 Scientific reports Discussion HBV T1674C;T1674G 54;54 62;62 Hepatocellular carcinoma 91 94 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. In addition, the effect of C1730G was reversed from a protective effect (adjusted OR = 0.18, 95% CI = 0.15-0.22) to a risk effect with borderline significance (adjusted OR = 2.07, 95% CI = 1.02-4.20) after being conditionally adjusted by the other mutations. 2015 Scientific reports Discussion HBV C1730G 27 33 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. In this study, the HBV mutations A1846T and G1896A, which have been reported to be associated with an increased risk of HCC by several studies, were not significantly associated with HCC. 2015 Scientific reports Discussion HBV A1846T;G1896A 33;44 39;50 Hepatocellular carcinoma;Hepatocellular carcinoma 120;183 123;186 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. There were also novel HBV mutations, including A1752G, G1915A/C and C1969T, which were found to be associated with HBV-related HCC. 2015 Scientific reports Discussion HBV A1752G;G1915A;G1915C;C1969T 47;55;55;68 53;63;63;74 Hepatocellular carcinoma 127 130 26568165 Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study. They sequenced the HBV EnhII/BCP/PC region successfully from 1,429 (52.2%) of the HBV-infected subjects and found that the interactions of rs9277535 AA with the T1674C/G or G1719T mutation in genotype C significantly decreased HCC risk. 2015 Scientific reports Discussion HBV T1674C;T1674G;G1719T 161;161;173 169;169;179 BCP;Enh II;Precore 29;23;33 32;28;35 Hepatocellular carcinoma;HBV infections 227;82 230;94 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Among them the C69stop codon mutation in the surface gene, the C1766T /T1768A mutation in the basal core promoter and the H94Y mutation in the x gene were found only in chronic patients showing its clear association with chronicity. 2015 PloS one Discussion HBV T1768A;C69X;C1766T;H94Y 71;15;63;122 77;22;69;126 BCP;S;X 94;45;143 113;52;144 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Interestingly, the frequency of the mutation G1896A in the pre-core region was relatively high among acute patients almost reaching to about half of the number found among chronic patients, thus revealing that this mutation is highly transmissible. 2015 PloS one Discussion HBV G1896A 45 51 Precore 59 67 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Moreover, we report that the highest difference in entropy was exhibited at positions A1762T and G1764A in the BCP region indicating that these two sites were most susceptible towards acquiring mutations, thus signifying that they were the strongest indicators of chronicity. 2015 PloS one Discussion HBV A1762T;G1764A 86;97 92;103 BCP 111 114 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. Notably, the M133I mutation was found in 2 acute isolates, but was missing from all chronic sequences indicating that this mutation might be a recent introduction into our population. 2015 PloS one Discussion HBV M133I 13 18 26571502 Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection. The M133I substitution in the major hydrophilic region of the surface gene is a known immune escape mutation. 2015 PloS one Discussion HBV M133I 4 9 S 62 69 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Clinically, the LAM-resistant viral mutations are rtL180M-rtM204V in HBV polymerase. 2014 Acta pharmaceutica Sinica. B Discussion HBV L180M;M204V 52;60 57;65 P;RT;RT 73;50;58 83;52;60 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. However, ETV remains potent on the model carrying triple mutations, which may be due to the enhancement of the viral replication caused by the third compensatory mutation rtV173L. 2014 Acta pharmaceutica Sinica. B Discussion HBV V173L 173 178 RT 171 173 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. In Delaney s observation, the rtL180M-rtM204V double mutations can reduce HBV replication in vitro compared with wild-type HBV, but the addition of rtV173L mutation to LAM-resistant HBV can increase HBV replication. 2014 Acta pharmaceutica Sinica. B Discussion HBV M204V;L180M;V173L 40;32;150 45;37;155 RT;RT;RT;S 30;38;148;11 32;40;150;12 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. In our experiment, rtL180M-rtM204V double mutations reduced HBV replication capacity in vivo compared with wild-type HBV. 2014 Acta pharmaceutica Sinica. B Discussion HBV L180M;M204V 21;29 26;34 RT;RT 19;27 21;29 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. In rtL180M-rtM204V double mutations HBV mouse model, low viral titer partially concealed the efficacy of ETV in serum, although ETV displayed efficacy in the liver. 2014 Acta pharmaceutica Sinica. B Discussion HBV M204V;L180M 13;5 18;10 RT;RT 3;11 5;13 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. Moreover, rtV173L was invariably found as a third compensatory mutation in conjunction with rtM204V and rtL180M in one of three patients who failed in lamivudine therapy, and it was not observed as a single change in chronic hepatitis B patients. 2014 Acta pharmaceutica Sinica. B Discussion HBV V173L;M204V;L180M 12;94;106 17;99;111 RT;RT;RT 10;92;104 12;94;106 Chronic Hepatitis B 217 236 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. rtM204V/I are primary resistance mutations which mapped in conserved YMDD motif within C domain of the viral RT and facilitate ongoing viral DNA synthesis in the presence of LAM. 2014 Acta pharmaceutica Sinica. B Discussion HBV M204V;M204I 2;2 9;9 RT;RT;P 0;109;69 2;111;73 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. The compensatory mutations include rtL180M and rtV173L within the B domain that restore viral fitness. 2014 Acta pharmaceutica Sinica. B Discussion HBV L180M;V173L 37;49 42;54 RT;RT 35;47 37;49 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. the replication of rtL180M-rtM204V-rtV173L triple mutant increased compared to wild-type HBV construct and double mutant in NOD/SCID mice. 2014 Acta pharmaceutica Sinica. B Discussion HBV M204V;L180M;V173L 29;21;37 34;26;42 RT;RT;RT 19;27;35 21;29;37 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. When treating with ETV, drug resistance arises less rapidly, amino acid substitutions compromise rtS202I, rtT184G and rtI169T, etc. 2014 Acta pharmaceutica Sinica. B Discussion HBV S202I;T184G;I169T 99;108;120 104;113;125 RT;RT;RT 97;106;118 99;108;120 26579395 Establishment of drug-resistant HBV small-animal models by hydrodynamic injection. When treating with LAM, drug resistance arises rapidly and amino acid substitutions compromise rtM204V/I, rtL180M and rtV173L, etc. 2014 Acta pharmaceutica Sinica. B Discussion HBV M204V;M204I;L180M;V173L 97;97;108;120 104;104;113;125 RT;RT;RT 95;106;118 97;108;120 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. From the analysis of the Malaysian HBV sequences, most isolates were found to confer C1858T mutation in the precore region. 2015 Hepatitis monthly Discussion HBV C1858T 85 91 Precore 108 115 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A mutation is located within the epsilon (epsilon) structure, a highly conserved stem-loop essential for the initiation of encapsidation during viral replication. 2015 Hepatitis monthly Discussion HBV G1896A 0 6 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. G1896A was thought to cause severe liver disease as it is frequently found in patients with chronic hepatitis B, liver cirrhosis and fulminant hepatitis. 2015 Hepatitis monthly Discussion HBV G1896A 0 6 Liver disease;Chronic Hepatitis B;Liver cirrhosis;Fulminant Hepatitis B 35;92;113;133 48;111;128;152 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Genotype predominance was not observed in subjects with C1858T mutation as it was equally distributed among HBV B and C genotypes and found in two of the D genotype. 2015 Hepatitis monthly Discussion HBV C1858T 56 62 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. However, heterozygous A1896 and G1896 peak observed in only one sequence direction may suggest the role of G1896A in triggering e-seroconversion. 2015 Hepatitis monthly Discussion HBV G1896A 107 113 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. However, our data suggested a significant association of G1896A with genotype B and patients with chronic hepatitis B and liver cirrhosis. 2015 Hepatitis monthly Discussion HBV G1896A 57 63 Chronic Hepatitis B;Liver cirrhosis 98;122 117;137 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. In accordance to the finding of this study, few other countries such as Indonesia, Vietnam and East Asia reported a significant association between genotype B and G1896A mutation. 2015 Hepatitis monthly Discussion HBV G1896A 163 169 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. In conclusion, the study findings showed an intermediate prevalence of G1896A mutation among Malaysian hepatitis B carriers. 2015 Hepatitis monthly Discussion HBV G1896A 71 77 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. In the present study, from 5 subjects with e-seroconversion, two conferred G1896A mutation. 2015 Hepatitis monthly Discussion HBV G1896A 75 81 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. No significant association was observed between G1896A mutations and its role in causing HBeAg-negativity. 2015 Hepatitis monthly Discussion HBV G1896A 48 54 C 89 94 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Our findings suggested that G1896A mutation was not significantly associated with HBeAg-negativity. 2015 Hepatitis monthly Discussion HBV G1896A 28 34 C 82 87 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Regarding the relation of G1896A mutation and clinical status of study subjects, it was observed that the stop codon mutation was significantly present in patients with asymptomatic chronic hepatitis B and liver cirrhosis. 2015 Hepatitis monthly Discussion HBV G1896A 26 32 Chronic Hepatitis B;Liver cirrhosis 182;206 201;221 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The basis behind genotype selectivity of G1896A mutant mainly points to the C1898T mutation, which is prominently present in genotypes B, D and E. 2015 Hepatitis monthly Discussion HBV G1896A;C1898T 41;76 47;82 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The G1896A mutation was more prevalent in HBV genotype B than genotype C in Malaysia. 2015 Hepatitis monthly Discussion HBV G1896A 4 10 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The mutation of interest G1896A was also present in HBV sequences. 2015 Hepatitis monthly Discussion HBV G1896A 25 31 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The present study also evidenced prominent prevalence of G1896A mutation among middle-aged adult group followed by older adult group and low prevalence in geriatric and pediatric groups. 2015 Hepatitis monthly Discussion HBV G1896A 57 63 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. The role of G1896A mutation in HBeAg-positive seroconversion has been reported. 2015 Hepatitis monthly Discussion HBV G1896A 12 18 C 31 36 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. There was one subject in the present study with fulminant hepatitis who had G1896A mutation. 2015 Hepatitis monthly Discussion HBV G1896A 76 82 Fulminant Hepatitis B 48 67 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. Therefore, development of G1896A mutation relies on the presence or absence of C or T at position 1858, which is genotype dependent. 2015 Hepatitis monthly Discussion HBV G1896A 26 32 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. These mutations include a change in DNA bases from guanine to adenine at position 1896 (G1896A), and from cytosine to thymine at position 1858 (C1858T) of the viral genome. 2015 Hepatitis monthly Discussion HBV G1896A;C1858T 88;144 94;150 26587040 G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B. When G1986A mutation is paired with C1858T, the epsilon structure is more stabilized, thus enhancing viral replication. 2015 Hepatitis monthly Discussion HBV G1986A;C1858T 5;36 11;42 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. determined three different S gene mutations (L109R, C137W, G145R) in a patient with occult hepatitis B, which led to false negative results for HBsAg but positive for HBsAb. 2015 Jundishapur journal of microbiology Discussion HBV L109R;C137W;G145R 45;52;59 50;57;64 S;S;S 167;144;27 172;149;28 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. have identified a deletion mutation in RNA splicing stage that delete nucleotides between positions 2986 and 202, which blocks 274 surface protein gene expression without affecting polymerase, core, and X-protein functions. 2015 Jundishapur journal of microbiology Discussion HBV del nt2986 63 104 C;P;S;X 193;181;131;203 197;191;138;204 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. In another study, Mu et al., reported that out of 46 HBsAg negative children, five children had OBI and a sequence analysis of the S region showed mutation in position C139S, which makes HBV vaccine inactive. 2015 Jundishapur journal of microbiology Discussion HBV C139S 168 173 S;S 53;131 58;132 Occult Hepatitis B 96 99 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. In our study, we detected a new substitution in position 153 (P153L), which can create escape mutant when placed in MHR. 2015 Jundishapur journal of microbiology Discussion HBV P153L 62 67 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. reported that out of 239 HBsAg negative patients, nine (3.8%) were HBV-DNA positive and seven of the nine (78%) showed mutations in the S region (G145R). 2015 Jundishapur journal of microbiology Discussion HBV G145R 146 151 S;S 25;136 30;137 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. reported that the T127R mutation is an escape mutant in the S region. 2015 Jundishapur journal of microbiology Discussion HBV T127R 18 23 S 60 61 26587212 Molecular Characterization of Pre-Core/Core and S Region of Hepatitis B Virus in Hemodialysis Patients With Occult Hepatitis B Infection. This result is similar to that reported by Sayan et al, who also reported a T to P substitution at position 127. 2015 Jundishapur journal of microbiology Discussion HBV T127P 76 111 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Additionally, once the rtM204I mutant prevailed over the rtA181T and wild-type viruses, we observed that VB developed quickly and that rtM204I predominated among the viral quasispecies, supporting the argument that the rtM204I mutant may have greater fitness than the rtA181T mutant under LdT treatment. 2015 Scientific reports Discussion HBV A181T;A181T;M204I;M204I;M204I 59;270;25;137;221 64;275;30;142;226 RT;RT;RT;RT;RT 23;57;135;219;268 25;59;137;221;270 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Although packaging-deficient rtA181T/sW172* mutant can dominate in viral populations during LAM or ADV treatment, our results showed that it always accounted for a minor proportion of the viral population during LdT treatment, thus suggesting that the composition of viral quasispecies may vary under the different selection pressures of various drugs. 2015 Scientific reports Discussion HBV W172X;A181T 37;31 43;36 RT;S 29;37 31;38 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Although we could not completely rule out the possibility that rtA181T and rtM204I simultaneously exist in the same genome due to the limited sequencing coverage in this study, our results indicated that most of the rtA181T and rtM204I mutants were derived from independent phylogenetic origins and therefore should be considered as two separate quasispecies. 2015 Scientific reports Discussion HBV A181T;A181T;M204I;M204I 65;218;77;230 70;223;82;235 RT;RT;RT;RT 63;75;216;228 65;77;218;230 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Among the 15 patients in this study who showed suboptimal virological responses and exhibited the rtA181T/sW172* quasispecies at week 12 or beyond, 7 of them eventually progressed to VB. 2015 Scientific reports Discussion HBV W172X;A181T 106;100 112;105 RT;S 98;106 100;107 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Because the rtA181T/sW172* mutant shows resistance to LdT, it is likely that rtA181T and wild-type viruses represented a complimentary pair of quasispecies that gained a certain extent of viral fitness and whose presence manifested as partial resistance to LdT. 2015 Scientific reports Discussion HBV W172X;A181T;A181T 20;14;79 26;19;84 RT;RT;S 12;77;20 14;79;21 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In conclusion, our in-depth analysis of rtA181T and rtM204I mutants suggests that patient virological responses to antiviral therapy are determined by the presence and composition of critical drug-resistant mutants at an early stage of treatment. 2015 Scientific reports Discussion HBV A181T;M204I 42;54 47;59 RT;RT 40;52 42;54 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In our study, both the rtM204I and rtA181T mutants were found at low frequencies (<1%) in some of the CVR, PVR and VB subjects at baseline (Supplementary Table S2). 2015 Scientific reports Discussion HBV A181T;M204I 37;25 42;30 RT;RT 23;35 25;37 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. In this regard, the rtM204I mutants, which carry both a drug-resistant RT enzyme and a functional S protein, clearly have superior fitness than either rtA181T/sW172* mutants or wild-type viruses in the presence of LdT. 2015 Scientific reports Discussion HBV W172X;A181T;M204I 159;153;22 165;158;27 RT;RT;RT;S;S 20;71;151;98;159 22;73;153;99;160 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Meanwhile, the rtA181T/sW172* mutants achieved evolutionary superiority by being functionally complementary with other quasispecies carrying the wild-type S gene (the quasispecies mutually share functional RT enzymes and S proteins). 2015 Scientific reports Discussion HBV W172X;A181T 23;17 29;22 RT;RT;S;S;S 15;206;23;155;221 17;208;24;156;222 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Our results showed that the rtA181T/sW172* mutant was present at time points after week 12 in most patients who showed a suboptimal response to LdT. 2015 Scientific reports Discussion HBV W172X;A181T 36;30 42;35 RT;S 28;36 30;37 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. Quasispecies with a functional drug-resistant RT enzyme and a defective S protein, such as rtA181T/sW172* mutants, may survive without requiring rescue from the defective S protein by additional mutations. 2015 Scientific reports Discussion HBV W172X;A181T 99;93 105;98 RT;RT;S;S;S 46;91;72;99;171 48;93;73;100;172 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. supporting the argument that synergistic growth of rtA181T/sW172* with the wild-type quasispecies may facilitate the development of VB. 2015 Scientific reports Discussion HBV W172X;A181T 59;53 65;58 RT;S 51;59 53;60 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. The independent origins of these two well-characterized drug-resistant mutants suggest that rtA181T and rtM204I double mutants may not possess a significantly greater evolutionary advantage than those carrying a single mutation. 2015 Scientific reports Discussion HBV A181T;M204I 94;106 99;111 RT;RT 92;104 94;106 26599443 Composition and Interactions of Hepatitis B Virus Quasispecies Defined the Virological Response During Telbivudine Therapy. We used a conservative cutoff of 1% to distinguish authentic mutations from sequencing errors; this cutoff may have also led to missing information about the rtA181T and rtM204I mutations if present at proportions less than 1%. 2015 Scientific reports Discussion HBV A181T;M204I 160;172 165;177 RT;RT 158;170 160;172 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. analyzed HBV sequences from 1236 CHB patients and found significantly higher frequency of rtA181T in HBV genotypes C isolates compared to genotypes D and A isolates (63.8% vs. 2015 Scientific reports Discussion HBV A181T 92 97 RT 90 92 Chronic Hepatitis B 33 36 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Another L-Nucleoside, LdT, shared some similar amino acid substitution in polymerase with LMV, namely rtM204I and rtL180M, which could increase the risk of cross-resistance. 2015 Scientific reports Discussion HBV M204I;L180M 104;116 109;121 P;RT;RT 74;102;114 84;104;116 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. But mutant rtL180M was more common in genotype C than genotype B again (63.7% vs. 2015 Scientific reports Discussion HBV L180M 13 18 RT 11 13 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. HBV mutation rtA181T/V and rtN236T could lead to drug resistance of ADV, and the influence of HBV genotypes on the resistance to ADV has not been clarified. 2015 Scientific reports Discussion HBV A181T;A181V;N236T 15;15;29 22;22;34 RT;RT 13;27 15;29 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. However, when analyzing rtL180M, a secondary mutation, genotype C showed a higher incidence than genotype B (54.7% vs. 2015 Scientific reports Discussion HBV L180M 26 31 RT 24 26 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. In 244 LdT-resistant patients from Sichuan Han population, HBV genotypes seemed not to be an important factor for the occurrence of antiviral resistance, with comparable prevalence of mutation sites rtM204I in genotype B and C (62.8% vs. 2015 Scientific reports Discussion HBV M204I 201 206 RT 199 201 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. In this study, we did not find any statistical difference in the frequency of rtM204V and rtM204I between genotype B and C (P = 0.119, P = 0.161, respectively) in LMV-resistant patients as well. 2015 Scientific reports Discussion HBV M204I;M204V 92;80 97;85 RT;RT 78;90 80;92 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. It was noteworthy that ADV-associated mutation rtA181T was considered as a cross-resistant mutation, which could induce resistance to LMV and LdT in patients never exposed to these antiviral drugs. 2015 Scientific reports Discussion HBV A181T 49 54 RT 47 49 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Patients infected with genotype C had a higher rate of mutant rtA181T/V and resistance to ADV than genotype B, while the incidence of resistant mutations to other NAs and clinical factors had no difference statistically among different genotypes. 2015 Scientific reports Discussion HBV A181T;A181V 64;64 71;71 RT 62 64 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. revealed that rtM204V was selected more frequently in genotype A patients compared to non-genotype A patients. 2015 Scientific reports Discussion HBV M204V 16 21 RT 14 16 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. The total frequency of rtA181T was higher in HBV genotype C isolates than genotype B isolates in Sichuan Hans (13.5% vs. 2015 Scientific reports Discussion HBV A181T 25 30 RT 23 25 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. which was supported by the higher rate of dual mutation rtL180M+rtM204I in genotype C. 2015 Scientific reports Discussion HBV L180M;M204I 58;66 63;71 RT;RT 56;64 58;66 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. while HBV genotype D strains had a higher rate of a combination of rtA181T/V and rtN236T than genotype B and C (53.9% vs. 2015 Scientific reports Discussion HBV A181T;A181V;N236T 69;69;83 76;76;88 RT;RT 67;81 69;83 26612031 Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China. Xinjiang Uygurs and Tibet Tibetans showed no incidence of rtA181T/V and rtN236T. 2015 Scientific reports Discussion HBV A181T;A181V;N236T 60;60;74 67;67;79 RT;RT 58;72 60;74 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. A previous study has shown that G1719T, A1726C, A1727T, T1753V and A1846T were associated with advanced liver diseases, indicating that other mutants other than A1762T/G1764A/G1896A should be took into account in evaluating the progressive liver diseases in the future. 2015 Scientific reports Discussion HBV G1896A;G1764A;G1719T;A1726C;A1727T;T1753V;A1846T;A1762T 175;168;32;40;48;56;67;161 181;174;38;46;54;62;73;167 Liver disease;Liver disease 104;240 118;254 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. In addition to BCP A1762T/G1764A and PC G1896A mutants, high prevalence of mutants were also observed at nt.1719, nt.1726, nt.1727, nt.1746, nt.1752, nt.1753, nt.1817, nt.1825 and nt.1846. 2015 Scientific reports Discussion HBV G1764A;A1762T;G1896A 26;19;40 32;25;46 BCP;Precore 15;37 18;39 26647737 Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients. Meanwhile, we found that A1762T, G1764A, G1719T and T1753V were significantly associated with genotype C, while A1726C and A1752G/T were genotype B related. 2015 Scientific reports Discussion HBV A1762T;G1764A;G1719T;T1753V;A1726C;A1752G;A1752T 25;33;41;52;112;123;123 31;39;47;58;118;131;131 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. Additionally, the present study revealed that YVDD-variant-dominated virological breakthrough was closely associated with the L180M mutation, and an identical trend in the changes of the M204V and L180M mutations was observed, which raised the question of the specific mechanism of rt204 and its supplementary sites. 2016 Molecular medicine reports Discussion HBV L180M;M204V;L180M 126;187;197 131;192;202 RT;P 282;46 284;50 26648309 Evaluation of the dynamic pattern of viral evolution in patients with virological breakthrough during treatment with nucleoside/nucleotide analogs by ultradeep pyrosequencing. The present study also revealed that the NUC-associated mutations existed in treatment naive patients, for example, patient D, who exhibited a high mutation rate of M204I at the baseline. 2016 Molecular medicine reports Discussion HBV M204I 165 170 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Importantly, we identified in our survey three natural M204V/I mutations in 3TC-naive patients, as already described in other settings. 2016 PloS one Discussion HBV M204V;M204I 55;55 62;62 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. Third, the M204V/I RAM were more common in HBV/A strains. 2016 PloS one Discussion HBV M204V;M204I 11;11 18;18 26764909 Broad Range of Hepatitis B Virus (HBV) Patterns, Dual Circulation of Quasi-Subgenotype A3 and HBV/E and Heterogeneous HBV Mutations in HIV-Positive Patients in Gabon. When considering HBV/A genotypes only, we observed a high (~50%) prevalence of M204V/I and L180M mutations. 2016 PloS one Discussion HBV M204V;M204I;L180M 79;79;91 86;86;96 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. At baseline, patient 1 harbored rtL180 M (2.09%), rtS202G (3.42%), and rtM204 V (3.45%) mutations, the frequencies of which rose to 19.12%, 18.33%, and 19.95%, respectively, after 1 year of treatment, but these changes did not cause virological breakthrough. 2016 Medicine Discussion HBV L180M;S202G;M204V 34;52;73 40;57;79 RT;RT;RT 32;50;71 34;52;73 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In addition to known NAr mutations, several novel mutations were identified, including rtN248H, rtS223A, rtS256C, and rtI224 V; whether these mutations are associated with curative effects remains to be further verified as well. 2016 Medicine Discussion HBV I224V;N248H;S223A;S256C 120;89;98;107 126;94;103;112 RT;RT;RT;RT 87;96;105;118 89;98;107;120 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In patient 5, when the resistant variants (rtL180 M, rtM204 V, rtS202G) began to rise to a high peak (84.60%, 79.56%, 76.88%) at 2 years, virological breakthrough occurred. 2016 Medicine Discussion HBV L180M;M204V;S202G 45;55;65 51;61;70 RT;RT;RT 43;53;63 45;55;65 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. In the present study, 7 patients harbored the rtL180 M, rtS202G, and rtM204I/V substitutions at a frequency of >1% at baseline, 5 of these patients belonged to the PVR group, and the other 2 belonged to the CVR group. 2016 Medicine Discussion HBV M204I;M204V;L180M;S202G 71;71;48;58 78;78;54;63 RT;RT;RT 46;56;69 48;58;71 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. One study reported that the most commonly detected mutations were M204 V/I, M250 V/I, A181T/V, and N236T. 2016 Medicine Discussion HBV M204V;M204I;M250V;M250I;A181T;A181V;N236T 66;66;76;76;86;86;99 74;74;84;84;93;93;104 26825915 Dynamics of Genotypic Mutations of the Hepatitis B Virus Associated With Long-Term Entecavir Treatment Determined With Ultradeep Pyrosequencing: A Retrospective Observational Study. UDPS indicated that NAr mutations were pre-existent at low percentages (ranging from 0.1% to 6.7%) at baseline, including rtV173A/M, rtL180 M, rtA181 V/T, rtS202G, rtM204I/V, rtV214A, rtQ215R/H, and rtN236T mutations. 2016 Medicine Discussion HBV V173A;V173M;A181V;A181T;M204I;M204V;Q215R;Q215H;L180M;S202G;V214A;N236T 124;124;145;145;166;166;186;186;135;157;177;201 131;131;153;153;173;173;193;193;141;162;182;206 RT;RT;RT;RT;RT;RT;RT;RT 122;133;143;155;164;175;184;199 124;135;145;157;166;177;186;201 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. A recent study reported that drug susceptibility of HBV rtA181V/T mutants was different, and the difference might be explained by a difference in HBV genotypes. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 58;58 65;65 RT 56 58 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. After rescue therapy for rtA181V/T mutants alone, newly developed mutants or disappearance of HBV rtA181V/T mutants were not evaluated in total. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T;A181V;A181T 27;27;100;100 34;34;107;107 RT;RT 25;98 27;100 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. As a result, the antiviral efficacy of ETV or ETV plus ADV as rescue therapy for HBV rtA181V/T mutants may be related to the genotypes of HBV. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 87;87 94;94 RT 85 87 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. As a result, the standard of care for HBV rtA181V/T mutants has not been established and clinical evidence of optimal treatment for HBV rtA181V/T mutants is also lacking. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T;A181V;A181T 44;44;138;138 51;51;145;145 RT;RT 42;136 44;138 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. As a substitute of ADV, antiviral efficacy of TDF for HBV rtA181V/T mutants is still unclear in practice. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 60;60 67;67 RT 58 60 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Clinical researches for rescue therapy for HBV rtA181V/T mutants should be performed considering the discrepancy in genotypes of HBV. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 49;49 56;56 RT 47 49 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Cross-resistance of HBV, including HBV rtA181V/T mutants, can result in development of serious liver-related diseases such as hepatic failure or progression to liver disease. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 41;41 48;48 RT 39 41 Liver disease;Liver disease;Liver disease 126;160;95 141;173;117 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. ETV alone was administered as rescue therapy for the HBV rtA181V mutant. 2016 Saudi journal of gastroenterology Discussion HBV A181V 59 64 RT 57 59 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Further investigation of rescue therapy, including TDF, for HBV rtA181V/T mutants alone will be necessary. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 66;66 73;73 RT 64 66 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. HBV rtA181V/T mutants are more important in practice because a single mutation can confer multidrug resistance against the L-nucleoside LMV, CLV, and LdT, as well as the alkyl phosphonates ADV and TDF. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 6;6 13;13 RT 4 6 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. In this study, all therapeutic responses of HBV rtA181V/T mutants alone, including decline of serum HBV DNA, virological, biochemical, and serological responses did not differ significantly between the ETV monotherapy group and the ETV plus ADV group (P > 0.05). 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 50;50 57;57 RT 48 50 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Newly developed HBV rtM204I and rtP237H mutants were detected, and the pre-existing HBV rtA181V mutant disappeared completely through rescue therapy. 2016 Saudi journal of gastroenterology Discussion HBV A181V;M204I;P237H 90;22;34 95;27;39 RT;RT;RT 20;32;88 22;34;90 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. The appearance of mutations other than HBV rtA181V/T mutants in this case may be associated with sequential antiviral monotherapy, as mentioned above, and is a problem to be solved before agreement on use of ETV monotherapy for HBV rtA181V/T mutants. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T;A181V;A181T 45;45;234;234 52;52;241;241 RT;RT 43;232 45;234 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. The patient had received CLV therapy prior to detection of the HBV rtA181V mutant. 2016 Saudi journal of gastroenterology Discussion HBV A181V 69 74 RT 67 69 26831605 Antiviral efficacy of entecavir versus entecavir plus adefovir for hepatitis B virus rtA181V/T mutants alone. Thus, to the best of our knowledge, this research appears to be valuable as it provides rare clinical evidence of treatment of HBV rtA181V/T mutants alone. 2016 Saudi journal of gastroenterology Discussion HBV A181V;A181T 133;133 140;140 RT 131 133 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. A previous report showed that HBeAg titers are closely correlated with BCP mutation, and HBeAg-positive patients of genotype C infection had a higher prevalence of the A1762T/G1764A mutations. 2016 Oncotarget Discussion HBV G1764A;A1762T 175;168 181;174 BCP;C;C 71;30;89 74;35;94 HBV infections 116 136 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Additionally, we performed a subgroup analysis that revealed no statistically significant difference in terms of the frequency of A1762T/G1764A dual mutations in liver cirrhotic HCC and non-cirrhotic HCC patients. 2016 Oncotarget Discussion HBV G1764A;A1762T 137;130 143;136 Liver cirrhosis;Liver cirrhosis;Liver cirrhosis 162;168;190 181;177;199 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. As the disease progressed, the risk of the A1762T/G1764A dual mutation in ASC, CHB, LC and HCC patients increased. 2016 Oncotarget Discussion HBV G1764A;A1762T 50;43 56;49 Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 79;91;84 82;94;86 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Based on our results, we could conclude that BCP A1762T/G1764A dual mutations are associated with disease progression and HCC occurrence in chronic HBV-infected patients. 2016 Oncotarget Discussion HBV G1764A;A1762T 56;49 62;55 BCP 45 48 Hepatocellular carcinoma;HBV infections 122;148 125;160 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Considered the frequency ratio of A1762T/G1764A dual mutation from ASC, CHB, LC and HCC, we suggested that BCP dual mutation should be screened in the CHB and LC patients. 2016 Oncotarget Discussion HBV G1764A;A1762T 41;34 47;40 BCP 107 110 Hepatocellular carcinoma;Chronic Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Liver cirrhosis 84;151;72;77;159 87;154;75;79;161 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. However, the BCP A1762T/G1764A dual mutation is increasingly more prevalent as chronic HBV infection progresses from the asymptomatic HBsAg carrier state to liver cirrhosis or HCC, indicating that these mutations accumulate before the diagnosis of HCC. 2016 Oncotarget Discussion HBV G1764A;A1762T 24;17 30;23 BCP;S 13;134 16;139 Chronic HBV infection;Liver cirrhosis;Hepatocellular carcinoma;Hepatocellular carcinoma 79;157;176;248 100;172;179;251 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. However, this analysis found no significance of BCP A1762T/G1764A mutations from HBeAg-positive and HBeAg-negative chronic HBV-infected patients. 2016 Oncotarget Discussion HBV G1764A;A1762T 59;52 65;58 BCP;C;C 48;81;100 51;86;105 HBV infections 123 135 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In HCC, patients with HBV genotype C suffered higher A1762T/G1764A dual mutations compared with those with genotype B. 2016 Oncotarget Discussion HBV G1764A;A1762T 60;53 66;59 Hepatocellular carcinoma 3 6 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. In this research, we found that chronic HBV-infected patients with genotype B had a significantly lower risk of A1762T/G1764A dual mutations compared with those with genotype C. 2016 Oncotarget Discussion HBV G1764A;A1762T 119;112 125;118 HBV infections 40 52 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. It has been suggested that the A1762T/G1764A double mutation in the BCP region can reduce the synthesis of HBeAg and enhance viral replication. 2016 Oncotarget Discussion HBV G1764A;A1762T 38;31 44;37 BCP;C 68;107 71;112 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Our meta-analysis showed that the A1762T/G1764A dual mutation was present at statistically significantly higher frequencies in HCC patients than in non-HCC controls, including LC, CHB and ASC patients. 2016 Oncotarget Discussion HBV G1764A;A1762T 41;34 47;40 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma;Liver cirrhosis 127;180;152;176 130;183;155;178 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. The most common naturally occurring mutations in the BCP A1762T/G1764A dual mutation has been associated with hepatocarcinogenesis, but conflicts still exist. 2016 Oncotarget Discussion HBV G1764A;A1762T 64;57 70;63 BCP 53 56 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Therefore, we hypothesized that A1762T/G1764A dual mutation might play a vital role in promoting disease progression in chronic HBV infection. 2016 Oncotarget Discussion HBV G1764A;A1762T 39;32 45;38 Chronic HBV infection 120 141 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Thus, we assumed that BCP A1762T/G1764A dual mutations might promote hepatocarcinogenesis even without progression to cirrhosis. 2016 Oncotarget Discussion HBV G1764A;A1762T 33;26 39;32 BCP 22 25 Liver cirrhosis 118 127 26848866 Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis. Transfection studies have shown that the T1762A/G1764A dual mutations decrease the level of pre-C mRNA by 50% to 70%, thereby inhibiting HBeAg production. 2016 Oncotarget Discussion HBV G1764A;T1762A 48;41 54;47 C;Precore 137;92 142;97 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. A clonal analysis of the virological breakthrough samples further revealed that rtT184F or rtS202G were linked with rtL180M and rtM204V and co-localized in the same viral strain. 2016 Experimental and therapeutic medicine Discussion HBV T184F;S202G;L180M;M204V 82;93;118;130 87;98;123;135 RT;RT;RT;RT 80;91;116;128 82;93;118;130 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. At month 24, a new resistant strain that carried all three mutations (rtM204V, rtL180M and rtT184F) emerged, which was accompanied by a virological breakthrough. 2016 Experimental and therapeutic medicine Discussion HBV M204V;L180M;T184F 72;81;93 77;86;98 RT;RT;RT 70;79;91 72;81;93 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. At month 24, the resistant variants rtM204V, rtL180M and rtS202G co-existed in the viral population and were co-localized in the same viral strain, while virological breakthrough occurred 6 months later, at month 30 of the therapy. 2016 Experimental and therapeutic medicine Discussion HBV S202G;M204V;L180M 59;38;47 64;43;52 RT;RT;RT 36;45;57 38;47;59 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. Furthermore, with prolonged treatment, whether the ADV-resistant variant (rtA181V/T or rtN236T) will be selected and linked with the ETV-resistant strain warrants additional investigation. 2016 Experimental and therapeutic medicine Discussion HBV A181V;A181T;N236T 76;76;89 83;83;94 RT;RT 74;87 76;89 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. However, the LAM-resistant variant, rtM204I, was detected after an 18-month period of ETV therapy, which is consistent with previous studies that observed that ETV-resistant variants preceded by LAM-resistant variants. 2016 Experimental and therapeutic medicine Discussion HBV M204I 38 43 RT 36 38 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. In patient B, the baseline sample contained the rtL180M and rtM204I/V variants. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204V;L180M 62;62;50 69;69;55 RT;RT 48;60 50;62 26889227 Evolution of entecavir-resistant hepatitis B virus during entecavir and adefovir dipivoxil combination therapy. The present results were inconsistent with a previous report, which indicated that a new resistant variant, rtS202G, emerged within the backgrounds of rtM204V and rtL180M, and was accompanied by virological breakthrough. 2016 Experimental and therapeutic medicine Discussion HBV S202G;M204V;L180M 110;153;165 115;158;170 RT;RT;RT 108;151;163 110;153;165 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. Although our phylogenetic analysis demonstrated that all viral strains in Saudi Arabia are members of genotype D [Figure 1], none of these strains showed the existence of G145R mutation. 2016 Saudi journal of gastroenterology Discussion HBV G145R 171 176 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. Another mutation with significant outcome on the protein level involves the change of the amino acid tryptophan into a stop codon at residue 111 within MHR of Riyadh 96/2012 strain. 2016 Saudi journal of gastroenterology Discussion HBV W111X 101 144 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. Conversely, a unique amino acid change F135S was identified in the 'a' determinant of Riyadh 108/2013 strain. 2016 Saudi journal of gastroenterology Discussion HBV F135S 39 44 S 68 82 26997220 Surface gene variants of hepatitis B Virus in Saudi Patients. The most stable and frequent amino acid change in HBsAg worldwide is G145R. 2016 Saudi journal of gastroenterology Discussion HBV G145R 69 74 S 50 55 27006468 C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties. As compared to the control, HBx-Delta14 or HBx-Delta35 resulted in a significant increase of the cells ability to self-renew, resist chemotherapy (5-FU) and the only targeted therapy approved for treatment of HCC (sorafenib), migrate and induce tube formation in endothelial cells. 2016 Oncotarget Discussion HBV del 35 47 54 X;X 28;43 31;46 Hepatocellular carcinoma 209 212 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. A1762T, G1764A, and T1753C/A mutations in the BCP region, and G1613A and C1653T mutations in the Enh II region were reported more frequent in HCC patients 27. 2016 Cancer medicine Discussion HBV T1753A;A1762T;G1764A;T1753C;G1613A;C1653T 20;0;8;20;62;73 28;6;14;28;68;79 BCP;Enh II 46;97 49;103 Hepatocellular carcinoma 142 145 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. Our previous study had also found several novel HBV mutations associated with HBV-related HCC, including A1752G, G1915A/C, and C1969T 20. 2016 Cancer medicine Discussion HBV G1915C;A1752G;G1915A;C1969T 113;105;113;127 121;111;121;133 Hepatocellular carcinoma 90 93 27075395 Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma. They found that the interactions of rs9277535 AA with the T1674C/G or G1719T mutation in genotype C significantly decreased HCC risk 28. 2016 Cancer medicine Discussion HBV T1674C;T1674G;G1719T 58;58;70 66;66;76 Hepatocellular carcinoma 124 127 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. Although there were differences in genotype, the dominant pattern of resistance among treatment-experienced patients with mutated strains, (rtM204V + rtL180M), was similar between the European multi-center study (29%) and the present study in Ghana (47.6%). 2017 Antiviral therapy Discussion HBV M204V;L180M 142;152 147;157 RT;RT 140;150 142;152 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. In our study, twenty (95.2%) of the 21 patients had at least one mutation that may confer clinical resistance to both telbivudine (rtM204V/I) and 3TC (rt180M + rtM204V/I, rtV173L + rtL180M + rtM204V/I, and rtL80I + rtM204I). 2017 Antiviral therapy Discussion HBV M204V;M204I;M204V;M204I;M204V;M204I;L80I;V173L;L180M;M204I 133;133;162;162;193;193;208;173;183;217 140;140;169;169;200;200;212;178;188;222 RT;RT;RT;RT;RT;RT;RT;RT 131;151;160;171;181;191;206;215 133;153;162;173;183;193;208;217 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. The 3TC mutations rtL80I, rtV173L, rtL180M, rtM204V, and/or rtM204I were observed in 21 patients. 2017 Antiviral therapy Discussion HBV L80I;V173L;L180M;M204V;M204I 20;28;37;46;62 24;33;42;51;67 RT;RT;RT;RT;RT 18;26;35;44;60 20;28;37;46;62 27167598 HBV genotypes and drug resistance mutations in antiretroviral treatment-naive and treatment-experienced HBV-HIV-coinfected patients. The 3TC mutations rtV173L, rtL180M, and rtM204V were observed in 3 patients, although ART information was not reported. 2017 Antiviral therapy Discussion HBV V173L;L180M;M204V 20;29;42 25;34;47 RT;RT;RT 18;27;40 20;29;42 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. In this study, sG145R was mainly detected in combination with other mutations in the MHR, including sI/T126V, sQ129N, and the s115-116 "INGTST" insertion. 2016 PloS one Discussion HBV T126V;G145R;I126V;Q129N 101;15;100;110 108;21;108;116 S;S;S;S 15;100;110;126 16;101;111;127 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. Our results showed that the sG145R mutation had little effect on the binding of anti-HBs to HBsAg (Fig 4) or intracellular replicative intermediate levels (Fig 3A), but significantly decreased supernatant HBV DNA levels (Fig 3B). 2016 PloS one Discussion HBV G145R 28 34 S;S;S 85;92;28 88;97;29 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. Our study verified that sQ129N and s131-133TSM NST significantly attenuated binding of anti-HBs to HBsAg, but that the s126-127 "RPCMNCTI" insertion, which also introduced an additional N-glycosylation site, had much weaker influence. 2016 PloS one Discussion HBV Q129N 24 30 S;S;S;S;S 92;99;24;35;119 95;104;25;36;120 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. Regarding the mechanism, some studies have suggested that the sG145R mutation reduces the antigenicity of HBsAg, while other studies have suggested that this mutation impairs the capacity for HBsAg or viral particles to be secreted. 2016 PloS one Discussion HBV G145R 62 68 S;S;S 106;192;62 111;197;63 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. sG145R has been reported as a classical immune escape mutation in the "a" determinant. 2016 PloS one Discussion HBV G145R 0 6 S 0 1 27182775 Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection. The 13 novel OBI-related preS/S-gene mutations were only detected in this patient, although the sQ129N, s131-133TSM NST, and sG145R mutations were detected in one, three, and one, respectively, of the other 34 subjects. 2016 PloS one Discussion HBV Q129N;G145R 96;125 102;131 PreS;S;S;S;S 25;30;96;104;125 29;31;97;105;126 Occult Hepatitis B 13 16 27226799 The Association of Pre-S/S Gene Mutations and Hepatitis B Virus Vertical Transmission. Studies have reported that ntA826G and ntC667T are associated with antiviral drug resistance, which can result in immune escape. 2016 Hepatitis monthly Discussion HBV A826G;C667T 28;40 34;46 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. A previous study reported that LAM-resistant variants, rtM204I/V and rtL180 M, were suppressed, but ADV-resistant variant rtA181 V/T emerged after 13-19 months of LAM-ADV sequential monotherapy. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204V;A181V;A181T;L180M 57;57;124;124;71 64;64;132;132;77 RT;RT;RT 55;69;122 57;71;124 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. ADV suppression of LAM-resistant variants, mainly due to rtL180 M and rtM204I/M, does not significantly affect sensitivity to ADV. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204M;L180M 72;72;59 79;79;65 RT;RT 57;70 59;72 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. However, LAM-resistant rtL180 M and rtM204I/V remained predominant during the 30-41 months of ADV-ETV combination therapy. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204V;L180M 38;38;25 45;45;31 RT;RT 23;36 25;38 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In the present study, regardless of the presence of LAM-resistant variants, it was observed that the replication of ADV-resistant variants rtA181 V and/or rtN236T was inhibited after 11-24 months of ADV-ETV combination therapy. 2016 Experimental and therapeutic medicine Discussion HBV A181V;N236T 141;157 147;162 RT;RT 139;155 141;157 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. In the present study, the data demonstrated that LAM-resistant variants rtL180 M and rtM204I/M were suppressed, whereas ADV-resistant variant rtA181 V/T or rtN236T was increased in patients with LAM resistance during 19-30 months of ADV sequential monotherapy. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204M;A181V;A181T;N236T;L180M 87;87;144;144;158;74 94;94;152;152;163;80 RT;RT;RT;RT 72;85;142;156 74;87;144;158 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. It should be noted that, even when the viral load decreases following the addition of ETV to ongoing ADV therapy, LAM-resistant variants rtL180 M and rtM204I/V persist after 30-41 months of ADV-ETV combination therapy. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204V;L180M 152;152;139 159;159;145 RT;RT 137;150 139;152 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. Second, persistence of LAM-resistant variants rtL180 M and rtM204 V increases the risk of ETV resistance, and therefore a more potent antiviral regimen, such as TDF-ETV combination therapy, may be considered in these rare cases. 2016 Experimental and therapeutic medicine Discussion HBV L180M;M204V 48;61 54;67 RT;RT 46;59 48;61 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. The results of the present study demonstrated that replication of ADV-resistant variants, rtA181T/V and rtN236T, was inhibited by combination therapy with ADV-ETV, whereas LAM-resistant rtL180 M and rtM204I/V were persistent during 30-41 months of combination therapy. 2016 Experimental and therapeutic medicine Discussion HBV A181T;A181V;M204I;M204V;N236T;L180M 92;92;201;201;106;188 99;99;208;208;111;194 RT;RT;RT;RT 90;104;186;199 92;106;188;201 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. These results may be attributed to an ADV-resistant variant, rtA181 V/T, which is responsible for cross-resistance to LAM and ADV. 2016 Experimental and therapeutic medicine Discussion HBV A181V;A181T 63;63 71;71 RT 61 63 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. These results were concordant with earlier findings from a previous study that determined that LAM-resistant variants (rtM204I/V and rtL180 M) decreased whereas ADV-resistant variants gradually increased during ADV monotherapy. 2016 Experimental and therapeutic medicine Discussion HBV M204I;M204V;L180M 121;121;135 128;128;141 RT;RT 119;133 121;135 27313669 Lamivudine-resistant rtL180M and rtM204I/V are persistently dominant during combination rescue therapy with entecavir and adefovir for hepatitis B. This result may be predictable as rtM204 V results in partial cross resistance to LAM and ETV. 2016 Experimental and therapeutic medicine Discussion HBV M204V 36 42 RT 34 36 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. A previous study reported that two core promoter mutations in the HBV BCP (C1768T and T1770A) resulted in enhanced viral encapsidation and replication.32 The A1762T and G1764A double mutation (TA mutation) has been reported to prevent the binding of liver-enriched factor to the BCP region, thus inhibiting precore RNA transcription and HBeAg secretion.13, 33, 34 Hussain et al. 2016 Cancer science Discussion HBV C1768T;T1770A;A1762T;G1764A 75;86;158;169 81;92;164;175 BCP;BCP;Core promoter;C;Precore 70;279;35;337;307 73;282;48;342;314 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. Our findings were consistent with two previous studies reporting that no tumor-specific hot-spot mutations, including the A1762T and G1764A double mutation, were found selectively in tumor tissues.40, 42 This similar frequency of HBx point mutations in tumor and non-tumor tissues indicates that different HBV variants derived from tumor and non-tumor pairs might have evolved from the same ancestor viral strain.43 Furthermore, progressive accumulation of naturally occurring viral mutants, especially the A1762T/G1764A double mutation accompanied by T1753A/T1768A point mutations, occurred only at or near the stage of HCC, indicating that the mutation combination plays a synergistic role in enhancing HBV carcinogenesis.5 Another possibility, however, is that activation of the Wnt/beta-catenin pathway might play an essential role in the early stage of malignant transformation but not in the late stage of HCC carcinogenesis. 2016 Cancer science Discussion HBV G1764A;T1768A;A1762T;G1764A;A1762T;T1753A 514;559;122;133;507;552 520;565;128;139;513;558 X 230 233 Hepatocellular carcinoma 621 624 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. substitutions (I127N/K130M/V131I/F132Y) that may lead to aberrant biological activity of HBx. 2016 Cancer science Discussion HBV K130M;V131I;F132Y;I127N 21;27;33;15 26;32;38;20 X 89 92 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. The TA double mutations always accompanied the T1753V or T1768A point mutations. 2016 Cancer science Discussion HBV T1753V;T1768A 47;57 53;63 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. Their results indicated that the A1762T and G1764A double mutation in the BCP, but not in the overlapping X gene, is responsible for the enhanced viral genome replication observed for BCP mutants.35 . 2016 Cancer science Discussion HBV A1762T;G1764A 33;44 39;50 BCP;BCP;X 74;184;106 77;187;107 27420729 HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway. Their results indicated that the A1762T and G1764A double mutation in the BCP, but not in the overlapping X gene, is responsible for the enhanced viral genome replication observed for BCP mutants.35. 2016 Cancer science Discussion HBV A1762T;G1764A 33;44 39;50 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. Again as regards the pre-S2 region in OBI, we detected the mutation P41H in the HCC tissue of 3 of the 6 patients with OBI investigated in the present study. 2016 Oncotarget Discussion HBV P41H 68 72 PreS2 21 27 Hepatocellular carcinoma;Occult Hepatitis B;Occult Hepatitis B 80;38;119 83;41;122 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. As regards the S region in OBI, we found the Q129H mutation in two HCC tissues and in one non-neoplastic liver tissue, a mutation located within the "a" determinant of HBsAg, already described as an escape mutation but never associated with hepatic carcinogenesis. 2016 Oncotarget Discussion HBV Q129H 45 50 S;S 168;15 173;16 Hepatocellular carcinoma;Liver disease;Occult Hepatitis B 67;241;27 70;263;30 27486882 Occult HBV infection in HCC and cirrhotic tissue of HBsAg-negative patients: a virological and clinical study. In accordance with this, we found an L54P AA mutation in the pre-S1 region in the HCC liver tissue of one of the 3 patients with OBI investigated for both HCC tissue and non-HCC liver tissue. 2016 Oncotarget Discussion HBV L54P 37 41 PreS1 61 67 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma;Occult Hepatitis B 82;155;174;129 85;158;177;132 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. It is interesting to note that mutants L180M and M204I that were detected during LAM and ADV breakthrough showed a high prevalence in the LAM-only group (25 and 50%, respectively), followed by a low frequency in the ADV-only group (9.9 and 23%, respectively), whereas they showed a very high frequency in group III in which the patients received ADV after LAM breakthrough (43.75 and 68.75%, respectively). 2016 Electronic physician Discussion HBV M204I;L180M 49;39 54;44 27504160 Mutational analysis of reverse transcriptase and surface proteins of patients with partial virological response during mono and combination antiviral therapies in genotype D chronic hepatitis B. Studies showed that the failure of therapy due to M204I/V could be related to the upstream substitutions in domains A and B. 2016 Electronic physician Discussion HBV M204V;M204I 50;50 57;57 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Although the lamivudine-induced rtM204I/V mutation might occur in any genotype, the compensatory mutations are not consistent in different genotypes. 2016 SpringerPlus Discussion HBV M204I;M204V 34;34 41;41 RT 32 34 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. Because the 3D structural modeling has shown that rt180 in the rt173-189 helix is close enough to interact with rtM204 of the YMDD loop (Allen et al.), the rtL180M is ever regarded as the rational explanation to the compensatory mutation. 2016 SpringerPlus Discussion HBV L180M 158 163 RT;RT;RT;RT;P 50;63;112;156;126 52;65;114;158;130 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. But here we provide new evidence that rtL180M hardly exists in rtM204I of genotype B and C, it means the rtL180M is not a unique key site to remain 3D structural balance, and other covariance also could contribute to the structural and functional stability of the RT. 2016 SpringerPlus Discussion HBV M204I;L180M;L180M 65;40;107 70;45;112 RT;RT;RT;RT 38;63;105;264 40;65;107;266 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. By the naive Bayes classification algorithm and the complete induction method based on the comparative sequence analysis, this study presents more detailed subsequent mutations followed with the lamivudine-induced rtM204I/V mutation. 2016 SpringerPlus Discussion HBV M204I;M204V 216;216 223;223 RT 214 216 27588233 Compensatory variances of drug-induced hepatitis B virus YMDD mutations. For instance, the previous studies reported a high incidence rate of rtL180M followed by YMDD variance, here we deeply figure out that the rtL180M is generally followed by rtM204V, but it is less followed by rtM204I in genotype C, and rare rtL180M by rtM204I in genotype B. 2016 SpringerPlus Discussion HBV L180M;M204I;L180M;M204V;L180M;M204I 71;210;141;174;242;253 76;215;146;179;247;258 RT;RT;RT;RT;RT;RT;P 69;139;172;208;240;251;89 71;141;174;210;242;253;93 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. According to the results of the high-sensitivity UDPS analysis, two resistance-associated variants (rtA181V/T, rtN236T) were detected at low prevalence in all treatment-naive patients (ranging from 1.1% to 6.1%). 2016 Oncotarget Discussion HBV A181V;A181T;N236T 102;102;113 109;109;118 RT;RT 100;111 102;113 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. After a long-term follow-up study, we did not detect the emergency of TDF-resistance-associated variants (rtA194T, rtP177G, and rtF249A), suggesting that this study will provide the basis for changing to a different medication in clinical trials. 2016 Oncotarget Discussion HBV A194T;P177G;F249A 108;117;130 113;122;135 RT;RT;RT 106;115;128 108;117;130 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. During treatment, the frequency of the rtA181T resistance sites increased in six of the eight patients (NOs. 2016 Oncotarget Discussion HBV A181T 41 46 RT 39 41 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In addition to the common substitutions, some unknown amino acid substitutions, such as rtD134N, rtL145M/S, rtF151Y/L, rtR153Q, rtS223A, rtI224V, and rtN248H, need to be further verified. 2016 Oncotarget Discussion HBV D134N;L145M;L145S;F151Y;F151L;N248H;R153Q;S223A;I224V 90;99;99;110;110;152;121;130;139 95;106;106;117;117;157;126;135;144 RT;RT;RT;RT;RT;RT;RT 88;97;108;119;128;137;150 90;99;110;121;130;139;152 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. In one article, the most commonly detected mutations were M204V/I(9/14) and M250V/I(11/14); other documented mutations include A181T/V(7/14) and N236T(3/14). 2016 Oncotarget Discussion HBV M204V;M204I;M250V;M250I;A181T;A181V;N236T 58;58;76;76;127;127;145 65;65;83;83;134;134;150 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. in whom the rate of rtA181T resistance was increasing showed high levels of rtN236T. 2016 Oncotarget Discussion HBV A181T;N236T 22;78 27;83 RT;RT 20;76 22;78 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. The virus communities in patients 1 and 2 harbored the A181T/V(4.7%/4.7%), N236T(6%/5.7%), L180M(2.4%/12.5%) and M204I/V(3.4%/7%), while those in patients 3 and 4 harbored only the A181T/V(1.4%/1.2%), and N236T(1.8%/1.4%). 2016 Oncotarget Discussion HBV A181T;A181V;N236T;L180M;M204I;M204V;A181T;A181V;N236T 55;55;75;91;113;113;181;181;205 62;62;80;96;120;120;188;188;210 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. They harbor the A181T/V(1.2%/8.7%) and N236T(1.8%/1.7%) substitutions; that of patient 6 harbored the L180M(10.5%) and M204I/V(7.5%), which are associated with resistance to LAM. 2016 Oncotarget Discussion HBV A181T;A181V;N236T;L180M;M204I;M204V 16;16;39;102;119;119 23;23;44;107;126;126 27602500 Pre-existing mutations related to tenofovir in chronic hepatitis B patients with long-term nucleos(t)ide analogue drugs treatment by ultra-deep pyrosequencing. This research demonstrates that the rtA181T mutation can cause drug resistance and increase viral replication, which are mainly dependent on the mutations in the overlapping surface gene. 2016 Oncotarget Discussion HBV A181T 38 43 RT;S 36;174 38;181 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. All these results indicate that the antigenic loops in the G145R mutant are not as exposed as those in the wild-type HBsAg, and it can reduce its availability to specific HBsAg antibodies, which may explain the lower immunogenic potential of the G145R mutant protein. 2016 Hepatitis monthly Discussion HBV G145R;G145R 59;246 64;251 S;S 117;171 122;176 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. An antigenic potential analysis of the wild-type HBsAg and the G145R mutant revealed a significant decrease of antigenicity in the mutant type. 2016 Hepatitis monthly Discussion HBV G145R 63 68 S 49 54 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Furthermore, an analysis of Rg demonstrated that the atoms of the G145R mutant were highly packed within the protein structure, resulting in increased protein stability. 2016 Hepatitis monthly Discussion HBV G145R 66 71 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. In conclusion, this study provides some in silico evidence about the impacts of the G145R mutation on the structure and immunogenic activity of the HBsAg. 2016 Hepatitis monthly Discussion HBV G145R 84 89 S 148 153 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. In contrast with the wild-type HBsAg, the RMSD of the coordinates of all Calpha atoms in the G145R mutant demonstrated that the HBsAg mutant remained very stable and folded over the course of 10 ns at 300 K. 2016 Hepatitis monthly Discussion HBV G145R 93 98 S;S 31;128 36;133 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. In this study, we found that the secondary structure of the G145R HBsAg was significantly affected, with a gain of a beta-strand as well as the loss of alpha-helix contents. 2016 Hepatitis monthly Discussion HBV G145R 60 65 S 66 71 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Indeed, we found that the G145R mutation reduced the ASA of the HBsAg by increasing the protein's compactness and rigidity. 2016 Hepatitis monthly Discussion HBV G145R 26 31 S 64 69 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Moreover, our results demonstrated that the G145R mutation was highly capable of increasing the compactness of the HBsAg. 2016 Hepatitis monthly Discussion HBV G145R 44 49 S 115 120 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Of these, G145R is the commonest and the most widely studied HBV immune escape mutation, emerging naturally or in response to vaccination or hepatitis B immunoglobulin (HBIG) therapy. 2016 Hepatitis monthly Discussion HBV G145R 10 15 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Our analyses revealed that the G145R mutation induces a local change in the "a" determinant conformation. 2016 Hepatitis monthly Discussion HBV G145R 31 36 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Reduced immunogenicity in "a" determinant mutants, especially the G145R mutant, has been observed in previous studies. 2016 Hepatitis monthly Discussion HBV G145R 66 71 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Taken together, the G145R mutation can increase the rigidity and aggregation potential of HBsAg's "a" determinant, which alters its immunogenic activity and secretion. 2016 Hepatitis monthly Discussion HBV G145R 20 25 S 90 95 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The G145R mutation is an immune escape mutation that causes problems with diagnostic assays and a poor response to vaccines. 2016 Hepatitis monthly Discussion HBV G145R 4 9 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The lower binding affinity between G145R and MAb12 compared with the wild-type protein indicated the intrinsic potential of this mutant to escape HBsAg neutralization using specific antibodies, as reported in previous studies. 2016 Hepatitis monthly Discussion HBV G145R 35 40 S 146 151 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. The present study showed that the average Calpha RMSF of the G145R mutant was clearly lower than that of the wild-type, especially in the antigenic regions. 2016 Hepatitis monthly Discussion HBV G145R 61 66 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. Therefore, R145 may change the arrangement of the H-bond network in the antigenic loops of the G145R mutant HBsAg. 2016 Hepatitis monthly Discussion HBV G145R 95 100 S 108 113 27642350 Impacts of the G145R Mutation on the Structure and Immunogenic Activity of the Hepatitis B Surface Antigen: A Computational Analysis. This finding may be an important factor involved in the antibody escape of HBsAgs that contain the G145R mutation. 2016 Hepatitis monthly Discussion HBV G145R 99 104 S 75 81 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. A number of previous reports demonstrated that mutations in the 'a' determinant (e.g., sG145R) influence antigenicity. 2017 Journal of hepatology Discussion HBV G145R 87 93 S;S 65;87 79;88 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. A third potential mechanism is that some mutants, especially the truncated mutations (e.g., sW182*), may lead to ER stress-induced oxidative DNA damage triggered by the unfolded protein response, which in turn could result in HBV genomic instability and reduction/loss of HBV DNA levels. 2017 Journal of hepatology Discussion HBV W182X 92 98 S 92 93 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Accordingly, our study on patients showed that the sW182* mutant was more prevalent in the HBsAg low group than that in the high group. 2017 Journal of hepatology Discussion HBV W182X 51 57 S;S 91;51 96;52 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. For example, in our previous study of 143 HBV genotype B sequences, two samples have the sL95W substitution (Supplementary Table 4). 2017 Journal of hepatology Discussion HBV L95W 89 94 S 89 90 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. In conclusion, we have identified several new HBV S protein substitutions (sE2G, sL21S, sR24K, sC69*, sL95W and sL98V) outside of the 'a' determinant of SHBs that are associated with lower serum HBsAg and HBV DNA levels. 2017 Journal of hepatology Discussion HBV E2G;L21S;R24K;C69X;L95W;L98V 75;81;88;95;102;112 79;86;93;100;107;117 S;S;S;S;S;S;S;S;S;S 135;195;50;75;81;88;95;102;112;153 149;200;51;76;82;89;96;103;113;157 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. In this study, we found that 12 samples with HBsAg level < 1000 IU/ml with median HBV DNA level 6.77 log10 IU/ml and 75.00% (9/12) of their sequences were found to harbor one or two our newly identified SHBs mutations (sL21R, sT47K, sL95W, sK122R, sI126T, sG145R and sW182*) (Supplementary Table 2). 2017 Journal of hepatology Discussion HBV L21R;T47K;L95W;K122R;I126T;G145R;W182X 219;226;233;240;248;256;267 224;231;238;246;254;262;273 S;S;S;S;S;S;S;S;S 45;219;226;233;240;248;256;267;203 50;220;227;234;241;249;257;268;207 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Indeed, Yan et al, reported that HBV BCP A1762T/G1764A mutations might be associated with low HBsAg levels, and Pollicino et al. 2017 Journal of hepatology Discussion HBV G1764A;A1762T 48;41 54;47 BCP;S 37;94 40;99 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Interestingly, the newly identified mutations (sE2G, sL21S, sR24K, sC69*, sL95W and sL98V) localize outside the 'a' determinant. 2017 Journal of hepatology Discussion HBV E2G;L21S;R24K;C69X;L95W;L98V 47;53;60;67;74;84 51;58;65;72;79;89 S;S;S;S;S;S;S 113;47;53;60;67;74;84 127;48;54;61;68;75;85 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Moreover, we discovered that HBV mutants sS117T, sK122R, sI126N/S/T, sG145R, and sW182*, reported in previous studies, were also associated with lower HBsAg levels. 2017 Journal of hepatology Discussion HBV S117T;K122R;I126N;I126S;I126T;G145R;W182X 41;49;57;57;57;69;81 47;55;67;67;67;75;87 S;S;S;S;S;S 151;41;49;57;69;81 156;42;50;58;70;82 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Our in vitro experiments suggest that mutations within the S protein may impair virion secretion (sE2G, sL95W and sL98V), change antigenicity (sL21R, sL95W and sL98V), or impact HBV replication (sC69*) thereby decreasing detectable levels of HBsAg. 2017 Journal of hepatology Discussion HBV E2G;L95W;L98V;L21R;L95W;L98V;C69X 98;104;114;143;150;160;195 102;109;119;148;155;165;200 S;S;S;S;S;S;S;S;S 242;59;98;104;114;143;150;160;195 247;60;99;105;115;144;151;161;196 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. reported that major hydrophilic region (MHR) mutations in the "a" determinant region (G119R, C124Y, I126S, Q129R, S136P, C139R, T140I, K141E, D144A, and G145R) can significantly decrease virion, HBsAg detection and apparent occult HBV infection. 2017 Journal of hepatology Discussion HBV G119R;C124Y;I126S;Q129R;S136P;C139R;T140I;K141E;D144A;G145R 86;93;100;107;114;121;128;135;142;153 91;98;105;112;119;126;133;140;147;158 S 195 200 HBV infections 231 244 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. reported that sW182* was associated with enhanced cell growth, indicating that HBV might also gain survival benefit by up-regulating proliferation of infected cells. 2017 Journal of hepatology Discussion HBV W182X 14 20 S 14 15 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. reported that the sE164G substitution, driven by vaccine escape and outside of the 'a' determinant, was also associated with occult HBV infection. 2017 Journal of hepatology Discussion HBV E164G 18 24 S;S 84;18 98;19 HBV infections 132 145 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. reported that the sW182* mutation induced retention of truncated S protein in the perinuclear ER and was associated with lower HBV transcript levels due to decreased stability, but without impact on HBV replication. 2017 Journal of hepatology Discussion HBV W182X 18 24 S;S 18;65 19;66 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. sE2G resides in the SHBs signal peptide sequence and may affect S protein translocation efficiency and secretion. 2017 Journal of hepatology Discussion HBV E2G 0 4 S;S;S 0;64;20 1;65;24 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Several mutations including sC69*, sL95W and sL98V were also identified in 60 samples of HBeAg-negative CHB patients (Supplementary Table 5). 2017 Journal of hepatology Discussion HBV C69X;L95W;L98V 28;35;45 33;40;50 C;S;S;S 89;28;35;45 94;29;36;46 Chronic Hepatitis B 104 107 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. Similarly, our results showed that substitutions sL21R, sL95W and sL98V, which unlike previous reports are located outside the 'a' determinant, affected extracellular and intracellular HBsAg levels by ELISA and Western blot with two different antibodies. 2017 Journal of hepatology Discussion HBV L21R;L95W;L98V 49;56;66 54;61;71 S;S;S;S;S 128;185;49;56;66 142;190;50;57;67 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. The sC69* also occurs in genotype D. 2017 Journal of hepatology Discussion HBV C69X 4 9 S 4 5 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. The sL95W and sL98V mutations are in a transmembrane segment and AA substitutions in this region could alter the conformation of S protein resulting in lower HBsAg secretion. 2017 Journal of hepatology Discussion HBV L95W;L98V 4;14 9;19 S;S;S;S 158;4;14;129 163;5;15;130 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. These included sE2G (near the N terminus), and sL95W and sL98V (in TM2). 2017 Journal of hepatology Discussion HBV E2G;L95W;L98V 15;47;57 19;52;62 S;S;S 15;47;57 16;48;58 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. This possibility is supported by experimental evidence from several previous reports showing that the mutant virion secretion could be rescued efficiently (i.e., sP127S) or moderately (i.e., sW172*) by co-expression of WT surface protein. 2017 Journal of hepatology Discussion HBV P127S;W172X 162;191 168;197 S;S;S 162;191;222 163;192;229 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. We also showed that impaired virion secretion for several mutants (sE2G, sC69* and sG145R) can be efficiently rescued by trans-complementation of the WT S protein. 2017 Journal of hepatology Discussion HBV E2G;C69X;G145R 67;73;83 71;78;89 S;S;S;S 67;73;83;153 68;74;84;154 27650283 Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA. We identified several new HBV mutations (sE2G, sL21S, sR24K, sC69*, sL95W and sL98V) with higher prevalence in the HBsAg low group than those in high group stratified by the median HBsAg levels. 2017 Journal of hepatology Discussion HBV E2G;L21S;R24K;C69X;L95W;L98V 41;47;54;61;68;78 45;52;59;66;73;83 S;S;S;S;S;S;S;S 115;181;41;47;54;61;68;78 120;186;42;48;55;62;69;79 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. In the other hand, the main substitutions observed in the S promoter region and CCAAT box were V80I in 7(8.5 %) and S90T in 6(7.3 %) of sequences. 2016 Infectious agents and cancer Discussion HBV V80I;S90T 95;116 99;120 S promoter 58 68 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The major mutation found in epitope B-cell and T-cell and hepatocyte binding site were R38K (17.1 %), H44L (13.4 %) and N29K in 8 (9.8 %) sequences. 2016 Infectious agents and cancer Discussion HBV R38K;H44L;N29K 87;102;120 91;106;124 27651827 Molecular characterization of hepatitis B virus among chronic hepatitis B patients from Pointe Noire, Republic of Congo. The phylogenetic analysis based on the sequencing of the HBV preS1 region have reported many substitutions; the most prevalent variant found were R38K in 14(17.1 %) sequences, following by H44L in 11(13.4 %) and K13E in 8(9.8 %) strains. 2016 Infectious agents and cancer Discussion HBV R38K;H44L;K13E 146;189;212 150;193;216 PreS1 61 66 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Among which, Thr118Val, Thr125Met, Pro127Thr, Ala128Val and Thr/Ser143Leu/Met were observed in genotype D sequences, which is thought to have strong impacts on functions of S gene. 2016 SpringerPlus Discussion HBV T143L;T143M;S143L;S143M;T118V;T125M;P127T;A128V 60;60;60;60;13;24;35;46 77;77;77;77;22;33;44;55 S 173 174 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. For example, substitution Pro127Thr has been alarmed as great public health significance. 2016 SpringerPlus Discussion HBV P127T 26 35 27652086 Molecular epidemiology of hepatitis B virus isolated from Bangladesh. Furthermore, Sequences of genotype C were found to have Thr126Ile and Thr131Ser mutations, and genotype A sequences have only Thr131Asn mutation in 'a' determinant region. 2016 SpringerPlus Discussion HBV T126I;T131S;T131N 56;70;126 65;79;135 S 149 163 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. A2159G and A2189Y mutations are missense mutations resulting in an amino acid change of HBcAg codons 87 (S87G) and 97 (I97L/F), respectively. 2016 International journal of molecular sciences Discussion HBV A2159G;A2189Y;S87G;I97L;I97F 0;11;105;119;119 6;17;109;125;125 C 88 93 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. After adjustment for age, history of cigarette smoking and alcohol consumption, unconditional logistic regression analyses showed that pre-S deletion, C1653T, A1762T/G1764A, A2159G, A2189Y, G2203W, and C2288R mutations were significantly associated with high HCC risk. 2016 International journal of molecular sciences Discussion HBV G1764A;C1653T;A1762T;A2159G;A2189Y;G2203W;C2288R 166;151;159;174;182;190;202 172;157;165;180;188;196;208 PreS 135 140 Hepatocellular carcinoma 259 262 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Among the 10 HCC-related mutations acquired from the full genome analysis in stage 1, four (A2159G, A2189Y, G2203W, and C2288R mutations) were located in the C gene. 2016 International journal of molecular sciences Discussion HBV A2159G;A2189Y;G2203W;C2288R 92;100;108;120 98;106;114;126 C 158 159 Hepatocellular carcinoma 13 16 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. demonstrated that A2189C and G2203W mutations were independent risk factors for HCC in another study from Qidong, showing odds ratios 3.99 and 9.70, respectively. 2016 International journal of molecular sciences Discussion HBV A2189C;G2203W 18;29 24;35 Hepatocellular carcinoma 80 83 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Furthermore, in this full HBV genome comparison between 30 HCC cases and 30 controls, we also identify some rarely reported or new HCC-related mutations, including G1613A in the X gene, and A2159G, A2189Y, G2203W, and C2288R mutations in the C gene. 2016 International journal of molecular sciences Discussion HBV G1613A;A2159G;A2189Y;G2203W;C2288R 164;190;198;206;218 170;196;204;212;224 C;X 242;178 243;179 Hepatocellular carcinoma;Hepatocellular carcinoma 59;131 62;134 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. However, in multivariate analysis, G2203W and C2288R mutations were not independent risk factors in predicting HCC occurrence. 2016 International journal of molecular sciences Discussion HBV G2203W;C2288R 35;46 41;52 Hepatocellular carcinoma 111 114 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. In accordance with the results of Zhu et al., in the present study, we confirmed that A2159G, A2189Y, G2203W, and C2288R mutations were associated with high HCC risk in univariate analysis. 2016 International journal of molecular sciences Discussion HBV A2159G;A2189Y;G2203W;C2288R 86;94;102;114 92;100;108;120 Hepatocellular carcinoma 157 160 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. In the present study, the risk of combined mutations in the C gene, including the A2159G, A2189Y, G2203W, and C2288R mutations, on HCC was explored. 2016 International journal of molecular sciences Discussion HBV A2159G;A2189Y;G2203W;C2288R 82;90;98;110 88;96;104;116 C 60 61 Hepatocellular carcinoma 131 134 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Meanwhile, the carcinogenic risk of pre-S deletion and pre-S2 start codon mutation in pre-S gene, C1653T, and A1762T/G1764A mutations in X gene has been extensively investigated in this cohort. 2016 International journal of molecular sciences Discussion HBV G1764A;C1653T;A1762T 117;98;110 123;104;116 PreS;PreS;PreS2;X 36;86;55;137 41;91;61;138 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Multivariate analysis indicated that pre-S deletion, A1762T/G1764A, A2159G, and A2189Y mutations were independent risk factors for HCC progression. 2016 International journal of molecular sciences Discussion HBV G1764A;A1762T;A2159G;A2189Y 60;53;68;80 66;59;74;86 PreS 37 42 Hepatocellular carcinoma 131 134 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. Similar to previous studies, pre-S deletion and pre-S2 start codon mutation in pre-S gene, C1653T, and A1762T/G1764A mutations in X gene were associated with significantly higher risk of HCC development. 2016 International journal of molecular sciences Discussion HBV G1764A;C1653T;A1762T 110;91;103 116;97;109 PreS;PreS;PreS2;X 29;79;48;130 34;84;54;131 Hepatocellular carcinoma 187 190 27727182 Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China. The key finding of this study was that the number and pattern of multiple mutations in the C gene (A2159G, A2189Y, G2203W, and C2288R mutations) showed the additive combined effects that related to HCC progression. 2016 International journal of molecular sciences Discussion HBV A2159G;A2189Y;G2203W;C2288R 99;107;115;127 105;113;121;133 C 91 92 Hepatocellular carcinoma 198 201 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. The mutation rtL180M found together with the rtM204V mutation in these patients is associated with resistance to telbivudine and also with enhanced replication. 2016 Virology journal Discussion HBV L180M;M204V 15;47 20;52 RT;RT 13;45 15;47 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. The replacement of methionine in the YMDD catalytic site motif by valine (rtM204V) in the seven patients is associated with resistance to lamivudine and other L-nucleoside analogues. 2016 Virology journal Discussion HBV M204V 76 81 RT;P 74;37 76;41 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. The rtL180M + rtT184S + rtM204V triple mutation found in one patient suggests resistance to entecavir, lamivudine and other L-nucleoside analogues. 2016 Virology journal Discussion HBV L180M;T184S;M204V 6;16;26 11;21;31 RT;RT;RT 4;14;24 6;16;26 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. The rtV173L mutation found in six of these patients is known to compensate for replication defects of lamivudine resistant HBV mutants. 2016 Virology journal Discussion HBV V173L 6 11 RT 4 6 27769271 Serologic and genotypic characterization of hepatitis B virus in HIV-1 infected patients from South West and Littoral Regions of Cameroon. There were three escape mutations identified which were previously associated with diagnostic failure (Y100C, R122K and Q129H) and two associated with vaccine escape (Q129H and T131N). 2016 Virology journal Discussion HBV Y100C;R122K;Q129H;Q129H;T131N 103;110;120;167;177 108;115;125;172;182 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. A previous study detected the G145R mutant as a minor population (22.66%) using ultra-deep pyrosequencing in a pregnant woman with a high viral load (7.83 lU/mL). 2016 PloS one Discussion HBV G145R 30 35 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Although the G145R mutant as a minor population was detected in pregnant women who were HBeAg-positive and had a high viral load, none of the infants born to the mothers infected with the G145R mutation showed breakthrough infection. 2016 PloS one Discussion HBV G145R;G145R 13;188 18;193 C 88 93 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. As the ratio reached the detection limit (wild:mutant = 200:1), the LNA-based probe real-time PCR could not accurately quantify the G145R mutant DNA level (data not shown). 2016 PloS one Discussion HBV G145R 132 137 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Deep sequencing detected the G145R mutant that was detected by the LNA-based probe real-time PCR in all but one patient. 2016 PloS one Discussion HBV G145R 29 34 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Deep sequencing showed that the highest frequency of amino acid changes, including minor populations in the "a" determinant region, was observed in patients who had the G145R or G145K mutant as a predominant strain. 2016 PloS one Discussion HBV G145R;G145K 169;178 174;183 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Except for the co-existence of HBsAg and anti-HBs, predictors of the presence of the G145R mutant remain unknown. 2016 PloS one Discussion HBV G145R 85 90 S;S 46;31 49;36 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Further studies are needed to confirm the association between HBeAg-positive status and the G145R mutant by sensitive detection systems or deep sequencing. 2016 PloS one Discussion HBV G145R 92 97 C 62 67 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. HBeAg-positive patients without a history of HB vaccinations, HBIG, or antiviral treatment tended to have the G145R mutant as a minor population, but HBeAg positivity did not show a significant association with the detection of the G145R mutant as a minor population. 2016 PloS one Discussion HBV G145R;G145R 110;232 115;237 C;C 0;150 5;155 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, the calculated frequency of the G145R mutant was much lower in deep sequencing than in LNA-based probe real-time PCR. 2016 PloS one Discussion HBV G145R 41 46 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. However, this previous study was a retrospective study and neither showed the viral load of VEMs nor detected the G145R mutant. 2016 PloS one Discussion HBV G145R 114 119 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. If HBeAg-positive status is significantly associated with the G145R mutant in pregnant mothers, these recommendations will also be effective in reducing breakthrough infections caused by the G145R mutant. 2016 PloS one Discussion HBV G145R;G145R 62;191 67;196 C 3 8 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In addition to the G145R mutant, these mothers showed very high levels of serum HBV DNA (7.8 log copies/mL or more). 2016 PloS one Discussion HBV G145R 19 24 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In conclusion, the frequency of the G145R mutant as a minor as well as major strain was approximately one-fourth in children who were infected due to immunoprophylaxis failure. 2016 PloS one Discussion HBV G145R 36 41 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In contrast to the previous study, the current study demonstrated that immunoprophylaxis with a series of 3 doses of HB vaccine plus HBIG could prevent breakthrough infection in children born to pregnant women infected with the G145R mutant existing as a minor population. 2016 PloS one Discussion HBV G145R 228 233 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In fact, although the 3 mothers showed high HBV DNA levels of the G145R mutant, which are considered to increase the risk of breakthrough infection, the selection of the preexisting G145R mutant did not occur in their infants after birth. 2016 PloS one Discussion HBV G145R;G145R 66;182 71;187 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. In the control cohort of this study, HBeAg-positive patients were prone to have the G145R mutant as a minor population. 2016 PloS one Discussion HBV G145R 84 89 C 37 42 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Moreover, treatment with lamivudine during the third trimester decreased the population of G145R mutants to 0.9% at 2 weeks after delivery (HBV DNA; 5.37 IU/mL), and breakthrough infection never occurred in the babies. 2016 PloS one Discussion HBV G145R 91 96 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Moreover, we compared the G145R mutant/wild DNA ratio quantified by the LNA-based probe real-time PCR with the G145R mutation frequency detected by deep sequencing. 2016 PloS one Discussion HBV G145R;G145R 26;111 31;116 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Neither the gLCR assay nor the LNA-based probe real-time PCR showed a ratio of G145R mutant DNA to wild-type DNA of less than 1%. 2016 PloS one Discussion HBV G145R 79 84 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Of the 3 patients who had the G145R mutant as a major population, HBsAg and anti-HBs co-existed in 2. 2016 PloS one Discussion HBV G145R 30 35 S;S 81;66 84;71 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. On the basis of the results of the quantitative real-time PCR and deep sequencing, the population with the G145R mutant ranged from 1% to 60% of the total population of pregnant mothers. 2016 PloS one Discussion HBV G145R 107 112 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Previous studies reported that G145R mutant was frequently detected in peripheral blood leukocytes from HBsAg-positive and negative patients. 2016 PloS one Discussion HBV G145R 31 36 S 104 109 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Taking these circumstances into consideration, the G145R mutant as a minor population does not always contribute to a breakthrough infection. 2016 PloS one Discussion HBV G145R 51 56 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The accuracy of the quantification depends on the ratio of the G145R mutant DNA to wild-type DNA. 2016 PloS one Discussion HBV G145R 63 68 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The G145R mutant was detected in 13% of pregnant women in this study, and this frequency was virtually identical to that detected in the control group. 2016 PloS one Discussion HBV G145R 4 9 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. The lowest frequency was observed in patients who did not have the G145R mutant as a minor population. 2016 PloS one Discussion HBV G145R 67 72 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Therefore, the blood in the mothers contained at least 6 log copies/mL of the G145R mutant, which represents a high viral load. 2016 PloS one Discussion HBV G145R 78 83 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings indicated that the emergence of the G145R mutant was accompanied by other amino acid changes in the "a" determinant region. 2016 PloS one Discussion HBV G145R 51 56 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. These findings suggest that both methods have the same sensitivity for the G145R mutant as the minor population among the predominant wild-type population. 2016 PloS one Discussion HBV G145R 75 80 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. This finding highlights the discrepancy in the frequency of the G145R mutant between the LNA-based probe real-time PCR and deep sequencing. 2016 PloS one Discussion HBV G145R 64 69 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Thus, it is speculated that approximately 10% of infants born to HBV carriers have been exposed to the G145R mutant existing as a minor strain for a long time. 2016 PloS one Discussion HBV G145R 103 108 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Thus, the pre-existence of the G145R mutation as a minor population in mothers does not always cause immunoprophylaixs failure after birth. 2016 PloS one Discussion HBV G145R 31 36 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Under the anti-HBs-specific humoral pressure, the compartmentalization of HBV in lymphocytes and the G145R escape mutation are advantageous for HBV to persist and survive. 2016 PloS one Discussion HBV G145R 101 106 S 15 18 27812178 Evaluation of the G145R Mutant of the Hepatitis B Virus as a Minor Strain in Mother-to-Child Transmission. Using the gLCR assay, the ratio of the G145R mutant DNA to wild-type DNA ranged from approximately 3% to 74% in serum from various HBV carriers. 2016 PloS one Discussion HBV G145R 39 44 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. As for the nucleotide substitution rate, medium/low MBL2 group has higher substitution rate in all investigated positions, except for mutation A1499G where the substitution rate was higher in high MBL2 production group. 2016 Aging Discussion HBV A1499G 143 149 27824315 Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naive patients. In an epidemiological study conducted in Hong Kong, A1499G mutation has been associated with the risk of HCC, the data revealed that the mutation rate of A1499 was 20% in chronic HBV patients while it elevated to 62.5% among HCC cases. 2016 Aging Discussion HBV A1499G 52 58 Hepatocellular carcinoma;Hepatocellular carcinoma;Chronic Hepatitis B 105;225;171 108;228;182 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. Besides, the Abbott assay may detect HBsAg produced by multiple S-escape mutants, including G145R. 2016 PloS one Discussion HBV G145R 92 97 S;S 37;64 42;65 27835694 Occult HBV Infection in Immunized Neonates Born to HBsAg-Positive Mothers: A Prospective and Follow-Up Study. S-escape mutants, such as G145R, unrecognized by diagnostic kits, may account for the absence of HBsAg observed in some cases. 2016 PloS one Discussion HBV G145R 26 31 S;S 97;0 102;1 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Apart from subgenotype specific differences, G145R - a potent immune escape mutation was specifically observed in the PBL related subgenotype A2 isolates. 2016 World journal of virology Discussion HBV G145R 45 50 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Earlier studies have demonstrated that by virtue of its definite advantages, G145R mutation helps HBV to dynamically evade anti-HBs specific immune response, thereby ensuring viral persistence in anatomical compartments, which are exposed to strong anti-HBs immunity. 2016 World journal of virology Discussion HBV G145R 77 82 S;S 128;254 131;257 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Interestingly, we further noted that nucleotide substitution 358C was also synonymous, while substitution 587A was non-synonymous and translated into the potent immune escape G145R mutation of HBsAg. 2016 World journal of virology Discussion HBV G145R 175 180 S 193 198 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Nevertheless, the finding of selective predominance of the point mutation leading to G145R in the present study is highly significant in the context of PBL, since PBLs are exposed to strong anti-HBs humoral immune response and HBV variants with G145R are capable of strongly neutralizing this immune response, without any compromise in the replicative competence, thereby ensuring viral perseverance. 2016 World journal of virology Discussion HBV G145R;G145R 85;245 90;250 S 195 198 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. On comparison of the pgRNA secondary structures, we observed that the invariable association of subgenotype A2 with the selection of nucleotide 587A (causing G145R) most possibly occur in the context of genotype A2 specific altered pgRNA base pairing patterns. 2016 World journal of virology Discussion HBV G145R 158 163 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. The association of these five synonymous nucleotide substitutions and a potent immune escape mutation with PBL associated Ae/A2 sequences led us to hypothesize that the advantageous 587A (G145R) might be selected at the pgRNA base pairing level and to verify this hypothesis, this comparative study was undertaken. 2016 World journal of virology Discussion HBV G145R 188 193 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Therefore, based on the predicted secondary structures, we hypothesized that, instead of selecting an altered nucleotide at this exceptionally essential position (359), a compensatory alteration of a single nucleotide (G to A) at position 587 is expected to serve dual purpose, firstly it may help stabilize the stem structure (by pairing with the highly conserved 359T/U) and secondly it results in the emergence of a potent immune escape G145R mutation, both of which appears to be highly advantageous for the virus. 2016 World journal of virology Discussion HBV G145R;G587A 440;218 445;242 27878103 Role of RNA secondary structure in emergence of compartment specific hepatitis B virus immune escape variants. Using computational prediction methods, the authors show that the PBL specific emergence of G145R occurs in the context of HBV subgenotype A2, due to altered base-pairing patterns, as compared to the HBV subgenotype A1. 2016 World journal of virology Discussion HBV G145R 92 97 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. Avellon reported M133T (2.2%), Q129H, M133I, F/Y134N (1.8%), F/Y134L, G145A (1.5%), and P120T (1.1%) as the most frequent mutations of S region, while G145R was found at a frequency of less than 1% (0.4%), while among them just Q129H was found in the current study. 2016 Hepatitis monthly Discussion HBV Y134N;Y134L;F134N;F134L;M133T;Q129H;M133I;G145A;P120T;G145R;Q129H 45;61;45;61;17;31;38;70;88;151;228 52;68;52;68;22;36;43;75;93;156;233 S 135 136 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. In a previous study in this estate of Iran, only P127L was present in one case and Q129H in two cases at MHR region in 25 patients. 2016 Hepatitis monthly Discussion HBV P127L;Q129H 49;83 54;88 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. In another study in Iran, P120T/S and R122K/T were found in 4% of patients, and G145R was found only in one case; which none of them occurred in the current project. 2016 Hepatitis monthly Discussion HBV P120T;P120S;R122K;R122T;G145R 26;26;38;38;80 33;33;45;45;85 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. Other mutation that observed in this study was L91I which reported as an Entecavir, lamivudine -related resistance mutation. 2016 Hepatitis monthly Discussion HBV L91I 47 51 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. Sayan reported multiple HBV vaccine-escape mutations (S143T, D144E, G145R, E164D, I195M), of which 3 of them (D144E, S143L and E164D, one case for each) were seen in the current study. 2016 Hepatitis monthly Discussion HBV S143T;D144E;G145R;E164D;I195M;D144E;S143L;E164D 54;61;68;75;82;110;117;127 59;66;73;80;87;115;122;132 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The most frequently identified HBsAg amino acid substitutions in previous studies include P120T, M33I, S143L, D144E/A, G145R, E164D, W172*, and W182* which are the most commonly occurring pattern. 2016 Hepatitis monthly Discussion HBV W172X;W182X;P120T;M33I;S143L;D144E;D144A;G145R;E164D 133;144;90;97;103;110;110;119;126 138;149;95;101;108;117;117;124;131 S 31 36 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The most prevalent escape mutation among the vaccinated was Q129H/P (6 cases), and S117G, P127L one case for each, while other escape mutations occurred just in the unvaccinated populations. 2016 Hepatitis monthly Discussion HBV Q129P;Q129H;S117G;P127L 60;60;83;90 67;67;88;95 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The most prevalent mutations in RT region of the study isolates was Q149K (9.83%) followed by N118D/T (6.55%), L157M (4.91%) and H124Y, A113Y/S, N131D/S, L145M, V173A/L, 3.27% for each one. 2016 Hepatitis monthly Discussion HBV Q149K;N118D;N118T;L157M;H124Y;A113Y;A113S;N131D;N131S;L145M;V173A;V173L 68;94;94;111;129;136;136;145;145;154;161;161 73;101;101;116;134;143;143;152;152;159;168;168 RT 32 34 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The Q129H was the most frequently detected escape mutant in this study (34.42%), followed by P127L/T (3.27%) and E164D, S117G/T, D144E, T125M, S143L, 1.63% for each; and their roles in the vaccine escape, Ig response and/or detection have already been established. 2016 Hepatitis monthly Discussion HBV Q129H;P127L;P127T;E164D;S117G;S117T;D144E;T125M;S143L 4;93;93;113;120;120;129;136;143 9;100;100;118;127;127;134;141;148 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The rare S78T mutation also observed in one patient can lead to tenofovir resistance. 2016 Hepatitis monthly Discussion HBV S78T 9 13 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The S135Y that occurred in one case is reported to be related to lamivudine resistance. 2016 Hepatitis monthly Discussion HBV S135Y 4 9 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The well known mutation rtV173L observed in two cases (3.2%), which is a compensatory mutation and could be selected in lamivudine-resistant patients due to an enhanced replication phenotype. 2016 Hepatitis monthly Discussion HBV V173L 26 31 RT 24 26 27882062 Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran. The well-known G145R mutation occurs in the S-gene with overlapping rtW153Q mutation in the Pol-gene (HBsAg classical vaccine escape strain), which was absent in isolates of the current project. 2016 Hepatitis monthly Discussion HBV W153Q;G145R 70;15 75;20 S;P;RT;S 102;92;68;44 107;95;70;45 27882070 Serological Patterns and Molecular Characterization of Occult Hepatitis B Virus Infection among Blood Donors. In contrast, in our OBI samples, 30.4% (21/69) of samples harbored mutations, and no G145R was found. 2016 Hepatitis monthly Discussion HBV G145R 85 90 Occult Hepatitis B 20 23 27882070 Serological Patterns and Molecular Characterization of Occult Hepatitis B Virus Infection among Blood Donors. The well-known G145R mutation is the major variation in HBV isolates responsible for OBI in southeast China. 2016 Hepatitis monthly Discussion HBV G145R 15 20 Occult Hepatitis B 85 88 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. After verification process, only miR-873-mediated downregulation of CSMD3 expression was consistently confirmed in an independent cohort of TgSW172* mice. 2016 Oncogenesis Discussion HBV W172X 142 148 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. As such, the increased ER stress in transgenic mice not only caused by pre-S/S-sW172* accumulation but also by miR-873 activation. 2016 Oncogenesis Discussion HBV W172X 79 85 PreS;S;S 71;77;79 76;78;80 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. In summary, we provided transgenic mouse evidence showing an increased oncogenicity of truncated HBV pre-S/S protein with sW172* mutation. 2016 Oncogenesis Discussion HBV W172X 122 128 PreS;S;S 101;107;122 106;108;123 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Recent studies using HBcAg/HBsAg-postive HCC tissues uncovered another frequent S gene truncation mutation, sW182*. 2016 Oncogenesis Discussion HBV W182X 108 114 C;S;S;S 21;27;80;108 26;32;81;109 Hepatocellular carcinoma 41 44 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. Such discrepancy urged us to search for other differentially regulated pathways between TgWT and TgSW172*. 2016 Oncogenesis Discussion HBV W172X 99 105 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. The actual prevalence of rtA181T/sW172* mutant in China is unknown, nor do we know whether it is capable of transmission among people. 2016 Oncogenesis Discussion HBV W172X;A181T 33;27 39;32 RT;S 25;33 27;34 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. The rtA181T/sW172* mutant exerts cross-resistance to both lamivudine and adeforvir. 2016 Oncogenesis Discussion HBV W172X;A181T 12;6 18;11 RT;S 4;12 6;13 27918551 Hepatocarcinogenesis in transgenic mice carrying hepatitis B virus pre-S/S gene with the sW172* mutation. When examining the regulatory cascade from pre-S/S-sW172* to CSMD3 suppression, it was found that activation of miR-873 only occurred in Hepa1-6 and HepY2 cells, suggesting that other cellular factors were involved in this process. 2016 Oncogenesis Discussion HBV W172X 51 57 PreS;S;S 43;49;51 48;50;52 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. And some other in vitro experiments also reported a decreased viral replication of HBV rtA181T/sW172*. 2016 Scientific reports Discussion HBV W172X;A181T 95;89 101;94 RT;S 87;95 89;96 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. And this may explain the lower levels of HBV DNA in cell supernatant and blood serum in HBV rtA181T/sW172* mutant strain as compared to that in HBV rtA181T/sW172L mutant and wild-type viral strains. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 100;156;94;150 106;162;99;155 RT;RT;S;S 92;148;100;156 94;150;101;157 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As the mutations can not directly affect protein synthesis, the low levels of HBsAg in cell supernatant and blood serum in rtA181T/sW172* mutant viral strain should be a direct result of the retention of HBsAg in liver cells. 2016 Scientific reports Discussion HBV W172X;A181T 131;125 137;130 S;S;RT;S 78;204;123;131 83;209;125;132 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As the sW172L and sW172* mutations of HBsAg gene are not inside the 'a' determinant, currently commercially antibody for substituted or truncated HBsAg is effective. 2016 Scientific reports Discussion HBV W172L;W172X 7;18 13;24 S;S;S;S;S 69;38;146;7;18 83;43;151;8;19 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. As we mentioned above, rtA181T/sW172L (TGG CTC TTA CTC) mutant viral strain codes substituted HBsAg protein and rtA181T/sW172*(TGG CTC TGA CTC) mutant viral strain codes truncated HBsAg protein. 2016 Scientific reports Discussion HBV W172L;W172X;A181T;A181T 31;122;25;116 37;128;30;121 S;S;RT;RT;S;S 96;184;23;114;31;122 101;189;25;116;32;123 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Based on those significantly differences, when we detected HBV rtA181T mutant in clinical practice, it is necessary and important for us to distinguish the sW172* truncated mutation from the sW172L substituted mutation. 2016 Scientific reports Discussion HBV A181T;W172X;W172L 65;156;191 70;162;197 RT;S;S 63;156;191 65;157;192 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. But in present study, similar findings were not observed in rtA181T/sW172L mutant strain. 2016 Scientific reports Discussion HBV W172L;A181T 68;62 74;67 RT;S 60;68 62;69 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. For rtA181T/sW172L mutant strains, the emergence of substituted HBsAg may not affect the assembly and secretion of virus particles, which may be similar to wild-type HBsAg. 2016 Scientific reports Discussion HBV W172L;A181T 12;6 18;11 S;S;RT;S 64;166;4;12 69;171;6;13 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, for rtA181T/sW172* mutant strains, the truncated HBsAg had significant changes in spatial structure of the protein, and the latter would inevitably impair the assembly and secretion of virus particles from intracellular to extracellular fluids. 2016 Scientific reports Discussion HBV W172X;A181T 21;15 27;20 S;RT;S 58;13;21 63;15;22 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. However, the HBV DNA RI level of HBV rtA181T/sW172* mutant strain in vivo was increased. 2016 Scientific reports Discussion HBV W172X;A181T 45;39 51;44 RT;S 37;45 39;46 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In another word, the HBsAg coding by rtA181T/sW172L mutant strain (substituted HBsAg) could be normally secreted or transferred to the outside of the cells, but the HBsAg coding by rtA181T/sW172* mutant strain (truncated HBsAg) could not. 2016 Scientific reports Discussion HBV W172L;W172X;A181T;A181T 45;189;39;183 51;195;44;188 S;S;S;S;RT;RT;S;S 21;79;165;221;37;181;45;189 26;84;170;226;39;183;46;190 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In fact, the pgRNA level of HBV rtA181T/sW172* was 1.2 time as much as pgRNA level of wild type (data unshown). 2016 Scientific reports Discussion HBV W172X;A181T 40;34 46;39 RT;S 32;40 34;41 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In our previous studies, we reported that the HBV DNA RI levels of the rtA181T/sW172* mutant strain were always higher and sustained longer as compared to wild-type HBV. 2016 Scientific reports Discussion HBV W172X;A181T 79;73 85;78 RT;S 71;79 73;80 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In summary, this is the first research to study the differences of HBV biological characteristics between rtA181T/sW172* and rtA181T/sW172L mutant strains. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 114;133;108;127 120;139;113;132 RT;RT;S;S 106;125;114;133 108;127;115;134 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In this study, the cell supernatant and blood serum levels of HBsAg were different between HBV rtA181T/sW172* and rtA181T/sW172L mutant strains. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 103;122;97;116 109;128;102;121 S;RT;RT;S;S 62;95;114;103;122 67;97;116;104;123 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In this study, the impact of different mutations in the rtA181T (rtA181T/sW172* and rtA181T/sW172L) on viral DNA replication and protein expression was investigated in both in vitro and in vivo conditions. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T;A181T 73;92;58;67;86 79;98;63;72;91 RT;RT;RT;S;S 56;65;84;73;92 58;67;86;74;93 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. In this study, there is a little difference in HBV DNA RI of HBV rtA181T/sW172* mutant strain in vitro and in vivo experiments. 2016 Scientific reports Discussion HBV W172X;A181T 73;67 79;72 RT;S 65;73 67;74 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. It must be noticed that just an in vitro experiment is not enough to fully reveal the differences between HBV rtA181T/sW172* and rtA181T/sW172L mutant strains. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 118;137;112;131 124;143;117;136 RT;RT;S;S 110;129;118;137 112;131;119;138 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Our results have indicated that the appearance of rtA181T/sW172L mutant has no obvious affection to the biological characteristics of HBV; while the appearance of rtA181T/sW172* mutant could cause the retention of HBsAg in hepatic cells, impairment of virus particles secretion from hepatic cells, and enhancement of viral replication in hepatic cells. 2016 Scientific reports Discussion HBV W172L;W172X;A181T;A181T 58;171;52;165 64;177;57;170 S;RT;RT;S;S 214;50;163;58;171 219;52;165;59;172 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. So the assembly and secretion of virus particles may be different between HBV rtA181T/sW172* and rtA181T/sW172L mutant strains. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 86;105;80;99 92;111;85;104 RT;RT;S;S 78;97;86;105 80;99;87;106 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. The major findings of present study were: (1) levels of HBsAg and HBV DNA in cell supernatant and blood serum in HBV rtA181T/sW172* mutant were significantly lower than in either HBV rtA181T/sW172L mutant or wild-type HBV; (2) levels of HBV DNA RI in HBV rtA181T/sW172* mutant were higher and more persistent than in HBV rtA181T/sW172L mutant and wild-type HBV; (3) significant higher levels of HBsAg and HBcAg in liver of HBV rtA181T/sW172* mutant as compare to HBV rtA181T/sW172L mutant and wild-type HBV; (4) the C promoter activity of HBV enhanced by truncated HBsAg, instead of by substitute or wild-type HBsAg. 2016 Scientific reports Discussion HBV W172X;W172L;W172X;W172X;W172L;W172L;A181T;A181T;A181T;A181T;A181T;A181T 125;191;263;435;329;475;119;185;257;323;429;469 131;197;269;441;335;481;124;190;262;328;434;474 Core promoter;C;S;S;S;S;RT;RT;RT;RT;RT;RT;S;S;S;S;S;S 516;405;56;395;565;610;117;183;255;321;427;467;125;191;263;329;435;475 526;410;61;400;570;615;119;185;257;323;429;469;126;192;264;330;436;476 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Thus, it is obvious that HBV rtA181T/sW172* and rtA181T/sW172L mutants have different biological characteristics. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 37;56;31;50 43;62;36;55 RT;RT;S;S 29;48;37;56 31;50;38;57 27976732 Biological characteristics comparison of HBV rtA181T mutants with truncated or substituted HBsAg expression in vitro and in vivo model systems. Thus, we speculated that the differences in DNA replication and protein secretion between rtA181T/sW172* and rtA181T/sW172L mutant viral strains should be closely related to the different HBsAg expression. 2016 Scientific reports Discussion HBV W172X;W172L;A181T;A181T 98;117;92;111 104;123;97;116 S;RT;RT;S;S 188;90;109;98;117 193;92;111;99;118 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Accordingly, the antigenic reactivity against a commercial HBsAg immunoassay was increased to some extent when phenylalanine at amino acid position 134 was substituted with valine (F134V) and it was not found to be responsible for the undetectability of HBsAg. 2017 PloS one Discussion HBV F134V;F134V 181;111 186;179 S;S 59;254 64;259 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Accordingly, we did not find any antigenic or secretory defect arising from the mutation at amino acid position 100 (Y100C), either when present singly (C100Y) or together with other mutations (VDCR98-101LDYQ), although Motta-Castro et al. 2017 PloS one Discussion HBV Y100C;C100Y 117;153 122;158 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Antigenic index (Ai) values of four or more amino acids around amino acid position 123 were altered by a magnitude of -0.4 to +0.2 or more by the T123A or T123N mutations, respectively. 2017 PloS one Discussion HBV T123A;T123N 146;155 151;160 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Consistent with previous reports, we also found significantly reduced antigenic reactivity of HBsAg in commercial immunoassays when independent mutation was made at position 120 with lysine (P120K) and at position 123 with aspartate (T123D). 2017 PloS one Discussion HBV P120K;T123D 191;234 196;239 S 94 99 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. found no reactivity of HBsAg using two commercial diagnostic assays whose sequences had simultaneous mutations at various positions, including an amino acid at 100 (Y100S), and this may have been due to mutations at other sites (T118V/R122K/M133I/Y134N/P142S/S143L/G145K). 2017 PloS one Discussion HBV R122K;M133I;Y134N;P142S;S143L;G145K;Y100S;T118V 235;241;247;253;259;265;165;229 240;246;252;258;264;270;170;234 S 23 28 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. G145R alone or in combination with others mutation in the HBs sequence may also affect the antigenic structure since it is located in the antigenic loop of "a" determinant. 2017 PloS one Discussion HBV G145R 0 5 S 58 61 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. G145R was also detected in patients with orthopedic liver transplantation even after having regular hepatitis B immune globulin prophylaxis. 2017 PloS one Discussion HBV G145R 0 5 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Glycine-to-alanine at 145 (G145A) and glutamine-to-arginine at 129 (Q129R) mutations were also found in the HBs amino acids sequence isolated from separate infants who already received recombinant hepatitis B vaccine. 2017 PloS one Discussion HBV G145A;Q129R;G145A;Q129R 27;68;0;38 32;73;25;66 S 108 111 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Glycine-to-arginine mutation at 145 (G145R) is a well-known mutation of HBsAg that is responsible for both immune escape and a reduction of the binding capacity in commercial diagnostic assays. 2017 PloS one Discussion HBV G145R;G145R 37;0 42;35 S 72 77 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. However, we found no effect of L213F mutation on the detection and the production by transient expression. 2017 PloS one Discussion HBV L213F 31 36 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. In addition, the combined mutations at these two positions with arginine (Q129R/G145R) affected twenty-eight amino acids surrounding the positions with significant degrees of Ai alteration. 2017 PloS one Discussion HBV G145R;Q129R 80;74 85;79 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. In this study, we found that seven up and three downstream amino acids were affected due to the mutation of threonine at position 123 by aspartate (T123D), with significant alteration of Ai values, and Ai degrees were notably changed from -0.4 to +1.48 due to simultaneous replacement of the amino acids at 120 and 123 with lysine and aspartate, respectively. 2017 PloS one Discussion HBV T123D;T123D 148;108 153;146 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Interestingly, the wt-HBs sequence (F134) was mutated to F134Y after orthopedic liver transplantation (OLT) or mutants I134F or Y134F were reverted to the wt (F134) after OLT and the predicted antigenic index was made slightly more positive due to amino acid substitution at this position either by tyrosine or isoleucine. 2017 PloS one Discussion HBV F134Y;I134F;Y134F 57;119;128 62;124;133 S 22 25 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. It might be suggested that the proline/lysine at amino acid position 120 and threonine/aspartate at 123 simultaneously determined the antigenic phenotype of HBsAg. 2017 PloS one Discussion HBV T123D;P120K 77;31 103;72 S 157 162 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Modification of the glycosylation pattern would alter the confirmation of HBsAg, since W3S showed more glycosylation than W1S (Fig 4A), which might be associated with immune escape. 2017 PloS one Discussion HBV W3S;W1S 87;122 90;125 S 74 79 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Natural mutation at the residue position 120 is very common, and has also been identified in patients with OBI, but the replacement of proline at this position (P120) with threonine (P120T) has been reported to have no effect on HBsAg antigenicity. 2017 PloS one Discussion HBV P120T 183 188 S 229 234 Occult Hepatitis B 107 110 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. observed a low level of HBV load in the serum with a C100Y mutation of the surface gene. 2017 PloS one Discussion HBV C100Y 53 58 S 75 82 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. On the other hand, when threonine at position 123 (T123) was substituted with asparagine (T123N), the reactivity of HBsAg in the supernatant of transfected cells was significantly reduced, but HBsAg retained some degree of its reactivity with the cell lysate or with other antibodies. 2017 PloS one Discussion HBV T123N 90 95 S;S 116;193 121;198 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Our synthetic mutant with substitutions of glycine-to-arginine at position 145 and glutamine-to-arginine at 129 (Q129R/G145R) showed significantly reduced binding efficiency especially in the supernatants (Fig 5B and 5D). 2017 PloS one Discussion HBV G145R;Q129R;G145R;Q129R 119;113;43;83 124;118;78;111 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Similarly, the antigenic sensitivity was fully recovered when we substituted the amino acid residues of these positions (120 and 123) with proline and threonine (K120P/D123T) and performed analyses using the same commercial immunoassay. 2017 PloS one Discussion HBV D123T;K120P 168;162 173;167 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Substitution of glutamine to arginine at position 129 (Q129R) was identified from the clinically HBV infected patients that also lied within the antigenic loop of "a" determinant. 2017 PloS one Discussion HBV Q129R;Q129R 55;16 60;53 HBV infections 97 109 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Surprisingly, we found that HBsAg lost antigenic reactivity when amino acid substitutions P120 and T123 were present simultaneously (P120K/T123D). 2017 PloS one Discussion HBV T123D;P120K 139;133 144;138 S 28 33 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Taken together, these results demonstrate that all the wt and synthetic mutants were well expressed and secreted into the culture medium except the mutant W1S Q129R/G145R, which had a secretion deficiency. 2017 PloS one Discussion HBV G145R;W1S;Q129R 165;155;159 170;158;164 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. Therefore, this double amino acid-substituted mutation might induce a greater inhibition of the efficiency of HBsAg secretion into the extracellular space and a greater reduction of antigenic reactivity compared to either of the individual mutations singly (Q129R or G145R), suggesting the importance of these positions. 2017 PloS one Discussion HBV Q129R;G145R 258;267 263;272 S 110 115 28045894 Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity. They also found reduced reactivity of HBsAg mutated at two positions simultaneously (Y100C/P120T). 2017 PloS one Discussion HBV P120T;Y100C 91;85 96;90 S 38 43 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. A LAM + ADV combination study showed YMDD mutation in 27-35 per cent of the cases while ADV-related mutation (A181V) was shown only in 5-7 per cent of the cases. 2016 The Indian journal of medical research Discussion HBV A181V 110 115 P 37 41 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. In addition, there was another compensatory mutation i.e., L180M + M204V. 2016 The Indian journal of medical research Discussion HBV L180M;M204V 59;67 64;72 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. In all patients on LAM therapy, the site of mutation was methionine in the YMDD motif for valine i.e., M204V at the end of second year. 2016 The Indian journal of medical research Discussion HBV M204V 103 108 P 75 79 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. M204V substitution was already reported earlier. 2016 The Indian journal of medical research Discussion HBV M204V 0 5 28139541 Comparative evaluation of long-term monotherapies & combination therapies in patients with chronic hepatitis B: A pilot study. Of the total 16.4 per cent with ADV mutation, sites detected were adenine substitution to threonine i.e., A181V (8.1%) and asparagine substitution to threonine (N236T: 8.3%). 2016 The Indian journal of medical research Discussion HBV A181V;N236T 106;161 111;166 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. At the same time, this may also suggest that sP203Q or sS210R and deletions in pre-S1/pre-S2 may lie on divergent evolutionary pathways contributing to HCC development. 2017 Oncotarget Discussion HBV P203Q;S210R 45;55 51;61 PreS1;PreS2;S;S 79;86;45;55 85;92;46;56 Hepatocellular carcinoma 152 155 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In addition, in a patient carrying the mutation sS210R, a pre-HCC HBV sequence was available and confirmed the presence of this mutation already 1 year before the diagnosis of HCC, further supporting the role of this mutation in promoted HBV-mediated hepatocarcinogenesis. 2017 Oncotarget Discussion HBV S210R 48 54 S 48 49 Hepatocellular carcinoma;Hepatocellular carcinoma 176;62 179;65 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In addition, sP203Q correlates with an increased percentage of cells in S phase, while sS210R with an increased percentage of cells in G2/M phase of cell cycle compared to wild-type, highlighting their ability to promote cell-cycle advancement and/or cell proliferation. 2017 Oncotarget Discussion HBV P203Q;S210R 13;87 19;93 S;S 13;87 14;88 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In line with this concept, we found that the presence of sP203Q and sS210R increases the % of cells in S- and G2/M phase of cell cycle, respectively, suggesting their contribution to the advancement of cell cycle that may pose the basis for an increased cell proliferation. 2017 Oncotarget Discussion HBV P203Q;S210R 57;68 63;74 S;S;S 57;68;103 58;69;104 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In line with this hypothesis, a previous study showed that the sS204R mutation in S-HBsAg C-terminus (along with G145R) exhibited a viral secretion defect compared to the wild-type. 2017 Oncotarget Discussion HBV S204R;G145R 63;113 69;118 S;S 63;82 64;89 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In our study, no deletions were found in HCC-patients with sP203Q or sS210R. 2017 Oncotarget Discussion HBV P203Q;S210R 59;69 65;75 S;S 59;69 60;70 Hepatocellular carcinoma 41 44 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. In our study, the presence of sP203Q and sS210R in HBsAg C-terminus determines a decrease of the extracellular on intracellular HBsAg ratio, reflecting the ability of these mutations to affect HBsAg secretion. 2017 Oncotarget Discussion HBV P203Q;S210R 30;41 36;47 S;S;S;S;S 51;128;193;30;41 56;133;198;31;42 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. Notably, sP203Q and sS210R introduce a negatively and positively charged amino acid, respectively. 2017 Oncotarget Discussion HBV P203Q;S210R 9;20 15;26 S;S 9;20 10;21 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. The increased amount of cyclin A observed in vitro for the mutant sS210R corroborates the impact of this mutation on cell cycle progression. 2017 Oncotarget Discussion HBV S210R 66 72 S 66 67 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. This may suggest that the co-presence of sP203Q/sS210R in HBsAg C-terminus and deletions in pre-S1 and pre-S2 may be lethal for HBV replication. 2017 Oncotarget Discussion HBV S210R;P203Q 48;41 54;47 S;PreS1;PreS2;S;S 58;92;103;41;48 63;98;109;42;49 28152517 Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro. This study shows that sP203Q and sS210R mutations, in HBsAg C-terminal domain (aa 179 to 226), significantly correlate with the presence of HBV-induced HCC. 2017 Oncotarget Discussion HBV P203Q;S210R 22;33 28;39 S;S;S 54;22;33 59;23;34 Hepatocellular carcinoma 152 155 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. Although it is unclear whether these mutants would survive during the treatment of capsid inhibitors, we could predict that the HAP-resistant mutant V124F could be suppressed by SBA_R01. 2017 Scientific reports Discussion HBV V124F 149 154 Capsid 83 89 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The contact areas are in similar order to the closed triangle format (444.4 to 484.9 A2 in Y132A-HAP_R01 structure). 2017 Scientific reports Discussion HBV Y132A 91 96 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. The type 1 (spike-to-contact) and type 2 (contact-to-spike) interfaces are formed by the spike domain (G63-G94) in one dimer and the intersubunit contact domain (G111-C terminus) from the symmetry-related dimer, with a contact surface area of 856.4 A2 and 414.8 A2, respectively. 2017 Scientific reports Discussion HBV G111C 162 168 S 227 234 28205569 Heteroaryldihydropyrimidine (HAP) and Sulfamoylbenzamide (SBA) Inhibit Hepatitis B Virus Replication by Different Molecular Mechanisms. We used the core protein Y132A mutant to trap the oligomer of dimers. 2017 Scientific reports Discussion HBV Y132A 25 30 C 12 16 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. 4B) indicates that the T1849A/T1850C and T1849G/ T1850C double mutations did not impair the epsilon signal function. 2017 Virology Discussion HBV T1850C;T1849A;T1849G;T1850C 30;23;41;49 36;29;47;55 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. A single nucleotide insertion at position 1821 did not increase core protein expression. 2017 Virology Discussion HBV ins 1821 2 46 C 64 68 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. A1846T has been associated with acute-on-chronic liver failure and HCC development, and can coexist with G1896A mutation (; our unpublished observation). 2017 Virology Discussion HBV A1846T;G1896A 0;105 6;111 Acute on chronic liver failure;Hepatocellular carcinoma 32;67 62;70 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Although the T1817C back mutation in clone g1 of genotype G was accompanied by selective loss of the RC DNA. 2017 Virology Discussion HBV T1817C 13 19 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Among HBeAg-negative precore mutations tested, G1896A in conjunction with G1899A was more effective than mutated precore ATG at increasing core protein expression. 2017 Virology Discussion HBV G1896A;G1899A 47;74 53;80 C;C;Precore;Precore 139;6;21;113 143;11;28;120 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. At the immune clearance phase genotypes B and C could develop the A1846T mutation, which according to this study will increase core protein expression and genome replication (Table 1). 2017 Virology Discussion HBV A1846T 66 72 C 127 131 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Both the G1896A and G1899A mutations convert a U:G pair in stem I into a UA pair. 2017 Virology Discussion HBV G1896A;G1899A 9;20 15;26 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. However, mutated precore ATG codon or the C1817T nonsense mutation at codon 2 will inactivate this mechanism to permit the packaging of pcRNA. 2017 Virology Discussion HBV C1817T 42 48 Precore 17 24 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. In addition, genotype B and subgenotype C2 can develop G1896A precore mutation, which was shown to increase core protein expression and genome replication. 2017 Virology Discussion HBV G1896A 55 61 C;Precore 108;62 112;69 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. In this regard, nucleotide 1846 lies outside the epsilon signal, while the G1888A mutation converts a wobble U:G pair in stem II into a more stable U:A pair. 2017 Virology Discussion HBV G1888A 75 81 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Optimization of the Kozak sequence of the uORF through the -3/-2 positions has complex impact: while the T1849A and T1849G mutations would both disrupt a U:A pair, the T1850C mutation converts a U:G pair into a much stronger C:G pair. 2017 Virology Discussion HBV T1849A;T1849G;T1850C 105;116;168 111;122;174 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. Similarly, alpha1 (which harbors G1896A mutation) had higher replication capacity than alpha1M0, which was nullified by addition of the C1817T mutation (mutant G). 2017 Virology Discussion HBV G1896A;C1817T 33;136 39;142 28260621 Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region. This interpretation was supported by the finding that adding an extra C1817T mutation, which shifted translational termination from codon 28 to codon 2, reverted core protein expression to a low level. 2017 Virology Discussion HBV C1817T 70 76 C 162 166 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. A previous study from North India reported the presence of rtM204V/I resistant mutants in 6% and 29% CHB patients receiving LMV for 12 and 18 months respectively while another study from South India detected M204V/I mutations in 27% of LMV-treated patients after a median treatment period of 13 months. 2017 Scientific reports Discussion HBV M204V;M204I;M204I;M204V 61;61;208;208 68;68;215;215 RT 59 61 Chronic Hepatitis B 101 104 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Among the non-classical RT substitutions detected in the study, rtL91I was earlier noted in HBV of genotype D, rtH124N and rtV278I were perceived in HBV of genotype G while rtN131D was encountered in HBV of genotype B derived from different CHB patients under LMV monotherapy in USA. 2017 Scientific reports Discussion HBV L91I;H124N;V278I;N131D 66;113;125;175 70;118;130;180 RT;RT;RT;RT;RT 24;64;111;123;173 26;66;113;125;175 Chronic Hepatitis B 241 244 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. By definition, a 5- to 10-fold increase in the IC50 correlates with partial resistance and hence our data clearly demonstrated partial resistance to tenofovir in the presence of rtH124N polymerase mutation and also strongly indicate the association of rt124N with a slower response to TDF therapy. 2017 Scientific reports Discussion HBV H124N 180 185 P;RT;RT 186;178;252 196;180;254 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. documented that HBV bearing the rtM204V + rtL180M mutations displayed a 3.33 and 2.1-fold increase in the IC50 for TDF compared to wild-type virus in cell culture suggesting that TDF was less efficacious on these LMV-resistant mutants. 2017 Scientific reports Discussion HBV M204V;L180M 34;44 39;49 RT;RT 32;42 34;44 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Following TDF therapy, the frequencies of rtM204I and rtL80I were found to decrease in both responders and non-responders although there was little change in the prevalence of rtM204V and rtL180M. 2017 Scientific reports Discussion HBV M204I;L80I;M204V;L180M 44;56;178;190 49;60;183;195 RT;RT;RT;RT 42;54;176;188 44;56;178;190 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Given that none of the TDF responders could achieve undetectable HBV DNA levels even after 1 year of therapy, it appears that the persistence of the novel RT variants in the quasispecies pool (such as, rtV278I) might cause a reduced sensitivity to TDF and could undermine the therapeutic benefit. 2017 Scientific reports Discussion HBV V278I 204 209 RT;RT 155;202 157;204 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Intriguingly, in-depth analysis of the baseline quasispecies pool showed that while both TDF responders and non-responders carried the well- known LMV resistance mutations in comparable proportions, there were significant differences in the basal frequencies of the one novel RT (rtH124N) and 6 S-substitutions (sS45A, sA/S113T, sT118V, sT125M, sA128V and sR210N) between the two groups. 2017 Scientific reports Discussion HBV S113T;H124N;S45A;A113T;T118V;T125M;A128V;R210N 320;282;312;319;329;337;345;356 327;287;317;327;335;343;351;362 RT;RT;S;S;S;S;S;S;S 276;280;295;312;319;329;337;345;356 278;282;296;313;320;330;338;346;357 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Of these, sI195M and sW196L had been shown to have reduced binding to anti-HBsAg antibodies while a decrease in the antigenicity of the S protein due to the presence of sP127T mutations had been documented. 2017 Scientific reports Discussion HBV I195M;W196L;P127T 10;21;169 16;27;175 S;S;S;S;S 75;10;21;136;169 80;11;22;137;170 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Our mutational analysis focusing on the RT domain of HBV Pol revealed that 75% of our cohort of HBV/D infected patients, who were under LMV for a median duration of 34 months carried the classical rtM204V/I mutation, of which rtM204V was predominant. 2017 Scientific reports Discussion HBV M204V;M204I;M204V 199;199;228 206;206;233 P;RT;RT;RT 57;40;197;226 60;42;199;228 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. Our results further extended these previous findings and raised doubts about the effectiveness of TDF on the heavily LMV experienced Indian patients, where rtM204V + rtL180M mutation is widely prevalent. 2017 Scientific reports Discussion HBV M204V;L180M 158;168 163;173 RT;RT 156;166 158;168 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. We assessed the susceptibility of rtH124N to tenofovir in transiently transfected Huh7 cells in vitro and noted that HBV harboring rt124N consistently demonstrated a 6.5-fold increase in the IC50 values as compared to WT-HBV. 2017 Scientific reports Discussion HBV H124N 36 41 RT;RT 34;131 36;133 28303969 HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy. We noted that the baseline frequency of rtM204V (18.3%) substitution was less than that of rtM204I (25%) in the clonal population of the LMV-failed patients who responded to TDF therapy in contrast to the non-responders where rtM204V was dominant. 2017 Scientific reports Discussion HBV M204V;M204I;M204V 42;93;228 47;98;233 RT;RT;RT 40;91;226 42;93;228 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Accompanying high levels of HBV DNA, the frequencies of G145R and other mutations (K160R, L173P, Q181R in the S region and R153Q, S256G, C332S, L336M in the RT region) were high both at baseline and in the 4th week. 2017 Emerging microbes & infections Discussion HBV G145R;K160R;L173P;Q181R;R153Q;S256G;C332S;L336M 56;83;90;97;123;130;137;144 61;88;95;102;128;135;142;149 RT;S 157;110 159;111 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Because the G145R mutation alters the projecting loop of the 'alpha' determinant, pre-existing neutralizing antibodies cannot adequately recognize the changed epitope. 2017 Emerging microbes & infections Discussion HBV G145R 12 17 S 62 80 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. However, the characteristics of the entire genomes of HBV quasispecies determined using ultra-deep sequencing during G145R mutant infection have not yet been reported. 2017 Emerging microbes & infections Discussion HBV G145R 117 122 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In addition, the Q181R mutation has been recently reported in a new vaccine escape mutant. 2017 Emerging microbes & infections Discussion HBV Q181R 17 22 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In contrast, the frequencies of L110I, T113S and I126T, which may be compensatory mutations, increased in the S region. 2017 Emerging microbes & infections Discussion HBV L110I;T113S;I126T 32;39;49 37;44;54 S 110 111 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In summary, our study shows the dynamic changes in the clinical features and quasispecies characteristics during infection with G145R mutant HBV. 2017 Emerging microbes & infections Discussion HBV G145R 128 133 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In the present study, data from ultra-deep sequencing revealed that mutants harboring different mutations, including G145R and I126T, coexisted in the patient. 2017 Emerging microbes & infections Discussion HBV G145R;I126T 117;127 122;132 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. In the present study, the clinical and quasispecies characteristics associated with G145R immune escape mutant HBV infection were described in detail. 2017 Emerging microbes & infections Discussion HBV G145R 84 89 HBV infections 111 124 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. Infection with G145R mutant HBV may involve a clinical onset that is insidious, as in our subject, who had a slightly elevated ALT level. 2017 Emerging microbes & infections Discussion HBV G145R 15 20 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. On the basis of the level of protective anti-HBs (129.57 mIU/mL) observed in 2009 and recent serological changes, hepatitis B caused by the G145R immune escape mutant was diagnosed. 2017 Emerging microbes & infections Discussion HBV G145R 140 145 S 45 48 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. The G145R mutation in the MHR, which is one of the most prevalent immune escape mutations, can impair HBsAg secretion and has been reported in patients with advanced liver diseases and even liver cancer. 2017 Emerging microbes & infections Discussion HBV G145R 4 9 S 102 107 Liver disease;Hepatocellular carcinoma 166;190 180;202 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. The G145R mutation in the S region is likely to be responsible for weak recognition by anti-HBs. 2017 Emerging microbes & infections Discussion HBV G145R 4 9 S;S 92;26 95;27 28325923 Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant. The presence of amino-acid substitutions in the MHR of HBsAg, such as G145R and I126T, can change the immunogenicity of HBsAg, thus resulting in HBsAg/anti-HBs coexistence and immune escape. 2017 Emerging microbes & infections Discussion HBV G145R;I126T 70;80 75;85 S;S;S;S 156;55;120;145 159;60;125;150 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. A mutation at aa120-aa123 (P120T and T123A) found in patient #10 was deemed essential for the antigenicity of HBs Ag in a previous report. 2017 Yonsei medical journal Discussion HBV P120T;T123A 27;37 32;42 S 110 116 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. According to a study by Svicher, et al., Y100S, found in patients #12 and 21, resulted in decreased antigen-antibody reactivity of HBs Ag, because other variants are incorporated in a step-by-step manner. 2017 Yonsei medical journal Discussion HBV Y100S 41 46 S 131 137 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Among the spontaneously occurring mutations, T123A and T131N were found in patient #10, but not in other patients. 2017 Yonsei medical journal Discussion HBV T123A;T131N 45;55 50;60 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. However, theses mutations were concurrently detected with other previously reported mutations, except for S132F. 2017 Yonsei medical journal Discussion HBV S132F 106 111 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. In our study, I84T was found in patient #22 and was also seen in a control patient, suggesting its origin as a natural polymorphism. 2017 Yonsei medical journal Discussion HBV I84T 14 18 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. In the same study, S17A, P32L, W43L/R, H51P/R, and I84T/M of the pre-S1 region and W3R/Stop and S5A of the pre-S2 region were found in occult HBV infections. 2017 Yonsei medical journal Discussion HBV W3R;W3X;S17A;P32L;W43L;W43R;H51P;H51R;I84T;I84M 83;83;19;25;31;31;39;39;51;51 91;91;23;29;37;37;45;45;57;57 PreS1;PreS2 65;107 71;113 HBV infections 142 156 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Mutations of A11T, D14N, R16K, G19D, F22L, G30E, I42T, and P54Q/T were found in pre-S2. 2017 Yonsei medical journal Discussion HBV A11T;D14N;R16K;G19D;F22L;G30E;I42T;P54Q;P54T 13;19;25;31;37;43;49;59;59 17;23;29;35;41;47;53;65;65 PreS2 80 86 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Only D144E and G145A were detected from patients #2 and 10, respectively, while other known mutations were not found. 2017 Yonsei medical journal Discussion HBV D144E;G145A 5;15 10;20 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Other than F22L and P54T also found in the control group, these pre-S2 mutations were previously not reported or mentioned. 2017 Yonsei medical journal Discussion HBV F22L;P54T 11;20 15;24 PreS2 64 70 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. P127T, found in four of six patients with mutations, appears to be a meaningful mutation contributing to the occurrence of occult HBV infection. 2017 Yonsei medical journal Discussion HBV P127T 0 5 HBV infections 130 143 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. Particularly, F34L and N46H were located in the hepatocyte binding site of the pre-S1. 2017 Yonsei medical journal Discussion HBV F34L;N46H 14;23 18;27 PreS1 79 85 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. S132F, found in patient #7 alone, seems to be associated with occult HBV infection of the host patient. 2017 Yonsei medical journal Discussion HBV S132F 0 5 HBV infections 69 82 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. The 'a' determinant mutations found in this study were I126M/N, P127S/T, T131N, S132F, M133T, F134L/T, D144E, and G145A. 2017 Yonsei medical journal Discussion HBV I126M;I126N;P127S;P127T;T131N;S132F;M133T;F134L;F134T;D144E;G145A 55;55;64;64;73;80;87;94;94;103;114 62;62;71;71;78;85;92;101;101;108;119 S 5 19 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. The newly detected mutations in this study were Q101K (patients #2 and 10), M103I (patients #12 and 21), L104S (patient #2), P105N/R (patients #2, 12, and 21), G112K (patients #12 and 21), T113A (patients #12 and 21), S132F (patient #7), S154P (patient #10), and P160K (patient #10). 2017 Yonsei medical journal Discussion HBV Q101K;M103I;L104S;P105N;P105R;G112K;T113A;S132F;S154P;P160K 48;76;105;125;125;160;189;218;238;263 53;81;110;132;132;165;194;223;243;268 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. The other mutations of F34L, N46H, P65S, T86A, L82H, G83S, and D114E seen in this study are mutations of previously unreported regions. 2017 Yonsei medical journal Discussion HBV F34L;N46H;P65S;T86A;L82H;G83S;D114E 23;29;35;41;47;53;63 27;33;39;45;51;57;68 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. The P127S mutation found in four (patients #2, 10, 12, and 21) patients and G145A found in one patient (patient #10) were previously reported to abolish the two loop structure of the 'a' determinant, resulting in altered hydrophilicity, electrical charge, or acidity of the loops. 2017 Yonsei medical journal Discussion HBV P127S;G145A 4;76 9;81 S 184 198 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. This Y100S mutation appears to be the route towards occult states. 2017 Yonsei medical journal Discussion HBV Y100S 5 10 28332361 Occult HBV among Anti-HBc Alone: Mutation Analysis of an HBV Surface Gene and Pre-S Gene. We found mutations of P65S, T86A, L82H, and G83S in this site, detecting G83S in 5 patients. 2017 Yonsei medical journal Discussion HBV P65S;T86A;L82H;G83S;G83S 22;28;34;44;73 26;32;38;48;77 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Among the missense mutations analyzed (D99G, P120T, C121Y, I126S, G145R, and R160G), only D99G caused HBsAg-negative phenotype. 2017 Virus research Discussion HBV D99G;P120T;C121Y;I126S;G145R;R160G;D99G 39;45;52;59;66;77;90 43;50;57;64;71;82;94 S 102 107 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. In our case, the sW172* mutation was silent at the P protein level and hence not selected by antiviral therapy. 2017 Virus research Discussion HBV W172X 17 23 P;S 51;17 52;18 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. More distal nonsense mutations in the S region include W172*, W182*, W201*, and L209*. 2017 Virus research Discussion HBV W172X;W182X;W201X;L209X 55;62;69;80 60;67;74;85 S 38 39 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. On the other hand, HBsAg secretion (the ratio of extracellular HBsAg/intracellular HBsAg) was completely blocked by the L209* mutation and diminished by the W182* and W201* mutations. 2017 Virus research Discussion HBV L209X;W182X;W201X 120;157;167 125;162;172 S;S;S 19;63;83 24;68;88 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. Site-directed mutagenesis using clones 4.2 and 19.3 confirmed a role of core promoter mutations (A1762T/G1764A in clone 4.2, and T1753C/A1762T/G1764A in clone 19.3) in the high replication capacity. 2017 Virus research Discussion HBV G1764A;A1762T;G1764A;A1762T;T1753C 104;136;143;97;129 110;142;149;103;135 Core promoter 72 85 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The C-terminal 10 residues of the core protein are dispensable for HBV replication, and the high replication capacity of clones 4.2, 4.9, 13.2, and 5.1 suggests that the E180G, S181P, and Q182K mutations present in these clones do not markedly suppress genome replication. 2017 Virus research Discussion HBV E180G;S181P;Q182K 170;177;188 175;182;193 C 34 38 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The G1896A precore mutation to abolish HBeAg expression occurred more often in HCC clones. 2017 Virus research Discussion HBV G1896A 4 10 C;Precore 39;11 44;18 Hepatocellular carcinoma 79 82 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The G72* and Q121* nonsense mutations in the preS region could explain the lack of L protein expression and HBsAg negative phenotype of clones 12.1, 12.3, 8.3, and 8.4, while the C69* and S61* nonsense mutations in the S region were confirmed to abolish HBsAg production. 2017 Virus research Discussion HBV G72X;Q121X;C69X;S61X 4;13;179;188 8;18;183;192 S;S;S;PreS;S 108;254;83;45;219 113;259;92;49;220 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. The W172* mutation is associated with resistance to nucleos(t)ide analogues and secondary to substitution in the reverse trancriptase (RT) domain of the P protein (rtA181T/ sW172*). 2017 Virus research Discussion HBV A181T;W172X;W172X 166;4;173 171;9;179 P;RT;RT;S 153;135;164;173 154;137;166;174 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. These include E180G, S181P, Q182K, and Q182* to remove the last 2 residues (Q182 and C183) of core protein. 2017 Virus research Discussion HBV Q182X;E180G;S181P;Q182K 39;14;21;28 44;19;26;33 C 94 98 28373061 Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer. We found the L209*, W182*, and especially W201* mutations markedly reduced intracellular S protein and HBsAg. 2017 Virus research Discussion HBV L209X;W182X;W201X 13;20;42 18;25;47 S;S 103;89 108;90 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. Additionally, two of our patients had sA184V, which was shown to impede detection by commercial assays of HBsAg in GTE infected Nigerian patients. 2017 Tropical medicine & international health Discussion HBV A184V 38 44 S;S 106;38 111;39 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. In the precore region, the G1896A mutation creates a stop codon in the precore gene abolishing HBeAg expression. 2017 Tropical medicine & international health Discussion HBV G1896A 27 33 C;Precore;Precore 95;7;71 100;14;78 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. In this cohort we found two patients with the well-described G145R mutation, as well as several patients with other mutations potentially leading to immune escape (including 'a' determinant sites 126, 129, 130, 131 and 144). 2017 Tropical medicine & international health Discussion HBV G145R 61 66 S 175 189 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. The double A1762T/G1764A ("TA" mutation) in the BCP region affects mRNA transcription and decreases HBeAg production. 2017 Tropical medicine & international health Discussion HBV G1764A;A1762T 18;11 24;17 BCP;C 48;100 51;105 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. The TA mutation frequency in this study was higher than that observed in other studies from Western Africa, although the frequency of G1896A was similar. 2017 Tropical medicine & international health Discussion HBV G1896A 134 140 28376292 Hepatitis B virus sequencing and liver fibrosis evaluation in HIV/HBV co-infected Nigerians. We found a high frequency of the "TA" mutation, (15/35, 43%) and G1896A mutation (20/35, 57%); mutations in these regions affect the production of HBeAg. 2017 Tropical medicine & international health Discussion HBV G1896A 65 71 C 147 152 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. A recent study has shown that rtA181T mutants with or without S truncation had different virological characteristics. 2017 Virology journal Discussion HBV A181T 32 37 RT;S 30;62 32;63 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. All therapeutic responses of ETV rescue, including decline of serum HBV DNA, virological, biochemical, and serological responses did not differ significantly between the rtA181T/V group and rtA181T/V + rtN236T group (P > 0.05). 2017 Virology journal Discussion HBV A181T;A181V;A181T;A181V;N236T 172;172;192;192;204 179;179;199;199;209 RT;RT;RT 170;190;202 172;192;204 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Antiviral efficacy of TDF for HBV rtA181V/T mutants is still unclear in practice. 2017 Virology journal Discussion HBV A181V;A181T 36;36 43;43 RT 34 36 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Further investigation of rescue therapy, including TDF, for HBV rtA181V/T mutants alone will be necessary. 2017 Virology journal Discussion HBV A181V;A181T 66;66 73;73 RT 64 66 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. However, Villet has reported rtA181V/T mutants had a slight decrease in susceptibility to TDF. 2017 Virology journal Discussion HBV A181V;A181T 31;31 38;38 RT 29 31 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In addition, the follow-up period of our study was relatively short, long-term studies were warranted to evaluate the long-time efficacy of ETV rescue therapy in patients with rtA181T/V mutation. 2017 Virology journal Discussion HBV A181T;A181V 178;178 185;185 RT 176 178 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In summary, this is the first study to investigate the efficacy of ETV in rescuing CHB patients in rtA181T/V mutation and rtA181T/V + rtN236T mutation patients. 2017 Virology journal Discussion HBV A181T;A181V;A181T;A181V;N236T 101;101;124;124;136 108;108;131;131;141 RT;RT;RT 99;122;134 101;124;136 Chronic Hepatitis B 83 86 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In the present study, mean HBV DNA level increased over 4 log10 IU/mL after rtA181T/V mutant emergence,but the total bilirubin, ALT and AST level raised moderately, which suggested that the antiviral drug still showed partial effect to rtA181T/V mutant strain, or the mutant virus defective. 2017 Virology journal Discussion HBV A181T;A181V;A181T;A181V 78;78;238;238 85;85;245;245 RT;RT 76;236 78;238 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. In this study, we evaluated the virological, serological, and biochemical outcomes of ETV rescue therapy in patients who developed HBV rtA181T/V mutation strains and compared the ETV rescue therapy efficacy between rtA181T/V mutation and rtA181T/V + rtN236T mutation patients. 2017 Virology journal Discussion HBV A181T;A181V;A181T;A181V;A181T;A181V;N236T 137;137;217;217;240;240;252 144;144;224;224;247;247;257 RT;RT;RT;RT 135;215;238;250 137;217;240;252 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Our study indicated the similar result that ETV was effective in rtA181T/V mutation patients. 2017 Virology journal Discussion HBV A181T;A181V 67;67 74;74 RT 65 67 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. The results of the present study indicate that ETV is efficient in rescuing rtA181T/V mutation patients and the HBV DNA level is the only predictor of 12 months antiviral outcomes. 2017 Virology journal Discussion HBV A181T;A181V 78;78 85;85 RT 76 78 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. The rtA181T/V is a cross-resistance mutation. 2017 Virology journal Discussion HBV A181T;A181V 6;6 13;13 RT 4 6 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. These explained that many patients who continued previously treatment could partly improve biochemical and virological results after occurring rtA181T/V mutant. 2017 Virology journal Discussion HBV A181T;A181V 145;145 152;152 RT 143 145 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. They found the serum levels of HBV DNA and HBsAg in pHBV-rtA181T/sW172* injected mice were significantly lower than that of pHBV-rtA181T/sW172L injected mice. 2017 Virology journal Discussion HBV W172X;W172L;A181T;A181T 65;137;59;131 71;143;64;136 S;RT;RT;S;S 43;57;129;65;137 48;59;131;66;138 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. Unfortunately, we could not demonstrate any difference between the two rtA181T mutants. 2017 Virology journal Discussion HBV A181T 73 78 RT 71 73 28376852 Antiviral efficacy of entecavir for hepatitis B virus rtA181V/T mutants. We evaluated the efficacy of ETV in rescuing patients with rtA181T/V mutation strain and rtA181T/V + rtN236T mutation strain. 2017 Virology journal Discussion HBV A181T;A181V;A181T;A181V;N236T 61;61;91;91;103 68;68;98;98;108 RT;RT;RT 59;89;101 61;91;103 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Although we did not examine the infectious ability of the isolates with sC69*, infection of new hepatocytes through alternative secretion of the isolates, as evidenced via exosomes in our study, is expected even if the incomplete structure of envelop proteins does not support the infectivity. 2017 Journal of hepatology Discussion HBV C69X 72 77 S 72 73 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Furthermore, the rtS78T exchange was also found to be increased in adefovir-treated patients suggesting a potential resistance to adefovir alone or in combination with other resistance mutations. 2017 Journal of hepatology Discussion HBV S78T 19 23 RT 17 19 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. However, these mutations are located 752 (rtS78T) and 1104 (preS1/S2del) nucleotides upstream of the known EnhI. 2017 Journal of hepatology Discussion HBV S78T 44 48 Enh I;PreS1;RT 107;60;42 111;65;44 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. However, we did not observe associated rtL80I substitutions by sequencing in our cases. 2017 Journal of hepatology Discussion HBV L80I 41 45 RT 39 41 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. In conclusion, we herein show the selection of functionally relevant rtS78T/sC69* mutation in two HBV-infected patients with TDF/ETV combination therapy. 2017 Journal of hepatology Discussion HBV C69X;S78T 76;71 81;75 RT;S 69;76 71;77 HBV infections 98 110 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. In this regard, the emergence of rtS78T/sC69* mutation has been occasionally reported in the literature. 2017 Journal of hepatology Discussion HBV C69X;S78T 40;35 45;39 RT;S 33;40 35;41 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. In this regard, the rtL80I was shown to be associated with restoring viral replication and increasing drug resistance properties of LAM-resistant isolates with impaired replication. 2017 Journal of hepatology Discussion HBV L80I 22 26 RT 20 22 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. In this study, we describe the development of the rtS78T/sC69* mutation during long-term antiviral therapy in two patients with chronic HBV infection. 2017 Journal of hepatology Discussion HBV C69X;S78T 57;52 62;56 RT;S 50;57 52;58 Chronic HBV infection 128 149 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. It has been speculated that truncated S proteins, like those having sC69*, may result in secretion incompetent variants due to the deletion of the HBsAg C-terminal domain. 2017 Journal of hepatology Discussion HBV C69X 68 73 S;S;S 147;38;68 152;39;69 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Moreover, based on computational studies rtS78T mutation implies a large affinity loss for TDF. 2017 Journal of hepatology Discussion HBV S78T 43 47 RT 41 43 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Our in vitro analyses indicated an enhanced replicative efficacy for rtS78T/sC69* as well as a partial resistance to ETV and to TDF. 2017 Journal of hepatology Discussion HBV C69X;S78T 76;71 81;75 RT;S 69;76 71;77 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The increased 3.5Kb HBV-RNA, pgDNA and HBeAg levels due to rtS78T and to a lesser extent preS1/S2del mutations, could possibly indicate a cis-acting role exerted by this domain of the viral genome to up-regulate transcription from PC. 2017 Journal of hepatology Discussion HBV S78T 61 65 C;Precore;PreS1;RT 39;231;89;59 44;233;94;61 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. The presence of rtS78T in addition to rtT184S, rtV173L, rtL180M, and rtM204V, was associated with a two-fold reduction in ETV susceptibility; however, in line with our results, the ETV resistance level for this mutation alone did not exceed 1.8-fold of the level of wild type HBV. 2017 Journal of hepatology Discussion HBV S78T;T184S;V173L;L180M;M204V 18;40;49;58;71 22;45;54;63;76 RT;RT;RT;RT;RT 16;38;47;56;69 18;40;49;58;71 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. Therefore, as also observed in the second serum analysis of patient A with detectable serum HBV-DNA in spite of 100% frequency of sC69*, a stop codon at S may not hinder the entire process of particle envelopment and release for mutated variants but possibly the stability of secreted virions. 2017 Journal of hepatology Discussion HBV C69X 130 135 S;S 130;153 131;154 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. They also reported a significant reduction in HBV genome levels, (DNA and RNA) both intra and extracellularly, under the influence of sC69*. 2017 Journal of hepatology Discussion HBV C69X 134 139 S 134 135 28392234 Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy. They showed that truncated S proteins with sC69* are only detectable intracellularly and through an HA Tag domain fused with HBs. 2017 Journal of hepatology Discussion HBV C69X 43 48 S;S;S 125;27;43 128;28;44 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Consistent with this, the results obtained by in vitro experiments showed that extracellular HBsAg with P120T was less detectable than wild type HBsAg or the mutant with S143L by CLEIA. 2017 World journal of hepatology Discussion HBV P120T;S143L 104;170 109;175 S;S 93;145 98;150 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. In conclusion, the prevalence of occult hepatitis B was detected in patients with hematological malignancies in South Egypt in association with two mutations in the HBsAg, P120T and S143L. 2017 World journal of hepatology Discussion HBV P120T;S143L 172;182 177;187 S 165 170 Hematologic Neoplasms 82 108 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. In vitro analysis of these two amino acid mutations revealed that P120T mutation reduces the antigenicity of HBsAg in vitro without affecting the HBV DNA replication capacity. 2017 World journal of hepatology Discussion HBV P120T 66 71 S 109 114 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. In vitro studies described the impairment of virion and/or S protein secretion in both Huh7 cells and hydrodynamic injected mice by Q129R MHR mutation. 2017 World journal of hepatology Discussion HBV Q129R 132 137 S 59 60 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Neither of these mutations affected the replication activity, virion or S protein secretion but one of the mutations, P120T, interfered with detection by current commercial assays probably by inducing a conformational change. 2017 World journal of hepatology Discussion HBV P120T 118 123 S 72 73 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Rather, the P120T mutation appeared to reduce the antigenicity of HBsAg. 2017 World journal of hepatology Discussion HBV P120T 12 17 S 66 71 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. The authors concluded that occult HBV infection is associated with P120T and S143L mutations and 120T mutation impairs the detection of HBsAg by chemiluminescence enzyme immunoassay. 2017 World journal of hepatology Discussion HBV P120T;S143L 67;77 72;82 S 136 141 HBV infections 34 47 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Two amino acid substitutions, P120T and S143L, were found in HBsAg. 2017 World journal of hepatology Discussion HBV P120T;S143L 30;40 35;45 S 61 66 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. Two prevalent amino acid substitutions P120T and S143L were associated with OBI in the present study. 2017 World journal of hepatology Discussion HBV P120T;S143L 39;49 44;54 Occult Hepatitis B 76 79 28396718 Characteristics of escape mutations from occult hepatitis B virus infected patients with hematological malignancies in South Egypt. We detected two previously reported escape mutations P120T and S143L that were associated with occult HBV infection, and investigated the mechanism by which these mutations cause occult infection using an in vitro system. 2017 World journal of hepatology Discussion HBV P120T;S143L 53;63 58;68 HBV infections;Occult Hepatitis B 102;179 115;195 28472081 HBV DNA genome co-transfection procedure for the evaluation of relative fitness. The G1896A mutation in pC region converts tryptophan (TGG) into a translational stop codon (TAG) which stops the production of HBeAg. 2017 PloS one Discussion HBV G1896A 4 10 C;Precore 127;23 132;25 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. As there were so few studies with a subgroup analysis of genotype A for patients with A1762T, G1764A, or A1762T/G1764A, it was not possible to make a comparison of the risk with other genotypes. 2017 Medicine Discussion HBV G1764A;A1762T;G1764A;A1762T 112;86;94;105 118;92;100;111 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Despite these limitations, we find that mutations G1896A, A1762T, G1764A, and A1762T/G1764A are associated with a higher risk of HCC. 2017 Medicine Discussion HBV G1764A;G1896A;A1762T;G1764A;A1762T 85;50;58;66;78 91;56;64;72;84 Hepatocellular carcinoma 129 132 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. First, although the correlation between the mutation G1896A and HCC was statistically significant, the correlations between the risk of HCC and the mutation G1896A for genotypes B, C, and D were not. 2017 Medicine Discussion HBV G1896A;G1896A 53;157 59;163 Hepatocellular carcinoma;Hepatocellular carcinoma 64;136 67;139 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. For patients with A1762T or G1764A, genotype C was most susceptible to HCC, while genotype B was most susceptible to HCC in patients with the double mutation A1762T/G1764A. 2017 Medicine Discussion HBV G1764A;A1762T;G1764A;A1762T 165;18;28;158 171;24;34;164 Hepatocellular carcinoma;Hepatocellular carcinoma 71;117 74;120 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. In contrast, Liao et al study concluded that genotype C was the most susceptible to HCC in patients with A1762T/G1764A. 2017 Medicine Discussion HBV G1764A;A1762T 112;105 118;111 Hepatocellular carcinoma 84 87 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. Mutation G1896A may suppress the expression of HBeAg by inducing a stop codon. 2017 Medicine Discussion HBV G1896A 9 15 C 47 52 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. The A1762G/G1764A mutation increased transcription of pregenomic RNA by the removing of the nuclear receptor-binding motif, thus creating a binding site for hepatocyte nuclear factor. 2017 Medicine Discussion HBV G1764A;A1762G 11;4 17;10 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. The data show a similar risk of HCC associated with A1762T, G1764A, and A1762T/G1764A with OR of 3.96, 3.48, and 3.96, respectively. 2017 Medicine Discussion HBV G1764A;A1762T;G1764A;A1762T 79;52;60;72 85;58;66;78 Hepatocellular carcinoma 32 35 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. The results support the conclusion that each of these mutations (A1762T, G1764A, and A1762T/G1764A) plays a significant role in the progression of chronic HBV infection to HCC. 2017 Medicine Discussion HBV G1764A;A1762T;G1764A;A1762T 92;65;73;85 98;71;79;91 Chronic HBV infection;Hepatocellular carcinoma 147;172 168;175 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. The risk of HCC associated with the double mutation A1762T/G1764A was similar to those described in previous meta-analyses. 2017 Medicine Discussion HBV G1764A;A1762T 59;52 65;58 Hepatocellular carcinoma 12 15 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. This may indicate that any 1 site of mutation of A1762T or G1764A constitutes a danger signal. 2017 Medicine Discussion HBV A1762T;G1764A 49;59 55;65 28489767 The association between hepatitis B mutants and hepatocellular carcinoma: A meta-analysis. This meta-analysis shows that the mutations G1896A, A1762T, G1764A, and A1762T/G1764A are each associated with a statistically significant increase in the risk of HCC. 2017 Medicine Discussion HBV G1764A;G1896A;A1762T;G1764A;A1762T 79;44;52;60;72 85;50;58;66;78 Hepatocellular carcinoma 163 166 28582431 Hepatitis B genotypes and surface antigen mutants present in Pakistani blood donors. The most common mutations were found in E2 at amino acid positions 143, 144, and 145, which have been shown to impact diagnostic assay sensitivity, as has P120S the most common E1 mutant observed in this study. 2017 PloS one Discussion HBV P120S 155 160 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Further sequence analysis revealed other mutations such as sR122K, sG145A andsW172* within the surface ORF of the OBI subjects (mainly belonging to HBV/D1 and D3) but at low frequencies. 2017 PloS one Discussion HBV R122K;G145A;W172X 59;67;77 65;73;83 S;S;S 59;67;95 60;68;102 Occult Hepatitis B 114 117 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Furthermore, 3TC resistance mutations (rtL180M + rtM204V) were also observed in one of the OBI patients, despite the population being treatment-naive. 2017 PloS one Discussion HBV L180M;M204V 41;51 46;56 RT;RT 39;49 41;51 Occult Hepatitis B 91 94 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. In one instance, Blaich et.al reported reactivation of HBV infection with mutated HBsAg harboring sQ129R in a liver transplant recipient, who previously received a graft from a complete seronegative individual. 2017 PloS one Discussion HBV Q129R 98 104 S;S 82;98 87;99 HBV infections 55 68 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. Of the many mutations that were detected, the major substitution to be associated with occult infection was sQ129R in the surface gene (Table 2). 2017 PloS one Discussion HBV Q129R 108 114 S;S 108;122 109;129 Occult Hepatitis B 87 103 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. On the other hand, some HBV/A1 isolates carried the sT118K mutation in their major hydrophilic loop, which has been previously reported to be associated with failure in HBsAg detection. 2017 PloS one Discussion HBV T118K 52 58 S;S 169;52 174;53 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The occult subjects were mainly of HBV/D1 and harbored a unique sQ129R mutation in their surface gene, which might affect their HBsAg secretion. 2017 PloS one Discussion HBV Q129R 64 70 S;S;S 128;64;89 133;65;96 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The presence of both sR122K and sG145A had been earlier reported among the occult patients from the US, where the combined presence of these two mutations resulted in decreased levels of HBsAg in vitro. 2017 PloS one Discussion HBV R122K;G145A 21;32 27;38 S;S;S 187;21;32 192;22;33 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The presence of sA128V substitution, an immune escape mutation, is often associated with HBV/D2 and is considered as a subgenotype specific change. 2017 PloS one Discussion HBV A128V 16 22 S 16 17 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. The salient findings of this study include 1) high prevalence of occult infection among the anti-HBc positive subjects, as well as the presence of seronegative OBI, 2) distinct differences with respect to subgenotype distribution and clonal diversity between occult and chronic HBV infection, and 3) potential association of OBI with HBV/D1 harboring a signature sQ129R mutation in its surface gene. 2017 PloS one Discussion HBV Q129R 363 369 C;S;S 97;363;386 100;364;393 Occult Hepatitis B;Occult Hepatitis B;Occult Hepatitis B 65;160;325 81;163;328 28591184 Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India. These HBV/D3 isolates exclusively carried the sT125M mutation in their surface gene and were different from the HBV/D3 isolates found among HBsAg positive patients. 2017 PloS one Discussion HBV T125M 46 52 S;S;S 140;46;71 145;47;78 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. also observed that PreC mutation (G1896A) is restricted to HBV strains with T1858 and hardly occurs in those with C1858. 2017 Electronic physician Discussion HBV G1896A 34 40 Precore 19 23 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. Mutation of G1896A in PreC region shuts off the HBe Ag synthesis by introducing a stop codon. 2017 Electronic physician Discussion HBV G1896A 12 18 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. The frequency of the G1896A mutation was significantly higher in the HBe Ag negative patients in our study, which was compatible with results of previous studies. 2017 Electronic physician Discussion HBV G1896A 21 27 C 69 72 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. The G1896A mutation occurs when nucleotide 1858 is composed of the thymine-nitrogen base, which leads to better stabilization in lower stem. 2017 Electronic physician Discussion HBV G1896A 4 10 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. These findings were in agreement with the theory that the relation between G1896A precore mutation and the HBV genotypes is due to different stabilization energy of each genotype as a result of the base pairing of the stem loop structure of the encapsidation sequence of pregenome RNA. 2017 Electronic physician Discussion HBV G1896A 75 81 Precore 82 89 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. This explains the high prevalence of G1896A in Asia and the Mediterranean region where the predominant HBV genotype is D, and its low prevalence in North America and Europe. 2017 Electronic physician Discussion HBV G1896A 37 43 28607644 Prevalence and Characteristics of Precore Mutation in Iran and Its Correlation with Genotypes of Hepatitis B. Two other studies also indicated the G1896A precore mutation was more frequent in the group of patients with genotype D than in the patients with genotype A. 2017 Electronic physician Discussion HBV G1896A 37 43 Precore 44 51 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. In the literature, there are no mutations in the S region associated with the rtA194T resistance mutation, confirming the results found. 2017 Infection and drug resistance Discussion HBV A194T 80 85 RT;S 78;49 80;50 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. One of the resistance mutations found in the Northeastern Region was rtA194T, which can be associated with resistance to TDF, which has shown in vitro reduced susceptibility to TDF when combined with the resistance mutations to LAM M204V and L180M. 2017 Infection and drug resistance Discussion HBV A194T;M204V;L180M 71;232;242 76;237;247 RT 69 71 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The clinical implication of the rtA194T mutation must be determined through long-term follow-up clinical studies. 2017 Infection and drug resistance Discussion HBV A194T 34 39 RT 32 34 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The HBeAg-patients may have an increased risk of selecting the rtA194T mutation, and there-fore, antiviral resistance, so another alternative would be an indication of ETV as a first drug of choice. 2017 Infection and drug resistance Discussion HBV A194T 65 70 C;RT 4;63 9;65 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The other two mutations are associated with resistance to LAM rtL180M + rtM204V and rtS202I. 2017 Infection and drug resistance Discussion HBV L180M;M204V;S202I 64;74;86 69;79;91 RT;RT;RT 62;72;84 64;74;86 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The resistance mutations rtL180M + rtM204V and rtS202I may be associated to the presence of mutations in the coding region of the HBsAg envelope region (S of the HBV), as found in the patterns I195M, W196L, and G145R, indicating vaccine escape. 2017 Infection and drug resistance Discussion HBV L180M;M204V;S202I;I195M;W196L;G145R 27;37;49;193;200;211 32;42;54;198;205;216 S;S;RT;RT;RT;S 136;130;25;35;47;153 144;135;27;37;49;154 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The rtM204V mutation is considered a primary resistance mutation due to the susceptibility of HBV to LAM, and the rtL180M mutations are considered compensatory or secondary mutations, which can increase the viral replication fitness. 2017 Infection and drug resistance Discussion HBV M204V;L180M 6;116 11;121 RT;RT 4;114 6;116 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. The rtM204V mutation was the most common in studies of naive patients, which is the resistance mutation associated with LAM. 2017 Infection and drug resistance Discussion HBV M204V 6 11 RT 4 6 28740410 Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B. Two major mutations of adefovir resistance are rtN236T and rtA181V/T, and in the current study we found the rtN236T mutation. 2017 Infection and drug resistance Discussion HBV A181V;A181T;N236T;N236T 61;61;49;110 68;68;54;115 RT;RT;RT 47;59;108 49;61;110 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Atypical substitutions of rtI169L, rtA181G, rtS202T/R, rtM204L, rtM250K were also detected. 2017 Viruses Discussion HBV A181G;S202T;S202R;M250K;I169L;M204L 37;46;46;66;28;57 42;53;53;71;33;62 RT;RT;RT;RT;RT 26;35;44;55;64 28;37;46;57;66 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Consistent with our findings, atypical substitutions of rtI169L, rtS202R, and rtM204L have been detected in six treatment-naive CHB patients with low proportions using a high-throughput sequencing method. 2017 Viruses Discussion HBV I169L;S202R;M204L 58;67;80 63;72;85 RT;RT;RT 56;65;78 58;67;80 Chronic Hepatitis B 128 131 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. found that three patients had an rtI169L substitution at a level of 1-8% using a clone sequencing method. 2017 Viruses Discussion HBV I169L 35 40 RT 33 35 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Furthermore, in vitro studies showed that substitutions rtS202R and rtM250K would severely impair the replication capability of HBV variants with LAM resistance substitutions (rtL180M + rtM204V), while substitution rtS202T played only a minor role in ETV resistance. 2017 Viruses Discussion HBV M250K;S202R;L180M;M204V;S202T 70;58;178;188;217 75;63;183;193;222 RT;RT;RT;RT;RT 56;68;176;186;215 58;70;178;188;217 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. However, rtT184A/S alone would not lead to clinical resistance to ETV. 2017 Viruses Discussion HBV T184A;T184S 11;11 18;18 RT 9 11 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. However, we should notice that only 7 of 16 sequences harbored typical NUCr AA substitution types, i.e., 6 of rtL80V and 1 of rtT184A. 2017 Viruses Discussion HBV L80V;T184A 112;128 116;133 RT;RT 110;126 112;128 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. In addition, we found that the detected atypical substitutions of rtI169L, rtA181G, rtS202T/R, rtM204L, and rtM250K were not reported in NUCs-treated patients by the Stanford HBV Drug Resistance Database (; accessing date: 17 January 2017). 2017 Viruses Discussion HBV A181G;S202T;S202R;M250K;I169L;M204L 77;86;86;110;68;97 82;93;93;115;73;102 RT;RT;RT;RT;RT 66;75;84;95;108 68;77;86;97;110 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. In conclusion, we confirmed the presence of naturally occurring typical NUCr substitutions of rtL80V, rtV173L and rtT184A/S with low frequencies before the clinical approval of NUCs. 2017 Viruses Discussion HBV L80V;T184A;T184S;V173L 96;116;116;104 100;123;123;109 RT;RT;RT 94;102;114 96;104;116 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Interestingly, 59.3% (16/27) had an atypical AA substitution type at these codons, meaning that their roles in NUCr and viral fitness are still unknown, as is the case for rtM204L. 2017 Viruses Discussion HBV M204L 174 179 RT 172 174 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. It has been related to ETV resistance in the presence of the rtM204V + rtL180M backbone. 2017 Viruses Discussion HBV M204V;L180M 63;73 68;78 RT;RT 61;71 63;73 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. No study has been performed to elucidate the relationship between substitution rtA181G and ADV resistance. 2017 Viruses Discussion HBV A181G 81 86 RT 79 81 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Notably, 4 of 6 rtL80V-containing sequences were from different clones of the same patient. 2017 Viruses Discussion HBV L80V 18 22 RT 16 18 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. reported that substitution at rtI169 could only modestly decrease the susceptibility to ETV in the recombinant viruses with LAM resistance and rtM250V substitutions, increasing the viral fitness for survival. 2017 Viruses Discussion HBV M250V 145 150 RT;RT 30;143 32;145 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Substitution rtM204L was shown to be sensitive to LAM in a study. 2017 Viruses Discussion HBV M204L 15 20 RT 13 15 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Substitution rtT184A/S (n = 2) was the only naturally occurring substitution detected as belonging to a typical primary NUCr substitution. 2017 Viruses Discussion HBV T184A;T184S 15;15 22;22 RT 13 15 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. Substitutions rtL80V (n = 7) or rtV173L (n = 2) are typical secondary substitutions that can restore functional defects of HBV polymerase caused by primary LAM or LdT resistance substitutions. 2017 Viruses Discussion HBV L80V;V173L 16;34 20;39 P;RT;RT 127;14;32 137;16;34 28749433 HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining. This suggests that these atypical substitutions might not play important roles in the emergence of NUCr as compared to rtA181T/V, rtS202C/G/I, rtM204I/V and rtM250I/L/V. 2017 Viruses Discussion HBV A181T;A181V;S202C;S202G;S202I;M204I;M204V;M250I;M250L;M250V 121;121;132;132;132;145;145;159;159;159 128;128;141;141;141;152;152;168;168;168 RT;RT;RT;RT 119;130;143;157 121;132;145;159 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Additionally, a small amount of P127T, A128V, G130E, T131P/N, M133T/I, F134L and D144N mutations was observed in our study, including the less frequent T131N/M133T double mutations. 2017 Scientific reports Discussion HBV M133T;P127T;A128V;G130E;T131P;T131N;M133T;M133I;F134L;D144N;T131N 158;32;39;46;53;53;62;62;71;81;152 163;37;44;51;60;60;69;69;76;86;157 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Again, an in vitro model revealed that HBV with a G145R mutation shared the replication efficacy with equal to wild-type virus. 2017 Scientific reports Discussion HBV G145R 50 55 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. confirmed that G145R virus could circulate as a stable strain for 8 years of follow-up. 2017 Scientific reports Discussion HBV G145R 15 20 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Four other types of VEMs (Q129H, S143L, D144A, D144E), which were known to be associated with virus secretion and lower reactivity in HBsAg assays, were also detected. 2017 Scientific reports Discussion HBV Q129H;S143L;D144A;D144E 26;33;40;47 31;38;45;52 S 134 139 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. Of the 11 positions where mutations occurred in "alpha" determinant region, the most frequent mutation position was aa 126 (I126S/N and T126A, 29.63%), and 145 (G145R/A, 25.93%), all of which were known to act as VEMs, accounting for more than half of the total mutation strains wither the "alpha" determinant. 2017 Scientific reports Discussion HBV I126S;I126N;T126A;G145R;G145A 124;124;136;161;161 131;131;141;168;168 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. T131N/M133T can create a novel N-linked glycosylation site, and play a role in some HBV immune escape mutants. 2017 Scientific reports Discussion HBV M133T;T131N 6;0 11;5 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. The well-known G145R/A mutations were often found in vaccination failure settings. 2017 Scientific reports Discussion HBV G145R;G145A 15;15 22;22 28751727 Temporal trend of hepatitis B surface mutations in the post-immunization period: 9 years of surveillance (2005-2013) in eastern China. To the best our knowledge, D144N is a new identified mutation in the present study. 2017 Scientific reports Discussion HBV D144N 27 32 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. But looking at the promoter region mutations, G1613A mutation was identified in 10.3% of these 31 strains, C1653T was 0%, T1753V was 3.2%, A1762T/G1764A was 16.1%, and C1766T /T1768A was 3.2%. 2017 PloS one Discussion HBV G1764A;T1768A;G1613A;C1653T;T1753V;A1762T;C1766T 146;176;46;107;122;139;168 152;182;52;113;128;145;174 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. Reported promoter mutations are G1613A, C1653T, and T1753V single mutations and A1762T/G1764A double mutations. 2017 PloS one Discussion HBV G1764A;G1613A;C1653T;T1753V;A1762T 87;32;40;52;80 93;38;46;58;86 28753615 Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family. reported that single G1613A mutation was associated with future emergence of HCC. 2017 PloS one Discussion HBV G1613A 21 27 Hepatocellular carcinoma 77 80 28859616 Molecular characterization of hepatitis B virus in Vietnam. A1762T & G1764 T double mutation). 2017 BMC infectious diseases Discussion HBV A1762T;G1764T 0;9 6;16 28859616 Molecular characterization of hepatitis B virus in Vietnam. Approximately one quarter of the genotype B patients had a G1896A mutation. 2017 BMC infectious diseases Discussion HBV G1896A 59 65 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Based on these findings, the accumulation of ROS followed by the activation of JNK may also be contributed to C1485T-HBx -dependent hepatocarcinogenesis. 2017 Scientific reports Discussion HBV C1485T 110 116 X 117 120 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Collectively, the findings obtained from human and mouse studies support our conclusion that the C1485T mutation in the HBx gene is a susceptible factor for the development of HBV-related hepatocarcinogenesis. 2017 Scientific reports Discussion HBV C1485T 97 103 X 120 123 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with the findings of human studies, experimental models of DEN-induced hepatocarcinogenesis revealed that C1485T-HBxTg mice were more susceptible to the development of HCC than WT-HBxTg and non-Tg mice. 2017 Scientific reports Discussion HBV C1485T 117 123 Hepatocellular carcinoma 179 182 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with the findings reported by Maeda et al., enhancements in DEN-induced hepatocarcinogenesis in C1485T-HBxTg mice were characterized by significant increase of ROS with the suppression of NF-kappaB activation in the liver, which are involved in hepatocarcinogenesis in C1485T-HBxTg mice treated with DEN. 2017 Scientific reports Discussion HBV C1485T;C1485T 107;280 113;286 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistent with this result, the activation of NF-kappaB was markedly suppressed in the livers of C1485T-HBxTg mice, as assessed by the expression of phospho-IkappaB alpha and degradation of IkappaB alpha. 2017 Scientific reports Discussion HBV C1485T 98 104 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Consistently, immunoblotting revealed that the expression of p-GSK3beta and beta-catenin in the liver was significantly stronger in C1485T-HBxTg mice than in WT-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 132 138 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. From a basic research standpoint, C1485T-HBxTg mice are a useful tool for the study of the molecular mechanisms underlying HBx-related hepatocarcinogenesis. 2017 Scientific reports Discussion HBV C1485T 34 40 X 123 126 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Furthermore, an immunohistochemical analysis revealed that the incorporation of BrdU and expression of cyclin D1 in hepatocytes were stronger in C1485T-HBxTg mice than in WT-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 145 151 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Furthermore, the nuclear translocation of p65, a major NF-kappaB subunit, in hepatocytes was more strongly inhibited in C1485T-HBxTg mice than in WT-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 120 126 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Furthermore, the occurrence of the C1485T mutation was markedly higher in HCC patients without LC than in those with LC in our cohort. 2017 Scientific reports Discussion HBV C1485T 35 41 Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 74;95;117 77;97;119 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Given the fact that WT-HBx also induces HBV-related carcinogenesis through the activation of the Wnt/beta-catenin signaling pathways, our results indicate that the presence of the C1485T HBx mutation further enhances hepatocarcinogenesis by augmenting Wnt/beta-catenin signaling pathways. 2017 Scientific reports Discussion HBV C1485T 180 186 X;X 23;187 26;190 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In addition, activation of JNK is reportedly contributed to the expansion and proliferation of stem-progenitor cells; the C1485T-HBxTg mice showed an increase of CD133+ stem-progenitor cells compared to WT-HBxTg mice after treated with DEN (data not shown). 2017 Scientific reports Discussion HBV C1485T 122 128 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In experimental models of hepatocarcinogenesis, C1485T-HBxTg mice were more susceptible to the development of HCC than WT-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 48 54 Hepatocellular carcinoma 110 113 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In human studies utilizing age, sex, and HBV-DNA-matched serum samples obtained from CHB patients, we found that the incidence of HCC was higher in patients bearing C1485T or C1653T HBx mutations than in those bearing wild type HBx. 2017 Scientific reports Discussion HBV C1485T;C1653T 165;175 171;181 X;X 182;228 185;231 Chronic Hepatitis B;Hepatocellular carcinoma 85;130 88;133 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In human studies, we found that the C1485T HBx mutation was more frequent in the sera of patients with HCC than in those without HCC. 2017 Scientific reports Discussion HBV C1485T 36 42 X 43 46 Hepatocellular carcinoma;Hepatocellular carcinoma 103;129 106;132 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In the present study, we demonstrated that the C1485T HBx mutation is involved in hepatocarcinogenesis in human and mice. 2017 Scientific reports Discussion HBV C1485T 47 53 X 54 57 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. In this regards, our preliminary studies show that C1485T mutation was successfully detected in the HCC tissue in 3 of 5 patients bearing such mutation in the serum (data not shown). 2017 Scientific reports Discussion HBV C1485T 51 57 Hepatocellular carcinoma 100 103 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. It should be noted, however, that no difference was detected in JNK activation in HepG2 cells overexpressing WT-HBx gene and C1485T-HBx gene in the reporter gene assay. 2017 Scientific reports Discussion HBV C1485T 125 131 X;X 112;132 115;135 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Our results suggest, from a clinical viewpoint, that a screening of C1485T-HBx mutation in serum might represent a promising approach for predicting the emergence of HCC for CHB, particularly in patients carrying HBV genotype C. 2017 Scientific reports Discussion HBV C1485T 68 74 X 75 78 Hepatocellular carcinoma;Chronic Hepatitis B 166;174 169;177 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Previous study also showed that the HBx codon-38 change in human HCC, which is attributed to the presence of C1485T, was detected in corresponding non-tumor tissues, and was consistent with those in serum. 2017 Scientific reports Discussion HBV C1485T 109 115 X 36 39 Hepatocellular carcinoma 65 68 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Regarding the mechanisms responsible for enhanced tumorigenesis in C1485T-HBxTg mice, we characterized cancer-related signaling pathways in the presence of C1485T-HBx genes. 2017 Scientific reports Discussion HBV C1485T;C1485T 67;156 73;162 X 163 166 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Reporter gene assays that the transactivation of Wnt signaling pathways was markedly enhanced in HepG2 cells overexpressing C1485T-HBx than in those expressing WT-HBx. 2017 Scientific reports Discussion HBV C1485T 124 130 X;X 131;163 134;166 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. showing that the C1485T mutation in the HBx gene was associated the development of HBV genotype C-related HCC. 2017 Scientific reports Discussion HBV C1485T 17 23 X 40 43 Hepatocellular carcinoma 106 109 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Since HBx is a multifunctional protein that not only activates transcriptional transactivation, but also mediates cell growth via proliferation and apoptosis, our results suggest that the C1485T mutation induces hepatocarcinogenesis through enhanced cell proliferation and cell cycle progression. 2017 Scientific reports Discussion HBV C1485T 188 194 X 6 9 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Since JNK signaling pathways are regarded as an important contributor to hepatocyte proliferation and HCC development, the activation of these pathways may be involved in enhanced hepatocarcinogenesis observed in C1485T-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 213 219 Hepatocellular carcinoma 102 105 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Since the activation of the Wnt signaling pathway induces the expression of downstream oncogenic proteins, such as c-myc and cyclin D1, which are overexpressed in the liver of C1485T-HBxTg mice, these results strongly suggest that C1485T-HBx enhances cell cycle progression through the activation of Wnt signaling pathways. 2017 Scientific reports Discussion HBV C1485T;C1485T 176;231 182;237 X 238 241 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Such suppression of NF-kappaB in the presence of C1485T- mutation is in contrast to previous findings showing that HBx induces malignant transformation through the inhibition of hepatocyte apoptosis and promotion of angiogenesis in an NF-kappaBeta-dependent manner. 2017 Scientific reports Discussion HBV C1485T 49 55 X 115 118 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The development of HCC in the presence of the C1485T-HBx mutation is associated with the enhanced activation of the Wnt and JNK signaling pathways, decreased activation of NF-kappaB signaling pathways, and accumulation of ROS. 2017 Scientific reports Discussion HBV C1485T 46 52 X 53 56 Hepatocellular carcinoma 19 22 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The increase of phosphorylated c-Jun is another characteristic associated with the development of HCC in the presence of C1485T-HBx in mice model. 2017 Scientific reports Discussion HBV C1485T 121 127 X 128 131 Hepatocellular carcinoma 98 101 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The relationship between the C1485T mutation and emergence of HCC has not been confirmed in HBV genotype A infection. 2017 Scientific reports Discussion HBV C1485T 29 35 Hepatocellular carcinoma 62 65 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The results obtained from male Tg mice revealed a higher incidence of HCC in C1485T-HBxTg mice than in WT-HBxTg mice following a challenge with DEN. 2017 Scientific reports Discussion HBV C1485T 77 83 Hepatocellular carcinoma 70 73 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. The suppression of NF-kappaB activation was significantly greater in HepG2 cells overexpressing C1485T-HBx than in those overexpressing WT-HBx. 2017 Scientific reports Discussion HBV C1485T 96 102 X;X 103;139 106;142 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Therefore, DEN-induced DNA damage may be a prerequisite for the increased susceptibility of C1485T-HBxTg mice to HCC. 2017 Scientific reports Discussion HBV C1485T 92 98 Hepatocellular carcinoma 113 116 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Therefore, the C1485T mutation in HBx appears to be involved in the development of HCC even in the cases without LC and thereby acts as a potent oncogenic accelerator independent from liver fibrosis. 2017 Scientific reports Discussion HBV C1485T 15 21 X 34 37 Hepatocellular carcinoma;Liver fibrosis;Liver cirrhosis 83;184;113 86;198;115 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Therefore, we established Tg mice carrying C1458T-HBx for the first time and performed a phenotypic analysis. 2017 Scientific reports Discussion HBV C1458T 43 49 X 50 53 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. This is consistent with our phenotypic analysis of C1485T-HBxTg mice in that the spontaneous development of HCC has not been observed in these mice without the administration of DEN (data not shown). 2017 Scientific reports Discussion HBV C1485T 51 57 Hepatocellular carcinoma 108 111 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, our results together with these findings suggest that the C1485T mutation in HBx might increase the risk of HCC associated with HBV genotype C. 2017 Scientific reports Discussion HBV C1485T 64 70 X 83 86 Hepatocellular carcinoma 114 117 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the accumulation of DNA damage due to persistent infection with HBV genotype C may act synergistically with the C1485T HBx mutation to promote hepatocarcinogenesis. 2017 Scientific reports Discussion HBV C1485T 118 124 X 125 128 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the C1485T mutation in HBx is involved in the pathogenesis of HCC in the presence of HBV genotype C, but not genotype A. 2017 Scientific reports Discussion HBV C1485T 10 16 X 29 32 Hepatocellular carcinoma 68 71 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the emergence of HCC caused by C1485T-HBx is also attributed to the suppression of NF-kappaB. 2017 Scientific reports Discussion HBV C1485T 37 43 X 44 47 Hepatocellular carcinoma 23 26 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. Thus, the higher incidence of hepatocarcinogenesis in C1485T-HBx Tg mice is linked to the abnormal regulation of the cell cycle and enhanced cell proliferation. 2017 Scientific reports Discussion HBV C1485T 54 60 X 61 64 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. To the best of our knowledge, this is the first study to conduct an in vivo phenotypic analysis on C1485T-HBxTg mice. 2017 Scientific reports Discussion HBV C1485T 99 105 28874700 Contribution of C1485T mutation in the HBx gene to human and murine hepatocarcinogenesis. We found that HBV carrying the C1485T mutation in the HBx gene is involved in the pathogenesis of HBV-related HCC. 2017 Scientific reports Discussion HBV C1485T 31 37 X 54 57 Hepatocellular carcinoma 110 113 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. As for mutation G130E, glycine is the smallest amino acid, and changes in this position could affect the tertiary conformation of the protein and likewise its antigenicity, being replaced the negatively charged glutamic acid with a longer side chain. 2017 PloS one Discussion HBV G130E 16 21 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Escape mutant G145R was the first one described in a serum sample obtained from an Italian vaccinated child. 2017 PloS one Discussion HBV G145R 14 19 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. G145R is considered as a potential cause of a public health problem in countries with a universal vaccination program. 2017 PloS one Discussion HBV G145R 0 5 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. In Latin America, the escape mutant D144A/G was characterized in a vaccinated child and potential escape mutants were identified in HBsAg+/anti-HBs+ patients in Argentina. 2017 PloS one Discussion HBV D144A;D144G 36;36 43;43 S;S 144;132 147;137 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. In regions with high prevalence of infection, where these variants have been found, the recommendation is to implement new vaccines containing the common escape mutants, mainly G145R. 2017 PloS one Discussion HBV G145R 177 182 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. In the case of the L109R mutation, leucine is a nonpolar, hydrophobic amino acid, in contrast to arginine, a hydrophilic and charged residue; although this mutation is located outside of the "a" determinant but within the B-cell epitope of the MHR, it classifies as a potential escape variant. 2017 PloS one Discussion HBV L109R 19 24 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Moreover, there are other reported escape mutants (P120T, T126A/S, and D144A/G) responsible for the evasion of vaccine-induced antibodies and therefore cause HBV infection in vaccinated individuals. 2017 PloS one Discussion HBV T126S;D144G;P120T;T126A;D144A 58;71;51;58;71 65;78;56;65;78 HBV infections 158 171 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Similar mutations induced by antiviral treatment resulting in a truncated protein have been reported in other studies, such as W196* (31 amino acid deletion) and W172* (55 amino acid deletion). 2017 PloS one Discussion HBV W196X;W172X 127;162 132;167 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. Studies carried out in Morocco and in Vietnam reported mutations in these same positions: L109Q and G130A/N in unvaccinated patients. 2017 PloS one Discussion HBV L109Q;G130A;G130N 90;100;100 95;107;107 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The mutation, W156*, was identified in a sample obtained from a child having undergone the complete vaccination schedule. 2017 PloS one Discussion HBV W156X 14 19 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The present study identified two HBV escape mutants (G145R, W156*), and two potential escape mutants (L109R and G130E) in a child and a two mothers belonging to Amerindian populations of the Amazonas state. 2017 PloS one Discussion HBV G145R;W156X;L109R;G130E 53;60;102;112 58;65;107;117 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The reduction of HBsAg binding to monoclonal and polyclonal antibodies of HBV strains having the mutation G145R, has been demonstrated, and could due to conformational changes in the tertiary structure of the protein, thus reducing its immunogenicity. 2017 PloS one Discussion HBV G145R 106 111 S 17 22 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The studies showed that mutation G145R is the most prevalent, 20 years after the introduction of the vaccine. 2017 PloS one Discussion HBV G145R 33 38 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The study identified the P120T and G130S mutations as the most frequent in both groups. 2017 PloS one Discussion HBV P120T;G130S 25;35 30;40 29016603 Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia. The two other mutations described in the study, L109R and G130E, have not been reported as HBV escape mutants, but they have the potential of being considered as such, since they are located in the MHR of HBsAg (amino acids 110 to 164). 2017 PloS one Discussion HBV L109R;G130E 48;58 53;63 S 205 210 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. However, there have been conflicting reports on the association between specific mutations in the HBV genome and fulminant hepatitis, especially the G1896A and A1762T/G1764A mutations. 2017 Virology journal Discussion HBV G1764A;G1896A;A1762T 167;149;160 173;155;166 Fulminant Hepatitis B 113 132 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. In our study the frequency of G1896A and A1762T/G1764A mutations was significantly greater in patients from HBeAg negative hepatitis groups compared to CHB patients with ACLF. 2017 Virology journal Discussion HBV G1764A;G1896A;A1762T 48;30;41 54;36;47 C 108 113 Chronic Hepatitis B;Acute on chronic liver failure;Hepatitis 152;170;123 155;174;132 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The G1896A precore mutation was reported in association with fulminant hepatitis B in patients from Japan Israel, and southern Mediterranean countries, and the A1762T/G174A mutations in BCP region was frequently showed in Japanese cohort. 2017 Virology journal Discussion HBV G1896A;A1762T 4;160 10;166 29065883 Chronic hepatitis B carriers with acute on chronic liver failure show increased HBV surface gene mutations, including immune escape variants. The G1896A precore mutation was reported in association with fulminant hepatitis B in patients from Japan Israel, and southern Mediterranean countries, and the A1762T/G1764A mutations in BCP region was frequently showed in Japanese cohort. 2017 Virology journal Discussion HBV G1764A 167 173 BCP;Precore 187;11 190;18 Fulminant Hepatitis B 61 80 29281718 The burden of hepatitis B virus (HBV) infection, genotypes and drug resistance mutations in human immunodeficiency virus-positive patients in Northwest Ethiopia. We found that more than half of these patients, for whom sequence data were available, had 3TC selected DRMs (rtV173L, rtL180M, and rtM204V). 2017 PloS one Discussion HBV V173L;L180M;M204V 112;121;134 117;126;139 RT;RT;RT 110;119;132 112;121;134 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. A study in Mongolian patients with HBV genotype D has shown that I127T mutation is significantly linked to HCC development. 2017 Oncotarget Discussion HBV I127T 65 70 Hepatocellular carcinoma 107 110 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. also have found H94Y mutation to be associated with HCC in patients with HBV genotype C2. 2017 Oncotarget Discussion HBV H94Y 16 20 Hepatocellular carcinoma 52 55 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Another combinational mutation observed in our study was K130M+V131I+F132Y. 2017 Oncotarget Discussion HBV K130M;V131I;F132Y 57;63;69 62;68;74 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Another study has proposed that K130M+V131I double mutation causes rapid progression to cirrhosis in HBV patients and, thus, has an indirect role in the development of HCC. 2017 Oncotarget Discussion HBV K130M;V131I 32;38 37;43 Liver cirrhosis;Hepatocellular carcinoma 88;168 97;171 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. As also stated by Iavarone et al., this suggested that the presence of K130M+V131I double mutation favors the occurrence of a polar mutation at position 127. 2017 Oncotarget Discussion HBV K130M;V131I 71;77 76;82 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Further, it was observed that H94Y and F132Y/I/R mutations were present with high frequency only in the HCC group, suggesting that these mutations were associated with an increased risk of HCC. 2017 Oncotarget Discussion HBV F132Y;F132I;F132R;H94Y 39;39;39;30 48;48;48;34 Hepatocellular carcinoma;Hepatocellular carcinoma 104;189 107;192 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. have demonstrated that the mutation at position 127 arises later than the K130M+V131I double mutation in the course of HBV infection. 2017 Oncotarget Discussion HBV K130M;V131I 74;80 79;85 HBV infections 119 132 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. have found an increased prevalence of V131I and K130M mutations proportional to progressive forms of HBV infection in patients. 2017 Oncotarget Discussion HBV V131I;K130M 38;48 43;53 HBV infections 101 114 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. have suggested that K130M+V131I double mutation increases NF-kappaB activity, which is known to play an important role in liver function and in regulation of oncogenic genes, leading to carcinogenesis. 2017 Oncotarget Discussion HBV K130M;V131I 20;26 25;31 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. However, some studies in the Indian population have reported that H94Y mutation was present at high frequencies in both LC and HCC groups, suggesting that population may increase or decrease the effect of this mutation on liver disease. 2017 Oncotarget Discussion HBV H94Y 66 70 Hepatocellular carcinoma;Liver disease;Liver cirrhosis 127;222;120 130;235;122 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. I127T+K130M+V131I triple mutation was present in increasing proportion with advancing clinical phases of HBV infection from AC to HCC. 2017 Oncotarget Discussion HBV I127T;K130M;V131I 0;6;12 5;11;17 HBV infections;Hepatocellular carcinoma 105;130 118;133 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. I127T+K130M+V131I triple mutation was significantly associated with AC, LC, and HCC stages. 2017 Oncotarget Discussion HBV I127T;K130M;V131I 0;6;12 5;11;17 Hepatocellular carcinoma;Liver cirrhosis 80;72 83;74 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. In addition, analysis of I127T mutation showed that its frequency was higher in the HCC (50%) than in the LC (19.23%) group. 2017 Oncotarget Discussion HBV I127T 25 30 Hepatocellular carcinoma;Liver cirrhosis 84;106 87;108 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Interestingly, in both cases where K130M+V131I double mutation was associated with adjacent mutation at position 127 or 132, the frequency of the mutation showed a striking increment from non-HCC phase to HCC phase, whereas that of only K130M+V131I double mutation was already high in non-HCC patients. 2017 Oncotarget Discussion HBV K130M;V131I;K130M;V131I 35;41;237;243 40;46;242;248 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 205;192;289 208;195;292 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. K130M+V131I double mutation is a common mutation present across different populations. 2017 Oncotarget Discussion HBV K130M;V131I 0;6 5;11 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. K130M+V131I double mutation showed a statistically significant increase in prevalence from IC to HCC stage. 2017 Oncotarget Discussion HBV K130M;V131I 0;6 5;11 Hepatocellular carcinoma 97 100 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Multivariate logistic regression analysis was informative as it confirmed our finding that H94Y, I127T and F132Y mutations in HBx can be useful as independent prognostic markers of HBV-associated liver disease evolution and advancement, especially when other contributing factors, such as viral load, exist. 2017 Oncotarget Discussion HBV H94Y;I127T;F132Y 91;97;107 95;102;112 X 126 129 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Our study found mutation V88F to be highly prevalent (100%) in the HCC group but its prevalence in LC was less than in both IC and AC groups in the Saudi population. 2017 Oncotarget Discussion HBV V88F 25 29 Hepatocellular carcinoma;Liver cirrhosis 67;99 70;101 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Previous data have established the specific presence of mutation at position 127 along with the double mutation at positions 130 and 131, a strong association between K130M+V131I mutation and the presence of a polar mutation at position 127 (I to T). 2017 Oncotarget Discussion HBV K130M;V131I 167;173 172;178 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Several previous studies on HBV genotypes have reported that H94Y, I127T, K130M, V131I, and F132Y/I/R mutations are frequently considered as associated risk factors of HCC and may promote progression of liver impairment. 2017 Oncotarget Discussion HBV F132Y;F132I;F132R;H94Y;I127T;K130M;V131I 92;92;92;61;67;74;81 101;101;101;65;72;79;86 Hepatocellular carcinoma;Liver disease 168;203 171;219 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. The biological mechanisms elucidating the association of V88F, H94Y, I127T, K130M, V131I, and F132Y/I/R mutations with the pathogenesis of HBV infection are unclear. 2017 Oncotarget Discussion HBV F132Y;F132I;F132R;V88F;H94Y;I127T;K130M;V131I 94;94;94;57;63;69;76;83 103;103;103;61;67;74;81;88 HBV infections 139 152 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. The mechanism by which K130M+V131I double mutation leads to progression of HBV related liver disease is not fully understood. 2017 Oncotarget Discussion HBV K130M;V131I 23;29 28;34 Liver disease 87 100 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. The prevalence of I127T, V131I, and F132Y/I/R mutations showed an increasing trend with increase in severity of disease from the IC to the HCC group. 2017 Oncotarget Discussion HBV F132Y;F132I;F132R;I127T;V131I 36;36;36;18;25 45;45;45;23;30 Hepatocellular carcinoma 139 142 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. These results were consistent with an earlier study that has found K130M+V131I double mutation with a mutation at position 132 to be associated with development of HCC. 2017 Oncotarget Discussion HBV K130M;V131I 67;73 72;78 Hepatocellular carcinoma 164 167 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. These results were in agreement with previous studies reporting an association between K130M+V131I mutation and disease progression. 2017 Oncotarget Discussion HBV K130M;V131I 87;93 92;98 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. This mutation was significantly associated with the development of HCC, though its prevalence in HCC was less than that of K130M+V131I (46.42%) and I127T+K130M+V131I (46.42%) mutations. 2017 Oncotarget Discussion HBV K130M;V131I;I127T;K130M;V131I 123;129;148;154;160 128;134;153;159;165 Hepatocellular carcinoma;Hepatocellular carcinoma 67;97 70;100 29285238 Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients. Two mutations (S42P and A47T) present within the B-cell epitope region did not show any significant association with the clinical stages of HBV infection. 2017 Oncotarget Discussion HBV S42P;A47T 15;24 19;28 HBV infections 140 153 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. C1485T, which is located in the RH domain overlapping with HBx, possesses RNase H activity that can degrade the pregenomic RNA template during minus-strand DNA elongation. 2017 PloS one Discussion HBV C1485T 0 6 X 59 62 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. Further functional research is required to determine whether the amino acid residue changes induced by G529A and T1078G would result in altered RT activity so as to modify HBV replication and cell proliferation in HCC. 2017 PloS one Discussion HBV G529A;T1078G 103;113 108;119 RT 144 146 Hepatocellular carcinoma 214 217 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. G529A and T1078G were located in the RT domain of polymerase, which possesses RT and DNA-dependent DNA polymerase activity. 2017 PloS one Discussion HBV G529A;T1078G 0;10 5;16 P;P;RT;RT 50;103;37;78 60;113;39;80 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. Our previous study identified C1485T as a prognostic factor, which causes a critical amino acid change (Pro38Ser) in the X protein. 2017 PloS one Discussion HBV C1485T;P38S 30;104 36;112 X 121 122 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. T1078G, which is located in the non-overlapping region of the RT domain, can induce an amino acid change from Ser to Ala (rtS316A). 2017 PloS one Discussion HBV S316A;T1078G 124;0 129;6 RT;RT 62;122 64;124 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. T31C, located in the spacer domain, is a highly variable region of polymerase. 2017 PloS one Discussion HBV T31C 0 4 P 67 77 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. The G529A mutation did not result in a structural change in HBsAg, which could induce changes in the antigenic properties of HBV. 2017 PloS one Discussion HBV G529A 4 9 S 60 65 29287068 Mutations in hepatitis B virus polymerase are associated with the postoperative survival of hepatocellular carcinoma patients. The lamivudine resistance-linked G529A (rtD134N) site in HBV was found to be associated with HCC outcomes, which implied potential correlation between resistance to the anti-HBV nucleoside analog lamivudine and HCC prognosis. 2017 PloS one Discussion HBV D134N;G529A 42;33 47;38 RT 40 42 Hepatocellular carcinoma;Hepatocellular carcinoma 93;211 96;214 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. A single HBV strain has an I169L mutation, at a position associated with resistance to Entecavir, although leucine (L) is not the amino acid involved. 2018 PloS one Discussion HBV I169L 27 32 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. Finally, among our ten HBV sequenced strains, we found only one strain with a G130N mutation like VEM as described, and associated with diagnostic failure, rarely described (1%). 2018 PloS one Discussion HBV G130N 78 83 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. For 3 patients, mutations M204V and M180V were present, for 1 patient only the M204I mutation was detected. 2018 PloS one Discussion HBV M204V;M180V;M204I 26;36;79 31;41;84 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. However, we found 20% of patient with G145K and K141R mutations, usually incriminated in the immune escape, mainly in patients with mutations for 3TC resistance. 2018 PloS one Discussion HBV G145K;K141R 38;48 43;53 29315352 Hepatitis B infection among HIV infected individuals in Gabon: Occult hepatitis B enhances HBV DNA prevalence. The mutation S143T in our results was common to all HBV-A genotype strains. 2018 PloS one Discussion HBV S143T 13 18 29326804 Occult Hepatitis B Virus Infection and Associated Genotypes among HBsAg-negative Subjects in Burkina Faso. In addition, the role of the G145R mutation has been clearly established by several studies in vaccine escape. 2018 Mediterranean journal of hematology and infectious diseases Discussion HBV G145R 29 34 29326804 Occult Hepatitis B Virus Infection and Associated Genotypes among HBsAg-negative Subjects in Burkina Faso. In this study, the L115I/A; H133F/A, and R149A/D mutations were found in OBI cases. 2018 Mediterranean journal of hematology and infectious diseases Discussion HBV L115I;L115A;H133F;H133A;R149A;R149D 19;19;28;28;41;41 26;26;35;35;48;48 Occult Hepatitis B 73 76 29326804 Occult Hepatitis B Virus Infection and Associated Genotypes among HBsAg-negative Subjects in Burkina Faso. The presence of same mutations in addition to that of G145R in "false OBI" cases of this study confirms the conclusion of the statements from the Taormina expert meeting on occult hepatitis B virus infection. 2018 Mediterranean journal of hematology and infectious diseases Discussion HBV G145R 54 59 Occult Hepatitis B 70 73 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. As the result of BCP polymorphism, clinically important multiple mutations per a study subject; such as T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A) were also the characteristics of the current study. 2018 PloS one Discussion HBV A1762T;G1764A;G1764A;C1766T;A1762T;T1768A;T1753V 111;118;136;143;129;154;104 117;124;142;149;135;160;110 BCP 17 20 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. In regard to PC mutations, although the overall mutant variants were found to be proportional among HIV co-infected and HBV mono-infected groups, none of the classical PC mutations (A1814C/C1816T, C1858T, G1862T and G1896) also associated with 3TC/ETV resistance gene mutations associated with the YMDD RT motif during HIV co-infection. 2018 PloS one Discussion HBV C1816T;A1814C;C1858T;G1862T 189;182;197;205 195;188;203;211 Precore;Precore;RT;P 13;168;303;298 15;170;305;302 HBV-HIV coinfections;HBV-HIV coinfections 100;319 115;335 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Interestingly, the premature stop codon (G1896A) that is known to abolish the synthesis of HBeAg in particular with C1858T was found to be 21.7% and commonly found in subjects with genotype D. 2018 PloS one Discussion HBV G1896A;C1858T 41;116 47;122 C 91 96 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Irrespective of the study groups, the majority of the classical BCP/PC mutants such as the Kozak sequences mutant, PC initiation and G1896A with C1858T mutations showed significantly higher rate in HBeAg negative subjects. 2018 PloS one Discussion HBV G1896A;C1858T 133;145 139;151 BCP;C;Precore;Precore 64;198;68;115 67;203;70;117 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Moreover, with a proportional HBeAg positive and negative status, 29.3% of HIV co-infected patients included in the current study were reported to have 3TC/ETV resistance due to rtM204V/I+rtL180M+rtV173L mutant gene variants. 2018 PloS one Discussion HBV M204V;M204I;L180M;V173L 180;180;190;198 187;187;195;203 C;RT;RT;RT 30;178;188;196 35;180;190;198 HBV-HIV coinfections 75 90 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. mutations which were absent in the current study, TA1 to TA3 rich BCP mutations such as A1752C/G/T (8.4%), T1753V (18.9%), A1762T (28.7%), G1764A (35.0%) and T1773C (37.1%) were common in the current study. 2018 PloS one Discussion HBV A1752C;A1752G;A1752T;T1753V;A1762T;G1764A;T1773C 88;88;88;107;123;139;158 99;98;98;113;129;145;164 BCP 66 69 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Nevertheless, the detection of the BCP double (A1762T and G1764A) mutations was unexpectedly negligible in these HIV co-infected individuals unlike that of the HBV drug resistance gene mutations which were affected by HIV co-infection and ART exposure. 2018 PloS one Discussion HBV A1762T;G1764A 47;58 53;64 BCP 35 38 HBV-HIV coinfections;HBV-HIV coinfections 113;218 128;234 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Other than YMDD RT motif resistance gene mutations, the observation of co-prevalence of PC mutations and ADV resistance mutants (rtI233V, rtQ215S/Q and rtV214A) in particular in the HBeAg negative cases was in line with earlier similar reports. 2018 PloS one Discussion HBV Q215S;Q215Q;V214A;I233V 140;140;154;131 147;147;159;136 C;Precore;RT;RT;RT;RT;P 182;88;16;129;138;152;11 187;90;18;131;140;154;15 29408943 Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia. Similarly, all sorts of PC mutant variants so far described and functionally known as the start codon mutations (A1814C/C1816; 15.4%) that abolish HBeAg expression and G1862T (44.8%) mutation that interferes with post-translational modification of the HBeAg-precursor were most common. 2018 PloS one Discussion HBV A1814C;G1862T 113;168 119;174 C;C;Precore 147;252;24 152;257;26 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. In present study, I126S/T mutants were detected only in HBsAg-positive cases, and it was suggested that the titre of HBsAg of these cases might decrease over a long-term follow-up period. 2018 Infectious agents and cancer Discussion HBV I126T;I126S 18;18 25;25 S;S 56;117 61;122 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Previously, the M1L, Q2K and S182Stop in the pre-S2 region and T105C in the pre-S/S region were reported as specific mutations in OBI patients. 2018 Infectious agents and cancer Discussion HBV M1L;Q2K;S182X;T105C 16;21;29;63 19;24;37;68 PreS;S;PreS2 76;82;45 81;83;51 Occult Hepatitis B 130 133 29434654 Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection. Several specific mutations, including G119R, C124Y, I126S, Q129R, S136P, C139R, T140I, K141E, D144A, and G145R, have been reported as being related to the decrease of HBsAg secretion. 2018 Infectious agents and cancer Discussion HBV I126S;G119R;C124Y;Q129R;S136P;C139R;T140I;K141E;D144A;G145R 52;38;45;59;66;73;80;87;94;105 57;43;50;64;71;78;85;92;99;110 S 167 172 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Additionally, the developed TG mouse model system carrying the full HBV genome with the W4P mutation in preS1 could be effectively used not only in basic research into the mechanisms of liver disease progression in HCC but also for the screening of antiHBV or antiinflammatory drugs. 2018 World journal of gastroenterology Discussion HBV W4P 88 91 PreS1 104 109 Liver disease;Hepatocellular carcinoma 186;215 199;218 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. First, by using the W4P TG mouse model of chronic HBV infection, we found that male W4P TG mice exhibited higher levels of secreted HBsAg and liver LHBs, which was indicative of higher HBV replication than in female W4P TG mice (Figure 4) and is one of the known HCC risk factors. 2018 World journal of gastroenterology Discussion HBV W4P;W4P;W4P 20;84;216 23;87;219 S;S 132;148 137;152 HBV infections;Hepatocellular carcinoma 42;263 63;266 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. However, in our recent molecular epidemiologic and cell-based studies, we have demonstrated that LHB harboring the W4P mutation in preS1 could also contribute to the sex disparity of HBV-associated HCC in an IL-6-dependent manner. 2018 World journal of gastroenterology Discussion HBV W4P 115 118 S;PreS1 97;131 100;136 Hepatocellular carcinoma 198 201 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. In addition, the relationships between increased hepatic production of IL-6 in mice expressing HBV genome with the W4P mutation and fat accumulation, increased liver weight and HCC development also remain to be elucidated in the future. 2018 World journal of gastroenterology Discussion HBV W4P 115 118 Hepatocellular carcinoma 177 180 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. In conclusion, we created W4P TG mice that constitutively express the full HBV genome with the W4P mutation in preS1 in the present study. 2018 World journal of gastroenterology Discussion HBV W4P;W4P 26;95 29;98 PreS1 111 116 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. In the present study, we constructed W4P TG mice that expressed the full HBV genome, which can help us to study sex disparity of the progression of liver diseases, including chronic hepatitis, steatohepatitis, cirrhosis and HCC, following chronic HBV infection. 2018 World journal of gastroenterology Discussion HBV W4P 37 40 Liver disease;Chronic Hepatitis B;Hepatitis;Liver cirrhosis;Hepatocellular carcinoma;Chronic HBV infection 148;174;193;210;224;239 162;191;208;219;227;260 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Our data showed significantly increased hepatomegaly, enhanced granule generation in liver tissue, higher HBsAg expression in the liver and serum, and higher serum ALT and IL-6 levels in W4P TG males compared to the values of these parameters in W4P TG females or littermate control groups. 2018 World journal of gastroenterology Discussion HBV W4P;W4P 187;246 190;249 S 106 111 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Our data using W4P TG mice indicate that this mutation likely contributes to sex disparity in the susceptibility to liver disease, including HCC, leading to increased HBV virion replication and enhanced IL-6-mediated inflammation in male individuals. 2018 World journal of gastroenterology Discussion HBV W4P 15 18 Liver disease;Hepatocellular carcinoma 116;141 129;144 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Recently, we identified the novel W4P substitution in the preS1 region of hepatitis B virus (HBV) related to HCC that occurs exclusively in male patients. 2018 World journal of gastroenterology Discussion HBV W4P 34 37 PreS1 58 63 Hepatocellular carcinoma 109 112 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Second, we found that male W4P TG mice showed increased incidence of hepatomegaly and lipid droplets (Figure 3), reflecting the imbalance of metabolic liver homeostasis, which could drive liver pathogenesis, including fatty liver and steatohepatitis, and further promote tumorigenesis. 2018 World journal of gastroenterology Discussion HBV W4P 27 30 Hepatitis 234 249 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. The obtained results suggest that W4P TG mice developed in this study could be effectively used not only for the basic research into the mechanisms of HBV-associated liver diseases, including HCC, but also for screening antiHBV and antiinflammatory drugs. 2018 World journal of gastroenterology Discussion HBV W4P 34 37 Liver disease;Hepatocellular carcinoma 166;192 180;195 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. The phenotypes of male W4P TG mice, namely higher levels of IL-6 and ALT in the serum, could provide a technical advantage in drug screening protocols, as it will be possible to analyze not only the inhibition of HBV replication but also the antiinflammatory activity. 2018 World journal of gastroenterology Discussion HBV W4P 23 26 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Therefore, further studies are necessary to demonstrate higher male susceptibility to liver carcinogenesis in our W4P TG mouse model and clarify its mechanism in the future. 2018 World journal of gastroenterology Discussion HBV W4P 114 117 Liver disease 86 106 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Third, we found that male W4P TG mice had increased IL-6-related liver inflammation and higher serum ALT levels (Figure 5), which were indications of liver damage, compared to those seen in female W4P TG mice. 2018 World journal of gastroenterology Discussion HBV W4P;W4P 26;197 29;200 Liver inflammation;Liver disease 65;150 83;162 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. This is the first study that used TG mice to uncover the role of the W4P mutation in HBV preS1 in sex disparity of liver disease progression due to concomitantly increased HBV virion replication and greater IL-6-mediated inflammation in male individuals. 2018 World journal of gastroenterology Discussion HBV W4P 69 72 PreS1 89 94 Liver disease 115 128 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Thus, our W4P TG model showing increased hepatic IL-6 production could provide a novel insight into the relationships between IL-6 production due to an infection caused by an HBV variant on the one hand, and development of nonalcoholic steatohepatitis, type 2 diabetes or HCC on the other hand. 2018 World journal of gastroenterology Discussion HBV W4P 10 13 Hepatitis;Diabetes mellitus type 2;Hepatocellular carcinoma 223;253;272 251;268;275 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. To gain further insight into the role of the W4P mutation in the preS1 region of HBV on sex disparity of HBV-induced liver inflammatory manifestations, we created a TG mouse that carried the full HBV genome with this mutation and evaluated HBV virion replication and IL-6-mediated inflammation in mutant and wild-type (WT) mice of both sexes. 2018 World journal of gastroenterology Discussion HBV W4P 45 48 PreS1 65 70 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. Unfortunately, we did not prove predominant carcinogenesis in males in our W4P TG mice. 2018 World journal of gastroenterology Discussion HBV W4P 75 78 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. We compared serum levels of hepatitis B surface antigen (HBsAg), IL-6, and the liver enzymes alanine aminotransferase (ALT) and aspartate transaminase (AST), as well as liver histopathology features in male and female W4P TG mice and their WT littermates. 2018 World journal of gastroenterology Discussion HBV W4P 218 221 S;S 57;40 62;47 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. We have also shown that the W4P mutation likely contributed to HCC development, particularly in male patients, in an interleukin (IL)-6-dependent manner. 2018 World journal of gastroenterology Discussion HBV W4P 28 31 Hepatocellular carcinoma 63 66 29563753 Sex disparity in viral load, inflammation and liver damage in transgenic mice carrying full hepatitis B virus genome with the W4P mutation in the preS1 region. We identified three noteworthy findings supporting the contribution of the W4P mutation in preS1 to liver disease progression in male patients. 2018 World journal of gastroenterology Discussion HBV W4P 75 78 PreS1 91 96 Liver disease 100 113 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Consistent with these findings, we previously reported that naturally occurring I110M, G119E, and R169P mutations inside the S domain impaired virion secretion through the S rather than L or M protein. 2018 Virology Discussion HBV I110M;G119E;R169P 80;87;98 85;92;103 S;S 125;172 126;173 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. For the glycosylation mutants, both N146Q and N146S continued to secrete HBsAg efficiently despite blocked virion release. 2018 Virology Discussion HBV N146Q;N146S 36;46 41;51 S 73 78 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Furthermore, mixed expression of L/M/S proteins of the G145R or N146Q mutant with just S protein of WT virus or the M133T mutant rescued virion secretion. 2018 Virology Discussion HBV G145R;N146Q;M133T 55;64;116 60;69;121 S 87 88 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Immune escape mutations such as G145R reduce the affinity of the mutant envelope proteins for anti-HBs antibody, thus leading to diagnostic failure, occult HBV infection, vaccine failure and breakthrough infection despite presence of neutralizing antibodies against WT S domain. 2018 Virology Discussion HBV G145R 32 37 S;S;S 72;99;269 80;102;270 HBV infections 156 169 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In our previous study, a G112N mutation (creating a glycosylation site at residue 112) partially rescued virion secretion of the G119E mutant but failed to rescue virion secretion of the G145R mutant. 2018 Virology Discussion HBV G112N;G119E;G145R 25;129;187 30;134;192 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In the current work we also performed limited study on four additional mutants creating novel N-linked glycosylation sites: T115N, G130N, 112NG113, and 114NT115. 2018 Virology Discussion HBV T115N;G130N 124;131 129;136 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. In the present study, we demonstrated its ability to moderately rescue virion secretion of the T114R, T115A, K141E, and D144G mutants as well. 2018 Virology Discussion HBV T114R;T115A;K141E;D144G 95;102;109;120 100;107;114;125 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Indeed, with the Abbott Architect i2000 assay, the K141E, D144G, and G145R escape mutants as well as M133T glycosylation mutant were associated with very little HBsAg in culture supernatant. 2018 Virology Discussion HBV K141E;D144G;G145R;M133T 51;58;69;101 56;63;74;106 S 161 166 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Introducing the M133T mutation could rescue virion secretion for both N146Q and N146S mutants, suggesting that N-linked glycosylation is essential for HBV virion secretion although the glycans can be attached to a site other than residue 146. 2018 Virology Discussion HBV M133T;N146Q;N146S 16;70;80 21;75;85 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. M133T mutation in the S rather than L or M protein rescued virion secretion of the N146Q mutant. 2018 Virology Discussion HBV M133T;N146Q 0;83 5;88 S 22 23 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Moreover, the M133T mutation in the S but not L/M proteins rescued virion secretion of the I110M mutant. 2018 Virology Discussion HBV M133T;I110M 14;91 19;96 S 36 37 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Of the other immune escape mutants with severely impaired virion secretion, I110M, G145R, and K141E mutants showed mild to moderate reduction in HBsAg secretion, while G119V, G130R, and C147R mutants had more or less WT efficiency of HBsAg secretion. 2018 Virology Discussion HBV I110M;G145R;K141E;G119V;G130R;C147R 76;83;94;168;175;186 81;88;99;173;180;191 S;S 145;234 150;239 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Similarly, introduction of the M133T mutation into the S protein construct alone sufficed to rescue virion production of the G145R mutant. 2018 Virology Discussion HBV M133T;G145R 31;125 36;130 S 55 56 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Similarly, Western blot analysis revealed very little intracellular S protein for the K141E, D144G, G145R, and M133T mutants (panel A in Figs. 2018 Virology Discussion HBV K141E;D144G;G145R;M133T 86;93;100;111 91;98;105;116 S 68 69 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. the 114NT115 insertion was very effective at rescuing virion secretion of the N146Q mutant, but none of the mutations rescued virion secretion of the G145R mutant as efficiently as M133T. 2018 Virology Discussion HBV N146Q;G145R;M133T 78;150;181 83;155;186 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T mutation could efficiently rescue virion secretion of the I110M, T118K, G119E, P127S, G145R, and R169H mutants to nearly WT level, and moderately improve virion secretion of the G130R, C138Y, C147R, and C149R mutants. 2018 Virology Discussion HBV M133T;I110M;T118K;G119E;P127S;G145R;R169H;G130R;C138Y;C147R;C149R 4;68;75;82;89;96;107;188;195;202;213 9;73;80;87;94;101;112;193;200;207;218 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The M133T/G145R double mutant did not display higher HBsAg titer in either cell lysate or culture supernatant than either G145R or M133T mutant. 2018 Virology Discussion HBV G145R;M133T;G145R;M133T 10;4;122;131 15;9;127;136 S 53 58 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The serious concern is: will vaccine escape mutants such as G145R with restored virion secretion capacity through M133T mutation gradually replace the WT virus and eventually make the current HBV vaccine obsolete? 2018 Virology Discussion HBV G145R;M133T 60;114 65;119 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The serious concern is: will vaccine escape mutants such as G145R with restored virion secretion capacity through M133T mutation gradually replace the WT virus and eventually make the current HBV vaccine obsolete. 2018 Virology Discussion HBV G145R;M133T 60;114 65;119 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. The T118K mutant actually had increased HBsAg release. 2018 Virology Discussion HBV T118K 4 9 S 40 45 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Therefore, adding the M133T mutation most likely does not alter the immune escape property of the G145R mutant. 2018 Virology Discussion HBV M133T;G145R 22;98 27;103 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Therefore, except for the C138Y, C149R, R169L, and R169P mutants, virion secretion phenotype of the immune escape mutants and glycosylation mutants did not correlate with the phenotype of subviral particle release. 2018 Virology Discussion HBV C138Y;C149R;R169L;R169P 26;33;40;51 31;38;45;56 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. Thus, M133T is a versatile compensatory mutation for virion secretion of a large number of immune escape mutants. 2018 Virology Discussion HBV M133T 6 11 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. We found that HBsAg secretion (ratio of extracellular HBsAg/intracellular HBsAg) was severely impaired by C138Y, C149R, R169L, and R169P mutants. 2018 Virology Discussion HBV C138Y;C149R;R169L;R169P 106;113;120;131 111;118;125;136 S;S;S 14;54;74 19;59;79 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. We further demonstrated that ability of the M133T mutation to rescue virion secretion of the I110M, G119E, and G145R mutants was abrogated by an additional N131Q or N131T mutation indicating that glycosylation at N131, rather than M133T mutation itself, restored virion secretion. 2018 Virology Discussion HBV M133T;I110M;G119E;G145R;N131Q;N131T;M133T 44;93;100;111;156;165;231 49;98;105;116;161;170;236 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. We previously reported that abolishing N-linked glycosylation in HBV envelope proteins by either N146Q or N146S mutation prevented HBV virion secretion. 2018 Virology Discussion HBV N146Q;N146S 97;106 102;111 S 69 77 29604477 Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein. While virion secretion was restored in the M133T/G145R double mutant in comparison with the G145R mutant, HBsAg secretion was rather reduced in the double mutant than G145R single mutant. 2018 Virology Discussion HBV G145R;M133T;G145R;G145R 49;43;92;167 54;48;97;172 S 106 111 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. And the difference in viral replication capacity of pHBV4.1-HBs(wt), pHBV4.1-HBs(sW172L) and pHBV4.1-HBs(sW172*) should be an important cause of different expression of Smad3/2 and CREB in present study. 2018 Virology journal Discussion HBV W172X;W172L 105;81 111;87 S;S;S;S;S 60;77;101;81;105 63;80;104;82;106 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. And this finding is also consistent with the clinical increased risk of developing HCC in CHB patients with evidence of HBV rtA181T/sW172* mutant. 2018 Virology journal Discussion HBV W172X;A181T 132;126 138;131 RT;S 124;132 126;133 Hepatocellular carcinoma;Chronic Hepatitis B 83;90 86;93 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. has been reported that the presence of HBV rtV191I/sW182* mutant may induce cell canceration via inhibiting TGFBI expression and increasing CyclinD1expression. 2018 Virology journal Discussion HBV W182X;V191I 51;45 57;50 RT;S 43;51 45;52 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In our previous study, we found that the viral replication in pHBV4.1-HBs(sW172*) mutant increased and maintained significantly longer than that in pHBV4.1-HBs(sW172L) mutant, and truncated mutant HBsAg also could increase the activity of HBV core promoter which could further increase transcription and replication of HBV genome. 2018 Virology journal Discussion HBV W172X;W172L 74;160 80;166 Core promoter;S;S;S;S;S 243;70;156;197;74;160 256;73;159;202;75;161 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, after restoration of TGFBI expression in L02 cells with stably transfected pHBV4.1-HBs(sW172*), the tumor volume was significantly reduced in nude mice; and the expression of CyclinD1 decreased in L02 cells accompanied by a decreasing of cell proliferation and increasing of cell apoptosis(data unshown). 2018 Virology journal Discussion HBV W172X 105 111 S;S 101;105 104;106 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, because of the deletion of 55 amino acids at the carboxyl terminus of HBsAg, the spatial structure HBsAg expressed by HBV rtA181T/sW172* has been changed, and this may be the molecular basis for enhanced pathogenicity of HBV rtA181T/sW172* mutant. 2018 Virology journal Discussion HBV W172X;W172X;A181T;A181T 148;251;142;245 154;257;147;250 S;S;RT;RT;S;S 88;117;140;243;148;251 93;122;142;245;149;252 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, there was no significant pathogenicity enhancement of sW172L mutation as compared to sW172*. 2018 Virology journal Discussion HBV W172L;W172X 72;103 78;109 S;S 72;103 73;104 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, we also investigated the molecular mechanism of tumorigenesis of truncated mutant HBsAg using L02 cells with stably transfected pHBV4.1-HBs(sW172*), and L02 cells with stably transfected pHBV-HBs(sW172L) and pHBV4.1-HBs(wt) were used as control. 2018 Virology journal Discussion HBV W172X;W172L 158;214 164;220 S;S;S;S;S;S 154;210;234;100;158;214 157;213;237;105;159;215 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. In present study, we also investigated the molecular mechanism of tumorigenesis of truncated mutant HBsAg using L02 cells with stably transfected pHBV4.1-HBs(sW172*), and L02 cells with stably transfected pHBV4.1-HBs (sW172L) and pHBV4.1-HBs(wt) were used as control. 2018 Virology journal Discussion HBV W172X;W172L 158;218 164;224 S;S;S;S;S;S 154;213;238;100;158;218 157;216;241;105;159;219 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Lee et al.found that the percentage of S-phase cells increased in the presence of HBV rtV191I/sW182* as compared to that in the presence of wide-type HBV, and the possible mechanism may be associated with the down-regulation of p53 and p21 and up-regulation of Cyclin A and CDK4 gene expressions, which also could promote cells from G1 phase to S phase thus accelerating cell proliferation. 2018 Virology journal Discussion HBV W182X;V191I 94;88 100;93 RT;S 86;94 88;95 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Though the changes of key molecules in LEF/Wnt pathway and proteinase C (PKC)-dependent c-Raf-1/Erk2 pathway were not significant than key molecules in TGF-beta/Smad pathway, we could not completely deny the possible role of LEF/Wnt and PKC- dependent c-Raf-1/Erk2 pathways in the tumorigenic mechanism of HBV-sW172* truncated mutant, and further research is still needed to clarify this issue. 2018 Virology journal Discussion HBV W172X 310 316 S 310 311 29609638 The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway. Thus, the transcriptional activation of truncated mutant HBsAg may be related to the increased possibility of tumorigenesis in HBV-rtA181T/sW172* mutant. 2018 Virology journal Discussion HBV W172X;A181T 139;133 145;138 S;RT;S 57;131;139 62;133;140 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. By assessing HBV DNA in liver tissue specimens, in 2010, Yeh et al from Taiwan showed for the first time that the BCP A1762T/G1764A mutation is independently predictive of postoperative survival in HCC patients. 2018 Cancer management and research Discussion HBV G1764A;A1762T 125;118 131;124 BCP 114 117 Hepatocellular carcinoma 198 201 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Chen et al also reported that the accumulation of A1762T/G1764A combined with other mutation(s) was more common in patients with poor prognosis than in patients with better prognosis. 2018 Cancer management and research Discussion HBV G1764A;A1762T 57;50 63;56 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. In the present study, most mutation regions that have been reported in the literature previously, were sequenced, and the results demonstrated that HBV DNA genomic mutations in A1762T/G1764A and Pre S deletion were associated with worse prognosis and early recurrence for HBV-HCC patients after surgery. 2018 Cancer management and research Discussion HBV G1764A;A1762T 184;177 190;183 PreS 195 200 Hepatocellular carcinoma 276 279 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. In the present study, we also revealed that the A1762T/G1764A mutation is correlated with tumor size, which indicates that A1762T/G1764A mutation might accelerate tumor proliferation through some unknown mechanism. 2018 Cancer management and research Discussion HBV G1764A;G1764A;A1762T;A1762T 55;130;48;123 61;136;54;129 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. In the present study, we sequenced most mutation regions that have been reported in the literature previously, and found that both A1762T/G1764A and Pre S deletion mutations related to worse OS and DFS. 2018 Cancer management and research Discussion HBV G1764A;A1762T 138;131 144;137 PreS 149 154 Hepatocellular carcinoma 198 201 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. More importantly, for the first time, we demonstrated that HBV-HCC with dual mutations in A1762T/G1764A and Pre S deletion related to the worst OS and DFS, and patients tended to have early recurrence. 2018 Cancer management and research Discussion HBV G1764A;A1762T 97;90 103;96 PreS 108 113 Hepatocellular carcinoma;Hepatocellular carcinoma 151;63 154;66 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. More recently, Chen et al reported that A1762T/G1764A double mutation and phosphorylated AKT (pAKT) correlated with proliferation and microvascularization but inversely correlated with apoptosis in HCC samples; levels of p21 and p27 were decreased in A1762T/G1764A double mutation or pAKT overexpressing HCC due to SKP2 upregulation; levels of E2F1, and both mRNA and protein of SKP2, were increased in A1762T/G1764A double mutation HCC. 2018 Cancer management and research Discussion HBV G1764A;G1764A;G1764A;A1762T;A1762T;A1762T 47;258;410;40;251;403 53;264;416;46;257;409 Hepatocellular carcinoma;Hepatocellular carcinoma;Hepatocellular carcinoma 198;304;433 201;307;436 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Other HBV mutations, which have been reported to relate to liver cirrhosis and HCC, including A1752T/G, T1753C, G1757A, C1766T, T1768A, A1775G, C1799G, A1846T, T1858C, and G1898A, failed to show the association with patients' prognosis in the present study. 2018 Cancer management and research Discussion HBV A1752T;A1752G;T1753C;G1757A;C1766T;T1768A;A1775G;C1799G;A1846T;T1858C;G1898A 94;94;104;112;120;128;136;144;152;160;172 102;102;110;118;126;134;142;150;158;166;178 Liver cirrhosis;Hepatocellular carcinoma 59;79 74;82 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Our findings also indicated that more aggressive anti-HBV therapy and more frequent follow-up should be suggested for those HBV-HCC patients with dual mutations in A1762T/G1764A and Pre S deletion. 2018 Cancer management and research Discussion HBV G1764A;A1762T 171;164 177;170 PreS 182 187 Hepatocellular carcinoma 127 131 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Patients with A1762T/G1764A double mutation tend to have poor liver function and serious cirrhosis, which will reduce time of survival after surgery. 2018 Cancer management and research Discussion HBV G1764A;A1762T 21;14 27;20 Liver cirrhosis 89 98 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. Previous studies had confirmed that A1762T/G1764A double mutation is not only an independent risk factor for HCC but also a predictor for poor survival in HBV-HCC patients. 2018 Cancer management and research Discussion HBV G1764A;A1762T 43;36 49;42 Hepatocellular carcinoma;Hepatocellular carcinoma 109;158 112;162 29628773 The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study. The A1762T/G1764A double mutation is the most frequent BCP mutation. 2018 Cancer management and research Discussion HBV G1764A;A1762T 11;4 17;10 BCP 55 58 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Due to the peculiar HBV-genome organization, drug-resistance mutations rtM204 V, rtM204I, and rtV173 L correspond to the NA-induced immune-escape mutations sI195M, sI196S, and sE164D. 2018 BMC infectious diseases Discussion HBV M204V;M204I;V173L;I195M;I196S;E164D 73;83;96;156;164;176 79;88;102;162;170;182 RT;RT;RT;S;S;S 71;81;94;156;164;176 73;83;96;157;165;177 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Notably, stop-codon at HBsAg-position 172 derives from the drug-resistance mutation rtA181T selected under ADV- and (in some cases) LAM-treatment. 2018 BMC infectious diseases Discussion HBV A181T 86 91 S;RT 23;84 28;86 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. Only the immune-associated escape mutation G130 N was detected more frequently in genotype-A than -D. 2018 BMC infectious diseases Discussion HBV G130N 43 49 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. This difference can be explained considering the fact that the number of nucleotide substitutions necessary to generate G130 N from the wild-type amino acid is lower in genotype-A than -D. 2018 BMC infectious diseases Discussion HBV G130N 120 126 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. This is consistent with an in-vitro study showing sP120T ability to rescue HBV-replication impaired by rtM204V/I. 2018 BMC infectious diseases Discussion HBV M204V;M204I;P120T 105;105;50 112;112;56 RT;S 103;50 105;51 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. This is in line with previous studies showing that genotype-A is more prone to develop rtM204V than genotype-D at lamivudine failure. 2018 BMC infectious diseases Discussion HBV M204V 89 94 RT 87 89 29859062 Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe. We observed that sP120T significantly correlated with rtM204V/I, and their co-presence is characterized by elevated serum HBV-DNA. 2018 BMC infectious diseases Discussion HBV M204V;M204I;P120T 56;56;17 63;63;23 RT;S 54;17 56;18 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. To the best of our knowledge, this is the first case describing breakthrough of HBV genotype F due to G145R, P120Q, and Q129P escape mutations in a transplant setting. 2018 World journal of hepatology Discussion HBV G145R;P120Q;Q129P 102;109;120 107;114;125 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. We also identified a P120Q mutation in the upstream region of the HBV core gene and two different mutations at positions Q129, Q129P, and H in our patient. 2018 World journal of hepatology Discussion HBV P120Q;Q129P 21;127 26;132 C 70 74 30079137 Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations: A case report and review of the literature. We identified the immune escape mutation G145R in our patient. 2018 World journal of hepatology Discussion HBV G145R 41 46 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. A European study demonstrated that the most frequent primary mutation was rtM204V/I, found in 49% of treatment experienced patients, while in China rtM204I, rtN236T and rtL180M+rtM204V+rtV173L/rtS202G were also the most prevalent RAMs. 2018 PLoS neglected tropical diseases Discussion HBV M204V;M204I;S202G;M204I;N236T;L180M;M204V;V173L 76;76;195;150;159;171;179;187 83;83;200;155;164;176;184;192 RT;RT;RT;RT;RT;RT;RT 74;148;157;169;177;185;193 76;150;159;171;179;187;195 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. A review of worldwide incidence of RAMs among treatment naive patients also described rtM204V/I as the most frequent, but with a much lower prevalence of 5%. 2018 PLoS neglected tropical diseases Discussion HBV M204V;M204I 88;88 95;95 RT 86 88 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. A study from Malawi demonstrated the rapid emergence of 3TC resistance in HIV coinfection, with virtually all treatment naive HBeAg positive individuals starting antiviral treatment showing emergence of rtM204I by six months. 2018 PLoS neglected tropical diseases Discussion HBV M204I 205 210 C;RT 126;203 131;205 HBV-HIV coinfections 74 89 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. In keeping with other settings, the most common RAM identified here was rtM204I/V, either alone or in combination with compensatory mutations rtL180M +- rtV173L. 2018 PLoS neglected tropical diseases Discussion HBV M204I;M204V;V173L;L180M 74;74;155;144 81;81;160;149 RT;RT;RT 72;142;153 74;144;155 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Individuals with rtM204V/I plus compensatory mutations typically exhibit high HBV DNA levels and are therefore highly infectious to others. 2018 PLoS neglected tropical diseases Discussion HBV M204V;M204I 19;19 26;26 RT 17 19 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Likewise, a study carried out in Italy revealed that patients with HIV coinfection were more likely to harbour the rtM204V mutation and to show multiple mutations compared to HBV monoinfected patients. 2018 PLoS neglected tropical diseases Discussion HBV M204V 117 122 RT 115 117 HBV-HIV coinfections;HBV infections 67;175 82;191 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. Of concern, rtM204V/I was seen in 76% of treatment experienced patients and 22% of treatment naive patients in South Africa. 2018 PLoS neglected tropical diseases Discussion HBV M204V;M204I 14;14 21;21 RT 12 14 30080852 A systematic review of hepatitis B virus (HBV) drug and vaccine escape mutations in Africa: A call for urgent action. The triple mutation rtM204V + rtL180M + rtV173L has been identified in East, West and Central Africa. 2018 PLoS neglected tropical diseases Discussion HBV M204V;L180M;V173L 22;32;42 27;37;47 RT;RT;RT 20;30;40 22;32;42 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Cross-resistance by HBV rtA181C was observed to LVD and LdT but not to ADV or TDF. 2018 Hepatology communications Discussion HBV A181C 26 31 RT 24 26 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Cross-resistance occurred between ETV and other approved anti-HBV drugs in analyses performed with recombinant clones expressing rt181C in combination with LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Discussion HBV L180M;M204V 177;185 182;190 RT;RT;RT 129;175;183 131;177;185 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. ETVr conferred by this substitution was always associated with the LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Discussion HBV L180M;M204V 88;96 93;101 RT;RT 86;94 88;96 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV rt181C was always detected in combination with the LVDr substitutions rtL180M+rtM204V and was observed as the major species in 3 of these patients by clonal analysis. 2018 Hepatology communications Discussion HBV L180M;M204V 76;84 81;89 RT;RT;RT 4;74;82 6;76;84 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. HBV rtA181 substitutions other than rt181C (G, N, S, T, or V) in combination with LVDr substitutions rtL180M+rtM204V showed a reduced ETV susceptibility similar to that previously observed for LVDr HBV. 2018 Hepatology communications Discussion HBV L180M;M204V 103;111 108;116 RT;RT;RT;RT 4;36;101;109 6;38;103;111 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. However, one of the patient-derived HBV RT sequences from 13 LVD-experienced patients with virologic breakthrough harbored a novel substitution (rtA181C) at an amino acid position associated with nucleos(t)ide resistance( 24, 25, 26, 27 ) in combination with LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Discussion HBV A181C;L180M;M204V 147;280;288 152;285;293 RT;RT;RT;RT 40;145;278;286 42;147;280;288 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. In our analysis, the only novel HBV RT substitution (rtA181C) shown to confer ETVr in vitro was detected in 0.5% (5/982) of evaluable patients who met the criteria for resistance testing. 2018 Hepatology communications Discussion HBV A181C 55 60 RT;RT 36;53 38;55 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Interestingly, this substitution was detected with the high-level ETVr substitution rtT184L and LVDr substitutions rtL180M+rtM204V during virologic breakthrough in all cases. 2018 Hepatology communications Discussion HBV T184L;L180M;M204V 86;117;125 91;122;130 RT;RT;RT 84;115;123 86;117;125 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. One of the novel emergent HBV RT substitutions (rtI169V) not associated with a loss in ETV susceptibility emerged in 6 LVD-experienced patients who were infected with HBV genotype C and had experienced virologic breakthrough. 2018 Hepatology communications Discussion HBV I169V 50 55 RT;RT 30;48 32;50 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous analyses have shown that the primary HBV substitutions at rtT184, rtS202, or rtM250 confer resistance to ETV when associated with LVDr substitutions rtM204V/I+-rtL180M( 15 ) and display varying degrees of ETV susceptibility depending on the specific resistance substitutions.( 12 ) While assessing HBV RT sequences from our integrated analysis, novel substitutions that emerged in at least 2 patients in WT, LVDr, and/or ETVr HBV RT backgrounds were observed. 2018 Hepatology communications Discussion HBV M204V;M204I;L180M 160;160;171 167;167;176 RT;RT;RT;RT;RT;RT;RT 67;75;86;158;169;311;439 69;77;88;160;171;313;441 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Previous findings have suggested that substitutions (e.g., rtI169T) at this amino acid position may act in a compensatory manner in ETVr HBV.( 14 ) Our data suggest that HBV rt169V may also have an adaptive role in ETVr HBV, specifically during the emergence of rtT184L with rtL180M+rtM204V in patients with virologic failure infected with genotype C HBV. 2018 Hepatology communications Discussion HBV I169T;T184L;L180M;M204V 61;264;277;285 66;269;282;290 RT;RT;RT;RT;RT 59;174;262;275;283 61;176;264;277;285 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. Reverse genetics confirmed the role of rtA181C in ETVr, although this loss in ETV sensitivity only resulted in the presence of the LVDr substitutions rtL180M+rtM204V. 2018 Hepatology communications Discussion HBV A181C;L180M;M204V 41;152;160 46;157;165 RT;RT;RT 39;150;158 41;152;160 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The HBV rtA181C substitution emerged infrequently in patients treated with ETV who had either experienced virologic breakthrough during treatment or had evidence of detectable HBV DNA throughout the course of treatment. 2018 Hepatology communications Discussion HBV A181C 10 15 RT 8 10 30202825 Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis. The HBV substitution rtA181C was identified from an integrated genotypic analysis of HBV RT sequences from ETV-treated patients. 2018 Hepatology communications Discussion HBV A181C 23 28 RT;RT 21;89 23;91 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. Both HBx S31A and S31D plasmids are resulted from missense mutation. 2018 Cancer medicine Discussion HBV S31A;S31D 9;18 13;22 X 5 8 30358169 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells. By transfecting the Huh7 cells with HBx S31A or S31D plasmid, we confirmed that the phosphorylation of HBx on at serine31 was responsible for the bond of HBx to 14-3-3zeta. 2018 Cancer medicine Discussion HBV S31A;S31D 40;48 44;52 X;X;X 36;103;154 39;106;157 30377627 Hepatitis B Virus (HBV) Infection and Re-activation During Nucleos(t)ide Reverse Transcriptase Inhibitor-Sparing Antiretroviral Therapy in a High-HBV Endemicity Setting. The viral sequence showed the major MHR mutations Y100C and Y161FY; in addition, the patient harbored HBV genotype A3, which circulates in Cameroon and carries arginine (R) rather than lysine (K) at surface position 122. 2018 Open forum infectious diseases Discussion HBV Y100C 50 55 S 199 206 30377627 Hepatitis B Virus (HBV) Infection and Re-activation During Nucleos(t)ide Reverse Transcriptase Inhibitor-Sparing Antiretroviral Therapy in a High-HBV Endemicity Setting. Y100C and K122R have been previously recognized in the context of HBsAg-negative HBV infection ("occult hepatitis B"); Y100C has also been previously described in a patient with co-circulating HBsAg and anti-HBs. 2018 Open forum infectious diseases Discussion HBV Y100C;K122R;Y100C 0;10;119 5;15;124 S;S;S 208;66;193 211;71;198 HBV infections 81 94 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. Additionally, WC33 had the dual secondary escape mutations sY134H and sD144A associated with HBV reactivation. 2019 Virus genes Discussion HBV Y134H;D144A 59;70 65;76 S;S 59;70 60;71 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. Although it was found exclusively among HBV isolates from blood donors, the change from Asp to Glu at position s144 (D144E) has been described also in HBV isolates from HBV/HIV infected patients. 2019 Virus genes Discussion HBV D144E 117 122 S 111 112 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. However, in the current study, sP120L was observed in HBV mono-infected as well. 2019 Virus genes Discussion HBV P120L 31 37 S 31 32 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. sD144A was the predominant mutation among genotype D sequences isolated from blood donors. 2019 Virus genes Discussion HBV D144A 0 6 S 0 1 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. sP120L mutation in genotype D sequences has been functionally characterized and linked with occult HBV (OBI). 2019 Virus genes Discussion HBV P120L 0 6 S 0 1 Occult Hepatitis B 104 107 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. sY134H causes a secondary co-variation with rtV142A in RT domain and is associated with failure to respond to immunoglobulin therapy in addition to HBV re-activation. 2019 Virus genes Discussion HBV V142A;Y134H 46;0 51;6 RT;RT;S 44;55;0 46;57;1 30382563 Molecular characterization of hepatitis B virus in blood donors in Botswana. Together with sD144A they reside in the immunogenic segment (aa 139 -149) and have been extensively discussed by Verheyen et al in correlation with reactivation. 2019 Virus genes Discussion HBV D144A 14 20 S 14 15 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Another precore mutation, which is usually detected alongside preC-W28*, is G29D; a recent meta-analysis combined the results of eleven individual studies and confirmed a significant correlation between G29D mutation and an increased risk of HCC (Liao et al.,). 2018 Frontiers in cellular and infection microbiology Discussion HBV W28X;G29D;G29D 67;76;203 71;80;207 Precore;Precore 62;8 66;15 Hepatocellular carcinoma 242 245 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Core mutation V91S/T was significantly associated with disease progression in HBV-infected patients, which is consistent with previous reports of an amino acid hot spot between residues 81-105 that is important for the progression of disease in chronically infected patients (Kim et al.,). 2018 Frontiers in cellular and infection microbiology Discussion HBV V91T;V91S 14;14 20;20 C 0 4 HBV infections 78 90 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Furthermore, progression from active HBV status to cirrhosis and HCC was associated with four core protein substitutions: E64D, E77Q, A80I/T/V, and L116I. 2018 Frontiers in cellular and infection microbiology Discussion HBV A80I;A80T;A80V;E64D;E77Q;L116I 134;134;134;122;128;148 142;142;142;126;132;153 C 94 98 Liver cirrhosis;Hepatocellular carcinoma 51;65 60;68 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In contrast, we observed the mutations A80I/V and L116I more frequently in active HBV carriers than in patients with severe liver disease. 2018 Frontiers in cellular and infection microbiology Discussion HBV A80V;A80I;L116I 39;39;50 45;45;55 Liver disease 124 137 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In the present study, three significant mutations were located within T-cell epitopes (F24Y, E64D, and V91S/T), and an equal number of significant mutations were present within B-cell epitopes (E77Q, A80I/V, and L116I), of the HBcAg protein. 2018 Frontiers in cellular and infection microbiology Discussion HBV F24Y;E64D;V91S;V91T;E77Q;A80I;A80V;L116I 87;93;103;103;194;200;200;212 91;97;109;109;198;206;206;217 C 227 232 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In the present study, two statistically significant core protein amino acid substitutions (E77Q and V91S/T) that may influence the progression of HBV infection from an inactive carrier stage to more advanced stages were identified. 2018 Frontiers in cellular and infection microbiology Discussion HBV V91T;E77Q;V91S 100;91;100 106;95;106 C 52 56 HBV infections 146 159 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In the present study, we observed a statistically significant increase in preC-W28* frequency in the LC+HCC group of patients as compared with active HBV carriers, which is consistent with previous reports of a positive association between this mutation and liver disease severity (Kim et al.,; Park et al.,; Xie et al.,). 2018 Frontiers in cellular and infection microbiology Discussion HBV W28X 79 83 Precore 74 78 Hepatocellular carcinoma;Liver disease;Liver cirrhosis 104;258;101 107;271;103 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. In this study, the HBcAg mutations E64D, E77Q, A80I/T/V, and L116I were significantly associated with cirrhosis and HCC. 2018 Frontiers in cellular and infection microbiology Discussion HBV A80I;A80T;A80V;E64D;E77Q;L116I 47;47;47;35;41;61 55;55;55;39;45;66 C 19 24 Liver cirrhosis;Hepatocellular carcinoma 102;116 111;119 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Indeed, both A80I/V and L116I were significantly associated with a decreased risk of cirrhosis and HCC in HBV-infected patients. 2018 Frontiers in cellular and infection microbiology Discussion HBV A80V;A80I;L116I 13;13;24 19;19;29 Liver cirrhosis;Hepatocellular carcinoma;HBV infections 85;99;106 94;102;118 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Interestingly, mutation E77Q, detected in our study, was also reported by Tong et al. 2018 Frontiers in cellular and infection microbiology Discussion HBV E77Q 24 28 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Multivariate logistic regression analysis indicated that the A80V and L116I mutations may also be useful independent prognostic markers of HBV-associated liver disease progression, particularly in combination with other contributing factors, such as viral load. 2018 Frontiers in cellular and infection microbiology Discussion HBV A80V;L116I 61;70 65;75 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Mutation E180A, which was significantly associated with liver disease development, was not located in a known epitopic region, suggesting that mechanisms other than immune evasion may be involved. 2018 Frontiers in cellular and infection microbiology Discussion HBV E180A 9 14 Liver disease 56 69 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. One of the most common precore mutations, detected in more than 50% of individuals with chronic hepatitis B in Asia and the Mediterranean area, is a G to A substitution at nucleotide 1896, resulting in a tryptophan to stop codon substitution at codon 28 (Tong et al.,). 2018 Frontiers in cellular and infection microbiology Discussion HBV G1896A;W28X 149;204 187;253 Precore 23 30 Chronic Hepatitis B 88 107 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Previously, a study of HBV core variability under antiviral therapy reported the presence of the E64D mutation during the course of HBV infection, and stated that this substitution significantly reduced T-cell proliferation in vitro when it occurred with mutation T67N (Homs et al.,). 2018 Frontiers in cellular and infection microbiology Discussion HBV E64D;T67N 97;264 101;268 C 27 31 HBV infections 132 145 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Similarly, four core protein mutations that were associated with the progression from active HBV status to cirrhosis were noted (F24Y, A80I/V, L116I, and E180A). 2018 Frontiers in cellular and infection microbiology Discussion HBV F24Y;A80I;A80V;L116I;E180A 129;135;135;143;154 133;141;141;148;159 C 16 20 Liver cirrhosis 107 116 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Similarly, the present analysis identified a significant positive association between the mutation G29D and progression toward severe liver disease in HBV-infected Saudi patients. 2018 Frontiers in cellular and infection microbiology Discussion HBV G29D 99 103 Liver disease;HBV infections 134;151 147;163 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. Some of these mutations, such as E77Q, A80I/V, and L116I, are present at multiple stages of HBV infection, whereas others are associated with a specific clinical stage. 2018 Frontiers in cellular and infection microbiology Discussion HBV E77Q;A80I;A80V;L116I 33;39;39;51 37;45;45;56 HBV infections 92 105 30406036 The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease. We identified four core protein mutations that were significantly associated with cirrhosis: F24Y, A80I/V, L116I, and E180A. 2018 Frontiers in cellular and infection microbiology Discussion HBV F24Y;A80I;A80V;L116I;E180A 93;99;99;107;118 97;105;105;112;123 C 19 23 Liver cirrhosis 82 91 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. In conclusion, G1896A precore mutation is highly prevalent in patients with HBeAg negative serology in particular with the clinical categories like FH, CH, Cirrhosis and HCC. 2018 Saudi journal of biological sciences Discussion HBV G1896A 15 21 C;Precore 76;22 81;29 Fulminant Hepatitis B;Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma 148;152;156;170 150;154;165;173 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Ligase chain reaction was used as a tool for screening G1896A mutation in all the clinical categories of HBV patients. 2018 Saudi journal of biological sciences Discussion HBV G1896A 55 61 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Mutant HBV with precore stop codon at position G1896A has been reported to be associated with severe liver damage in chronic liver disease patients. 2018 Saudi journal of biological sciences Discussion HBV G1896A 47 53 Precore 16 23 Liver disease 101 113 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Preliminary studies conducted in South India suggests that G to A switch at nucleotide G1896A is a most common mutation of HBV genome in patients with chronic liver disease from the Indian subcontinent. 2018 Saudi journal of biological sciences Discussion HBV G1896A 87 93 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The detection of the G1896A mutation or Wild type samples by LCR was in 100% agreement with the results of direct sequencing. 2018 Saudi journal of biological sciences Discussion HBV G1896A 21 27 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. The LCR technology can be a suitable tool for screening G1896A mutations. 2018 Saudi journal of biological sciences Discussion HBV G1896A 56 62 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. Therefore, it is of immense importance to screen precore G1896A mutations in patients with HBeAg negative serology and we have tried to establish LCR as a mutation screening tool. 2018 Saudi journal of biological sciences Discussion HBV G1896A 57 63 C;Precore 91;49 96;56 30505167 Hepatitis B virus precore G1896A mutation in chronic liver disease patients with HBeAg negative serology from North India. This observation suggests the need of screening HBV precore G1896A mutation in this region particularly in HBeAg negative cases. 2018 Saudi journal of biological sciences Discussion HBV G1896A 60 66 C;Precore 107;52 112;59 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Meanwhile, 5 women out of 40, harboured mutations that confer resistance to NNRTIs of which K103 N (12.5%) and Y181C (10.0%) were the most frequent. 2018 BMC pregnancy and childbirth Discussion HBV K103N;Y181C 92;111 98;116 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Of the 9 RAMs identified, K103 N was identified in 5 women, which predicts resistance to nevirapine. 2018 BMC pregnancy and childbirth Discussion HBV K103N 26 32 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Of the nine mutations, M184 V (12.5%) and K70R (10.0%) were most frequently identified. 2018 BMC pregnancy and childbirth Discussion HBV M184V;K70R 23;42 29;46 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. On the other hand, two women were found with RAMs to protease inhibitors which were M46 L (2.5%) and L90 M (2.5%). 2018 BMC pregnancy and childbirth Discussion HBV M46L;L90M 84;101 89;106 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. The high frequency of M184 V found in our study could be explained by the fact that lamivudine and zidovudine are part of PMTCT regimens in Cameroon. 2018 BMC pregnancy and childbirth Discussion HBV M184V 22 28 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. The M184 V is known to confer high levels of resistance to lamivudine (3TC) and emtricitabine (FTC), while K70R is known to confer intermediate levels of resistance to zidovudine (AZT). 2018 BMC pregnancy and childbirth Discussion HBV M184V;K70R 4;107 10;111 30577760 Rates of HBV, HCV, HDV and HIV type 1 among pregnant women and HIV type 1 drug resistance-associated mutations in breastfeeding women on antiretroviral therapy. Y181C as well as K103 N confer intermediate to high level resistance to nevirapine and efavirenz, two NNRTIs commonly used in Cameroon. 2018 BMC pregnancy and childbirth Discussion HBV Y181C;K103N 0;17 5;23 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. demonstrated that 3 of 230 (1.3%) hepatitis B e antigen-positive chronic hepatitis B patients were infected with sE2G variants, 9 of 230 (3.9%) were infected with sL98V variants, and 3 of 230 (1.3%) were infected with sG145R variants in the small S protein. 2018 Scientific reports Discussion HBV E2G;L98V;G145R 113;163;218 117;168;224 C;S;S;S;S 46;113;163;218;241 55;114;164;219;248 Chronic Hepatitis B 65 84 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Indeed, sE2G, sL77R, sL98V, sT118K, sQ129H, and sG145R, all of which cause reduced virion secretion, were found in the sera from 9 of 24 (38%) patients with HBV reactivation. 2018 Scientific reports Discussion HBV E2G;L77R;L98V;T118K;Q129H;G145R 8;14;21;28;36;48 12;19;26;34;42;54 S;S;S;S;S;S 8;14;21;28;36;48 9;15;22;29;37;49 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Interestingly, 4 of 16 (25%) patients in the non-HSCT group developed HBV reactivation by variants with the M1V/I substitution at the PreS2 start codon, leading to ablation of the middle S protein. 2018 Scientific reports Discussion HBV M1V;M1I 108;108 113;113 S;PreS2 180;134 188;139 Hematopoietic stem cell transplantation 49 53 30584239 Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection. Moreover, 6 of 24 (25%) patients had sL21S and/or sF220C amino acid variants in the MHC class II-restricted T-cell epitope of the small S protein, potentially leading to a complete loss of T-cell reactivity and anti-HBs production. 2018 Scientific reports Discussion HBV L21S;F220C 37;50 42;56 S;S;S;S 216;37;50;130 219;38;51;137 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Although C18T, G82A, A115C and G120A showed similar behaviors regarding regulation of HBsAg expression in three different in vitro systems, respectively, the up-regulation effect of A138G and C189A on HBsAg expression found in luciferase reporter system was not confirmed in pLMS and p1.2/PC systems. 2019 Viruses Discussion HBV C18T;G82A;A115C;G120A;A138G;C189A 9;15;21;31;182;192 13;19;26;36;187;197 S;S 86;201 91;206 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Although G120A was only a single mutation, our results suggest that it might up-regulate the transcriptional activity of SPII. 2019 Viruses Discussion HBV G120A 9 14 S promoter II 121 125 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. At the same time, C18T, A115C, G120A and A138G could regulate HBV total RNA levels, but they have no effect on pgRNA levels. 2019 Viruses Discussion HBV C18T;A115C;G120A;A138G 18;24;31;41 22;29;36;46 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. By luciferase assay in cell culture system, we demonstrated that only C18T mutation among the 12 SPII novel mutations significantly inhibited SPII activity. 2019 Viruses Discussion HBV C18T 70 74 S promoter II;S promoter II 97;142 101;146 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Firstly, it is speculated that A115C, G120A and A138G in the C region of SPII may enhance the promoter activity, since the C region is a positive regulatory region. 2019 Viruses Discussion HBV A115C;G120A;A138G 31;38;48 36;43;53 C;C;S promoter II 61;123;73 62;124;77 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Further functional study on some novel mutations in SPII region, such as G82A, A115C, G120A and A138G and so on, revealed that these mutations could affect the transcription activity of SPII promoter regulating HBsAg levels and HBV replication. 2019 Viruses Discussion HBV G82A;A115C;G120A;A138G 73;79;86;96 77;84;91;101 S;S promoter II;S promoter II 211;52;186 216;56;190 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. However, C18T locates in TF unbinding region, the significant impact of this mutation hints that the inter-functional regions might have unrevealed functions. 2019 Viruses Discussion HBV C18T 9 13 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. However, other mutations led to increased SPII activity, especially the G120A mutation showing 15-fold higher activity than WT. 2019 Viruses Discussion HBV G120A 72 77 S promoter II 42 46 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Interestingly, the G120A mutation increased HBV DNA levels in vitro (see Figure 7), which was consistent with the patient results. 2019 Viruses Discussion HBV G120A 19 24 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Moreover, we found that most of these hotspot mutations were not prone to mutate in combinations (C18T + G82A (n = 1), C18T + A115C (n = 1), C18T + A138G (n = 1) and A115C + G120A (n = 1)), however, G82A + A138G combination mutations were detected in 17.2% (15/87) of C2 sequences. 2019 Viruses Discussion HBV C18T;G82A;C18T;A115C;C18T;A138G;A115C;G120A;G82A;A138G 98;105;119;126;141;148;166;174;199;206 102;109;123;131;145;153;171;179;203;211 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Mutants A115C, G120A and A138G upregulated extracellular/intracellular HBsAg levels (Figure 6), and C18T downregulated those (Figure 6), which were consistent with luciferase assay (Figure 4). 2019 Viruses Discussion HBV A115C;G120A;A138G;C18T 8;15;25;100 13;20;30;104 S 71 76 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Results showed that HBsAg and HBV DNA levels were significantly higher in the G120A mutation group than those of WT (p < 0.05). 2019 Viruses Discussion HBV G120A 78 83 S 20 25 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. The A115C mutation in SPII corresponds to PreS1-I84L substitution, but G120A and A138G do not cause any AA changes of PreS1. 2019 Viruses Discussion HBV A115C;I84L;G120A;A138G 4;48;71;81 9;52;76;86 PreS1;PreS1;S promoter II 42;118;22 47;123;26 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Therefore, it is speculated that A115C mutation may affect HBsAg expression. 2019 Viruses Discussion HBV A115C 33 38 S 59 64 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. These results indicate that G120A mutation may impact viral replication. 2019 Viruses Discussion HBV G120A 28 33 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Thirdly, due to the spacer region of the P gene overlapping with SPII, mutations A115C, G120A, and A138G of SPII correspond to spacer-H87P, D89N and T95N AA substitution, respectively. 2019 Viruses Discussion HBV A115C;G120A;A138G;H87P;D89N;T95N 81;88;99;134;140;149 86;93;104;138;144;153 P;S promoter II;S promoter II 41;65;108 42;69;112 30669266 Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients. Whether single-site mutations may have such a significant effect on activity, we refer to the effects of the A1762T/G1764A mutation in HBV. 2019 Viruses Discussion HBV G1764A;A1762T 116;109 122;115 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Addition of classical ETV-resistance mutation rtS202G or rtM250V into LAMr+rtA181C mutant reduced N-H:O hydrogen bonds from three to two, leading to further decrease of the binding affinity of HBV RT to ETV-TP. 2019 Emerging microbes & infections Discussion HBV M250V;A181C;S202G 59;77;48 64;82;53 RT;RT;RT;RT 46;57;75;197 48;59;77;199 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. From the view of resistance history, the five representative rtA181C-positive patients all had rtA181V and/or rtA181V-containing mutations (as shown in Figure 1). 2019 Emerging microbes & infections Discussion HBV A181V;A181V;A181C 97;112;63 102;117;68 RT;RT;RT 61;95;110 63;97;112 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. identified ETV-resistance features in the mutants rtL180M+M204V (LAMr), LAMr+rtT184L, LAMr+rtS202G, LAMr+rtM250V, and LAMr+rtT184G+rtS202I, showing they had 27, 246, 402, 1028, and >1333-fold respective decreases in drug susceptibility when compared to the wild-type strain. 2019 Emerging microbes & infections Discussion HBV M250V;L180M;T184L;S202G;T184G;S202I;M204V 107;52;79;93;125;133;58 112;57;84;98;130;138;63 RT;RT;RT;RT;RT;RT 50;77;91;105;123;131 52;79;93;107;125;133 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition, artificial elimination of rtA181C obviously restored its sensitivity to ETV, verifying the critical role of rtA181C mutation in ETV-resistance contribution. 2019 Emerging microbes & infections Discussion HBV A181C;A181C 41;123 46;128 RT;RT 39;121 41;123 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In addition, we identified two novel ETV-resistance mutants, rtL180M+A181C+M204V+M250V and rtL180M+A181C+S202G+M204V. 2019 Emerging microbes & infections Discussion HBV L180M;L180M;M204V;A181C;M250V;M204V;A181C;S202G 63;93;75;69;81;111;99;105 68;98;80;74;86;116;104;110 RT;RT 61;91 63;93 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In conclusion, this study is the first to demonstrate that rtL180M+A181C+M204V is a non-classical ETV-resistance mutation pattern and identified two other rtA181C-containing ETV-resistance mutation patterns, rtL180M+A181C+S202G+M204V and rtL180M+A181C+M204V+M250V. 2019 Emerging microbes & infections Discussion HBV A181C;L180M;L180M;L180M;A181C;M204V;S202G;M204V;A181C;M204V;A181C;M250V 157;61;210;240;67;73;222;228;216;252;246;258 162;66;215;245;72;78;227;233;221;257;251;263 RT;RT;RT;RT 59;155;208;238 61;157;210;240 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In contrast, rtA181C mutation requires a two-nucleotide change (GCT to TGT), which would increase the genetic barrier of the mutation and largely explain its low clinical incidence. 2019 Emerging microbes & infections Discussion HBV A181C 15 20 RT 13 15 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In the five ETV-resistance patients with rtL180M+A181C+M204V presented in this study, two received TDF and the other three received ADV+ETV. 2019 Emerging microbes & infections Discussion HBV L180M;A181C;M204V 43;49;55 48;54;60 RT 41 43 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In this study, the occurrence of an rtA181C mutation was independent of HBV genotypes. 2019 Emerging microbes & infections Discussion HBV A181C 38 43 RT 36 38 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In this study, we identified that the LAMr+rtA181C (rtL180M+A181C+M204V) mutant had 85.6-fold decreased susceptibility to ETV in vitro, which was lower than the decrease values of two classical ETV-resistance mutants simultaneously identified in the study (137.7 and 110.4 folds, Table 3), as well as reported values above. 2019 Emerging microbes & infections Discussion HBV A181C;L180M;M204V;A181C 45;54;66;60 50;59;71;65 RT;RT 43;52 45;54 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. In this study, we identified the rtA181C mutation through sequence analysis of a large number of chronic HBV-infected patients' samples, and managed to follow-up with five of the 18 rtA181C-positive patients. 2019 Emerging microbes & infections Discussion HBV A181C;A181C 35;184 40;189 RT;RT 33;182 35;184 HBV infections 105 117 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. It has been suggested rt181 mutation (rtA181 T/V) is involved in a shared pathway for resistance of several NAs. 2019 Emerging microbes & infections Discussion HBV A181T;A181V 40;40 48;48 RT;RT 22;38 24;40 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Most rtA181 T mutation only needed one-nucleotide change as we previously analysed, and so did for rtA181V mutation (Supplementary Table 1). 2019 Emerging microbes & infections Discussion HBV A181V;A181T 101;7 106;13 RT;RT 5;99 7;101 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Overall, the occurrence frequency of rtL180M+A181C+M204V in NAs-treated patients was rather low, and none of ETV naive treated patients were detected with rtL180M+A181C+M204V. 2019 Emerging microbes & infections Discussion HBV L180M;L180M;A181C;A181C;M204V;M204V 39;157;45;163;51;169 44;162;50;168;56;174 RT;RT 37;155 39;157 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Phenotypic analysis verified that three rtA181C-containing mutants only had a 2.7-3.2-fold decrease in TDF susceptibility, similar with the susceptibility of the two classical ETV-resistance mutants (2.0-2.2-fold decrease) in our study and rtL180M+S202G+M204V mutant (2.5-fold decrease) reported by other investigators. 2019 Emerging microbes & infections Discussion HBV A181C;L180M;M204V;S202G 42;242;254;248 47;247;259;253 RT;RT 40;240 42;242 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The LAMr rtL180M+M204V had decreased susceptibility to ETV but the decrease was not sufficient to cause clinical ETV resistance. 2019 Emerging microbes & infections Discussion HBV L180M;M204V 11;17 16;22 RT 9 11 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The modelling of viral RT indicated that the introduction of rtA181C mutation into LAMr mutant changed hydrogen bonds from O-H:O form to relatively less stable N-H:O form, leading to the decrease of the binding affinity of HBV RT to ETV-TP. 2019 Emerging microbes & infections Discussion HBV A181C 63 68 RT;RT;RT 23;61;227 25;63;229 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The results of molecular dynamics simulation also indicated LAMr+rtA181C together reduced the overall flexibility of the mutant proteins and prevented the ETV-TP from interacting with them. 2019 Emerging microbes & infections Discussion HBV A181C 67 72 RT 65 67 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtL180M+A181C+M204V mutant sequences were not found being documented previously in GenBank. 2019 Emerging microbes & infections Discussion HBV L180M;A181C;M204V 6;12;18 11;17;23 RT 4 6 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The rtL180M+A181C+M204V mutation pattern reported herein meets these conditions for ETV resistance: it was only detected in the patients who were receiving ETV and had experienced LAM treatment, it emerged in multiple patients with virological breakthrough or inadequate virological response against ETV monotherapy, and it conferred a > 50-fold increased EC50 for ETV. 2019 Emerging microbes & infections Discussion HBV L180M;A181C;M204V 6;12;18 11;17;23 RT 4 6 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The successive resistance history to LAM and ADV was likely a favourite factor for the development of the rtL180M+A181C+M204V mutation, which could contribute to the rare occurrence of rtA181C as an ETV resistance mutation. 2019 Emerging microbes & infections Discussion HBV L180M;A181C;M204V;A181C 108;187;120;114 113;192;125;119 RT;RT 106;185 108;187 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. The two mutants successively emerged during ADV+ETV treatment (Figure 1(E)), and the rtL180M+A181C+M204V+M250V mutant also emerged in patient 1 and patient 2 during ETV treatment. 2019 Emerging microbes & infections Discussion HBV L180M;M204V;A181C;M250V 87;99;93;105 92;104;98;110 RT 85 87 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. These data suggest that the rtM250V or rtS202G mutation contributed to the rtL180M+A181C+M204V template to adapt to selective drug pressure, while they had no persistent advantage for replication competency to overcome the continuous pressure of ADV+ETV. 2019 Emerging microbes & infections Discussion HBV M250V;S202G;L180M;M204V;A181C 30;41;77;89;83 35;46;82;94;88 RT;RT;RT 28;39;75 30;41;77 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. These modelling results reinforced that rtL180M+A181C+M204V to be a novel ETV-resistance mutation pattern analysis and supplied likelihood resistance mechanisms for the mutation pattern. 2019 Emerging microbes & infections Discussion HBV L180M;A181C;M204V 42;48;54 47;53;59 RT 40 42 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. These rtA181C mutants remained sensitive to TDF treatment. 2019 Emerging microbes & infections Discussion HBV A181C 8 13 RT 6 8 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. They had a higher ETV resistance but much lower replication capacity compared to the rtL180M+A181C+M204V mutant that emerged previously. 2019 Emerging microbes & infections Discussion HBV L180M;M204V;A181C 87;99;93 92;104;98 RT 85 87 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. This might partly account for the infrequency of LAMr+rtA181C-causative ETV resistance in clinic. 2019 Emerging microbes & infections Discussion HBV A181C 56 61 RT 54 56 30866789 Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice. Unlike rtA181 T mutation which may cause sW172stop and non-stop (sW172S, sW172L) mutations and the stop mutation will delete an HLA-A2-restricted s172-180 (env335-343) epitope of cytotoxic T lymphocytes (CTL) the rtA181C mutation only caused sW172C mutation in this study without deleting the CTL epitope. 2019 Emerging microbes & infections Discussion HBV A181T;A181C;W172S;W172L;W172C;W172X 9;215;65;73;242;41 15;220;71;79;248;50 RT;RT;S;S;S;S;S 7;213;41;65;73;146;242 9;215;42;66;74;147;243 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. A recent meta-analysis has shown that the incidence of spontaneous primary and secondary mutations among untreated chronic hepatitis B patients was 4.9% for primary mutations of rtM204V/I, while the natural incidence of secondary rtL180M mutations was 2.7%. 2019 PeerJ Discussion HBV M204V;M204I;L180M 180;180;232 187;187;237 RT;RT 178;230 180;232 Chronic Hepatitis B 115 134 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. For example, dual rtL180M and M204V/I mutants were frequently found in patients in Italy, with three patients having triple mutation of rtV173L, rtL180M and M204V. 2019 PeerJ Discussion HBV L180M;V173L;L180M;M204V;M204I;M204V 20;138;147;30;30;157 25;143;152;37;37;162 RT;RT;RT 18;136;145 20;138;147 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. In Turkey, the most frequent mutations observed were T143M and K122R, whereas in Egypt 14.8% presented with mutations in the MHR, and eight different mutations were discovered: R122K, S143L, L109P, S114P, S117N, P127S, P127T and Y134F. 2019 PeerJ Discussion HBV T143M;K122R;R122K;S143L;L109P;S114P;S117N;P127S;P127T;Y134F 53;63;177;184;191;198;205;212;219;229 58;68;182;189;196;203;210;217;224;234 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. M204I/V mutations are frequently accompanied by compensatory mutations in other domains such as 59 rtV173L, rtL180M, rtT184S/G, 58 rtI169T, rtS202I, rtL80V/I and rtQ215S which enhanced the replication efficiency of rt204I/V mutants without significantly affecting lamivudine resistance, by compensating the decrease in efficiency due to resistance-associated changes. 2019 PeerJ Discussion HBV T184S;T184G;L80V;L80I;Q215S;V173L;L180M;I169T;S202I;M204I;M204V 119;119;151;151;164;101;110;133;142;0;0 126;126;157;157;169;106;115;138;147;7;7 RT;RT;RT;RT;RT;RT;RT;RT 99;108;117;131;140;149;162;215 101;110;119;133;142;151;164;217 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Previous literature suggests that lamivudine is the main cause of YMDD (tyrosine-methionine-aspartateaspartate) mutations (M204I/V) within the catalytic sites (C domain) in HBV P-ORF. 2019 PeerJ Discussion HBV M204I;M204V 123;123 130;130 P;P 177;66 178;70 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. The prevalence of HBsAg escape mutants in Jordan was 18.9%, with the R122K mutation which affects HBV detection being the most prevalent type. 2019 PeerJ Discussion HBV R122K 69 74 S 18 23 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. This is comparable to a study done in Iran, which showed that the frequency of 14% major hydrophilic region mutations (MHR), with the most frequent ones of P120T/S and R122K/T. 2019 PeerJ Discussion HBV P120T;P120S;R122K;R122T 156;156;168;168 163;163;175;175 30867996 Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan. Upon comparing the mutant strains with wild HBV strains, patients with rtM204V/I more frequently presented with severe acute hepatitis B and lower serum HBV DNA values. 2019 PeerJ Discussion HBV M204V;M204I 73;73 80;80 RT 71 73 Acute Hepatitis B 112 136 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Although the in vivo transfection by hydrodynamic injection showed a relatively strong and prolonged expression of the LHBs sW182* protein in the mouse liver, this method is considered as transient transfection with a limited efficiency (only part of the liver cells are transfected). 2019 PloS one Discussion HBV W182X 124 130 S;S 119;124 123;125 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Because of the labile nature of the mutant in the cultured liver cells, we only transiently expressed the sW182* in Huh-7 cells, which showed a low, but reasonable amount of the protein expression (Fig 1). 2019 PloS one Discussion HBV W182X 106 112 S 106 107 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. Consistently, depletion of Jab1 from the liver cells impaired the effect of the LHBs sW182* to downregulate the tumor suppressors and their target genes (Figs 4 and 5). 2019 PloS one Discussion HBV W182X 85 91 S;S 80;85 84;86 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. From the observations above, we reasoned that mechanistic analysis of the sW182* mutant in the cultured liver cells is relevant, although it is unclear at present what causes the mutant protein unstable in the cultured liver cells. 2019 PloS one Discussion HBV W182X 74 80 S 74 75 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In conclusion, the current study identified that the oncogenic LHBs truncation mutant sW182* downregulates multiple tumor suppressors through a Jab1-mediated pathway in the liver cells. 2019 PloS one Discussion HBV W182X 86 92 S;S 63;86 67;87 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In contrast, the sW182* mutant was not detected in the blood but retained in the liver at a relatively high level. 2019 PloS one Discussion HBV W182X 17 23 S 17 18 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In NIH3T3 cells, the sW182* elevated pro-oncogenic signals that include JNK, JAK1,2 and STAT3. 2019 PloS one Discussion HBV W182X 21 27 S 21 22 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. In the current study, we therefore examine the effects of the LHBs sW182* mutant in a liver cell line. 2019 PloS one Discussion HBV W182X 67 73 S;S 62;67 66;68 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. It would be worthwhile to analyze more putative Jab1 targets if any of them is affected to further understand the signaling pathways that are influenced by the LHBs sW182* mutant. 2019 PloS one Discussion HBV W182X 165 171 S;S 160;165 164;166 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The expression of the sW182* mutant in the mouse liver in vivo resolved the concern, as we confirmed a prolonged expression of the mutant protein in the liver cells in the living mice (Fig 2). 2019 PloS one Discussion HBV W182X 22 28 S 22 23 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The instability of the sW182* mutant in the cultured liver cells raised a concern about its functional role in liver tumorigenesis. 2019 PloS one Discussion HBV W182X 23 29 S 23 24 Hepatocellular carcinoma 111 130 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The sW182* mutant can also epigenetically affects gene expression. 2019 PloS one Discussion HBV W182X 4 10 S 4 5 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. The three nonsense mutants, designated sL95*, sW182* and sL216*, have been shown to have oncogenic property and sW182* was the most potent. 2019 PloS one Discussion HBV L95X;W182X;L216X;W182X 39;46;57;112 44;52;63;118 S;S;S;S 39;46;57;112 40;47;58;113 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. These effects may account in part for the sW182* mutant-induced tumorigenesis in the mouse xenograft model. 2019 PloS one Discussion HBV W182X 42 48 S 42 43 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. To examine the functional effect of the LHBs sW182* protein on the mouse liver, a transgenic mouse model would be necessary. 2019 PloS one Discussion HBV W182X 45 51 S;S 40;45 44;46 30870427 A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1. We observed two major tumor suppressors p53 and Smad4, and their downstream target genes, were downregulated by the LHBs sW182* mutant, but not by the wild-type protein (Figs 4 and 5). 2019 PloS one Discussion HBV W182X 121 127 S;S 116;121 120;122 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. A previous study reported that the P5T mutation (strain: Shanghai adr) enhanced the intracellular viral DNA replication and rescued the immature secretion phenotype of I97L mutation in Huh7 cells. 2019 Antiviral research Discussion HBV P5T;I97L 35;168 38;172 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Among the 7 concurrent core mutations of GYF isolate, the I97L mutation has been reported to promote HBV DNA replication in cell cultures. 2019 Antiviral research Discussion HBV I97L 58 62 C 23 27 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Based on that, we changed I97L mutant back to its wild type sequence within the GYF background. 2019 Antiviral research Discussion HBV I97L 26 30 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Further investigation revealed that the mutation from proline (P) to threonine (T) at codon 5 (P5T) of core protein led to enhanced viral replication competency. 2019 Antiviral research Discussion HBV P5T 95 98 C;P 103;63 107;64 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Here, our result demonstrated that P5T alone promoted the viral ssDNA replication but reduced intracellular rcDNA level in HepG2. 2019 Antiviral research Discussion HBV P5T 35 38 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. However, the P5T mutation of WT HBV alone does not completely recapitulate the replication phenotype of GYF isolate, inferring that other core mutation(s) and/or the pol mutation(s) may work together with P5T to further promote virus replication and rcDNA maturation. 2019 Antiviral research Discussion HBV P5T;P5T 13;205 16;208 C;P 138;166 142;169 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. indicating that I97L mutation does not play a role in enhancing HBV replication, at least not in HepG2 cells. 2019 Antiviral research Discussion HBV I97L 16 20 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. It has been reported that the P5T mutation of HBcAg is common in HBV-related acute-on-chronic liver failure (ACLF) patients. 2019 Antiviral research Discussion HBV P5T 30 33 C 46 51 Acute on chronic liver failure;Acute on chronic liver failure 109;77 113;107 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. It is worth noting that the previous study indeed observed a much weaker phenotype of I97L-mediated enhancement of HBV replication in HepG2 cells compared to Huh7 cells. 2019 Antiviral research Discussion HBV I97L 86 90 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Moreover, P5T mutation enhanced the EIA signal of capsid in the native gel assay, indicating that P5T may promote capsid assembly and the subsequent pgRNA encapsidation. 2019 Antiviral research Discussion HBV P5T;P5T 10;98 13;101 Capsid;Capsid 50;114 56;120 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. One limitation of this study is that, though P5T and I97L mutations are commonly found in HBV patients, limited reports are available on the co-existence of multiple core compensatory mutations in NA-resistant patients. 2019 Antiviral research Discussion HBV P5T;I97L 45;53 48;57 C 166 170 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. reversely, T5P restoration reduced the DNA replication of GYF isolate but enhanced intracellular rcDNA production. 2019 Antiviral research Discussion HBV T5P 11 14 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. Structurally, HBV core protein has a four helix bundle structure, and according to the previously published three-dimensional structure of HBcAg dimer, amino acid 5 appears to be located at the interface of two monomers at the N-terminus of HBcAg, indicating that the P5T mutation may regulate the core dimerization/oligomerization to affect nucleocapsid assembly and viral DNA maturation. 2019 Antiviral research Discussion HBV P5T 268 271 C;C;C;C 18;298;139;241 22;302;144;246 30902704 Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate. The mechanistic link between P5T mutation and CHB exacerbation including ACLF remains elusive, but may be related to the enhanced virus replication and/or HBcAg-mediated liver inflammation. 2019 Antiviral research Discussion HBV P5T 29 32 C 155 160 Chronic Hepatitis B;Acute on chronic liver failure;Liver inflammation 46;73;170 49;77;188 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Furthermore, rtW284* was detected in one RS patient (4 of 25 clones) at baseline. 2019 Experimental and therapeutic medicine Discussion HBV W284X 15 20 RT 13 15 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. In addition to these well-documented major and compensatory mutations, 2 more mutations (rtS256G/C and rtM337H/T) were detected at a high rate. 2019 Experimental and therapeutic medicine Discussion HBV S256G;S256C;M337H;M337T 91;91;105;105 98;98;112;112 RT;RT 89;103 91;105 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. In addition, the substitution mutation rtA194T, which has been associated with TDF resistance, was not detected. 2019 Experimental and therapeutic medicine Discussion HBV A194T 41 46 RT 39 41 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Other mutations, including rtV84M, rtN118H/D/T, rtI169T, rtT184A/L/S, rtV191I, rtV207I/M, rtS213T, rtQ215P/S/H, rtI233L, rtP237H/T and rtS202G, which have been previously reported to be associated with ADV or ETV resistance, were detected at baseline or after six months of LAM/ADV treatment. 2019 Experimental and therapeutic medicine Discussion HBV V84M;N118H;N118D;N118T;T184A;T184L;T184S;V207I;V207M;Q215P;Q215S;Q215H;P237H;P237T;I169T;V191I;S213T;I233L;S202G 29;37;37;37;59;59;59;81;81;101;101;101;123;123;50;72;92;114;137 33;46;46;46;68;68;68;88;88;110;110;110;130;130;55;77;97;119;142 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 27;35;48;57;70;79;90;99;112;121;135 29;37;50;59;72;81;92;101;114;123;137 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. rtA181T was detected in one patient in the RS group. 2019 Experimental and therapeutic medicine Discussion HBV A181T 2 7 RT 0 2 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. Similar to previous studies, the present study suggested that truncation mutations (rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182*) occurred at the highest frequency. 2019 Experimental and therapeutic medicine Discussion HBV W172X;W196X;W182X;A181T;M204I;V191I 92;108;127;86;102;121 98;114;133;91;107;126 RT;RT;RT;S;S;S 84;100;119;92;108;127 86;102;121;93;109;128 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. sP120T and sG145R) that may be associated with LAM resistance, were not detected in the present study. 2019 Experimental and therapeutic medicine Discussion HBV P120T;G145R 0;11 6;17 S;S 0;11 1;12 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. The ADV resistance- associated rtN236T mutation was not detected at all in the present study. 2019 Experimental and therapeutic medicine Discussion HBV N236T 33 38 RT 31 33 30906435 Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy. The rtA181T mutation has been suggested as an atypical mutation associated with LAM and ADV resistance. 2019 Experimental and therapeutic medicine Discussion HBV A181T 6 11 RT 4 6 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. Hydrophilicity analysis of the second loop of the HBsAg major hydrophilic region by the Hopp & Woods method indicated that a mutation to asparagine at amino acid 144 would result in a reduction in hydrophilicity similar to that for the A/H mutations, suggesting that the D144N mutation may affect the presentation or conformation of this epitope in the 'a' determinant. 2019 Virology journal Discussion HBV D144N 271 276 S;S 354;50 368;55 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. Neither the precore stop codon mutation G1896A which abolishes HBeAg production or the basal core promoter mutations which cause reduced HBeAg production were found in any samples from either panel. 2019 Virology journal Discussion HBV G1896A 40 46 BCP;C;C;Precore 87;63;137;12 106;68;142;19 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. The D144N mutation (aspartic acid to asparagine) is a recently identified, rare mutation that has been reported only four times previously: a vaccine breakthrough infection (genotype A2) in a patient who received a liver transplant from an anti-HBc positive donor, and in three HBV infected individuals from Iran, Tanzania, and China (genotypes D, A1, and C, respectively) . 2019 Virology journal Discussion HBV D144N 4 9 C 245 248 HBV infections 278 290 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. The most frequently reported mutations at amino acid 144 result in substitution of alanine, histidine, or glutamic acid for aspartic acid (D144A/E/H). 2019 Virology journal Discussion HBV D144A;D144E;D144H 139;139;139 148;148;148 30943997 Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors. To our knowledge, the current study is the first report of the D144N mutation in association with a vaccine breakthrough case in the United States. 2019 Virology journal Discussion HBV D144N 63 68 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. All results shown here confirm that HBx-B K130M/V131I mutant variant displayed a stronger tumorigenic effect than its wild-type counterpart. 2019 Molecular cancer research Discussion HBV V131I;K130M 48;42 53;47 X 36 39 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. Taken together, these results provide a potential mechanism whereby HBV encoding X_K130M/V131I (BCP_A1762T/G1764A) may contribute to the high rate of HCC observed clinically in patient cohorts containing these mutations. 2019 Molecular cancer research Discussion HBV V131I;G1764A;K130M;A1762T 89;107;82;99 94;113;88;106 BCP;X 96;81 99;82 Hepatocellular carcinoma 150 153 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. The X_K130M/V131I amino acid changes are encoded by nucleotide changes at BCP_A1762T/G1764A, which also result in a decrease in PC/C mRNA and subsequent HBeAg expression. 2019 Molecular cancer research Discussion HBV V131I;G1764A;K130M;A1762T 12;85;5;77 17;91;11;84 BCP;C;Precore;X 74;153;128;4 77;158;130;5 30975706 HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism. Using the Fah/SB11 mouse model, K130M/V131I mutant variant of HBx-B induced a higher tumor burden than its wild-type counterpart and significantly increased the liver weight of the experimental animals. 2019 Molecular cancer research Discussion HBV V131I;K130M 38;32 43;37 X 62 65 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Another limitation of the study was our failure to clarify whether HBV with the G2765A substitution is actually less infectious to hepatocytes, and we could not directly show whether the mutation is associated with a decrease in the L/S protein ratio in patient sera due to technical reasons. 2019 Virology journal Discussion HBV G2765A 80 86 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. In fact, G2765A mutant HBV-infected patients showed less severe disease. 2019 Virology journal Discussion HBV G2765A 9 15 HBV infections 23 35 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. In fact, the aminotransferase levels of patients infected with the G2765A mutant HBV tend to be low, indicating that the immune responses of those patients are weak. 2019 Virology journal Discussion HBV G2765A 67 73 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Our data from the clinical samples showed that the G2765A substitution was associated with a lower HBV DNA load. 2019 Virology journal Discussion HBV G2765A 51 57 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Our results suggest the possibility that the G2765A substitution reduced L protein levels, leading to an increase in the number of cccDNA, which is difficult to eliminate from hepatocytes. 2019 Virology journal Discussion HBV G2765A 45 51 S 73 82 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. proposed that either a sufficiently high or low L/S protein ratio inhibited virion secretion, and this was corroborated by our finding that patients infected with the G2765A mutant HBV showed a lower HBV DNA load. 2019 Virology journal Discussion HBV G2765A 167 173 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Reduced levels of L protein caused by the G2765A substitution may enable HBV to escape immune pressure, making it possible to persist in the hepatocytes of patients. 2019 Virology journal Discussion HBV G2765A 42 48 S 18 27 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. The A1762T and G1764A mutations in the basic core promoter region are associated with an increased risk of HCC in genotype C patients. 2019 Virology journal Discussion HBV A1762T;G1764A 4;15 10;21 BCP 39 58 Hepatocellular carcinoma 107 110 31046787 A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus. Therefore, the G2765A substitution is considered to serve as a marker of good prognosis. 2019 Virology journal Discussion HBV G2765A 15 21 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Among 435 patients, non-classical mutations were detected at nine sites (V191I, V207I/M, S213T, E218D, F221Y, I224V, L229V, N/H238 and R242D) with virological breakthrough and without classical mutations (Table 4). 2019 Scientific reports Discussion HBV V191I;V207I;V207M;S213T;E218D;F221Y;I224V;L229V;R242D 73;80;80;89;96;103;110;117;135 78;87;87;94;101;108;115;122;140 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. By contrast, it is selected more frequently than M204V in genotype D. 2019 Scientific reports Discussion HBV M204V 49 54 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. considered that N238H variant did neither influence the susceptibilities to LAM or ADV nor weak the viral replication efficiency in vitro. 2019 Scientific reports Discussion HBV N238H 16 21 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Even so, the main mutants of A181T and F221Y might closely relate to TDF therapy. 2019 Scientific reports Discussion HBV A181T;F221Y 29;39 34;44 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. For L-nucleosides resistance, M204I/V was the most critical mutation site. 2019 Scientific reports Discussion HBV M204I;M204V 30;30 37;37 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. found that V207I restored viral replication fitness in LAM-resistant HBV, exhibiting YMDD mutations, and indicating the compensatory function of the rtV207I mutation. 2019 Scientific reports Discussion HBV V207I;V207I 151;11 156;16 RT;P 149;85 151;89 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. However, L180 + M204I formed the basis of ETV resistance, which together with the higher mutation rates at other three ETV-resistant mutation sites (180, 200 and 202) in genotype C (Table 3), contributed to more favorable for further evolution towards ETV resistance in genotype C. 2019 Scientific reports Discussion HBV M204I 16 21 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In addition, mutations of A181T/V and N236T showed intermediate susceptibility to TDF. 2019 Scientific reports Discussion HBV A181T;A181V;N236T 26;26;38 33;33;43 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In another case in this study, the patient experienced viral breakthrough after 22 months of TDF monotherapy with the mutant HBV bearing mutation pattern of A181T + F221Y. 2019 Scientific reports Discussion HBV A181T;F221Y 157;165 162;170 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In both genotypes L180 was practically necessary for M204V. 2019 Scientific reports Discussion HBV M204V 53 58 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In current study, mutation of L229 was not a single mutation site: 75% mutations of this site associated to M204I or V. 2019 Scientific reports Discussion HBV M204I 108 113 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. In this study, F221Y was observed in cases not only under ADV therapy but also under LAM treatment (Table 4). 2019 Scientific reports Discussion HBV F221Y 15 20 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Interestingly, in vitro test, the V191I mutant remained sensitive to ADV. 2019 Scientific reports Discussion HBV V191I 34 39 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. It revealed that L229W did not change the susceptibility to NA in one vitro mutational analysis. 2019 Scientific reports Discussion HBV L229W 17 22 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Notably, in present study, the mutation pattern of A181T associated with F221Y was observed in one case after 22 months of TDF monotherapy with virological and biochemical breakthrough. 2019 Scientific reports Discussion HBV A181T;F221Y 51;73 56;78 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Other studies have suggested that V207I moderately decreased the sensitivity to LAM and ADV. 2019 Scientific reports Discussion HBV V207I 34 39 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Our data showed no significant difference was found in frequencies of M204I or V mutation. 2019 Scientific reports Discussion HBV M204I 70 75 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. proved that N238H mutation had little effect on ETV resistance. 2019 Scientific reports Discussion HBV N238H 12 17 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported F221Y was detected in one case suffering viral breakthrough under TDF monotherapy following an initial unsuccessful LAM and ADV combination therapy. 2019 Scientific reports Discussion HBV F221Y 9 14 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that A194T conferred a reduced susceptibility to TDF in vitro in two HBV and human immunodeficiency virus (HIV) co-infected patients. 2019 Scientific reports Discussion HBV A194T 14 19 HBV-HIV coinfections 78 132 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that an combined mutation pattern of L80M, L180M, M204V/I, A200V, F221Y, S223A, T184A/L, R153Q, and rtV191I was detected at the time of virological and biochemical breakthrough emerged during TDF monotherapy, following an unsuccessful LAM, ETV and ADV sequential or combined treatment. 2019 Scientific reports Discussion HBV V191I;L80M;L180M;M204V;M204I;A200V;F221Y;S223A;T184A;T184L;R153Q 111;46;52;59;59;68;75;82;89;89;98 116;50;57;66;66;73;80;87;96;96;103 RT 109 111 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that F221Y was found under ADV therapy in genotype A, Lee et al. 2019 Scientific reports Discussion HBV F221Y 14 19 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that M204I appeared in a minority of resistant strains in genotype A and usually existed as an isolated one. 2019 Scientific reports Discussion HBV M204I 14 19 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that single mutation of N238H did not affect replication under clevudine treatment, while the replication efficiency was significantly reduced by N238H + K333N double mutant in vitro. 2019 Scientific reports Discussion HBV N238H;N238H;K333N 33;155;163 38;160;168 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. reported that V191I was observed after 6 months of treatment with ADV, similar with that in present study (Table 4). 2019 Scientific reports Discussion HBV V191I 14 19 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. showed that L229F and L229V might act as a compensatory mutation for M204I, although the susceptibility to LAM was not reduced, similarly to another study. 2019 Scientific reports Discussion HBV L229F;L229V;M204I 12;22;69 17;27;74 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. These data indicated that F221Y might associate with LAM, ADV and TDF treatment. 2019 Scientific reports Discussion HBV F221Y 26 31 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. Unlike M204V, variant of M204I was highly resistant to LDT. 2019 Scientific reports Discussion HBV M204V;M204I 7;25 12;30 31147594 Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection. When taking into account the associated sites, M204I mutation itself was more prevalent in genotype B, while L180 + M204I was more common in genotype C. 2019 Scientific reports Discussion HBV M204I;M204I 47;116 52;121 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. Currently, the well-known classical NA resistance mutations are mainly located in domains B, C, D, and E, such as rtI169T, rtA181T/V, and rtT184A/C/F/G/I/L/M (located in domain B), rtS202C/G/I and rtM204I/V/S (located in domain C), rtN236T (located in domain D), and rtM250I/L/V (located in domain E). 2019 Journal of clinical microbiology Discussion HBV A181T;A181V;T184A;T184C;T184F;T184G;T184I;T184L;T184M;S202C;S202G;S202I;M204I;M204V;M204S;M250I;M250L;M250V;I169T;N236T 125;125;140;140;140;140;140;140;140;183;183;183;199;199;199;269;269;269;116;234 132;132;157;157;157;157;157;157;157;192;192;192;208;208;208;278;278;278;121;239 RT;RT;RT;RT;RT;RT;RT 114;123;138;181;197;232;267 116;125;140;183;199;234;269 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. In this study, except rtA181T, the classical primary drug resistance mutations (i.e., I169T, A181T/V, T184A/C/F/G/I/L/M/S, A194T, S202C/G/I, M204I/V/S, N236T, and M250I/L/V) were not detected by Sanger sequencing in treatment-naive patients (Table 3), which was consistent with previous reports. 2019 Journal of clinical microbiology Discussion HBV A181T;T184A;T184C;T184F;T184G;T184I;T184L;T184M;T184S;S202C;S202G;S202I;M204I;M204V;M204S;A181V;N236T;M250I;M250L;M250V;I169T;A181T;A194T 24;102;102;102;102;102;102;102;102;130;130;130;141;141;141;93;152;163;163;163;86;93;123 29;121;121;121;121;121;121;121;121;139;139;139;150;150;150;100;157;172;172;172;91;100;128 RT 22 24 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. In this study, using next-generation sequencing, mutations were found at rt202 (rtS202R/I/N/C/G), rt204 (rtM204L/R/I), rt236 (rtN236T/K/H), and rt250 (rtM250I/L) (Table 5). 2019 Journal of clinical microbiology Discussion HBV S202R;S202I;S202N;S202C;S202G;N236K;N236H;M250I;M250L;M204L;M204R;M204I;N236T 82;82;82;82;82;128;128;153;153;107;107;107;128 95;95;95;95;95;137;137;160;160;116;116;116;137 RT;RT;RT;RT;RT;RT;RT;RT 73;80;98;105;119;126;144;151 75;82;100;107;121;128;146;153 31189581 Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing. such as rtS/C256G, which is associated with ETV treatment, should be noticed. 2019 Journal of clinical microbiology Discussion HBV C256G;S256G 12;10 17;17 RT 8 10 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. The mutation S117C has not been shown to occur in other genotype A sequences but is found in genotypes B, C, and F and among nucleoside reverse transcriptase inhibitor-treated persons. 2019 Viruses Discussion HBV S117C 13 18 RT 136 157 31248149 Frequency of Hepatitis B Virus Resistance Mutations in Women Using Tenofovir Gel as Pre-Exposure Prophylaxis. Three of these less well-characterised amino acid substitutions:rtM129L, rtI163V, and rtL217R:are commonly observed in other genotype A sequences, occurring in treatment naive individuals at frequencies of 44.1%, 5.7% and 36.3%, respectively. 2019 Viruses Discussion HBV L217R;M129L;I163V 88;66;75 93;71;80 RT;RT;RT 64;73;86 66;75;88 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. As mentioned above, some of our results were different from other studies, such as the influence of sC69* on viral replication. 2019 Frontiers in microbiology Discussion HBV C69X 100 105 S 100 101 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. As shown in our previous report, the sC69* mutant had impaired replication and secretion. 2019 Frontiers in microbiology Discussion HBV C69X 37 42 S 37 38 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, in a recent study, reported that sC69* in genotype A HBV had a higher viral replication. 2019 Frontiers in microbiology Discussion HBV C69X 42 47 S 42 43 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, sC69* could inhibit some immune factors expression (RIG-I, IL29, and ISG15) with or without WT. 2019 Frontiers in microbiology Discussion HBV C69X 9 14 S 9 10 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. However, the issue of how sC69* inhibits host innate immune response remains to be elucidated in a future study. 2019 Frontiers in microbiology Discussion HBV C69X 26 31 S 26 27 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, HBV DNA levels in patients with the sC69* mutant were significantly lower than those where sC69* was not detected. 2019 Frontiers in microbiology Discussion HBV C69X;C69X 49;104 54;109 S;S 49;104 50;105 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In addition, how sC69* mutant antagonizes immune response is needed to be studied in the future. 2019 Frontiers in microbiology Discussion HBV C69X 17 22 S 17 18 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In our study, we could detect HBV pgRNA levels, which supports the possible origin of sC69* from cccDNA. 2019 Frontiers in microbiology Discussion HBV C69X 86 91 S 86 87 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In our study, we found that both in patient serum and in in vitro studies the sC69* mutant showed lower HBV DNA levels than the WT HBV. 2019 Frontiers in microbiology Discussion HBV C69X 78 83 S 78 79 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In this study, we also found that sC69* alone also resulted in deficient virion infection and spread in HepG2-NTCP. 2019 Frontiers in microbiology Discussion HBV C69X 34 39 S 34 35 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In this study, we reported that the sC69* mutant was highly prevalent in the 435 CHB patients with and without antiviral treatment. 2019 Frontiers in microbiology Discussion HBV C69X 36 41 S 36 37 Chronic Hepatitis B 81 84 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In this study, we tested the impact of the sC69* on viral infectivity and spread in the HepG2-NTCP cell line. 2019 Frontiers in microbiology Discussion HBV C69X 43 48 S 43 44 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In this study, we used both the HepG2-NTCP cell line and HLCs derived from hESCs as HBV infection systems to study the sC69* mutant influence on innate immune responses. 2019 Frontiers in microbiology Discussion HBV C69X 119 124 S 119 120 HBV infections 84 97 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. In vitro studies showed that the sC69* mutant could inhibit viral infection and spread, but could be rescued by WT surface protein. 2019 Frontiers in microbiology Discussion HBV C69X 33 38 S;S 33;115 34;122 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Interestingly, among 19 patients with the sC69* mutant, 15 patients mutation were found to have a mixture of WT sC69 and sC69* encoded by TGC + TGA. 2019 Frontiers in microbiology Discussion HBV C69X;C69X 42;121 47;126 S;S;S 42;112;121 43;113;122 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Moreover sC69* was found to inhibit expression of a number of ISGs in vitro and this may possibly lead to attenuation of the innate immune response. 2019 Frontiers in microbiology Discussion HBV C69X 9 14 S 9 10 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Moreover, the sC69* mutant could attenuate host innate immune responses to help the WT and itself to escape the host immune surveillance. 2019 Frontiers in microbiology Discussion HBV C69X 14 19 S 14 15 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Patients with the sC69* mutant were significantly older than those with WT infection. 2019 Frontiers in microbiology Discussion HBV C69X 18 23 S 18 19 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. reported that sW182* mutant showed lower HBV DNA levels and existed preferentially in older patients. 2019 Frontiers in microbiology Discussion HBV W182X 14 20 S 14 15 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. showed that sW172* mutant could be rescued by WT for secretion. 2019 Frontiers in microbiology Discussion HBV W172X 12 18 S 12 13 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The less innate immune response of sC69* mutant was shown not to be caused by its lower replication, which lead to less virus production. 2019 Frontiers in microbiology Discussion HBV C69X 35 40 S 35 36 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The results showed that sC69* might have stronger inhibition on the innate immune responses compared to that of the WT HBV. 2019 Frontiers in microbiology Discussion HBV C69X 24 29 S 24 25 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant exists mostly in HBeAg-negative CHB patients and usually coexisted with WT as quasispecies. 2019 Frontiers in microbiology Discussion HBV C69X 4 9 C;S 34;4 39;5 Chronic Hepatitis B 49 52 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69* mutant was reported in several published papers including our previous reports. 2019 Frontiers in microbiology Discussion HBV C69X 4 9 S 4 5 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. The sC69*, with the concomitant rtS78T mutation impaired viral replication in vitro, which may explain the association of sC69* with low HBV DNA levels in patient sera. 2019 Frontiers in microbiology Discussion HBV S78T;C69X;C69X 34;4;122 38;9;127 RT;S;S 32;4;122 34;5;123 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. These indicate that sC69* mutant could persist in the host through escape host innate immune response. 2019 Frontiers in microbiology Discussion HBV C69X 20 25 S 20 21 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. Thus, the questions came out why the sC69* coexisted with WT and how sC69* survived in the host. 2019 Frontiers in microbiology Discussion HBV C69X;C69X 37;69 42;74 S;S 37;69 38;70 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We also established effective cell models for HBV infection and used them to study the impact of the sC69* mutant on viral infection and spread. 2019 Frontiers in microbiology Discussion HBV C69X 101 106 S 101 102 HBV infections 46 59 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. We suspect that the sC69* mutant might show stronger inhibition on the innate immune response than WT. 2019 Frontiers in microbiology Discussion HBV C69X 20 25 S 20 21 31249567 The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response. When infected HepG2-NTCP cells were treated with poly (I:C), the pgRNA and HBV total RNA levels of sC69* were similar to WT. 2019 Frontiers in microbiology Discussion HBV C69X 99 104 S 99 100 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Although previous studies have already confirmed that the mutations in MHR, especially in the 'a' determinant influenced the virus antigenicity and were significantly associated with vaccine escape, we observed that the vaccine escaped mutations occurred frequently in the 'a' determinant (T116 N (4.3%), P120S (4.3%), T126A (8.7%), Q129R/H (17.3%), D144A/E (8.7%) and G145A/R (21.7%) for OBIB and T116 N (4.3%), I126S (8.7%), Q129R (8.7%), D144E (4.3%) and G145A/R (17.4%) for OBIC). 2019 BMC infectious diseases Discussion HBV T116N;P120S;T126A;Q129R;Q129H;D144A;D144E;G145A;G145R;T116N;I126S;Q129R;D144E;G145A;G145R 290;305;319;333;333;350;350;369;369;398;413;427;441;458;458 296;310;324;340;340;357;357;376;376;404;418;432;446;465;465 S;S 95;274 109;288 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Consistently, a Chinese study reported that a mutation L95 W could impair virion secretion and change antigenicity. 2019 BMC infectious diseases Discussion HBV L95W 55 60 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Moreover, mutations outside MHR including T47K (13%) and L95 W (4.3%) were also observed in our population. 2019 BMC infectious diseases Discussion HBV T47K;L95W 42;57 46;62 31269905 Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China. Some mutations such as Q101R, S167 L, V168A, R169H, S174 N, L175S, V177A, Q129R, D144E/A and G145A/R were in concordance with previous studies. 2019 BMC infectious diseases Discussion HBV Q101R;S167L;V168A;R169H;S174N;L175S;V177A;Q129R;D144E;D144A;G145A;G145R 23;30;38;45;52;60;67;74;81;81;93;93 28;36;43;50;58;65;72;79;88;88;100;100 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. A predominant double mutation in the basic core promoter region involves a G to A change at nucleotide 1764 and an A to T change at nucleotide 1762. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764A;A1762T 75;115 107;147 BCP 37 56 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. A prevalent mutation in the PC region of the HBV genome is a substitution at position G1896A (codon 28), resulting in the disappearance of HBeAg. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1896A 86 92 C;Precore 139;28 144;30 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Another frequent dual mutation detected in the present study was a G to T change at nucleotide 1764 and a C to G change at nucleotide 1766. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764T;C1766G 67;106 99;138 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Another study performed in Korea indicated that all isolates with a G to A change at position 1899, had a concomitant G1896A change. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1899A;G1899G;G1896A;G1899A 68;68;118;68 123;123;124;98 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. However, the present study showed a higher rate of G1896A than other studies in Iran by Ghabeshi et al. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1896A 51 57 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. in 120 CHB patients and Soleimani in 69 CHB patients which demonstrated the presence of G1896A in 46.0%, 36.66% and 17.3% of patients, respectively. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1896A 88 94 Chronic Hepatitis B;Chronic Hepatitis B 7;40 10;43 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. in 97 CHB patients with HBeAg negative reporting that 30.0% of subjects had G1764T/C1766G double mutation, and the combined mutational patterns T1762/A1764/G1766 or T1762/T1764/G1766 which would not generate binding sites for HNF1 or HNF3 were not seen. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV C1766G;G1764T 83;76 89;82 C 24 29 Chronic Hepatitis B 6 9 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. In our data, the G1764T/C1766G mutant was seen in 26.0% (7/26) of patients (6 CHB patients, 1 inactive carrier). 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV C1766G;G1764T 24;17 30;23 Chronic Hepatitis B 78 81 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. In our study, G1896A mutation was detected in 16 (61.0%) out of 26 isolates (12 CHB patients, 1 cirrhosis, 3 inactive carriers). 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1896A 14 20 Chronic Hepatitis B;Liver cirrhosis 80;96 83;105 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. In this study, another common pre-core mutation at position G1899A was detected in 6 (23.0%) patients (4 CHB patients, 1 cirrhosis, 1 inactive carrier). 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1899A 60 66 Precore 30 38 Chronic Hepatitis B;Liver cirrhosis 105;121 108;130 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. It has been suggested that the G1764T/C1766G mutant creates a new binding site for the hepatocyte nuclear factor 3 (HNF3), and increases core promoter activity. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV C1766G;G1764T 38;31 44;37 Core promoter 137 150 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. It was observed that all subjects with the G1899A variant carried G1896A. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1899A;G1896A 43;66 49;72 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. More extensive research work is needed to explore the tendency to either A1762T/G1764A or C1766G/G1764T. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764A;G1764T;A1762T;C1766G 80;97;73;90 86;103;79;96 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Nevertheless, the simultaneous presence of the A1762T/G1764A in conjunction with G at position 1757 is more efficient. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764A;A1762T 54;47 60;53 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. None of the patients with G1764T/C1766G mutation carried A1762T/G1764A substitution. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV C1766G;G1764A;G1764T;A1762T 33;64;26;57 39;70;32;63 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Our finding is comparable with a study which showed G1899A in 29.3% of patients. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1899A 52 58 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Some studies revealed that G1899A is found to be associated with the severity of liver diseases. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1899A 27 33 Liver disease 81 95 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. Some studies revealed that the A1762/G1764A mutant accompanied by G1757A is associated with lower viral load and ALT level; hence, G1757A acts as an inhibitor to the A1762/G1764A mutant. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764A;G1764A;G1757A;G1757A 37;172;66;131 43;178;72;137 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The mechanism by which the G1764A/A1762T dual mutation enhances the virulence of HBV is not fully understood. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV A1762T;G1764A 34;27 40;33 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The proportion of patients with A1762T/G1764A dual mutant in our study (23.0%,6/26) (3 CHB patients, 3 cirrhosis) is consistent with recent findings from Iran (19.6%), Malaysia (26.9%) in 93 HBV carriers (26.9%) and Morocco in 221 chronic carriers (22.9%). 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764A;A1762T 39;32 45;38 Chronic Hepatitis B;Liver cirrhosis 87;103 90;112 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. The result of the present study revealed the presence of A1762T and G1764A mutations in 30% (4 CHB patients, 3 cirrhosis, 1 inactive carrier) and 26% (3 CHB patients, 3 cirrhosis, 1 inactive carrier) of subjects, respectively. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV A1762T;G1764A 57;68 63;74 Chronic Hepatitis B;Liver cirrhosis;Chronic Hepatitis B;Liver cirrhosis 95;111;153;169 98;120;156;178 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. This finding is in line with other studies in France in 252 HBsAg positive carriers and Korea in 472 patients with chronic HBV infection, which reported the substitution of G1896A in 54.9% and 55.0% of subjects, respectively. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1896A 173 179 S 60 65 Chronic HBV infection 115 136 31308922 Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients. When there is G1757A, the C1766G/G1764T double mutant is more efficient than the A1762T/G1764A mutation. 2019 Mediterranean journal of hematology and infectious diseases Discussion HBV G1764T;G1764A;G1757A;C1766G;A1762T 33;88;14;26;81 39;94;20;32;87 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Although G1896A had the most significant association with HBeAg status, we identified other variants that were important for understanding a patient's HBeAg status. 2019 Scientific reports Discussion HBV G1896A 9 15 C;C 58;151 63;156 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Although patients with high frequency of C1817T and A1838G variants experienced earlier viral suppression while on treatment, given the effectiveness of the latest reverse transcriptase inhibitors, the difference in viral load reduction diminishes after 48 weeks. 2019 Scientific reports Discussion HBV C1817T;A1838G 41;52 47;58 RT 164 185 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. C1653T exhibited only marginal signal with viral load. 2019 Scientific reports Discussion HBV C1653T 0 6 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Given its proximity to the transcription start site, we hypothesize that C1817T affects the transcriptional regulation of pgRNA leading to the reduction of the viral load. 2019 Scientific reports Discussion HBV C1817T 73 79 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. It is worth mentioning that G1896A variants in HBV genotype A and some genotype C strains are rare due to genotype-specific constraints in the base-pairing of the pgRNA secondary structure and other mutations become solely responsible for the disruption of HBeAg production. 2019 Scientific reports Discussion HBV G1896A 28 34 C 257 262 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Our data show that increased frequency of viral variants C1817T and A1838G were associated with significantly lower serum levels of HBV DNA at baseline. 2019 Scientific reports Discussion HBV C1817T;A1838G 57;68 63;74 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. Previous studies described additional variants in the core promoter including C1653T, T1753C, A1762T, and G1764A and their correlation with the downregulation of precore mRNA. 2019 Scientific reports Discussion HBV C1653T;T1753C;A1762T;G1764A 78;86;94;106 84;92;100;112 Core promoter;Precore 54;162 67;169 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. The A1838G variant is located within this h3E region where nucleotide substitutions in the in vitro model resulted in a significant decrease in the production of rcDNA. 2019 Scientific reports Discussion HBV A1838G 4 10 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. The C1817T variant lies in the second codon of precore inducing a stop codon. 2019 Scientific reports Discussion HBV C1817T 4 10 Precore 47 54 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. While G1896A disrupts the production of HBeAg via a premature stop codon in the precore region, other variants likely inhibit dimerization or protein folding of HBeAg. 2019 Scientific reports Discussion HBV G1896A 6 12 C;C;Precore 40;161;80 45;166;87 31324819 Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients. While our study did not identify any significant association with A1762T and G1764A, we found T1753C to be strongly associated with HBeAg status in our dataset (Supplementary Table 2). 2019 Scientific reports Discussion HBV A1762T;G1764A;T1753C 66;77;94 72;83;100 C 132 137 31341412 Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations. In summary, our study provides evidence using GWAS that host genetic polymorphisms are associated with the immune selection of HCC-related double mutations (A1762T and G1764A) in the basal core promoter of HBV. 2019 International journal of medical sciences Discussion HBV A1762T;G1764A 157;168 163;174 BCP 183 202 Hepatocellular carcinoma 127 130 31402915 rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. Second, our further epidemiologic data showed that HBeAg seronegative status observed in patients with rt269I was due to a higher frequency of preC mutations (G to A at 1896) induced via IFN-I mediated APOBEC3G (Table 2 and Figure 2). 2019 Frontiers in immunology Discussion HBV G1896A 159 173 C;Precore;RT 51;143;103 56;147;105 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. Among 24 Cambodian C1 isolates, the double mutation at A1762T/G1764A was most frequent and found in 75.0% of them, and combination mutation at C1653T or T1753V and A1762T/G1764A was found in 58.3% of them. 2019 Scientific reports Discussion HBV G1764A;G1764A;A1762T;C1653T;T1753V;A1762T 62;171;55;143;153;164 68;177;61;149;159;170 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. As for HBV genotype C1 genome, some reports were published; the report in the hospital-based study from South China reported a combination mutation rate at T1753V and A1762T/G1764A in CH and HCC patients of 4.8% and 14.7%, respectively. 2019 Scientific reports Discussion HBV G1764A;T1753V;A1762T 174;156;167 180;162;173 Hepatocellular carcinoma;Chronic Hepatitis B 191;184 194;186 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. The double mutation at A1762T/G1764A in genotype C2 has been shown to be present at a high rate in HCC in previous reports and the combination mutation at C1653T and/or T1753V and A1762T/G1764A increases the risk of occurrence of HCC among HBV genotype C2 carriers. 2019 Scientific reports Discussion HBV G1764A;G1764A;A1762T;C1653T;T1753V;A1762T 30;187;23;155;169;180 36;193;29;161;175;186 Hepatocellular carcinoma;Hepatocellular carcinoma 99;230 102;233 31434918 High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank. We could not reach all residents of these regions, but according to the results of this study among 24 Cambodian isolates of genotype C1, double mutation at A1762T/G1764A was observed in 78.3% and combination mutation was observed in 58.3% of the isolates. 2019 Scientific reports Discussion HBV G1764A;A1762T 164;157 170;163 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. A lower level of mutant I97L DNA was also observed in the extracellular virions at 1 or 2 weeks postinjection in both immunocompetent BALB/c and immunodeficient NOD/SCID mouse models. 2019 Journal of virology Discussion HBV I97L 24 28 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. a superefficient interaction between the viral envelope protein and the nucleocapsid particles could be responsible for the intra- and extracellular phenotypes of mutant I97L. 2019 Journal of virology Discussion HBV I97L 170 174 S 47 55 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Another novel finding in the time course experiments was the poor persistence of the intracellular and extracellular viral DNAs of mutant I97L relative to the WT HBV. 2019 Journal of virology Discussion HBV I97L 138 142 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Because NOD/SCID mice are deficient in mature T and B cells, more rapid clearance of mutant I97L virions could not be related to the humoral immunity. 2019 Journal of virology Discussion HBV I97L 92 96 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. By immunohistochemical staining, we noted no apparent histopathological difference between liver sections from mice injected with WT HBV versus those injected with mutant I97L. 2019 Journal of virology Discussion HBV I97L 171 175 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Compared to WT HBc, mutant F97L showed an enhanced rate and extent and a stronger temperature dependence of empty capsid assembly in vitro. 2019 Journal of virology Discussion HBV F97L 27 31 Capsid;C 114;15 120;18 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Comparison of the secretion kinetics of mature virions in cell culture revealed no detectable difference between mutant F97L and WT HBV. 2019 Journal of virology Discussion HBV F97L 120 124 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Even though the intracellular mutant I97L DNA was even stronger in signal intensity than WT DNA at day 3 postinjection, no viral DNA from mutant I97L was detected at 2 weeks postinjection, when the WT DNA remained clearly detectable. 2019 Journal of virology Discussion HBV I97L;I97L 37;145 41;149 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Finally, mutation F97L also does not have any apparent effect on HBc phosphorylation in Escherichia coli coexpressing the SRPK1 kinase. 2019 Journal of virology Discussion HBV F97L 18 22 C 65 68 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Here, we have not performed the same cis-trans test in vivo for mutant I97L. 2019 Journal of virology Discussion HBV I97L 71 75 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. However, unlike the cell culture system, the immature secretion phenotype from mutant I97L could only be partially rescued by P130T in the double mutant I97L/P130T (only partially upshifted RC DNA in the day 3 panel). 2019 Journal of virology Discussion HBV P130T;I97L;P130T;I97L 158;86;126;153 163;90;131;157 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. If host immunity is not the primary mechanism for poor persistence of mutant I97L, what could then be the mechanism behind the phenomenon of poor persistence of mutant I97L? The most apparent clue for the mechanism of poor persistence is its correlation with the genome immaturity of the extracellular HBV DNA. 2019 Journal of virology Discussion HBV I97L;I97L 168;77 172;81 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. If less infectious in vivo, then how can mutant I97L emerge to predominance in chronic hepatitis B patients in the first place? In longitudinal studies, putative immune-selected HBc variants can emerge after a single or repeated acute exacerbations. 2019 Journal of virology Discussion HBV I97L 48 52 C 178 181 Chronic Hepatitis B 79 98 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In an in vivo experimental setting, mutant P130T still exhibited more highly abundant fully mature RC-form DNA than did the WT HBV. 2019 Journal of virology Discussion HBV P130T 43 48 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. In fact, in HepG2 cells, we detected no apparent deficiency in the intracellular DNA synthesis of mutant I97L. 2019 Journal of virology Discussion HBV I97L 105 109 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Indeed, immature genomes of low-MW HBV DNA can be detected by Southern blotting using serum HBV samples containing a predominant HBc mutation I97L. 2019 Journal of virology Discussion HBV I97L 142 146 C 129 132 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Indeed, in our previous study, when virion secretion of mutant F97L was genetically blocked with another surface antigen knockout mutation (SK/O), intracellular genome maturation to full-length RC DNA was well restored (~30%) in the double mutant F97L/SK/O. 2019 Journal of virology Discussion HBV F97L;F97L 247;63 256;67 S 105 112 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Indeed, we noted that the stronger intensity of the extracellular virion-associated DNA of mutant I97L. 2019 Journal of virology Discussion HBV I97L 98 102 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It is tempting to speculate here that the mature RC DNA in the nucleocapsids of P130T might shuttle back to the nucleus for cccDNA amplification. 2019 Journal of virology Discussion HBV P130T 80 85 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It remains to be investigated whether these in vitro capsid assembly properties of mutant F97L could also influence the efficiency of envelopment in virion secretion in mouse models. 2019 Journal of virology Discussion HBV F97L 90 94 Capsid 53 59 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. It was reported that HBc of mutant F97L exhibited faster kinetics in empty capsid assembly. 2019 Journal of virology Discussion HBV F97L 35 39 Capsid;C 75;21 81;24 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. mutant I97L deficient in the intracellular mature genome was less persistent than was WT HBV. 2019 Journal of virology Discussion HBV I97L 7 11 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Previously, we demonstrated that a mutation A119F in the pre-S1 domain of the envelope protein can rescue the immature secretion phenotype of mutant I97L. 2019 Journal of virology Discussion HBV A119F;I97L 44;149 49;153 S;PreS1 78;57 86;63 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Previously, we reported a naturally occurring mutation, P130T, which displayed a hypermaturation phenotype with more abundant amount of the fully mature RC form-DNA than did WT HBV in cell culture. 2019 Journal of virology Discussion HBV P130T 56 61 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. relative to WT HBV, there was a more prolonged persistence of HBV DNA of the hypermaturation mutant P130T in the mouse liver at 1 and 2 weeks postinjection. 2019 Journal of virology Discussion HBV P130T 100 105 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Similarly, more rapid decay of the intracellular DNA of mutant I97L may not be related to the innate immunity, since the same phenomenon was observed in immunocompetent BALB/c mice and immunodeficient IFNAR-/- or STAT1-/- mice. 2019 Journal of virology Discussion HBV I97L 63 67 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Similarly, mutant F97L exhibited no differential secretion kinetics between its mature and immature virions. 2019 Journal of virology Discussion HBV F97L 18 22 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Similarly, we speculate here that HBc mutation I97L could generate a mutant nucleocapsid with a subtly altered structure, leading to pleiotropic phenotypes, including a relaxed stringency in envelopment for immature nucleocapsids, as well as a cis-defect in viral DNA synthesis. 2019 Journal of virology Discussion HBV I97L 47 51 C 34 37 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The most prominent feature of mutant I97L is the relaxed stringency in the release of virions containing immature genomes of low-MW RC and SS DNA. 2019 Journal of virology Discussion HBV I97L 37 41 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The other complication is that the HBV DNA from human patients always contains multiple mutations in addition to I97L or F97L (e.g., coexisting with known or unknown compensatory mutations). 2019 Journal of virology Discussion HBV I97L;F97L 113;121 117;125 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. The other plasmid contains double mutations, with an additional F97L mutation. 2019 Journal of virology Discussion HBV F97L 64 68 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Therefore, mutation F97L is pleiotropic in both cis- and trans-defects in cell culture. 2019 Journal of virology Discussion HBV F97L 20 24 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Therefore, the cis-defect in viral DNA synthesis of mutant F97L contributes to approximately 70% of the reduction in the total intracellular viral DNA. 2019 Journal of virology Discussion HBV F97L 59 63 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This inverse correlation suggests that mutant I97L is more efficient in virion secretion than WT HBV, leading to the depletion of the intracellular pool of viral DNA, including the RC and SS DNAs. 2019 Journal of virology Discussion HBV I97L 46 50 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. This mutation P130T can efficiently rescue the immature secretion of mutation I97L in the cell culture system. 2019 Journal of virology Discussion HBV P130T;I97L 14;78 19;82 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. To our knowledge, this is the first in vivo demonstration of an immature secretion phenotype of a frequent naturally occurring HBc variant I97L in a mouse model. 2019 Journal of virology Discussion HBV I97L 139 143 C 127 130 31462567 Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model. Upon systematic substitution at HBc amino acid 97 from a wild-type isoleucine to 18 other amino acids via site-directed mutagenesis, only the mutant I97L exhibited immature secretion. 2019 Journal of virology Discussion HBV I97L 149 153 C 32 35 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. An L11Q point mutation was also located in the hepatocyte binding site (p10-36 in pre-S1). 2019 Clinical and experimental hepatology Discussion HBV L11Q 3 7 PreS1 82 88 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. As mentioned above, nt 2,879 A>T and nt 2,960 A>G variations that were located in this region were found significantly more frequently in ASCs individuals. 2019 Clinical and experimental hepatology Discussion HBV A879T;A960G 25;42 32;49 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Certain substitutions, including L11Q, A28T and K38R, at the pre-S1 region, and S130F/L in the pre-S2 region, were detected significantly more frequently in the ASC individuals than in those with LC/HCC. 2019 Clinical and experimental hepatology Discussion HBV L11Q;A28T;K38R;S130F;S130L 33;39;48;80;80 37;43;52;87;87 PreS1;PreS2 61;95 67;101 Hepatocellular carcinoma;Liver cirrhosis 199;196 202;198 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. In conclusion, according to the present results, the point mutations L11Q, N37S and K38R, as well as certain deletion mutations, may correlate with the development of a healthy carrier state. 2019 Clinical and experimental hepatology Discussion HBV L11Q;N37S;K38R 69;75;84 73;79;88 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. On the other hand, a higher frequency of A49V in LC/HCC patients implies that this substitution is possibly associated with HBV infection progression toward LC/HCC. 2019 Clinical and experimental hepatology Discussion HBV A49V 41 45 Hepatocellular carcinoma;HBV infections;Hepatocellular carcinoma;Liver cirrhosis;Liver cirrhosis 52;124;160;157;49 55;137;163;159;51 31501793 Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals. Therefore, L11Q substitution may interfere with the HBV life cycle and lead to an ASC state in infected individuals. 2019 Clinical and experimental hepatology Discussion HBV L11Q 11 15 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. However, in a previous study the OBI-associated P178R substitution prevented HBsAg secretion in two distinct OBI clones and in M88. 2019 Emerging microbes & infections Discussion HBV P178R 48 53 S 77 82 Occult Hepatitis B;Occult Hepatitis B 33;109 36;112 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. In contrast, Q16R appeared to enhance HBsAg secretion by reducing the IC level of HBsAg when introduced in P38.II. 2019 Emerging microbes & infections Discussion HBV Q16R 13 17 S;S 38;82 43;87 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Mutations T116N, T123N, G130N, and T131N + M133 T have been reported to reduce antigenicity and immunogenicity and rescue virion secretion in N146 mutants. 2019 Emerging microbes & infections Discussion HBV T116N;T123N;G130N;T131N;M133T 10;17;24;35;43 15;22;29;40;49 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. The extremely low EIA reactivity observed for mutant TCT123-125NFT may be related to the combined effect of creation of an N-glycosylation site by T123N substitution and disruption of a putative disulfide bridge by the C124F substitution. 2019 Emerging microbes & infections Discussion HBV T123N;C124F 147;219 152;224 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. The Q16R substitution in the central part of TMD1 in M88 did not significantly affect the total amount of HBsAg produced but slightly decreased its secretion (Figure 4). 2019 Emerging microbes & infections Discussion HBV Q16R 4 8 S 106 111 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. The separate introduction of substitutions C85R, L87R, L88R, and C90R in the TMD2 alpha-helix significantly impaired both HBsAg production and secretion (Figure 4). 2019 Emerging microbes & infections Discussion HBV C85R;L87R;L88R;C90R 43;49;55;65 47;53;59;69 S 122 127 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. The substitutions Q181R and W182R had no significant impact on HBsAg production pattern, suggesting that TMD3 is not essential for S protein oligomerization and HBsAg formation. 2019 Emerging microbes & infections Discussion HBV Q181R;W182R 18;28 23;33 S;S;S 63;161;131 68;166;132 31516090 Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains. Two types of mutations in the S region were significantly associated with occult HBV carriage: (i) mutations creating new N-linked glycosylation sites at positions s116, s123, s130, and s131 + s133 or removing the existing site at position s146; and (ii) mutations C85R, L87R, L88R, and C90R within the hydrophobic alpha-helix of transmembrane domain TMD2. 2019 Emerging microbes & infections Discussion HBV C85R;L87R;L88R;C90R 265;271;277;287 269;275;281;291 S;S;S;S;S;S;S 30;164;170;176;186;193;240 31;165;171;177;187;194;241 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. Amongst the detected immune escape mutations, we found the HBsAg D144E mutation in two ALF and three non-ALF patients. 2019 Viruses Discussion HBV D144E 65 70 S 59 64 Liver disease;Liver disease 87;105 90;108 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. Furthermore, the sequencing of the whole HBV genome per NGS and the functional analysis of the HBsAg L216* mutation allows us to investigate in more depth viral aspects of HBV reactivation-induced ALF. 2019 Viruses Discussion HBV L216X 101 106 S 95 100 Liver disease 197 200 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. HBsAg stop codon mutations leading to a truncated HBsAg such as W172* have been described in patients with chronic hepatitis B patients in the past and have been associated with lamivudine/entecavir resistance, cirrhosis, and hepatocellular carcinoma, as well as defective HBsAg secretion like L216*. 2019 Viruses Discussion HBV W172X;L216X 64;294 69;299 S;S;S 0;50;273 5;55;278 Chronic Hepatitis B;Liver cirrhosis;Hepatocellular carcinoma 107;211;226 126;220;250 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. One of them, the SHB L216* mutation, was associated with reduced HBsAg production and secretion. 2019 Viruses Discussion HBV L216X 21 26 S;S 65;17 70;20 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. The functional evaluation of L216* demonstrated that this mutation led to reduced production and secretion of HBsAg compared to wildtype HBsAg. 2019 Viruses Discussion HBV L216X 29 34 S;S 110;137 115;142 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. This effect was not observed with the D144E mutant. 2019 Viruses Discussion HBV D144E 38 43 31527514 Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure. Thus, one could hypothesize that the L216* may contribute to hepatocyte apoptosis and ALF. 2019 Viruses Discussion HBV L216X 37 42 Liver disease 86 89 31542053 Hepatitis B virus reactivation sustained by a hepatitis B virus surface antigen immune-escape mutant isolate in a patient who was hepatitis B core antibody positive during treatment with sofosbuvir and velpatasvir for hepatitis C virus infection: a case report. In the first case, genome sequencing revealed a T118K mutation in the S region, but in contrast to our description, the HBV viremia occurred 5 months after the EOT with daclatasvir and asunaprevir. 2019 Journal of medical case reports Discussion HBV T118K 48 53 S 70 71 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Although the mechanism is unclear, a possible reason for the significant association between spontaneous rtM204I variants and liver fibrosis might also be related to HBV genotype C. 2019 World journal of gastroenterology Discussion HBV M204I 107 112 RT 105 107 Liver fibrosis 126 140 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Among these variants, spontaneous rtM204I/V variants were detected in approximately 1.5% of NAs-native patients, and the rtM204I variant was the dominant type. 2019 World journal of gastroenterology Discussion HBV M204I;M204V;M204I 36;36;123 43;43;128 RT;RT 34;121 36;123 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Another finding of this study is that spontaneous rtM204I variants could affect antiviral responsiveness in treatment-naive patients when they are treated with NAs. 2019 World journal of gastroenterology Discussion HBV M204I 52 57 RT 50 52 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. But there is still controversy regarding prevalence of the naturally occurring rtM204I mutations prior to antiviral treatments. 2019 World journal of gastroenterology Discussion HBV M204I 81 86 RT 79 81 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Hence, this study suggested that progression of fibrosis might be related to spontaneous occurrence of rtM204I mutations prior to NAs, as well as infection with naturally occurring pre-S variants, in treatment-naive patients infected with HBV genotype C2 strains. 2019 World journal of gastroenterology Discussion HBV M204I 105 110 PreS;RT 181;103 186;105 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. In conclusion, the LNA-RT-PCR method can detect pre-existing rtM204I variants with high sensitivity in NAs-naive CHB patients. 2019 World journal of gastroenterology Discussion HBV M204I 63 68 RT 61 63 Chronic Hepatitis B 113 116 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. In contrast, only one of six patients carrying pre-existing rtM204I mutations achieved CVR at 12 mo of entecavir treatment, and one of four patients achieved CVR at 12 mo of low genetic barrier agents. 2019 World journal of gastroenterology Discussion HBV M204I 62 67 RT 60 62 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. In this study, we have confirmed that spontaneous rtM204I mutations exist in NAs-naive patients with CHB genotype C infection, and their prevalence is approximately 4%. 2019 World journal of gastroenterology Discussion HBV M204I 52 57 RT 50 52 Chronic Hepatitis B 101 104 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Indeed, rtM204I variants are the predominant mutations causing resistance to NAs with low genetic barriers, such as LAM, L-dT, and CLV. 2019 World journal of gastroenterology Discussion HBV M204I 10 15 RT 8 10 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Moreover, the clinical characteristics of the naturally occurring rtM204I mutations have not been fully elucidated. 2019 World journal of gastroenterology Discussion HBV M204I 68 73 RT 66 68 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Our data showed that CVR rate to antiviral therapy was significantly lower in patients infected with spontaneous rtM204I variants. 2019 World journal of gastroenterology Discussion HBV M204I 115 120 RT 113 115 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. rtM204I mutations can occur spontaneously with a rate of approximately 4% in treatment-naive patients infected with HBV genotype C2. 2019 World journal of gastroenterology Discussion HBV M204I 2 7 RT 0 2 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Spontaneous M204I mutations were more frequently detected in patients with higher scores on the FIB-4 index, which is considered to be a noninvasive marker of liver fibrosis, and multivariate analysis showed that pre-existing M204I mutations were more frequently detected in patients with significant fibrosis. 2019 World journal of gastroenterology Discussion HBV M204I;M204I 12;226 17;231 Liver fibrosis 159 173 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The detection of pre-existing rtM204I variants with the newly developed LNA-RT-PCR method could play a relevant role in the clinical management of NA-naive patients with CHB genotype C2 infection. 2019 World journal of gastroenterology Discussion HBV M204I 32 37 RT 30 32 Chronic Hepatitis B;HBV infections 170;183 173;195 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The most common substitutions are methionine at amino acid position 204 to either isoleucine (rtM204I, YIDD mutations) or valine (rtM204V, YVDD mutations). 2019 World journal of gastroenterology Discussion HBV M204I;M204V 96;132 101;137 RT;RT;P;P 94;130;103;139 96;132;107;143 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The newly developed LNA-RT-PCR method can detect pre-existing rtM204I variants with high sensitivity in NAs-naive CHB patients. 2019 World journal of gastroenterology Discussion HBV M204I 64 69 RT 62 64 Chronic Hepatitis B 114 117 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The objective of this study was to determine the prevalence and clinical characteristics of naturally occurring rtM204I mutations in treatment-naive patients infected with HBV genotype C2 strains by using a newly developed locked nucleotide probe (LNA probe) based real time PCR (LNA-RT-PCR) method, which can detect subspecies at 5% of the circulating HBV population. 2019 World journal of gastroenterology Discussion HBV M204I 114 119 RT 112 114 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The rtM204I variants more frequently pre-existed in patients with significant fibrosis, and the pre-existence of rtM204I variants was associated with incomplete responses to NAs. 2019 World journal of gastroenterology Discussion HBV M204I;M204I 6;115 11;120 RT;RT 4;113 6;115 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. The rtM204I variants were analyzed by a newly developed LNA RT-PCR method. 2019 World journal of gastroenterology Discussion HBV M204I 6 11 RT 4 6 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Therefore, tenofovir is the preferred treatment since its higher barrier to resistance provides the best chance for successful long-term therapy in treatment-naive patients carrying spontaneous rtM204I variants. 2019 World journal of gastroenterology Discussion HBV M204I 196 201 RT 194 196 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Therefore, the detection of pre-existing rtM204I variants with the newly developed LNA-RT-PCR method could play a relevant role in the clinical management of NA-naive patients with CHB genotype C2 infection. 2019 World journal of gastroenterology Discussion HBV M204I 43 48 RT 41 43 Chronic Hepatitis B;HBV infections 181;194 184;206 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. These data suggest that spontaneous rtM204I variants might be risk factors for the progression of liver fibrosis. 2019 World journal of gastroenterology Discussion HBV M204I 38 43 RT 36 38 Liver fibrosis 98 112 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. This result might be related to the fact that tenofovir therapy can more effectively suppress HBV-DNA compared to entecavir therapy and consequently decrease the risk of LC progression or HCC development in Korean patients infected with HBV genotype C strains, some of whom have spontaneous rtM204I variants. 2019 World journal of gastroenterology Discussion HBV M204I 293 298 RT 291 293 Hepatocellular carcinoma;Liver cirrhosis 188;170 191;172 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. This study also revealed that all seven patients carrying pre-existing rtM204I mutations achieved CVR to tenofovir, which can effectively suppress not only WT HBV strains but also rtM204I variants. 2019 World journal of gastroenterology Discussion HBV M204I;M204I 73;182 78;187 RT;RT 71;180 73;182 31543688 Tenofovir is a more suitable treatment than entecavir for chronic hepatitis B patients carrying naturally occurring rtM204I mutations. Thus, in this research, we focused on the spontaneous rtM204I variants, and they were evaluated using an LNA-RT-PCR method, which is a more sensitive method than sequence analysis. 2019 World journal of gastroenterology Discussion HBV M204I 56 61 RT 54 56 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. Combinational mutation occurrences were mainly L180M + M204I/V. 2019 Scientific reports Discussion HBV L180M;M204I;M204V 47;55;55 52;62;62 31558731 Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018. The results showed that the HBV mutation rtM204I/V together with rtL180M were the three mutations with the highest incidence, thus demonstrating that LAM-resistance and LdT were the most common resistances in Shenzhen. 2019 Scientific reports Discussion HBV M204I;M204V;L180M 43;43;67 50;50;72 RT;RT 41;65 43;67 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. H94Y and I127L/T/N/S mutations have been associated to K130M/V131I in previous studies. 2019 Biomedical reports Discussion HBV V131I;I127L;I127T;I127N;I127S;H94Y;K130M 61;9;9;9;9;0;55 66;20;20;20;20;4;60 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. In this study, the presence of K130M/V131I mutations constituted an independent risk factor for CLD progression. 2019 Biomedical reports Discussion HBV V131I;K130M 37;31 42;36 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The H94Y mutation causes changes in the alpha box, an element strongly activating the EnhII/core promoter, and increase the binding affinity of the alpha box and EnhII/core promoter. 2019 Biomedical reports Discussion HBV H94Y 4 8 Core promoter;Core promoter;Enh II;Enh II 92;168;86;162 105;181;91;167 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The present study found 12 types of X gene mutation, among which the K130M/V131I mutations were significantly correlated with CLD progression. 2019 Biomedical reports Discussion HBV V131I;K130M 75;69 80;74 X 36 37 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The rate of the P38S mutation was reported to be significantly higher in HCC than in asymptomatic carriers, but not significantly different from the rates in CH and LC patients. 2019 Biomedical reports Discussion HBV P38S 16 20 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 73;158;165 76;160;167 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. The rate of the T36P mutation was reported to be higher in HCC patients, presumably due to its location at the B epitope, which affects the immune response. 2019 Biomedical reports Discussion HBV T36P 16 20 Hepatocellular carcinoma 59 62 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. There were significant differences in viral load levels between patients with X gene mutations, including R87W/G, I127L/T/N/S and K130M/V131I mutations. 2019 Biomedical reports Discussion HBV V131I;I127L;I127T;I127N;I127S;R87W;R87G;K130M 136;114;114;114;114;106;106;130 141;125;125;125;125;112;112;135 X 78 79 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. While further studies are required to examine the clinical value of these results, the presence of K130M/V131I mutations may serve as a predictive marker for the progression of CLD in Indonesia and may also be applicable for other countries where chronic HBV infections are prevalent. 2019 Biomedical reports Discussion HBV V131I;K130M 105;99 110;104 Chronic HBV infection 247 269 31565220 Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients. X gene mutations, including R87W/G, I127L/T/N/S and K130M/V131I mutations, were correlated with HBV viral load. 2019 Biomedical reports Discussion HBV V131I;I127L;I127T;I127N;I127S;R87W;R87G;K130M 58;36;36;36;36;28;28;52 63;47;47;47;47;34;34;57 X 0 1 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. As the BCP region overlaps with the X gene reading frame, this double mutation results in amino acid changes in the X protein also (Met130Leu/Ile131Val). 2019 Scientific reports Discussion HBV I131V;M130L;M130I;M130V 142;132;132;132 151;141;141;141 BCP;X;X 7;36;116 10;37;117 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Demonstration of a common M125T mutation amongst all samples sequenced resonates with the fact that point mutations are frequently observed in the first loop of the "a" epitope (a.a.124-147) of the surface antigen in OBI isolates. 2019 Scientific reports Discussion HBV M125T 26 31 S 198 205 Occult Hepatitis B 217 220 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. In four patients, two core mis-sense mutations, yielding Asp96Thr and Ala101Val were also from the carboxy domain of the core protein and may alter nucleic acid binding and assembly of the core protein. 2019 Scientific reports Discussion HBV D96T;A101V 57;70 65;79 C;C;C 22;121;189 26;125;193 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Intra-host missense variants across compartments in X gene were located in the transactivation domain (Phe73Val), the X binding region (Ala44Val) and the p53 binding domains (Ser146Ala, Ser147Pro). 2019 Scientific reports Discussion HBV F73V;A44V;S146A;S147P 103;136;175;186 111;144;184;195 X;X 52;118 53;119 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Mis-sense variants across compartments were localized to this domain - Arg94Leu and Glu86Arg in B cell compartment and Ser41Thr in tumor compartment. 2019 Scientific reports Discussion HBV R94L;E86R;S41T 71;84;119 79;92;127 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Most notable of these and found in all seven tumor samples analyzed in our study was the classic double mutation T1762A/A1764G, in the basal core promoter region (BCP) which has been reported in several studies and is known to be an important pro-oncogenic mutation. 2019 Scientific reports Discussion HBV A1764G;T1762A 120;113 126;119 BCP;BCP 135;163 154;166 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Of these, Ala44Val has earlier been implicated in probable etiopathogenesis of Hepatocellular carcinoma with an odds ratio of over seven and hence may play a role in lymphomas too. 2019 Scientific reports Discussion HBV A44V 10 18 Hepatocellular carcinoma;Lymphomas 79;166 103;175 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Presence of Ser41Thr specifically in tumor compartment in a patient is noteworthy as it may be a likely candidate for etiopathogenic association with DLBCL. 2019 Scientific reports Discussion HBV S41T 12 20 B cell lymphoma 150 155 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. The G1630A mutation was also detected in another study and showed an increased association with hepatocellular carcinoma, albeit not clinically significant. 2019 Scientific reports Discussion HBV G1630A 4 10 Hepatocellular carcinoma 96 120 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. The G1635A mutation can be mapped to the HBV Enhancer 2 within the core promoter gene and is known to augment the enhancer and core promoter activities and subsequently HBV replication. 2019 Scientific reports Discussion HBV G1635A 4 10 Core promoter;Core promoter 67;127 80;140 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. Two core promoter mutations found in all samples were the G1630A and G1635A. 2019 Scientific reports Discussion HBV G1630A;G1635A 58;69 64;75 Core promoter 4 17 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. We also found double mutation T1809G/T1812C in the X gene region in all the tumor samples. 2019 Scientific reports Discussion HBV T1812C;T1809G 37;30 43;36 X 51 52 31601912 Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection. We found mutant T528C (Met125Thr) within this region in all ten of our patients analyzed which may explain HBsAg negativity accounting for OBI. 2019 Scientific reports Discussion HBV T528C;M125T 16;23 21;32 S 107 112 Occult Hepatitis B 139 142 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. In addition to the three IEMs identified, several surface protein mutations were identified (sP56Q, sT57I, sN59S, sP62L, sI110L, sS140T, sE164G, sS207N, and sL216*), which have also been reported in previous studies (Mello et al.,; Lin et al.,; Munshi et al.,; Qin and Liao,). 2020 International journal of infectious diseases Discussion HBV P56Q;T57I;N59S;P62L;I110L;S140T;E164G;S207N;L216X 93;100;107;114;121;129;137;145;157 98;105;112;119;127;135;143;151;163 S;S;S;S;S;S;S;S;S;S 93;100;107;114;121;129;137;145;157;50 94;101;108;115;122;130;138;146;158;57 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. It has also been reported that the naturally occurring mutation sM133T can create a novel N-linked glycosylation site in the viral envelope proteins (Ito et al.,). 2020 International journal of infectious diseases Discussion HBV M133T 64 70 S;S 131;64 139;65 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. Many studies (Protzer-Knolle et al.,; Beckebaum et al.,; Cheung et al.,) have demonstrated that M133T itself is frequently associated with occult HBV infection and is also often associated with some mutations in the 'a' determinant such as G130N, F134L, D144A, D144G, G145A, G145K, and G145R or failed hepatitis B immune globulin (HBIG) prophylaxis. 2020 International journal of infectious diseases Discussion HBV M133T;G130N;F134L;D144A;D144G;G145A;G145K;G145R 96;240;247;254;261;268;275;286 101;245;252;259;266;273;280;291 S 217 231 HBV infections 146 159 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. Mutation sY100C was previously assessed by Mello et al. 2020 International journal of infectious diseases Discussion HBV Y100C 9 15 S 9 10 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. Mutations sP56Q and sP62L, harbored by two HBeAg-negative patients, have previously been reported to be associated with an increased risk of hepatocellular carcinoma (HCC) (Lin et al.,; Munshi et al.,; Qin and Liao,); the serological analysis identified 102/118 patients in this study to be HBeAg-negative. 2020 International journal of infectious diseases Discussion HBV P56Q;P62L 10;20 15;25 C;C;S;S 43;291;10;20 48;296;11;21 Hepatocellular carcinoma;Hepatocellular carcinoma 141;167 165;170 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. other mutations like K122R and F134I detected in the 'a' determinant support the idea of IEMs associated with strains harboring the sY100C as discussed in the present study. 2020 International journal of infectious diseases Discussion HBV Y100C;K122R;F134I 132;21;31 138;26;36 S;S 54;132 68;133 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. sG145R is the most identified of the HBV IEMs and has been well-characterized, but was not identified in this study. 2020 International journal of infectious diseases Discussion HBV G145R 0 6 S 0 1 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. The most frequently identified polymerase mutation was rtL91I, harbored by six isolates. 2020 International journal of infectious diseases Discussion HBV L91I 57 61 P;RT 31;55 41;57 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. The most frequently occurring surface protein mutation was sN59S, harbored by 46/51 isolates. 2020 International journal of infectious diseases Discussion HBV N59S 59 64 S;S 59;30 60;37 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. The mutation sA128V was confirmed by geno2pheno HBV, and this IEM was associated with vaccine escape in a recent study conducted by Cremer et al. 2020 International journal of infectious diseases Discussion HBV A128V 13 19 S 13 14 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. The three IEMs identified in the present study (sY100C, sA128V, and sM133T) were confirmed by geno2pheno HBV. 2020 International journal of infectious diseases Discussion HBV Y100C;A128V;M133T 48;56;68 54;62;74 S;S;S 48;56;68 49;57;69 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. The two subgenotype A1 isolates (Pol33 and Pol40) harbored 14 and 13 amino acid exchanges, respectively, in the polymerase gene, among which nine (rtN122H, rtN124H, rtM129L, rtS137T, rtW153R, rtV163I, rtS256C, rtT259S, and rtI269L) were not present in genotype E (of the 49 isolated genotype E, 22 did not have any amino acid exchanges in the polymerase gene), showing that genotype A circulating in CAR is likely to undergo mutations that will affect the diagnosis, as well as the prevention and control measures for HBV in the CAR population. 2020 International journal of infectious diseases Discussion HBV N122H;N124H;M129L;S137T;W153R;V163I;S256C;T259S;I269L 149;158;167;176;185;194;203;212;225 154;163;172;181;190;199;208;217;230 P;P;P;P;RT;RT;RT;RT;RT;RT;RT;RT;RT 33;43;112;343;147;156;165;174;183;192;201;210;223 36;46;122;353;149;158;167;176;185;194;203;212;225 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. This study detected three IEMs, sY100C, sA128V, and sM133T, similar to previous studies (Mello et al.,; Kwei et al.,; Cremer et al.,). 2020 International journal of infectious diseases Discussion HBV Y100C;A128V;M133T 32;40;52 38;46;58 S;S;S 32;40;52 33;41;53 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. This study identified several known polymerase mutations (rtL91I, rtM129L, rtW153R, rtS213T, rtV214A, rtN238T, rtN248H, and rtI269L), recorded in many previous studies (Locarnini,; Abdelnabi et al.,; Gomes-Gouvea et al.,; Zhang and Ding,; Kim et al.,; Yamani et al.,; Choi et al., 2018; Shaha et al.,; Ababneh et al.,). 2020 International journal of infectious diseases Discussion HBV L91I;M129L;W153R;S213T;V214A;N238T;N248H;I269L 60;68;77;86;95;104;113;126 64;73;82;91;100;109;118;131 P;RT;RT;RT;RT;RT;RT;RT;RT 36;58;66;75;84;93;102;111;124 46;60;68;77;86;95;104;113;126 31682960 Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic. who showed a reduction in HBsAg detection level by commercial ELISA kit, but without statistical significance, leading the authors to conclude that mutation sY100C alone did not play a role in reducing the HBsAg affinity of this commercial ELISA assay. 2020 International journal of infectious diseases Discussion HBV Y100C 157 163 S;S;S 26;206;157 31;211;158 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. (2) The other unexplained observation is the discrepancy in the frequency of G145A in the nail samples between the direct sequencing and deep sequencing. 2019 BMC infectious diseases Discussion HBV G145A 77 82 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Although the deep sequencing did not detect the G145A mutant in the nails of the 2nd-born child, the LNA-based probe real-time PCR detected the G145A mutant as a minor population in the nails of the 2nd-born child. 2019 BMC infectious diseases Discussion HBV G145A;G145A 48;144 53;149 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. However, D144A and G145A mutants were detected by the deep sequencing as minor populations in the serum of the 2nd-born child of Family 2. 2019 BMC infectious diseases Discussion HBV D144A;G145A 9;19 14;24 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. However, T126A and T143S were detected as minor populations in serum. 2019 BMC infectious diseases Discussion HBV T126A;T143S 9;19 14;24 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. However, the G145A mutant existed as a major population in the nails of the mother of Family 2, and it is thus plausible that the G145A mutant, which was transmitted from the mother to the 2nd-born child, was present as < 1% of the viral population in the umbilical cord. 2019 BMC infectious diseases Discussion HBV G145A;G145A 13;130 18;135 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. In addition to T143S, T126A was present as a minor population in the umbilical cord of the 1st-born child of Family 1. 2019 BMC infectious diseases Discussion HBV T143S;T126A 15;22 20;27 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. In the animal experiment, chimpanzees were protected from infection of VEMs (G145R) by a recombinant HB vaccine. 2019 BMC infectious diseases Discussion HBV G145R 77 82 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Moreover, the frequencies of T126A and T143S showed almost the same levels in the umbilical cord samples and serum after the breakthrough infections. 2019 BMC infectious diseases Discussion HBV T126A;T143S 29;39 34;44 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. Notably, T126A has often been reported as a VEM, and the combination of T126A plus T143S was often detected in Indonesian children with breakthrough infections. 2019 BMC infectious diseases Discussion HBV T126A;T126A;T143S 9;72;83 14;77;88 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. One of our previous studies demonstrated that four of six children who were chronically infected with HBV due to a breakthrough infection had the G145R mutant had a minor population in their serum. 2019 BMC infectious diseases Discussion HBV G145R 146 151 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The electropherogram of the direct sequencing showed that the G145A mutant was predominant in the nails. 2019 BMC infectious diseases Discussion HBV G145A 62 67 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The frequency of G145A was therefore calculated as 34.8% in the nails. 2019 BMC infectious diseases Discussion HBV G145A 17 22 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The G145A mutant was detected as a major population in the nails of the mother of Family 2. 2019 BMC infectious diseases Discussion HBV G145A 4 9 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The LNA-based probe real-time PCR results confirmed that the HBV DNA level of G145A was higher than that of the wild-type in the nail samples. 2019 BMC infectious diseases Discussion HBV G145A 78 83 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The other possibility is that the G145A mutant was caused by de novo mutation. 2019 BMC infectious diseases Discussion HBV G145A 34 39 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. The reverse read of the deep sequencing showed G145A mutant at the frequency of 69.6% (not shown). 2019 BMC infectious diseases Discussion HBV G145A 47 52 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. There are two possibilities to explain why the deep sequencing failed to identify the G145A mutant in the umbilical cord; one possibility is based on the detection limit of the frequencies in deep sequencing. 2019 BMC infectious diseases Discussion HBV G145A 86 91 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. We cannot clearly explain the causes of two observations: (1) The reason for the successful immunoprophylaxis in the 3rd-born child of Family 1 despite the exposure to T143S mutant at delivery is not known. 2019 BMC infectious diseases Discussion HBV T143S 168 173 31752732 Deep sequencing of hepatitis B surface antigen gene in the preserved umbilical cords in immunoprophylaxis failure against mother-to-child HBV transmission. We observed that VEMs were not detectable in the umbilical cord samples by direct sequencing, but the deep sequencing showed that VEMs (T143S) were present as minor populations in all of the umbilical cord samples from Family 1. 2019 BMC infectious diseases Discussion HBV T143S 136 141 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. In the current study, among 68 patients, there were 25 (37%) secondary/compensatory resistance mutations (rtL91I, rtQ149K, rtQ215H/P/S, rtN238D) which are related to LdT, LAM, and ADV resistance. 2019 Polish journal of microbiology Discussion HBV L91I;Q215H;Q215P;Q215S;N238D;Q149K 108;125;125;125;138;116 112;134;134;134;143;121 RT;RT;RT;RT 106;114;123;136 108;116;125;138 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. In the current study, we detected rtV173M partial resistance mutation in one patient according to Geno2pheno Drug Resistance Program, however, the rtV173L substitution has been reported more commonly in the literature. 2019 Polish journal of microbiology Discussion HBV V173M;V173L 36;149 41;154 RT;RT 34;147 36;149 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. LAM-associated resistance triple mutation pattern (rtV173L + rtL180M + rtM204V) has also been shown to enhance viral replication compared with rtL180M + rtM204V. 2019 Polish journal of microbiology Discussion HBV V173L;L180M;M204V;L180M;M204V 53;63;73;145;155 58;68;78;150;160 RT;RT;RT;RT;RT 51;61;71;143;153 53;63;73;145;155 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. Sayan has shown in one of his studies that rtV173L mutation combined with sD144E produced HBV vaccine escape +HBIG escape. 2019 Polish journal of microbiology Discussion HBV V173L;D144E 45;74 50;80 RT;S 43;74 45;75 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. sP120T, Sm133I, Ss143L, sD144A/E, sD145R and Se164D are the most frequently detected typical HBsAg escape mutations in CHB patients. 2019 Polish journal of microbiology Discussion HBV P120T;D144A;D144E;D145R 0;24;24;34 6;32;32;40 S;S;S;S 93;0;24;34 98;1;25;35 Chronic Hepatitis B 119 122 31880877 Evaluation of the pol/S Gene Overlapping Mutations in Chronic Hepatitis B Patients in Northern Cyprus. The most common compensatory mutations have been reported to be rtQ149K, rtQ215H/P/S and rtL91I. 2019 Polish journal of microbiology Discussion HBV Q215H;Q215P;Q215S;L91I;Q149K 75;75;75;91;66 84;84;84;95;71 RT;RT;RT 64;73;89 66;75;91 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. sQ129H, sM133I, and sY134N mutations are associated with occult infection with D genotype; also they impair S protein secretion. 2019 Polish journal of microbiology Discussion HBV Q129H;M133I;Y134N 0;8;20 6;14;26 S;S;S;S 0;8;20;108 1;9;21;109 Occult Hepatitis B 57 73 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. These were rtM204I/sW196L mutations (Table II). 2019 Polish journal of microbiology Discussion HBV W196L;M204I 19;13 25;18 RT;S 11;19 13;20 31880889 Molecular Epidemiology of Hepatitis B Virus in Turkish Cypriot. When analyzed in greater details, rtM204I, rtI233V, rtL80I, and rtL180M mutations were not detected before, and these mutations, particularly rtL80I and rtL180M, restore the activity of viral polymerase to near wild type levels, which helps to promote the replication of mutants. 2019 Polish journal of microbiology Discussion HBV L80I;L80I;M204I;I233V;L180M;L180M 54;144;36;45;66;155 58;148;41;50;71;160 P;RT;RT;RT;RT;RT;RT 192;34;43;52;64;142;153 202;36;45;54;66;144;155 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Furthermore, the NTCP-binding region of preS1 showed two mutations (D27G and H39N) that require further investigations into whether these mutations affect the HBV infection efficiency. 2020 International journal of molecular sciences Discussion HBV D27G;H39N 68;77 72;81 PreS1 40 45 HBV infections 159 172 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. identified HBV with a C2964A mutation in the preS1 region as a novel factor associated with HCC; this mutation has also been reported in the present study. 2020 International journal of molecular sciences Discussion HBV C2964A 22 28 PreS1 45 50 Hepatocellular carcinoma 92 95 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. In addition, the D27G mutation has been identified in patients with active chronic hepatitis. 2020 International journal of molecular sciences Discussion HBV D27G 17 21 Chronic Hepatitis B 75 92 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. In this study, four mutations (D27G, H39N, H51Q, and E54A) were identified within residues 21-59. 2020 International journal of molecular sciences Discussion HBV D27G;H39N;H51Q;E54A 31;37;43;53 35;41;47;57 31952213 PreS1 Mutations Alter the Large HBsAg Antigenicity of a Hepatitis B Virus Strain Isolated in Bangladesh. Some RT mutations, such as rtI91L, have been positively associated with HCC; however, this has not been experimentally confirmed in vitro and is considered a putative nucleotide analogues-resistant mutation. 2020 International journal of molecular sciences Discussion HBV I91L 29 33 RT;RT 5;27 7;29 Hepatocellular carcinoma 72 75 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Considering the N-linked glycosylation sites observed in our study, recent studies have shown that the mutational profile T131N+M133T reduces HBsAg antigenicity and fails to induce anti-HBs response without altering HBV replicative capacity. 2020 Viruses Discussion HBV T131N;M133T 122;128 127;133 S;S 186;142 189;147 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Furthermore, another study has shown that the N-linked glycosylation site T123N can strongly reduce virion assembly when introduced in a HBV genotype C backbone. 2020 Viruses Discussion HBV T123N 74 79 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. In our study, T123N did not affect HBV replicative efficiency when present in a HBV genotype D backbone. 2020 Viruses Discussion HBV T123N 14 19 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Other studies have also shown the capability of T131N+M133T to rescue HBsAg secretion impaired by the vaccine escape mutation G145R. 2020 Viruses Discussion HBV T131N;M133T;G145R 48;54;126 53;59;131 S 70 75 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. Similarly, the detection of T123N is capable to affect HBsAg antigenic properties and has been observed in patients with atypical serological profiles for HBV infection. 2020 Viruses Discussion HBV T123N 28 33 S 55 60 HBV infections 155 168 32102257 A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro. This is in agreement with a previous study by our group, showing the associated of T115N and T123N with occult HBV infection in the setting of HBV genotype D. 2020 Viruses Discussion HBV T115N;T123N 83;93 88;98 HBV infections 111 124 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Last, patients with rtM204I/V develop VB with relatively high viral loads, which also facilitate the amplification and sequencing of LAMR in serum samples. 2021 Hepatology (Baltimore, Md.) Discussion HBV M204I;M204V 22;22 29;29 RT 20 22 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. Second, the development or reversion of the rtM204I/V mutant in serum can occur rapidly (within several months) with continuation or withdrawal of antiviral therapy. 2021 Hepatology (Baltimore, Md.) Discussion HBV M204I;M204V 46;46 53;53 RT 44 46 32189364 Rapid Turnover of Hepatitis B Virus Covalently Closed Circular DNA Indicated by Monitoring Emergence and Reversion of Signature-Mutation in Treated Chronic Hepatitis B Patients. The selection of rtM204I/V as the signature biomarker was based on several reasons: First, rtM204I/V is a high-frequency LAMR mutation site, especially in patients with LAM or LdT antiviral therapy. 2021 Hepatology (Baltimore, Md.) Discussion HBV M204I;M204V;M204I;M204V 19;19;93;93 26;26;100;100 RT;RT 17;91 19;93 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. A discrepancy is observed for S210N and S210N + F220L. 2020 Emerging microbes & infections Discussion HBV S210N;S210N;F220L 30;40;48 35;45;53 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Indeed, in in vitro experiments, both S210N and S210N + F220L determined a significant decrease in HBsAg amount compared to wild-type. 2020 Emerging microbes & infections Discussion HBV S210N;S210N;F220L 38;48;56 43;53;61 S 99 104 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Nevertheless, the decrease observed for S210N + F220L was not significantly stronger than that observed for S210N, paralleling results observed in patients. 2020 Emerging microbes & infections Discussion HBV S210N;F220L;S210N 40;48;108 45;53;113 32312174 Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection. Notably, for the pair of mutation S204N + L205P a 90% decrease in HBsAg secretion efficiency was observed. 2020 Emerging microbes & infections Discussion HBV S204N;L205P 34;42 39;47 S 66 71 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. In this study, the A1762T/G1764A double mutations were observed in 27.93% in HBV CD recombinant sequences. 2020 Virology journal Discussion HBV G1764A;A1762T 26;19 32;25 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Other mutations, such as T53C, G1613A, C1653T, T1753C, A2189C, T3098C and PreS deletions were also reported associated with clinical progress. 2020 Virology journal Discussion HBV T53C;G1613A;C1653T;T1753C;A2189C;T3098C 25;31;39;47;55;63 29;37;45;53;61;69 PreS 74 78 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. Previous studies reported that A1762T/G1764A double mutation in BCP (nt.1742-1849) was the strongest viral factor associated with the development of liver disease. 2020 Virology journal Discussion HBV G1764A;A1762T 38;31 44;37 BCP 64 67 Liver disease 149 162 32532295 Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies. The same result was also found in frequencies of mutation A2189C (12.85%), G1613A (8.94%), T1753C (8.38%), C1653T (5.59%), T53C (4.47%), T3098C (1.68%) and PreS deletion (2.23%, 4/179), which were also lower than mutation frequencies of genotype C in CHB patients in Asia. 2020 Virology journal Discussion HBV A2189C;G1613A;T1753C;C1653T;T53C;T3098C 58;75;91;107;123;137 64;81;97;113;127;143 PreS 156 160 Chronic Hepatitis B 251 254 32545313 Impact of Lamivudine-Based Antiretroviral Treatment on Hepatitis B Viremia in HIV-Coinfected South Africans. The current study also detected the M204I variant at baseline in treatment-naive patients, and other mutations such as A181T, L180M, or M204V during follow-up of individuals on a lamivudine-based regimen. 2020 Viruses Discussion HBV M204I;A181T;L180M;M204V 36;119;126;136 41;124;131;141 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. An increase in deuterium exchange is consistent with increased disorder in this region in the WHV Cp149-Y132A as compared to the HBV Cp149-Y132A. 2020 ACS chemical biology Discussion HBV Y132A;Y132A 104;139 109;144 C;C 98;133 100;135 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Both the hCp149-Y132A and wCp149-Y132A mutants are blocked from assembling into capsids. 2020 ACS chemical biology Discussion HBV Y132A;Y132A 16;33 21;38 Capsid 80 87 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. If increased stability in the spike tip causes the capsid to assemble more readily, the decrease in stability of this region in the hCp149-Y132A mutant should contribute to the inability of this mutant to assemble into capsids. 2020 ACS chemical biology Discussion HBV Y132A 139 144 Capsid;Capsid 51;219 57;226 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In our data, the spike tip (intra-dimer interface) shows more deuterium incorporation in the hCp149-Y132A mutant than in the WT hCp149 dimer at later time points (Figure 5, panel A). 2020 ACS chemical biology Discussion HBV Y132A 100 105 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In the alpha5 helix (Figure 1C), both the human and the woodchuck Cp149-Y132A mutants take up less deuterium than the respective WT dimers (Figure 5), as the helix becomes more structured upon mutation of Y132. 2020 ACS chemical biology Discussion HBV Y132A 72 77 C 66 68 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In the inter-dimer contact region, hCp149-Y132A takes up more deuterium than hCp149 (Figure 5A), indicating that this could be another region where an increase in dynamics blocks capsid assembly. 2020 ACS chemical biology Discussion HBV Y132A 42 47 Capsid 179 185 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. In Zhao et al., it was determined that a decrease in stability at the intra-dimer interface caused by the mutation D78S reduced the rate of capsid assembly . 2020 ACS chemical biology Discussion HBV D78S 115 119 Capsid 140 146 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Loss of structure in the loop of the contact region and a gain of structure in the alpha5 helix may contribute to the inability of the hCp149-Y132A and wCp149-Y132A mutants to assemble into capsids. 2020 ACS chemical biology Discussion HBV Y132A;Y132A 142;159 147;164 Capsid 190 197 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Of the four dimers, hCp149-Y132A was the least stable in NMS and had the most deuterium exchange in the spike region (Figure 3C, Figure 4), which is consistent with a less stable intra-dimer interface and more dynamic spike tip. 2020 ACS chemical biology Discussion HBV Y132A 27 32 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. One interpretation of this is that the effect of the Y132A mutation on the spike tip and contact regions is to increase entropy. 2020 ACS chemical biology Discussion HBV Y132A 53 58 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. Our data also show that both the hCp149-Y132A and wCp149-Y132A mutations, which are well removed from the spike tip, none-the-less decreases stability at the intra-dimer interface. 2020 ACS chemical biology Discussion HBV Y132A;Y132A 40;57 45;62 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The loop containing residue 132, located within the contact region, takes up more deuterium in both the hCp149-Y132A and wCp149-Y132A mutants than in the WT dimers at early time points (Figure 5). 2020 ACS chemical biology Discussion HBV Y132A;Y132A 111;128 116;133 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The loop within the contact region shows similar deuterium exchange between the wCp149-Y132A and the hCp149-Y132A, however, there is more deuterium exchange in the wCp149-Y132A as compared to the hCp149-Y132A in the alpha5 helix (Supplemental Figure 4). 2020 ACS chemical biology Discussion HBV Y132A;Y132A;Y132A;Y132A 87;108;171;203 92;113;176;208 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. The Y132A mutation, located in the inter-dimer contact region, causes changes throughout the protein including stability of the intra-dimer interface. 2020 ACS chemical biology Discussion HBV Y132A 4 9 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. To understand the role of allostery in the capsid assembly process of the HBV Cp149 protein, we compared the melting temperature, the strength of the intra-dimer interface, and protein dynamics of hCp149, hCp149-Y132A, wCp149, and wCp149-Y132A. 2020 ACS chemical biology Discussion HBV Y132A;Y132A 212;238 217;243 Capsid;C 43;78 49;80 32662972 Dynamics of Hepatitis B Virus Capsid Protein Dimer Regulate Assembly through an Allosteric Network. when investigating the oxidized wild-type human dimer and the oxidized D78S mutant dimer assembly at differing salt concentrations. 2020 ACS chemical biology Discussion HBV D78S 71 75 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. (2013) have similarly detected such mutations (S45 T/A, N131T, I194V, and S207N) in the S region and recommended further research in this domain. 2020 Heliyon Discussion HBV S45T;S45A;N131T;I194V;S207N 47;47;56;63;74 54;54;61;68;79 S 88 89 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. G145R is a well-known immune escape mutation which results in the lowest capacity of binding to all monoclonal antibodies. 2020 Heliyon Discussion HBV G145R 0 5 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. In contrast, the G145R mutation of S gene was not observed in our sequences. 2020 Heliyon Discussion HBV G145R 17 22 S 35 36 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. In fact, concerning our sequences, several immune epitope mutations including S45T, T113S, N131T, I194V and P142L in MK355500 and S207N in MK355501 were detected in S gene. 2020 Heliyon Discussion HBV S45T;T113S;N131T;I194V;P142L;S207N 78;84;91;98;108;130 82;89;96;103;113;135 S 165 166 32695898 In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D. In this study, T126N mutation was observed in one of HBV isolates (MK355501) which may lead to the failure of HBsAg detection by ELISA tests. 2020 Heliyon Discussion HBV T126N 15 20 S 110 115 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. (2005) on the nonclassical rtV207M/I mt:the most frequent nonclassical mt found in treatment-naive patients:that rtV207M/I is regarded as a compensatory or secondary mt which led to suppression of the wt and predominance of the mt, possibly due to an increased replication competence. 2020 Diagnostics (Basel, Switzerland) Discussion HBV V207M;V207I;V207M;V207I 29;29;115;115 36;36;122;122 RT;RT 27;113 29;115 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. (2009) on 472 samples collected from treatment-naive American adults using conventional PCR combined Sanger DNA sequencing, 389 cases (82.4%) were found to not carry any NA-drug resistance mt, 79 cases (16.7%) were found with rtV207M, and only 4 cases (0.9%) were found with other "putative" mt. 2020 Diagnostics (Basel, Switzerland) Discussion HBV V207M 228 233 RT 226 228 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. (2015) on 168 treatment-naive Chinese adults that the majority of mutants were nonclassical ones found in genotypes B and C, including rtV207M. 2020 Diagnostics (Basel, Switzerland) Discussion HBV V207M 137 142 RT 135 137 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Additional mt including rtS256G for resistance to LMV and rtL229V, rtI233V, rtP237T, and rtN238A/K/T for resistance to ADF were detected based on the work of Liu and his colleagues. 2020 Diagnostics (Basel, Switzerland) Discussion HBV N238A;N238K;N238T;S256G;L229V;I233V;P237T 91;91;91;26;60;69;78 100;100;100;31;65;74;83 RT;RT;RT;RT;RT 24;58;67;76;89 26;60;69;78;91 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Additionally, 6 mt including rtI187V, rtK212T, rtL235V, rtN248H, rtV253I, and rtS256C were found either independently (23 cases) or combined with NA drug-resistance-associated mt (11 cases), but their role in drug resistance in previous reports has not been determined. 2020 Diagnostics (Basel, Switzerland) Discussion HBV S256C;I187V;K212T;L235V;N248H;V253I 80;31;40;49;58;67 85;36;45;54;63;72 RT;RT;RT;RT;RT;RT 29;38;47;56;65;78 31;40;49;58;67;80 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Among those mt, we found only 2 cases of respective HBV genotypes B and C that have rtM204V and rtM204I primary mt coexisting with rtL180M compensatory/secondary mt. 2020 Diagnostics (Basel, Switzerland) Discussion HBV M204V;M204I;L180M 86;98;133 91;103;138 RT;RT;RT 84;96;131 86;98;133 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. In our data, the LMV-associated rtV207M was the most abundant (38.0%), followed by ADF-associated rtN238T (9.9%), ADF-associated rtN238A (5.6%), LMV-associated rtV207L (1.4%), LMV-associated rtS213T (1.4%), LMV-associated rtS256G (1.4%), LMV-associated rtL229V (0.7%), ADF-associated rtN238K (0.7%), and ADF-associated rtP237T (0.7%). 2020 Diagnostics (Basel, Switzerland) Discussion HBV N238A;N238K;V207M;N238T;V207L;S213T;S256G;L229V;P237T 131;286;34;100;162;193;224;255;321 136;291;39;105;167;198;229;260;326 RT;RT;RT;RT;RT;RT;RT;RT;RT 32;98;129;160;191;222;253;284;319 34;100;131;162;193;224;255;286;321 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Multiple-point mt are found to be rare, including rtV207M + rtV207I; rtV207M + rtS213T; rtV207M + rtL229V; rtV207M + rtI233V; rtN238A + rtS256G; rtL180M + rtM204I + rtN238T; rtV207M + rtS213T + rtS256G; and rtL180M + rtM204V + rtV207I + rtV207M. 2020 Diagnostics (Basel, Switzerland) Discussion HBV N238A;L180M;V207M;V207I;V207M;S213T;V207M;L229V;V207M;I233V;S256G;M204I;N238T;V207M;S213T;S256G;L180M;M204V;V207I;V207M 128;147;52;62;71;81;90;100;109;119;138;157;167;176;186;196;209;219;229;239 133;152;57;67;76;86;95;105;114;124;143;162;172;181;191;201;214;224;234;244 RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT;RT 50;60;69;79;88;98;107;117;126;136;145;155;165;174;184;194;207;217;227;237 52;62;71;81;90;100;109;119;128;138;147;157;167;176;186;196;209;219;229;239 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. Our data confirms that these two samples are actually positive with mt rtV207I (G750A) and mt rtV207I (G750T). 2020 Diagnostics (Basel, Switzerland) Discussion HBV V207I;V207I;G750A;G750T 73;96;80;103 78;101;85;108 RT;RT 71;94 73;96 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. We also detected rtI187V with a high prevalence of 14.1%. 2020 Diagnostics (Basel, Switzerland) Discussion HBV I187V 19 24 RT 17 19 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. While our reported spectrum of mt in treatment-naive resembles that of Nguyen et al., with the majority of mt being rtV207M, we also speculated that, with our improved COLD-PCR assay, several mt that were presumably assigned as non-mutation in the Nguyen et al. 2020 Diagnostics (Basel, Switzerland) Discussion HBV V207M 118 123 RT 116 118 32708399 COLD-PCR Method for Early Detection of Antiviral Drug-Resistance Mutations in Treatment-Naive Children with Chronic Hepatitis B. With the design of COLD-PCR for the amplification of P1 and P2 fragments, corresponding to the B, C, D, and E domains in HBV RT, the developed method can be applied for sensitive detection of major NA-drug resistance mutations, including three mt (rtV173L, rtL180M, and rtM204I/V) that are associated not only with LMV and ETV resistance but also with vaccine escape. 2020 Diagnostics (Basel, Switzerland) Discussion HBV M204I;M204V;V173L;L180M 272;272;250;259 279;279;255;264 RT;RT;RT;RT 125;248;257;270 127;250;259;272 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. However, these in vivo findings are in contrast with our in vitro results in which secreted HBV RNA from the A1762T/G1764A double mutant were not significantly reduced in comparison to the wild-type HBV. 2020 Frontiers in microbiology Discussion HBV G1764A;A1762T 116;109 122;115 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. In the current study, HBeAg expression was reduced and we found noticeable differences in the replication of G1896A and A1762T/G1764A mutations in vitro. 2020 Frontiers in microbiology Discussion HBV G1764A;A1762T;G1896A 127;120;109 133;126;115 C 22 27 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Interestingly, the investigators also reported that the presence of BCP mutations (i.e., A1762T/G1764A) correlated to lower levels of serum HBV RNA. 2020 Frontiers in microbiology Discussion HBV G1764A;A1762T 96;89 102;95 BCP 68 71 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. It is intriguing to note that a consistent elevation of numerous immune markers was observed, as well as elevated ALT, within the G1896A variant which might suggest overall heightened immune activity and hepatic inflammation within these individuals. 2020 Frontiers in microbiology Discussion HBV G1896A 130 136 Liver inflammation 204 224 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. Prior epidemiological and population-based studies have demonstrated the associations of X/BCP/PC variants, especially the G1896A pre-core and the A1762T/G1764A double mutation to cirrhosis and HCC. 2020 Frontiers in microbiology Discussion HBV G1764A;G1896A;A1762T 154;123;147 160;129;153 BCP;Precore;Precore;X 91;95;130;89 94;97;138;90 Liver cirrhosis;Hepatocellular carcinoma 180;194 189;197 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. The A1762T/G1764A mutations are responsible for the K130M/V131I mutations found in the HBx. 2020 Frontiers in microbiology Discussion HBV G1764A;V131I;A1762T;K130M 11;58;4;52 17;63;10;57 X 87 90 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. To enhance the clinical relevance of the in vitro cytokine analysis, we evaluated serum derived from CHB patients with predominantly wild-type, G1896A, and A1762T/G1764A. 2020 Frontiers in microbiology Discussion HBV G1764A;G1896A;A1762T 163;144;156 169;150;162 Chronic Hepatitis B 101 104 32760388 Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants. We also found increased HBV DNA levels and detection within the A1762T/G1764A mutant compared to the G1896A mutant in agreement with these in vitro results. 2020 Frontiers in microbiology Discussion HBV G1764A;A1762T;G1896A 71;64;101 77;70;107 32765014 Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues. Furthermore, some variants were related to DR to entecavir and tenofovir disoproxil fumarate, such as rtI169T, rtl180M, rtM204I/V, rtH126Y and rtD134E, which have been previously reported, and were also found in the present study. 2020 Infection and drug resistance Discussion HBV I169T;M204I;M204V;H126Y;D134E 104;122;122;133;145 109;129;129;138;150 RT;RT;RT;RT;RT 102;111;120;131;143 104;113;122;133;145 32790777 A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants. The immune escape mutant G145R is a notable one found in many cases of occult HBV infection and often undetected by routine assays, which has been attributed to the low level of circulating antigen as well as the reduced affinity to diagnostic antibodies. 2020 PloS one Discussion HBV G145R 25 30 HBV infections 78 91 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. As for rtM204I/sW196* (YIDDst in this study), a mutant less commonly encountered than rtM204I/sW196S/L (* 8.2%, L 76.4%, S 10.2%, and L/S 5.1%) in 3TC or Telbivudine-experienced patients, we proved that YIDDst-transfected cells presented a transformation and tumorigenesis potential. 2020 International journal of molecular sciences Discussion HBV W196X;W196S;W196L;M204I;M204I 15;94;94;9;88 21;102;102;14;93 RT;RT;S;S 7;86;15;94 9;88;16;95 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. C-terminal truncated surface gene mutations, including sW172*, sW182*, and sW196* in this study, coincidentally resulted in TGFbi downregulation in transfected-cells, which presented transforming characteristics and mouse xenograft tumorigenesis. 2020 International journal of molecular sciences Discussion HBV W172X;W182X;W196X 55;63;75 61;69;81 S;S;S;S 55;63;75;21 56;64;76;28 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Other researchers also identified sW182* in HCC tissues, and demonstrated its enhanced tumorigenesis and migration ability in vitro. 2020 International journal of molecular sciences Discussion HBV W182X 34 40 S 34 35 Hepatocellular carcinoma 44 47 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. Previously, we identified rtA181T/sW172* in HCC patients, either 3TC-treated or -naive. 2020 International journal of molecular sciences Discussion HBV W172X;A181T 34;28 40;33 RT;S 26;34 28;35 Hepatocellular carcinoma 44 47 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. The downregulated TGFbi expression was revealed by cDNA microarray study of the sW182*-transfected cells due to the hypermethylation of its promoter. 2020 International journal of molecular sciences Discussion HBV W182X 80 86 S 80 81 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. This finding coincided with that in the sW182* study by Jiang et al. 2020 International journal of molecular sciences Discussion HBV W182X 40 46 32887289 Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi. We also explored the oncogenesis mechanism in transgenic mice carrying the preS/S sW172* mutation. 2020 International journal of molecular sciences Discussion HBV W172X 82 88 PreS;S;S 75;80;82 79;81;83 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Although decreased susceptibility to ETV may be expected in presence of HBV rtM204V and rtL180M mutants, doubling the dose of ETV overcomes the effects of these two mutations. 2020 PloS one Discussion HBV M204V;L180M 78;90 83;95 RT;RT 76;88 78;90 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Lamivudine resistance mutations detected in the RT region resulted in sE164D, sI195M, and sW196L/S changes in the surface gene. 2020 PloS one Discussion HBV E164D;I195M;W196L;W196S 70;78;90;90 76;84;98;98 RT;S;S;S;S 48;70;78;90;114 50;71;79;91;121 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Resistance to lamivudine is best recognized in association with the rtM204V/I mutation, which is also associated with decreased viral replication fitness, leading to the subsequent selection of the compensatory mutants rtL180M, rtV173L, and rtL80I/V. 2020 PloS one Discussion HBV M204V;M204I;L180M;V173L;L80I;L80V 70;70;221;230;243;243 77;77;226;235;249;249 RT;RT;RT;RT 68;219;228;241 70;221;230;243 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Selection of the sW182 stop codon (sW182*) arose from rtV191I. 2020 PloS one Discussion HBV V191I;W182X;W182X 56;17;35 61;27;41 RT;S;S 54;17;35 56;18;36 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. sW182* causes termination in the SHB gene, leading to intracellular accumulation of HBsAg protein; which may increase apoptosis of hepatocytes, potentially driving hepatocarcinogenesis. 2020 PloS one Discussion HBV W182X 0 6 S;S;S 84;0;33 89;1;36 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. The G1764T/C1766G BCP double mutation is enriched among cirrhotic patients, and combined core mutations are more common in children with liver cirrhosis. 2020 PloS one Discussion HBV C1766G;G1764T 11;4 17;10 BCP;C 18;89 21;93 Liver cirrhosis;Liver cirrhosis 137;56 152;65 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. The Pre-C stop codon G1896A (W28*) mutation, observed in two children, interrupts HBeAg production. 2020 PloS one Discussion HBV W28X;G1896A 29;21 33;27 C;Precore 82;4 87;9 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. The presence of both W28* and wild-type virus (W28*W) explained the HBeAg positive status noted in these two patients. 2020 PloS one Discussion HBV W28X;W28X 21;47 25;51 C 68 73 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. The rtL80I mutant was most often found in presence of rtM204I as opposed to rtM204V, and most prevalent among genotype D strains; as has been previously reported. 2020 PloS one Discussion HBV L80I;M204I;M204V 6;56;78 10;61;83 RT;RT;RT 4;54;76 6;56;78 32915862 Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia. Though the diagnostic sensitivity of APRI to identify liver fibrosis is relatively low (reported to be around 47%), it is worth noting that this patient also harboured HBV mutations associated with severe liver disease including sW182* and BCP G1764T/C1766G, and presented with a HBeAg positive status and high viraemia; these are known independent risk factors for the development of liver cirrhosis and HCC. 2020 PloS one Discussion HBV C1766G;W182X;G1764T 251;229;244 257;235;250 BCP;C;S 240;280;229 243;285;230 Liver fibrosis;Liver disease;Liver cirrhosis;Hepatocellular carcinoma 54;205;385;405 68;218;400;408 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. According to the reports, the "a" determinant of OBI patients contains Gly145Arg/Ala/Ile/Trp/Glu (G145R/A/I/W/E), Leu109Arg (L109R), Gly119Arg (G119R), Pro120Thr (P120T), Lys122Ile (K122I), Thr126Asn (T126N), Thr127Arg (T127R), Gln129Asn (Q129N), Thr131Asn (T131N), Met133Thr/Leu (M133T/L), Phe134Leu (F134L), Cys139Ser (C139S), Thr140Leu (T140L), Asp144Glu (D144E) and Pro153Leu (P153L) mutants. 2020 International journal of medical sciences Discussion HBV G145R;G145R;G145A;G145I;G145W;G145E;G145A;G145I;G145W;G145E;L109R;L109R;G119R;G119R;P120T;P120T;K122I;K122I;T126N;T126N;T127R;T127R;Q129N;Q129N;T131N;T131N;M133T;M133T;M133L;F134L;F134L;C139S;C139S;T140L;T140L;D144E;D144E;P153L;P153L;M133L 71;98;98;98;98;98;71;71;71;71;114;125;133;144;152;163;171;182;190;201;209;220;228;239;247;258;266;281;281;291;302;310;321;329;340;348;359;370;381;266 96;111;111;111;111;111;96;96;96;96;123;130;142;149;161;168;180;187;199;206;218;225;237;244;256;263;279;288;288;300;307;319;326;338;345;357;364;379;386;279 Occult Hepatitis B 49 52 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. The presence of Thr131Asn (T131N), Phe134Leu (F134L) and Asp144Glu (D144E) mutants was showed in other studies. 2020 International journal of medical sciences Discussion HBV T131N;T131N;F134L;F134L;D144E;D144E 16;27;35;46;57;68 25;32;44;51;66;73 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. Therefore, it's the first time Gln129Arg (Q129R) and Met133Ser (M133S) mutants are reported. 2020 International journal of medical sciences Discussion HBV Q129R;Q129R;M133S;M133S 31;42;53;64 40;47;62;69 32922195 Occult Hepatitis B Virus Infection in Maintenance Hemodialysis Patients: Prevalence and Mutations in "a" Determinant. We found Gln129Arg (Q129R), Thr131Asn (T131N), Met133Ser (M133S), Phe134Leu (F134L), Asp144Glu (D144E) mutants in the "a" determinant of the S gene in one of the patients. 2020 International journal of medical sciences Discussion HBV Q129R;Q129R;T131N;T131N;M133S;M133S;F134L;F134L;D144E;D144E 9;20;28;39;47;58;66;77;85;96 18;25;37;44;56;63;75;82;94;101 S 141 142 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. A phylogenetic analysis of Patient A-derived viral strains showed that sA159V+rtM204I (rtL180M) and sA159V+rtM204V (rtL180M) mutants are likely derived from the sA159V mutant as an adaptation to LAM pressure. 2020 World journal of gastroenterology Discussion HBV M204I;L180M;M204V;L180M;A159V;A159V;A159V 80;89;109;118;71;100;161 85;94;114;123;77;106;167 RT;RT;RT;RT;S;S;S 78;87;107;116;71;100;161 80;89;109;118;72;101;162 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. HBV sA159V reduced the hepatitis B surface antigen production but increased the replication capacity of lamivudine (LAM)/entecavir (ETV)-resistant mutants. 2020 World journal of gastroenterology Discussion HBV A159V 4 10 S;S 4;35 5;42 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. However, sA159V-positive patients had similar serum HBsAg levels to those of sA159V-negative patients. 2020 World journal of gastroenterology Discussion HBV A159V;A159V 9;77 15;83 S;S;S 52;9;77 57;10;78 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In a longitudinal analysis of five patients, the coexistence of sA159V with LAM/ADV/ETV-resistance mutations was frequently detected in the viral pool along with virological breakthrough or an inadequate virological response upon NA therapy. 2020 World journal of gastroenterology Discussion HBV A159V 64 70 S 64 65 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In addition, the sA159V mutation alone was detected before the emergence of the resistance mutation and was recovered after the sA159V-containing resistant mutants were effectively suppressed by rescue therapy. 2020 World journal of gastroenterology Discussion HBV A159V;A159V 17;128 23;134 S;S 17;128 18;129 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In contrast, the HBV DNA levels were partially restored in the LAM- or ETV-resistance viral strains with sA159V compared to the levels in the WT strain, suggesting that the sA159V mutation has a compensatory effect on replication in resistant viral strains. 2020 World journal of gastroenterology Discussion HBV A159V;A159V 105;173 111;179 S;S 105;173 106;174 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In our study, the sA159V mutant had lower HBsAg production than the WT strain. 2020 World journal of gastroenterology Discussion HBV A159V 18 24 S;S 42;18 47;19 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. In view of these results, it is possible that the sA159V mutation increases the fitness of resistant mutants by alleviating anti-HB immune stress and enhancing viral replication competency rather than by directly increasing drug resistance. 2020 World journal of gastroenterology Discussion HBV A159V 50 56 S 50 51 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Notably, the sA159V mutation had no effect on LAM and ETV sensitivity. 2020 World journal of gastroenterology Discussion HBV A159V 13 19 S 13 14 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. sA159V mutants had lower HBsAg levels than the WT strain. 2020 World journal of gastroenterology Discussion HBV A159V 0 6 S;S 25;0 30;1 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. The sA159V+rtL180M+rtT184L+rtM204V mutant is probably derived from sA159V+rtL180M+rtM204V as an adaptation to ETV pressure. 2020 World journal of gastroenterology Discussion HBV L180M;T184L;M204V;L180M;M204V;A159V;A159V 13;21;29;76;84;4;67 18;26;34;81;89;10;73 RT;RT;RT;RT;RT;S;S 11;19;27;74;82;4;67 13;21;29;76;84;5;68 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. This bias could be explained by the frequent coexistence of the sA159V mutant with the WT virus in these patients. 2020 World journal of gastroenterology Discussion HBV A159V 64 70 S 64 65 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. This is supported by a previous study demonstrating that two classical immune escape-associated mutations, sG145R and sP120T, significantly reduce HBsAg production and increase the replication capacity of LAM-resistant HBV mutants. 2020 World journal of gastroenterology Discussion HBV G145R;P120T 107;118 113;124 S;S;S 147;107;118 152;108;119 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Upon follow-up, hepatitis B virus (HBV) sA159V was found to have contributed to resistance in several patients. 2020 World journal of gastroenterology Discussion HBV A159V 40 46 S 40 41 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. Viral strains harboring both sA159V and LAM- or ETV-resistance mutations exhibited significantly lower HBsAg levels than their counterpart strains lacking sA159V mutations. 2020 World journal of gastroenterology Discussion HBV A159V;A159V 29;155 35;161 S;S;S 103;29;155 108;30;156 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. We also found that the sA159V mutation might increase the fitness of LAM/ETV-resistant mutants by decreasing the HBsAg levels and increasing the viral replication capacity. 2020 World journal of gastroenterology Discussion HBV A159V 23 29 S;S 113;23 118;24 32994690 Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations. We selected the sA159V mutation for detailed analyses because: (1) Its frequency was significantly higher in resistance mutation-positive patients than in resistance mutation-negative patients; (2) It was frequently detected together with LAM-, ADV-, and ETV-resistance mutations; and (3) Its virological features have not been documented by phenotypic analyses. 2020 World journal of gastroenterology Discussion HBV A159V 16 22 S 16 17 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. Furthermore, the A194V polymorphism observed among genotype A1 sequences in this study may represent a molecular signature for the HBV Mozambican infected population; however, further studies must be conducted to evaluate this hypothesis. 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV A194V 17 22 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. In particular, T123A escape mutation located in the MHR of the S gene was distinctly present in one patient (sample BSM590). 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV T123A 15 20 S 63 64 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. Interestingly, amino acid substitution E164G was also observed in a study conducted among Nigerian blood donor samples. 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV E164G 39 44 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. Substitutions V190 and F134I in genotype A samples have been reported in some studies, however their contribution to occult hepatitis has not yet been described. 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV F134I 23 28 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. This finding is in concordance with several studies reporting the occurrence of T123A mutation in OBI individuals, changing its immunogenicity and making HBsAg unrecognizable by available commercial kits. 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV T123A 80 85 S 154 159 Occult Hepatitis B 98 101 32997000 Molecular and serological characterization of occult hepatitis B among blood donors in Maputo, Mozambique. With regards to additional analysis for sample BSM1498 belonging to genotype E, amino acid substitution E164G was observed within the MHR. 2020 Memorias do Instituto Oswaldo Cruz Discussion HBV E164G 104 109 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. As recently described, the BCP double mutation A1762T/G1764A is frequently (61%) found in the overall study population. 2020 JCI insight Discussion HBV G1764A;A1762T 54;47 60;53 BCP 27 30 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. In our study, we observed a strong association of GCAC1809-1812TTCT with BCP double mutation A1762T/G1764A in the inactive carrier group. 2020 JCI insight Discussion HBV G1764A;A1762T 100;93 106;99 BCP 73 76 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. In the present study, 560 patients from this cohort were analyzed for additional core mutations associated with BCP double mutation A1762T/G1764A. 2020 JCI insight Discussion HBV G1764A;A1762T 139;132 145;138 BCP;C 112;81 115;85 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. Interestingly, BCP double mutation was found in both HBeAg-positive and HBeAg-negative patients, underlining that this mutation does not completely abolish HBeAg, like, for example, the precore mutation G1896A, which converts TGG to the stop codon TAG. 2020 JCI insight Discussion HBV G1896A 203 209 BCP;C;C;C;Precore 15;53;72;156;186 18;58;77;161;193 33055418 Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers. The double point mutation G1809T/C1812T was observed to reduce HBeAg synthesis in vitro. 2020 JCI insight Discussion HBV C1812T;G1809T 33;26 39;32 C 63 68 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Concretely, we have identified putative resistance mutations rtL229V/M/F whose frequency significantly increased in treated patients. 2020 Emerging microbes & infections Discussion HBV L229V;L229M;L229F 63;63;63 72;72;72 RT 61 63 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Determining whether a similar phenomenon is observed in rtL229 V mutants may call for a further enzyme kinetic study. 2020 Emerging microbes & infections Discussion HBV L229V 58 64 RT 56 58 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Followed by the further investigation of some given sites, we found substitutions at two NA-r mutation sites rtV191I and rtA181T/V, were of interest due to detection much more frequently in genotype C than genotype B (Figure 3(C), Figure 3(D)), indicating different genomic variability by each genotype. 2020 Emerging microbes & infections Discussion HBV V191I;A181T;A181V 111;123;123 116;130;130 RT;RT 109;121 111;123 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Furthermore, the significant difference of the prevalence of rtL229V/M/F mutations between treatment-naive and NAs-treated patients was consistent with that observed from rtM204V, indicating that this mutation may contribute to the antiviral resistance. 2020 Emerging microbes & infections Discussion HBV L229V;L229M;L229F;M204V 63;63;63;173 72;72;72;178 RT;RT 61;171 63;173 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. However, the rtL229V, which accounts for the majority of rtL229 substitutions in Chinese people, was not analyzed in detail in these papers. 2020 Emerging microbes & infections Discussion HBV L229V 15 20 RT;RT 13;57 15;59 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. In addition, considering that rtL229 substitutions emerged and displayed significant virological breakthrough in 83.3% (5/6) of the cases who have received LMV only (Table 2), it suggested that the reduced ETV susceptibility from rtL229V might be easily developed together with or subsequent to the emergence of rtM204V among the cases of LMV therapy failure. 2020 Emerging microbes & infections Discussion HBV L229V;M204V 232;314 237;319 RT;RT;RT 30;230;312 32;232;314 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. In phenotypic resistance testing, rtL229V single mutation showed a >1000-fold increased IC50 value for LMV, in line with the results from the rtM204V phenotypic testing and the clinical profile of patients shown in Table 2. 2020 Emerging microbes & infections Discussion HBV L229V;M204V 36;144 41;149 RT;RT 34;142 36;144 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. It was described in several reports that rtL229 mutants, mainly involving rtL229F and rtL229W, conferred resistance to LMV and showed a capacity of restored viral replication in vitro when coexisted with rtM204 V/I. 2020 Emerging microbes & infections Discussion HBV L229F;L229W;M204V;M204I 76;88;206;206 81;93;214;214 RT;RT;RT;RT 41;74;86;204 43;76;88;206 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. ntG753T,>40% among genotype B), which might play a role in the existence of genotype-dependent nucleotide polymorphic sites, whereas most of them actually tended to have no pathogenic efficacy in phenotype. 2020 Emerging microbes & infections Discussion HBV G753T 1 7 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Of particular concern, the potential effects of rtV191I might result in decreased viral replication, impaired secretion of HBsAg and the LMV, ADV related resistance. 2020 Emerging microbes & infections Discussion HBV V191I 50 55 S;RT 123;48 128;50 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Of these mutations, rtL180M and rtM204V/I were predominant in both genotype B and C, and probably favored by genotype D according to another report in Italian people, supporting that rtL180M and rtM204V/I could be joint resistance mutations across most genotypes of HBV. 2020 Emerging microbes & infections Discussion HBV M204V;M204I;M204V;M204I;L180M;L180M 34;34;197;197;22;185 41;41;204;204;27;190 RT;RT;RT;RT 20;32;183;195 22;34;185;197 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Our data partly confirmed these findings with even more significant replication inhibition in rtL229V mutants compared to rtM204V mutants, and argued against the observations of enhanced viral replication through adaptive changes. 2020 Emerging microbes & infections Discussion HBV L229V;M204V 96;124 101;129 RT;RT 94;122 96;124 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Our in-vitro testing results revealed that the rtL229V and rtL229V + rtM204V produced the most potent suppression of viral replication, followed by rtM204V single mutation (Figure 6(A)). 2020 Emerging microbes & infections Discussion HBV L229V;L229V;M204V;M204V 49;61;71;150 54;66;76;155 RT;RT;RT;RT 47;59;69;148 49;61;71;150 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. rtL229V as putative resistance mutation, was critically selected by drug pressure and showed an increased IC50 value for ETV in vitro when coexisting with LMV resistance mutation rtM204V, suggesting that rtL229V had a negative efficacy of ETV mutation, in agreement with the discovery from our analysis of sequencing, clinical data and molecular modeling. 2020 Emerging microbes & infections Discussion HBV L229V;L229V;M204V 2;206;181 7;211;186 RT;RT;RT 0;179;204 2;181;206 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. rtV191I as a putative resistance mutation, was the only mutation with genotype-specificity identified in the treatment-naive patients. 2020 Emerging microbes & infections Discussion HBV V191I 2 7 RT 0 2 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Taking into account the comprehensive analysis of both phenotypic and molecular modeling we have described here (Figure 5), it was reasonable to hypothesize that the highly decreased viral fitness and binding affinity restriction of the rtL229V substitution were much more similar to the ETV-resistant mutation, rather than other substitutions at rt229, such as rtL229F or rtL229W. 2020 Emerging microbes & infections Discussion HBV L229V;L229F;L229W 239;364;375 244;369;380 RT;RT;RT;RT 237;347;362;373 239;349;364;375 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. The introduction of rtL229V into HBV RT might confer resistance through the mechanism of restricting the size of the ETV-TP binding pocket to sterically impede the ETV-TP binding, and presumably interact with rtM204V through steric repositioning of the YMDD loop. 2020 Emerging microbes & infections Discussion HBV L229V;M204V 22;211 27;216 RT;RT;RT;P 20;37;209;253 22;39;211;257 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. Therefore, the sequential treatment with LMV and ETV should be avoided, while an early diagnosis of rtL229V which was supported as important clinical marker of ETV resistance were recommended, as far as our study was concerned. 2020 Emerging microbes & infections Discussion HBV L229V 102 107 RT 100 102 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. These properties interestingly corroborated with those of ETV resistance mutations rtT184G/rtS202I in a study of the mechanistic basis underlying ETV resistance. 2020 Emerging microbes & infections Discussion HBV T184G;S202I 85;93 90;98 RT;RT 83;91 85;93 33124952 Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients. These results demonstrated that rtL229V displayed a negative efficacy of ETV compensatory mutation, and could confer as much resistance to ETV as rtT184G/rtS202I/rtM250V mutants. 2020 Emerging microbes & infections Discussion HBV T184G;S202I;L229V;M250V 148;156;34;164 153;161;39;169 RT;RT;RT;RT 32;146;154;162 34;148;156;164 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. More importantly, the zero cross-reactivity to HBcAg of the NTR-HBeAg assay was demonstrated by systematic testing of cell culture samples and patient's sera of G1896A viral strains (Figure 4 and Figure 6). 2021 Emerging microbes & infections Discussion HBV G1896A 161 167 C;C 47;64 52;69 33296295 Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection. Moreover, several previous studies found some serum samples from patients who were infected by G1896A HBeAg-minus HBV strains were positive in commercial HBeAg assays, suggesting possible false-positive detection attributed to the cross-reactivity to circulating HBcAg. 2021 Emerging microbes & infections Discussion HBV G1896A 95 101 C;C;C 263;102;154 268;107;159 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. A previous meta-analysis showed that Pre-S deletions, C1653T in enhancer II, and T1753V and A1762T/G1764A in BCP are associated with increased risk of HCC compared with HBV without mutations. 2020 Frontiers in microbiology Discussion HBV G1764A;C1653T;T1753V;A1762T 99;54;81;92 105;60;87;98 BCP;Enh II;PreS 109;64;37 112;75;42 Hepatocellular carcinoma 151 154 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Consistently, genotype H showed the lowest rates of T1753V and A1762T/G1764A and no Pre-S deletions, and was identified as the HBV genotype with fewer HCC-associated mutant sequences. 2020 Frontiers in microbiology Discussion HBV G1764A;T1753V;A1762T 70;52;63 76;58;69 PreS 84 89 Hepatocellular carcinoma 151 154 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Genotype C displayed the highest frequency of Pre-S deletions (3.3%) and the second highest rates of C1653T, T1753V and A1762T/G1764A variations. 2020 Frontiers in microbiology Discussion HBV G1764A;C1653T;T1753V;A1762T 127;101;109;120 133;107;115;126 PreS 46 51 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Genotype G showed by far the highest frequency (>=95%) of C1653T, T1753V, and A1762T/G1764A. 2020 Frontiers in microbiology Discussion HBV G1764A;C1653T;T1753V;A1762T 85;58;66;78 91;64;72;84 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. In fact, both subgenotypes showed similar frequencies of A1762T/G1764A (F1, 29.3%; F2, 27.6%), which were higher than those observed for subgenotypes F3 and F4 (15.4% and 10.7%, P = 0.027). 2020 Frontiers in microbiology Discussion HBV G1764A;A1762T 64;57 70;63 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Moreover, significantly higher frequency of T1753V was observed in subgenotype F2 (44.8%, P < 0.001), whereas F1 was the only subgenotype that contained Pre-S deletions. 2020 Frontiers in microbiology Discussion HBV T1753V 44 50 PreS 153 158 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Only 4 of the 25 escape mutations had total frequencies of >=1% (I/T126S, 1.8%; G145R, 1.2%; M133T, 1.2%; and Q129R, 1.0%), consistent with a previous large-scale analysis showing frequencies of no less than 1% for most escape mutations. 2020 Frontiers in microbiology Discussion HBV T126S;I126S;G145R;M133T;Q129R 65;65;80;93;110 72;72;85;98;115 33381105 Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region. Particularly, the most common escape mutation identified, I/T126S, was previously associated with vaccine failure in Chinese adults undergoing the HBV vaccination program and most prevalent among patients under 15 years of age after mass vaccination in China. 2020 Frontiers in microbiology Discussion HBV T126S;I126S 58;58 65;65 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. Amino acid (aa) substitutions found in this study include rtL180M, rtV173L, rtM204V/I among individuals on ART however, in one drug-naive individual, aa substitutions L180M, M204V and S202I have also been detected. 2021 Virology journal Discussion HBV L180M;V173L;M204V;M204I;L180M;M204V;S202I 60;69;78;78;167;174;184 65;74;85;85;172;179;189 RT;RT;RT 58;67;76 60;69;78 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. Here, we found a high prevalence of resistance mutations to nucleoside analogues and predominantly mutations usually selected by lamivudine (rtL180M (25%; n = 9/36), rtV173L (22.2%), n = 8/36; rtM204V/I (27.8%; n = 10/36) and rtS202I (2.8%; n = 1/36) (Table 2) in the HIV/HBV co-infected individuals collectively. 2021 Virology journal Discussion HBV V173L;M204I;L180M;M204V;S202I 168;195;143;195;228 173;202;148;202;233 RT;RT;RT;RT 141;166;193;226 143;168;195;228 HBV-HIV coinfections 268 287 33446224 Prevalence and characteristics of hepatitis B and D virus infections among HIV-positive individuals in Southwestern Nigeria. Primary aa-substitution rtM204V was the most common in this study, conferring lamivudine-like resistance which has been reported previously to emerge at an annual rate of 15-20% in HIV-1/HBV co-infected individuals in developed countries. 2021 Virology journal Discussion HBV M204V 26 31 RT 24 26 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Fifteen cases of T1719G mutations in the BCP/PC region were identified in 16 samples in the present study, which can inhibit in vitro HBV replication, and may lead to a low HBV DNA viral load. 2021 BMC infectious diseases Discussion HBV T1719G 17 23 BCP;Precore 41;45 44;47 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. G1896A is another typical mutation in the pre-C region, which generates a stop codon at the 28th amino acid position of the HBeAg sequence, resulting in the inhibition of protein synthesis. 2021 BMC infectious diseases Discussion HBV G1896A 0 6 C;Precore 124;42 129;47 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Mutations in the MHR and non-MHR in the S region, such as Y100C, Y103I, Q129H, T131I, M133L/S/T, F134L, T143M, G145R, and L175S, were found in this study, and could reduce the affinity of monoclonal antibodies for "a" epitopes by altering the structure of HBsAg protein, which may contribute to the failure of commercial reagents. 2021 BMC infectious diseases Discussion HBV M133L;M133S;M133T;Y100C;Y103I;Q129H;T131I;F134L;T143M;G145R;L175S 86;86;86;58;65;72;79;97;104;111;122 95;95;95;63;70;77;84;102;109;116;127 S;S 256;40 261;41 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. The N40S mutation in the S region was identified in both samples. 2021 BMC infectious diseases Discussion HBV N40S 4 8 S 25 26 33468062 Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China. Typically, BCP mutations (A1762T and G1764A) can reduce the mRNA synthesis of the pre-C region, which is reflected as a very low level of HBV DNA. 2021 BMC infectious diseases Discussion HBV A1762T;G1764A 26;37 32;43 BCP;Precore 11;82 14;87 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Additionally, as its region is not overlapped with surface gene either, the effect of the rtT301A mutation may be solely attributed to itself. 2021 International journal of molecular sciences Discussion HBV T301A 92 97 RT;S 90;51 92;58 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. As the next step, molecular modeling of RT mutants would be helpful to elucidate the role and mechanism of the rtT301A mutation in viral fitness. 2021 International journal of molecular sciences Discussion HBV T301A 113 118 RT;RT 40;111 42;113 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Discovery of the rtT301A mutation at the nadir point of HBV DNA during TDF treatment may have captured the evolution process of the tenofovir-resistant virus. 2021 International journal of molecular sciences Discussion HBV T301A 19 24 RT 17 19 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Further investigation is required to know whether endogenous cofactors are possibly associated with HBV polymerase, and if so, whether their properties are altered by rtT301A substitution. 2021 International journal of molecular sciences Discussion HBV T301A 169 174 P;RT 104;167 114;169 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Herein, we report a novel rtT301A mutation accompanying previously reported tenofovir-resistant mutations (CYELMVI) in a tenofovir-treated CHB patient without complete virological suppression. 2021 International journal of molecular sciences Discussion HBV T301A 28 33 RT 26 28 Chronic Hepatitis B 139 142 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. However, the nucleotide position of rtT301A is far from the YMDD motif, indicating that this particular substitution might not directly affect binding and catalysis of polymerase substrates. 2021 International journal of molecular sciences Discussion HBV T301A 38 43 P;RT;P 168;36;60 178;38;64 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In addition, we found that the rtT301A substitution was concomitant with these mutations at a high rate. 2021 International journal of molecular sciences Discussion HBV T301A 33 38 RT 31 33 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In ADV-treated patients, the reduced replication capacity of rtN236T mutant, which is well-known for ADV resistance, was restored by a compensatory mutation rtI233V. 2021 International journal of molecular sciences Discussion HBV I233V;N236T 159;63 164;68 RT;RT 61;157 63;159 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In other words, the function of host protein(s), possibly interacting at the rtT301A mutation site, may be impaired in hepatoma cell lines, while they remained authentic in PHHs. 2021 International journal of molecular sciences Discussion HBV T301A 79 84 RT 77 79 Hepatocellular carcinoma 119 127 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. In summary, we herein show that the novel, naturally present rtT301A mutation significantly impaired viral replication, while slightly increasing tenofovir resistance in hepatoma cell lines. 2021 International journal of molecular sciences Discussion HBV T301A 63 68 RT 61 63 Hepatocellular carcinoma 170 178 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Nevertheless, predominant survival of HBV variants harboring the rtT301A CYELMVI mutation was present in the patient's serum. 2021 International journal of molecular sciences Discussion HBV T301A 67 72 RT 65 67 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Nevertheless, some recent studies have shown that rtS78T/sC69*, rtS106C/rtH126Y/rtD134E/rtL269I, and rtL180M/T184L/M204V/rtA200V are related to TDF resistance. 2021 International journal of molecular sciences Discussion HBV C69X;T184L;M204V;S78T;S106C;H126Y;D134E;L180M;A200V;L269I 57;109;115;52;66;74;82;103;123;90 62;114;120;56;71;79;87;108;128;95 RT;RT;RT;RT;RT;RT;RT;S 50;64;72;80;88;101;121;57 52;66;74;82;90;103;123;58 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Nonetheless, the exact utility of the C-terminal RT domain, which is also known as the "thumb subdomain", where the rtT301A mutation is located, has not been understood well. 2021 International journal of molecular sciences Discussion HBV T301A 118 123 RT;RT 49;116 51;118 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. One possibility is that the defective replication of rtT301A mutants might be compensated by unknown cellular factors in PHHs, which requires further examination. 2021 International journal of molecular sciences Discussion HBV T301A 55 60 RT 53 55 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. One study showed that the F501L substitution exhibited a decreased pregenomic RNA encapsidation level, resulting in defective DNA synthesis. 2021 International journal of molecular sciences Discussion HBV F501L 26 31 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Possible compensatory mutations capable of restoring the disrupted replication by rtT301A is the next step in the evolutionary process of tenofovir-resistant mutations, which should be further explored. 2021 International journal of molecular sciences Discussion HBV T301A 84 89 RT 82 84 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Quantitative real-time PCR exhibited abolished replication efficiency and enhanced tenofovir resistance in rtT301A-containing mutants in two hepatoma cell lines, Huh7 and HepG2. 2021 International journal of molecular sciences Discussion HBV T301A 109 114 RT 107 109 Hepatocellular carcinoma 141 149 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The abolished replication levels of clones with an rtT301A mutation from in vitro experiments in hepatoma cell lines were restored to a similar extent to the clones without rtT301A mutation in PHHs. 2021 International journal of molecular sciences Discussion HBV T301A;T301A 53;175 58;180 RT;RT 51;173 53;175 Hepatocellular carcinoma 97 105 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. The novel rtT301A mutation accompanying CYELMVI mutations resulted in increased resistance but a decrease in replication capacity. 2021 International journal of molecular sciences Discussion HBV T301A 12 17 RT 10 12 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. This clinically relevant finding provides rationale that HBV variants bearing both CYELMVI and rtT301A could dominantly exist in the patient's serum. 2021 International journal of molecular sciences Discussion HBV T301A 97 102 RT 95 97 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Thus, here we characterized the impact of this novel rtT301A substitution on replication ability and susceptibility to tenofovir treatment. 2021 International journal of molecular sciences Discussion HBV T301A 55 60 RT 53 55 33562603 Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes. Thus, we believe that the rtT301A might be an important site in polymerase-mediated replication. 2021 International journal of molecular sciences Discussion HBV T301A 28 33 P;RT 64;26 74;28 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Analysis of protein stability showed that HBx was less stable in the presence of both patterns, more evidently so in relation to the T36D pattern, indicating that the specific threonine to aspartate change may further affect HBx stability and consequently, its trans-activating activity. 2021 Scientific reports Discussion HBV T36D 133 137 X;X 42;225 45;228 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. Here, we detected a pattern of aa changes (A12S/P33S/P46S/T36G-D) that was highly represented in low-replicative groups, mainly genotype D CI haplotypes. 2021 Scientific reports Discussion HBV T36G;P46S;P33S;A12S 58;53;48;43 62;57;52;47 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. In vitro investigation of HBV expression in the presence of the A12S/P33S/P46S/T36G pattern showed an approximately 1 log reduction in HBV expression. 2021 Scientific reports Discussion HBV T36G;P33S;P46S;A12S 79;69;74;64 83;73;78;68 33603102 Sophisticated viral quasispecies with a genotype-related pattern of mutations in the hepatitis B X gene of HBeAg-ve chronically infected patients. More marked inhibition was detected in relation to A12S/P33S/P46S/T36D. 2021 Scientific reports Discussion HBV T36D;P33S;P46S;A12S 66;56;61;51 70;60;65;55 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. A missense mutation observed in this study is the G1899A mutation which occurred in 12.5% of the participants [Table 1]. 2021 International journal of health sciences Discussion HBV G1899A 50 56 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. Although there were no statistically significant differences in the median HBV DNA load or serum AFP levels between the participants with the different specific mutations and those with the WT strains, the occurrence of G1899A mutation was marked with a higher level of HBV DNA and serum AFP, and a trend toward statistical significance for both parameters (P = 0.057 and P = 0.056, respectively) was evident. 2021 International journal of health sciences Discussion HBV G1899A 220 226 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. Furthermore, the core gene mutations previously reported to be associated with liver disease progression in chronic patients and particularly in HCC patients such as C1913A/G, C1914G, and G1915T were not identified in any of the sequences from this study. 2021 International journal of health sciences Discussion HBV C1913A;C1913G;C1914G;G1915T 166;166;176;188 174;174;182;194 C 17 21 Liver disease;Hepatocellular carcinoma 79;145 92;148 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. However, in contrast, a study done in Cameroun reported the occurrence of the G1862C mutation in patients infected with HBV genotype/subgenotype E and A3. 2021 International journal of health sciences Discussion HBV G1862C 78 84 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. In this study, this mutation occurred in 87.5% of the participants [Table 1] and caused a nucleotide change from guanine to cytosine (G1862C), leading to a change in the translated amino acid from valine to leucine at position 17 of the precore region. 2021 International journal of health sciences Discussion HBV G1862C;V17L 134;197 140;229 Precore 237 244 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. It was not the regular wild-type GCACC sequence, but TCATC, as a result of a double mutation (G1809T and C1812T) which occurred in all the participants infected with HBV subgenotype A1 [Table 2]. 2021 International journal of health sciences Discussion HBV G1809T;C1812T 94;105 100;111 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. Mutations occurring at nucleotide positions 1821-1828, the region important for pregenomic RNA initiation and synthesis, which have not been widely reported such as T1821C, C1826T, and A1827C mutations were observed in this study. 2021 International journal of health sciences Discussion HBV T1821C;C1826T;A1827C 165;173;185 171;179;191 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. Some novel mutations observed in this study which may also be of clinical importance include the G/A1951T, G1957A, and nucleotide 1812 deletion of cytosine (C). 2021 International journal of health sciences Discussion HBV A1951T;G1951T;G1957A 97;97;107 105;105;113 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The case was different with the G1888A and G1862C mutations, in which lower HBV DNA and serum AFP levels were observed in participants infected with the mutant strains than the WT strains, and the differences also showed a trend toward statistical significance. 2021 International journal of health sciences Discussion HBV G1888A;G1862C 32;43 38;49 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The G1888A HBV mutation is a silent mutation of clinical relevance which was detected in 87.5% of the participants [Table 1]. 2021 International journal of health sciences Discussion HBV G1888A 4 10 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The G1896A mutation has previously been reported among HIV/HBV co-infected Nigerians in a study done in Jos, North-central, Nigeria as 57%. 2021 International journal of health sciences Discussion HBV G1896A 4 10 HBV-HIV coinfections 55 74 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The G1896A mutation is a nonsense mutation occurring in the HBV precore region leading to a G-to-A shift, which causes a conversion of codon 28 from TGG (tryptophan) to a premature stop codon TAG, and subsequent termination of the expression of HBeAg. 2021 International journal of health sciences Discussion HBV G1896A 4 10 C;Precore 245;64 250;71 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The G1896A mutation occurs frequently in genotypes/subgenotypes which have 1858T, such as C1, D, E, and F and was reported to be least frequently observed in genotype A. 2021 International journal of health sciences Discussion HBV G1896A 4 10 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The G1899A precore mutation causing the amino acid variation G29D have also been reported to be significantly associated with the development of cirrhosis and HCC. 2021 International journal of health sciences Discussion HBV G1899A;G29D 4;61 10;65 Precore 11 18 Liver cirrhosis;Hepatocellular carcinoma 145;159 154;162 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The report from this study is higher than the report from India which recorded a prevalence rate of 6.1% for G1899A precore mutation. 2021 International journal of health sciences Discussion HBV G1899A 109 115 Precore 116 123 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. The report from this study is in concordance with a report from India where the G1896A mutation was not detected among the patients infected with HBV subgenotype A1 but in the genotype D infected patients. 2021 International journal of health sciences Discussion HBV G1896A 80 86 33708042 Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria. This mutation caused a change from guanine to adenine at nucleotide 1899 which resulted to a glycine to aspartic acid amino acid substitution at residue 29 of the precore region. 2021 International journal of health sciences Discussion HBV G29D 93 155 Precore 163 170 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Also, the HIV infection may influence the association between rtA194T mutation and TDF resistance. 2021 Infection and drug resistance Discussion HBV A194T 64 69 RT 62 64 HBV-HIV coinfections 10 23 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Apart from rtL180M, rtM204V and rtA194T mutations, rtM187V and rtV207L were also detected. 2021 Infection and drug resistance Discussion HBV L180M;M204V;A194T;M187V;V207L 13;22;34;53;65 18;27;39;58;70 RT;RT;RT;RT;RT 11;20;32;51;63 13;22;34;53;65 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. But these results do not agree with the previous study that a clear association between rtA194T and viral load rebound reported by Sheldon. 2021 Infection and drug resistance Discussion HBV A194T 90 95 RT 88 90 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Furthermore, previous studies reported that rtA194T mutant can be observed in treatment-naive patients. 2021 Infection and drug resistance Discussion HBV A194T 46 51 RT 44 46 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. HBV rtA194T mutant emerged prior TDF treatment in this case, whereas Sheldon reported that rtA194T mutation occurred under the treatment with TDF for 11.2+-6.7 months in two HIV/HBV-coinfected patients. 2021 Infection and drug resistance Discussion HBV A194T;A194T 6;93 11;98 RT;RT 4;91 6;93 HBV-HIV coinfections 174 192 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. However, G1896A or A1762T/G1764A mutations were not found in this patient with genotype C HBV by DNA sequencing, while A1727T, C1730G and C1799G mutations were found in BCP region, which were reported to be associated significantly with cirrhosis. 2021 Infection and drug resistance Discussion HBV G1764A;G1896A;A1762T;A1727T;C1730G;C1799G 26;9;19;119;127;138 32;15;25;125;133;144 BCP 169 172 Liver cirrhosis 237 246 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. In addition, only one patient had a transient viral increase and the other one had continuous viral decrease after the occurrence of rtA194T mutant under TDF treatment in his study. 2021 Infection and drug resistance Discussion HBV A194T 135 140 RT 133 135 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. In conclusion, our case reported that the emergence of rtA194T mutants within the HBV polymerase after LAM treatment is sensitive to TDF rescue therapy. 2021 Infection and drug resistance Discussion HBV A194T 57 62 P;RT 86;55 96;57 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. In this case, we report the occurrence of rtA194T mutant during the long-term LAM monotherapy in a CHB patient who remains sensitive to TDF. 2021 Infection and drug resistance Discussion HBV A194T 44 49 RT 42 44 Chronic Hepatitis B 99 102 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Interestingly, genotypic drug resistance testing showed that rtA194T mutation was present in this patient, along with rtL180M and rtM204V mutations. 2021 Infection and drug resistance Discussion HBV A194T;L180M;M204V 63;120;132 68;125;137 RT;RT;RT 61;118;130 63;120;132 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. It is coincided with an in vitro study that the rtA194T mutation did not confer to TDF as a single mutation or in a LAM-resistant viral background, using a HepG2 cell system. 2021 Infection and drug resistance Discussion HBV A194T 50 55 RT 48 50 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Notedly, close virological monitoring is necessary, because CHB patients with HBeAg negative may be at particular risk to rtA194T mutations on account of precore (PC) and basic core promoter (BCP) substitutions enhancing the reduced replicative capacity of rtA194T mutants. 2021 Infection and drug resistance Discussion HBV A194T;A194T 124;259 129;264 BCP;BCP;C;Precore;Precore;RT;RT 171;192;78;163;154;122;257 190;195;83;165;161;124;259 Chronic Hepatitis B 60 63 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Three mutations associated with LAM resistance have been mostly described: rtM204V/I in C domain, rtV173L and rtL180M in B domain. 2021 Infection and drug resistance Discussion HBV M204V;M204I;V173L;L180M 77;77;100;112 84;84;105;117 RT;RT;RT 75;98;110 77;100;112 33758517 The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report. Whether the rtA194T mutation conferring resistance against TDF is still controversial and more clinical evidences are needed to reveal the true relevance of the rtA194T mutation. 2021 Infection and drug resistance Discussion HBV A194T;A194T 14;163 19;168 RT;RT 12;161 14;163 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. In rt269I signature NS mutations, several types, including preC-W28Stop (1896 preC mutation) and two types in the X region, V/L5M and V131I, are strongly related to HBeAg seronegative infections, which can lead to enhanced persistent rt269I type HBV infections by increasing mutation frequencies within the HBV genome, particularly in the Pol region, perhaps because of a host immune response. 2021 Microorganisms Discussion HBV L5M;W28X;V5M;V131I 124;64;124;134 129;71;129;139 C;P;Precore;Precore;RT;RT;X 165;339;59;78;3;234;114 170;342;63;82;5;236;115 HBV infections 246 260 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. In this study, we found a total of 19 NS signature mutation types, of which all 17 types, except for two types specific to rt269L (I68T in S region and T36P/S/A in X), were rt269I signature type. 2021 Microorganisms Discussion HBV I68T;T36P;T36S;T36A 131;152;152;152 135;160;160;160 RT;RT;S;X 123;173;139;164 125;175;140;165 33803998 rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome. Indeed, we found several rt269I signature mutation types related to lower HBV replication (I84T/M/L/V in PreS1, preC-W28Stop, V/L5M in X region, C-I97F/L in C region and rtM204I/V in RT region) or liver disease progression (three types in preC/C region (preC-W28Stop, C-I97F/L and C-Q182K/*), F141L in PreS2, L213I/S in S region, three types in X region (V/L5M, T36P/S/A and V131I), three types in Pol region (rtN139K/H, rtM204I/V and rtI224V)) (Table 3 and Figure 5). 2021 Microorganisms Discussion HBV L5M;L5M;M204I;M204V;N139K;N139H;M204I;M204V;I224V;W28X;V5M;W28X;V5M;I84T;I84M;I84L;I84V;I97F;I97L;I97F;I97L;Q182K;F141L;L213I;L213S;T36P;T36S;T36A;V131I 126;355;172;172;412;412;423;423;437;117;126;259;355;91;91;91;91;147;147;270;270;283;293;309;309;362;362;362;375 131;360;179;179;419;419;430;430;442;124;131;266;360;101;101;101;101;153;153;276;276;290;298;316;316;370;370;370;380 C;C;C;C;P;Precore;Precore;Precore;C;PreS1;PreS2;RT;RT;RT;RT;RT;RT;S;X;X 145;157;268;281;398;112;254;239;244;105;302;25;170;183;410;421;435;320;135;345 146;158;269;282;401;116;258;243;245;110;307;27;172;185;412;423;437;321;136;346 Liver disease 197 210 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. A previous meta-analysis estimated the prevalence of M204I/V as 4.9% among >12,000 treatment-naive individuals, and another review reported a prevalence of M204I/V of 5.9% among 8435 treatment-naive individuals. 2021 Journal of viral hepatitis Discussion HBV M204I;M204V;M204I;M204V 53;53;156;156 60;60;163;163 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. For example, RAMs in HBV reverse transcriptase, A181T/V, M204I and M204V, cause corresponding changes in the overlapping region of HBsAg (W172 stop, W196S/L/Stop and I195M, respectively). 2021 Journal of viral hepatitis Discussion HBV W196S;W196L;W196X;A181T;A181V;M204I;M204V;W172X;I195M 149;149;149;48;48;57;67;138;166 161;161;161;55;55;62;72;147;171 S;RT 131;25 136;46 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. For example, T118A/R/V, A128V and D144A/E/G/N variants are more common in Europe, which may relate to better vaccine coverage that drives the selection of resistant variants. 2021 Journal of viral hepatitis Discussion HBV T118A;T118R;T118V;D144A;D144E;D144G;D144N;A128V 13;13;13;34;34;34;34;24 22;22;22;45;45;45;45;29 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. For example, TFV resistance might be selected more easily in genotype A given that RAMs H126Y and R/W153W are wild type in this genotype. 2021 Journal of viral hepatitis Discussion HBV W153W;R153W;H126Y 98;98;88 105;105;93 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. M204I/V is one of the best recognized drug resistance motifs in HBV and had the highest overall prevalence of 3.8% within our sequence database. 2021 Journal of viral hepatitis Discussion HBV M204I;M204V 0;0 7;7 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. The global prevalence of the VEM G145A/R in our data was 1.3%, which is comparable to a previous report across genotypes A-F. 2021 Journal of viral hepatitis Discussion HBV G145A;G145R 33;33 40;40 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Unlike these two studies, we took a lenient approach by reporting the overall prevalence of ETV resistance considering sequences with RAMs M204I/V+L180M, with or without an additional compensatory mutation. 2021 Journal of viral hepatitis Discussion HBV M204I;M204V;L180M 139;139;147 146;146;152 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. Using phylogenetic dating, we estimate that RAMs M204V and L180M, and VEM G145R were already present around the mid 20th century. 2021 Journal of viral hepatitis Discussion HBV M204V;L180M;G145R 49;59;74 54;64;79 33893696 Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations. While evidence is lacking for a mechanistic relationship between the presence of common RAMs such as M204I/V+L180M and HCC, an association has been reported. 2021 Journal of viral hepatitis Discussion HBV M204I;M204V;L180M 101;101;109 108;108;114 Hepatocellular carcinoma 119 122 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. Analysis of HBV resistance was not performed prior to treatment in the present case, and thus, whether the baseline rtM204I substitution was present before the treatment is not known. 2021 Molecular and clinical oncology Discussion HBV M204I 118 123 RT 116 118 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. For example, Kim et al , by comparing frequencies and types of pre-existing RT mutations in treatment-naive patients, found a significantly higher rate of RT mutations in patients with HCC compared with patients with chronic hepatitis, and also identified three mutations that induced NA resistance (rtL80I, rtN139K/T/H and rtM204I/V) and were significantly associated with the progression of HCC. 2021 Molecular and clinical oncology Discussion HBV L80I;N139K;N139T;N139H;M204I;M204V 302;310;310;310;326;326 306;319;319;319;333;333 RT;RT;RT;RT;RT 76;155;300;308;324 78;157;302;310;326 Hepatocellular carcinoma;Chronic Hepatitis B;Hepatocellular carcinoma 185;217;393 188;234;396 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. Furthermore, data in the literature show that, among primary drug resistance mutations, M204I/V is the most frequently encountered in treatment-naive patients. 2021 Molecular and clinical oncology Discussion HBV M204I;M204V 88;88 95;95 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. Furthermore, the presence of only the M204I substitution makes this case uncommon and unique. 2021 Molecular and clinical oncology Discussion HBV M204I 38 43 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. In fact, a systematic review by Zhang et al revealed that the global incidence of rtM204I/V/S is 4.85%. 2021 Molecular and clinical oncology Discussion HBV M204S;M204I;M204V 84;84;84 93;93;93 RT 82 84 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. In the present case report, despite the presence of only one RT substitution (rtM204I), the case showed both genotypical and clinical resistance to ETV, requiring a therapeutic switch to a higher barrier treatment, such as TDF. 2021 Molecular and clinical oncology Discussion HBV M204I 80 85 RT;RT 61;78 63;80 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. The substitution rtM204V/I in the tyrosine/methionine/aspartate/aspartate (YMDD) motif of the pol gene domain in HBV-DNA is the most common mutation linked to LVD resistance, which was observed at a rate of 14-32% after 1 year, and 60-70% after 5 years of LVD treatment. 2021 Molecular and clinical oncology Discussion HBV M204V;M204I 19;19 26;26 P;RT;P 94;17;75 97;19;79 33903819 Entecavir resistance in a patient with treatment-naive HBV: A case report. There were 8 mutations in the RT region, rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V and rtM309K that were significantly associated with the progression of HCC in treatment-naive patients. 2021 Molecular and clinical oncology Discussion HBV L80I;D134N;N139K;N139T;N139H;Y141F;M204I;M204V;F221Y;I224V;M309K 43;51;60;60;60;73;82;82;93;102;114 47;56;69;69;69;78;89;89;98;107;119 RT;RT;RT;RT;RT;RT;RT;RT;RT 30;41;49;58;71;80;91;100;112 32;43;51;60;73;82;93;102;114 Hepatocellular carcinoma 179 182 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Although both mutants share the same phenotype, they show very different thermal stability, with P5T-HBc having a 9 K lower transition temperature (Tm) as L60V-HBc. 2021 Microorganisms Discussion HBV P5T;L60V 97;155 100;159 C;C 101;160 104;163 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. As the mutations L60V and P5T have opposite effects on the stability, it is unlikely that changes in their direct interaction are causative for the low-secretion phenotypes. 2021 Microorganisms Discussion HBV P5T;L60V 26;17 29;21 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. At a resolution of 3.2 A, the mutants P5T-HBc and L60V-HBc have the same overall structure as WT-HBc without rearrangements in the protein's backbone. 2021 Microorganisms Discussion HBV P5T;L60V 38;50 41;54 C;C;C 42;55;97 45;58;100 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Binding probably disrupts the intra-dimer interaction similarly as described for D78S-HBc in the absence of a binding partner. 2021 Microorganisms Discussion HBV D78S 81 85 C 86 89 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Both variants differ only in positions, T33N and A80I. 2021 Microorganisms Discussion HBV T33N;A80I 40;49 44;53 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. Compared to the WT-HBc and P5T-HBc, which bind P2 with intermediate micromolar affinity (68 microM and 74 microM), the premature (F97L-HBc) and low secretion (L60V-HBc) variants bind P2 much weaker (160 microM and 127 microM). 2021 Microorganisms Discussion HBV P5T;F97L;L60V 27;130;159 30;134;163 C;C;C;C 19;31;135;164 22;34;138;167 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. However, local cross-correlation maps and DSC indicate that the mutations P5T and L60V impact differently on the capsid properties: While the mutation P5T weakens the stability of the whole capsids (lowest TM), but leaves the spikes unchanged (high local correlation), L60V stabilizes the capsid slightly (largest TM) and changes the spike around the pocket (lower local correlation). 2021 Microorganisms Discussion HBV P5T;P5T;L60V;L60V 74;151;82;269 77;154;86;273 Capsid;Capsid;Capsid 113;289;190 119;295;197 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. However, two of the residues, V74N and S87N, are in the ascending helix alpha3 and in the descending helix alpha4 of the upper spike, which moves upon peptide binding. 2021 Microorganisms Discussion HBV V74N;S87N 30;39 34;43 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. In addition, the side chain of F97 in L60V-HBc can adopt two alternate positions. 2021 Microorganisms Discussion HBV L60V 38 42 C 43 46 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. In this context, it is interesting to note that WT-HBc with bound "SLLGRM" also exhibits mobility of the F97 side-chain (Figure 7) and has a similar low affinity for this shorter binder as F97L-HBc and L60V-HBc have for the longer P2. 2021 Microorganisms Discussion HBV F97L;L60V 189;202 193;206 C;C;C 51;194;207 54;197;210 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. In this respect, the mutations D78A-HBc or E77A-HBc that reduce binding of P2-related peptides must be evaluated in a new light. 2021 Microorganisms Discussion HBV D78A;E77A 31;43 35;47 C;C 36;48 39;51 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. In this study, we present the first structures of capsids of the HBc mutants P5T-HBc and L60V-HBc, with a low-secretion phenotype. 2021 Microorganisms Discussion HBV P5T;L60V 77;89 80;93 Capsid;C;C;C 50;65;81;94 57;68;84;97 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. MD-simulations show that the mutation D78S destabilizes the descending helix alpha4, where we see the largest mobility upon P2-binding (Figure S5). 2021 Microorganisms Discussion HBV D78S 38 42 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. One of them increases the size of the adjacent pocket similar to in F97L-HBc for the smaller Leu side chain. 2021 Microorganisms Discussion HBV F97L 68 72 C 73 76 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The differences between our ayw strain and the much tighter-binding CW-variant are four residues (V74N; S87N, F97I, I116L), which do not contact the peptide directly. 2021 Microorganisms Discussion HBV V74N;S87N;F97I;I116L 98;104;110;116 102;108;114;121 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The pivot points G63 and G94 and the mutation L60V and F97L are direct neighbors in adjacent turns of the helix. 2021 Microorganisms Discussion HBV L60V;F97L 46;55 50;59 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The two mutations of the low-secretion phenotype mutants, P5T and L60V, are at the entrance of a hydrophobic pocket in the center of the spikes. 2021 Microorganisms Discussion HBV P5T;L60V 58;66 61;70 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. The two stronger binders (P5T-HBc and WT-HBc) have essentially the same spike structure, whereas, in the two weaker binders (L60V-HBc and F97L-HBc), a large hydrophobic side chain is exchanged for a smaller hydrophobic side chain, increasing the size of the adjacent pocket. 2021 Microorganisms Discussion HBV P5T;L60V;F97L 26;125;138 29;129;142 C;C;C;C 30;41;130;143 33;44;133;146 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. These mutations probably induce a conformational change at the tips of the spikes that similarly weakens the dimer interface as D78S rather than being involved in the direct interaction with P2. 2021 Microorganisms Discussion HBV D78S 128 132 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. This open conformation is also adopted in the absence of binding partners by certain mutants Y132A-HBc and D78S-HBc that affect HBc-assembly. 2021 Microorganisms Discussion HBV Y132A;D78S 93;107 98;111 C;C;C 99;112;128 102;115;131 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. While L60V is part of the spike, P5T is in the N-terminus at the dimer interface and occludes the entrance to the pocket. 2021 Microorganisms Discussion HBV P5T;L60V 33;6 36;10 33946808 Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype. While Y132A-HBc forms planar trimers of dimers but no capsids, D78S-HBc assembles slowly into stable capsids but has weakened dimer stability. 2021 Microorganisms Discussion HBV Y132A;D78S 6;63 11;67 Capsid;Capsid;C;C 54;101;12;68 61;108;15;71 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Besides, rtN236 T/A mutation that was related to decreasing sensitivity of TDF presented in 53.4% of the pregnant women, which had no difference with the proportion of the patients with rtM204I/V mutation. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV N236T;N236A;M204I;M204V 11;11;188;188 19;19;195;195 RT;RT 9;186 11;188 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Furthermore, some pregnant women had multibase mutations combined with rtM204I/V at baseline, including rtM204I + rtA181 T/V, rtM204I/V + rtL80I/V, rtM204I/V + rtN236 T, and rtM204I/V + rtI233 V, which may affect their sensitivity to LAM, TBV, ADV, and TDF. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I;M204V;M204I;A181T;A181V;M204I;M204V;L80I;L80V;M204I;M204V;N236T;M204I;M204V;I233V 73;73;106;116;116;128;128;140;140;150;150;162;176;176;188 80;80;111;124;124;135;135;146;146;157;157;168;183;183;194 RT;RT;RT;RT;RT;RT;RT;RT;RT 71;104;114;126;138;148;160;174;186 73;106;116;128;140;150;162;176;188 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. High frequency of rtM204I mutation (more than 20%) can be tested in approximately 30% of patients after 104 weeks of TBV treatment, and virological breakthrough was observed as well. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 20 25 RT 18 20 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. In our study, TBV, a low resistance barrier agent, was administrated in the pregnant women and the HBV RT sequences were tested before and after TBV treatment; we found that the overall viral quasispecies complexity was 0.40 +- 0.09 and 30 of 73 patients (41.1%) had rtM204I/V positive at baseline, while 71.2% of pregnant women had serum HBV DNA load more than 103 IU/mL at delivery. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I;M204V 269;269 276;276 RT;RT 103;267 105;269 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. In the present study, 41.1% of patients were rtM204I/V positive, while only 9.6% (7/73) patients had rtM204I/V frequency of 20% or more. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I;M204V;M204I;M204V 47;47;103;103 54;54;110;110 RT;RT 45;101 47;103 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. It was reported that the preexisting primary resistance mutations could reduce the susceptibility of anti-HBV monotherapy or even combined-therapy; for example, rtM204I was refractory to LAM and TBV, and the efficacy of the corresponding NAs could be affected. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 163 168 RT 161 163 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Moreover, mutation frequency more than 30% was also analyzed; the pregnant women with higher mutation frequency did not have more proportion of HBV DNA load >=103 IU/mL at delivery compared with those patients with rtM204I < 30% (50.0% vs. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 217 222 RT 215 217 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. No increases of the viral quasispecies complexity and the frequency of rtM204I mutation were observed, which supplemented the safety of TBV treatment in late pregnancy. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 73 78 RT 71 73 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. reported 22.2% (4/18) NA-naive patients had rtM204I/V mutation by peptide nucleic acid mediated polymerase chain reaction clamping which could detect mutation rate as low as 0.01-0.001%, and Ayres et al. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I;M204V 46;46 53;53 RT 44 46 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. The complexity of viral quasispecies and the frequency of rtM204I mutation had no significant increase after TBV treatment in those pregnant women; however, caution has to be taken for them to choose NAs in subsequent long-term therapy due to the drug resistance mutations. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 60 65 RT 58 60 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. Two previous studies conducted rtM204I/V mutation testing with sensitive methods. 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I;M204V 33;33 40;40 RT 31 33 33986897 High Prevalence of Preexisting HBV Polymerase Mutations in Pregnant Women Does Not Limit the Antiviral Therapy Efficacy. We tested the association between the mutation frequency of rtM204I and the HBV DNA load decrease; no significant association was found in either the high mutation frequency group or low mutation frequency group (Figure 3). 2021 The Canadian journal of infectious diseases & medical microbiology Discussion HBV M204I 62 67 RT 60 62 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. All sequences obtained in this study were classified as HBV genotype E, which is known to show a clear genotypic divergence from all genotypes within the a determinant, where escape mutations can occur, reported that the types of polymorphisms at positions associated with escape mutations observed in HBV vary from one genotype to another and that the most common of these polymorphisms found in genotype E are T116N, P120L/S, Q129H/R, M133I, D144E, and G145I. 2021 Viruses Discussion HBV T116N;P120L;P120S;Q129H;Q129R;M133I;D144E;G145I 412;419;419;428;428;437;444;455 417;426;426;435;435;442;449;460 S 154 167 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Although the existence and circulation of escape mutants was already reported in 1990, the first case reported in Nigeria was the G145K/R escape mutation, detected in an asymptomatic pregnant woman in Ibadan, Oyo State, among samples collected in 2012. 2021 Viruses Discussion HBV G145K;G145R 130;130 137;137 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Apart from corroborating the occurrence of IEMs in Nigeria, this study reports for the first time the detection of the Q129H mutation from samples collected in Ekiti and Ondo States, southwestern Nigeria. 2021 Viruses Discussion HBV Q129H 119 124 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. Different studies report the presence of the Q129H mutation in different HBV genotypes, including genotype E, whereas the escape mutation Q129R has been detected in genotypes A, C, and D and Q129L in genotype F only. 2021 Viruses Discussion HBV Q129H;Q129R;Q129L 45;138;191 50;143;196 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. However, the detection of Q129H among pregnant women and prospective blood donors detected in this study calls for more studies on its transmissibility, other likely effects on its carriers, as well as its interaction with the existing HBV vaccine, in order to prevent its further spread. 2021 Viruses Discussion HBV Q129H 26 31 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. In both studies other IEMs were also detected; however, these did not include the IEM sQ129H, which was detected in this study. 2021 Viruses Discussion HBV Q129H 86 92 S 86 87 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. In this study, the sQ129H mutation was detected in sequences of 18.2% (n = 8/44) of HBV-positive individuals, which is the highest IEM prevalence reported so far in Nigeria. 2021 Viruses Discussion HBV Q129H 19 25 S 19 20 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. None of the eight study participants carrying the sQ129H escape mutation in this study had blood transfusion records and only two, a male and a pregnant woman, claimed to have received an HBV vaccination. 2021 Viruses Discussion HBV Q129H 50 56 S 50 51 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The presence of sQ129H in Africa has so far only been reported from HBV-HIV-coinfected patients on antiretroviral therapy (ART) in Cote D'Ivoire, Ethiopia, and Angola. 2021 Viruses Discussion HBV Q129H 16 22 S 16 17 HBV-HIV coinfections 68 86 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. The sG145R mutation is one of the most widely reported escape mutations and its horizontal transmission has been proven frequently. 2021 Viruses Discussion HBV G145R 4 10 S 4 5 34210073 Detection of Q129H Immune Escape Mutation in Apparently Healthy Hepatitis B Virus Carriers in Southwestern Nigeria. There is no information about the transmissibility of sQ129H/L/R/N until today. 2021 Viruses Discussion HBV Q129H;Q129L;Q129R;Q129N 54;54;54;54 66;66;66;66 S 54 55 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. Carman et al described the first vaccine escape mutation resulted from the substitution of a glycine (G) residue at position 145 by an arginine (A) residue (G145R). 2021 Infection and drug resistance Discussion HBV G145R 157 162 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. HBV variants with combinations of HBs Ag (G145R or P120T) and polymerase (L526M plus M550V) mutations showed increased HBV replication resulting in a severe clinical course in transplanted patients. 2021 Infection and drug resistance Discussion HBV G145R;P120T;L526M;M550V 42;51;74;85 47;56;79;90 S;P 34;62 40;72 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. In addition, this study shows the presence of different vaccine mutants circulating among Egyptian CHB patients, some mutants such as G145R/A, and D144E/A are recognized as the commonly known vaccine escape mutants. 2021 Infection and drug resistance Discussion HBV G145R;G145A;D144E;D144A 134;134;147;147 141;141;154;154 Chronic Hepatitis B 99 102 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. In the region aa115-123, we found two mutations, the first mutation at the position aa115 (T115S) in three patients and the second mutation at the position aa120 (P120T) in three patients. 2021 Infection and drug resistance Discussion HBV T115S;P120T 91;163 96;168 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. In the region aa124-147, we found 6 different mutations at the positions 126 (T126S), 129 (Q129R), 133 (M133T), 143 (S143L), 144 (D144E/A) and 145 (G145R/A). 2021 Infection and drug resistance Discussion HBV T126S;Q129R;M133T;S143L;D144E;D144A;G145R;G145A 78;91;104;117;130;130;148;148 83;96;109;122;137;137;155;155 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. Ma and Wang reported that eight mutations (P120T, T126S, Q129H, G130N, S143L, D144A, and G145A/R) are associated with diagnostic failure and mutations in the positions 120, 126, 129, 130, 133, 134, 137, 140, 143, 144, and 145 are recorded in escape variants hat evade vaccine or immunoglobulin therapy. 2021 Infection and drug resistance Discussion HBV P120T;T126S;Q129H;G130N;S143L;D144A;G145A;G145R 43;50;57;64;71;78;89;89 48;55;62;69;76;83;96;96 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. S143L, G145R/A, and D144E/A were the highest reported mutations among our cohort, which were detected in 25%, 20%, and 15% of the patients, respectively. 2021 Infection and drug resistance Discussion HBV S143L;G145R;G145A;D144E;D144A 0;7;7;20;20 5;14;14;27;27 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. Several other studies reported other substitutions in the "a" determinant region and associated with vaccine escape, such as T116N, P120S/E, I/T126A/N/I/S, Q129H/R, M133L, K141E, and D144A/E. 2021 Infection and drug resistance Discussion HBV I126A;I126N;I126I;I126S;T126A;T126N;T126I;T126S;T116N;P120S;P120E;Q129H;Q129R;M133L;K141E;D144A;D144E 141;141;141;141;141;141;141;141;125;132;132;156;156;165;172;183;183 154;154;154;154;154;154;154;154;130;139;139;163;163;170;177;190;190 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. Similar to our findings, Zeid et al reported that S143L mutation is the predominant mutation (6.8%) among Egyptian CHB patients. 2021 Infection and drug resistance Discussion HBV S143L 50 55 Chronic Hepatitis B 115 118 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. T115S, P120T, T125M, P127T, Q129R, K141R, and S143L were HBV mutants recorded among Egyptian blood donors with occult infection. 2021 Infection and drug resistance Discussion HBV T115S;P120T;T125M;P127T;Q129R;K141R;S143L 0;7;14;21;28;35;46 5;12;19;26;33;40;51 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. The well-characterized escape mutations in the HBsAg are P120T, D144E/A, and G145R, the latter mutant affects the polymerase gene. 2021 Infection and drug resistance Discussion HBV P120T;D144E;D144A;G145R 57;64;64;77 62;71;71;82 S;P 47;114 52;124 34234472 Characterization of Antigen Escape Mutations in Chronic HBV-Infected Patients in Upper Egypt. While Q129R, M133T, and T126S were recorded in 10%, 10%, and 5% of the patients, respectively. 2021 Infection and drug resistance Discussion HBV Q129R;M133T;T126S 6;13;24 11;18;29 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. In addition, resistance mutation rtV173L, rtL180M, and rtM204V can cause alterations in the S gene resulting to immune escape variants hence greater number of viral strains with cross-resistance. 2021 International journal of health sciences Discussion HBV V173L;L180M;M204V 35;44;57 40;49;62 RT;RT;RT;S 33;42;55;92 35;44;57;93 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. In addition, the presence of secondary mutation in amino acid position 180 (rtL180M) in pol gene can reinstate hepatitis B capacity to replicate. 2021 International journal of health sciences Discussion HBV L180M 78 83 P;RT 88;76 91;78 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. In addition, there was no rtM204I mutation detected in the study; absence of this mutation with detection of rtM204V mutation confirms the predominance of genotype A in drug resistance mutations. 2021 International journal of health sciences Discussion HBV M204I;M204V 28;111 33;116 RT;RT 26;109 28;111 34234632 Hepatitis B virus genetic heterogeneity and drug resistance among jaundiced patients at Coast General Teaching and Referral Hospital, Mombasa County, Kenya. Mutation rtM204V occurred predominantly followed by rtL180M; rtM204V [Table 2] mutation known to be primary mutation since it is susceptible to HBV and lamivudine while rtL180M mutation is taken to be secondary mutation due to its ability to enhance viral replication. 2021 International journal of health sciences Discussion HBV M204V;L180M;M204V;L180M 11;54;63;171 16;59;68;176 RT;RT;RT;RT 9;52;61;169 11;54;63;171 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. A higher rate of ALT within the normal range achieved was also detected in patients with HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 93 97 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Although the production of virions with immature single-stranded genomes by HBV-I97L has been demonstrated, the effects of this amino acid substitution on the clinical course of CHB and the HBV life cycle, especially for the infectivity of HBV-I97L or the synthesis of cccDNA, have not yet been clarified. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L;I97L 80;244 84;248 Chronic Hepatitis B 178 181 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. At the end of the observation, the levels of HBsAg and HBV DNA were significantly lower in patients with HBV-I97L than in those with HBV-I97wt. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 109 113 S 45 50 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. By Southern blotting analysis, we detected the release of immature HBV particles with a single-stranded genome from HBV-I97L-transfected cells, as reported by other researchers. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 120 124 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. However, the efficiency of cccDNA synthesis by infection with HBV-I97L was significantly lower than that of HBV-I97wt. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 66 70 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. However, we and other researchers found that HBV-I97L predominantly generates immature virions with the single-stranded genome, whereas HBV-I97wt preferentially generates mature virions with the partially double-stranded relaxed-circular genome. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 49 53 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In addition, iodixanol density gradient analysis revealed that the profile patterns of HBsAg, HBcrAg, and NL DNA were similar between I97L-HBV/NL and I97wt-HBV/NL, although the rate of HBc protein coexisting with HBsAg was higher in I97L-HBV/NL than in I97wt-HBV/NL. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L;I97L 134;233 138;237 C;S;S 185;87;213 188;92;218 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In conclusion, we found that the amino acid substitution I97L in the HBc region is associated with stable hepatitis characterized by ALT within the normal range and undetectable levels of HBsAg and HBV DNA. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 57 61 C;S 69;188 72;193 Hepatitis 106 115 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In our density gradient analysis of cell culture-generated HBV-I97L, we detected the predominant coexistence of HBc and HBs proteins. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 63 67 C;S 112;120 115;123 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In our previous study, we found that the amino acid substitution I97L mainly emerges in HBeAg-negative patients and is associated with low HBV DNA, normal ALT, and HBsAg clearance. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 65 69 C;S 88;164 93;169 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In the HBV reporter virus infection system, the luciferase activity in I97L-HBV/NL-infected cells was lower than that in I97wt-HBV/NL-infected cells, even after infection with virus adjusted by the NL DNA level. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 71 75 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. In this study, we used a cohort of HBeAg-negative patients with HBV-wt or -I97L. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 75 79 C 35 40 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Luciferase activity after infection of the peak fraction of infectivity was lower for I97L-HBV/NL than for I97wt-HBV/NL. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 86 90 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Moreover, we assessed the effects of the emergence of I97L in the HBV genome on the HBV life cycle by using an in vitro HBV infection system and found that introduction of I97L in the HBc region reduces the infectivity of HBV. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L;I97L 54;172 58;176 C 184 187 HBV infections 120 133 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Recently, Wu et al investigated this amino acid substitution in vivo by using the mouse-hydrodynamic injection system of HBV molecular clones and suggested that HBV-I97L releases HBV virions with single-stranded genomes. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 165 169 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Sex, age, and clinical backgrounds were matched between the patients with HBV-wt and -I97L, and the mean observation periods for these groups were similar. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 86 90 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Taken together, our in vitro data clearly indicated that the production level of cccDNA by either infection or recycling was reduced in HBV-I97L. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 140 144 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The amino acid substitution I97L may be associated with modification of this signal. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 28 32 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The amount of cccDNA generated by the recycling of encapsidated HBV DNA was also lower in HBV-I97L-transfected cells than in HBV-I97wt-transfected cells. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 94 98 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The capsid with the I97L substitution may have a high affinity for envelope proteins and easily be able to interact with the L-HBs protein contained in the envelope. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 20 24 Capsid;S;S;S 4;67;156;127 10;75;164;130 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The compensatory substitutions of amino acid at 5 and 130 have also been reported to improve the immature secretion phenotype by the I97L substitution. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 133 137 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The difference in infectivity between the peak fractions of I97wt- and I97L-HBV/NL was almost identical to that of the difference in infectivity of unpurified culture media. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 71 75 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The efficiencies of attachment and internalization by infection after adjusting the HBV DNA titers of cell culture-generated HBV-I97wt and -I97L viruses were comparable. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 140 144 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The higher affinity of HBc protein with I97L to L-HBs protein compared with that of HBc protein with I97wt was confirmed by a split-reporter system for the protein-protein interactions. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 40 44 C;C;S 23;84;50 26;87;53 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The increase in the SS HBV DNA genome by the I97L substitution is suggested not to be restricted by the HBeAg status. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 45 49 C 104 109 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The mechanisms of I97L-dependent predominance of the single-stranded genome are still obscure. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 18 22 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The number of HBc-positive cells by infection of the peak fraction of HBV-I97L infectivity was approximately 3-fold lower than that of HBV-I97wt, even though the HBV DNA levels were comparable. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 74 78 C 14 17 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The predominance of the single-stranded genome in HBV-I97L-transfected cells was confirmed by Southern blotting, and the amounts of HBV DNA were quantified by targeting HBc and HBx regions. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 54 58 C;X 169;177 172;180 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The production efficiency of core-associated HBV DNA was lower in HBV-I97L-transfected cells than in HBV-I97wt-transfected cells, but the transcription level of pgRNA was comparable. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 70 74 C 29 33 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. The rates of undetectable HBsAg and HBV DNA and the mean annual reduction in these markers were also higher in patients with HBV-I97L than in those with HBV-I97wt. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 129 133 S 26 31 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. These data imply that HBV-I97L containing a single-stranded genome can attach to the cell and invade as well as HBV-wt can, but HBV-I97L cannot synthesize cccDNA at a similar level after internalization. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L;I97L 26;132 30;136 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. These data indicate that the lower infectivity of I97L-HBV/NL can be attributed to the infectivity of the viruses generated and not to the efficiencies of encapsidation or envelopment of the virion. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 50 54 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. They also indicated a lower amount of genomic DNA in hepatocytes and less persistence in the liver after hydrodynamic injection of the HBV molecular clone of HBV-I97L in comparison with HBV-wt, irrespective of the immune status of the mice. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 162 166 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. This lower infectivity of HBV with I97L was also confirmed by infection of HBVcc. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 35 39 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. This reduction in the efficiency of cccDNA synthesis by HBV-I97L can explain the in vivo data of the low amount of genomic DNA in hepatocytes or reduced persistence in the liver after hydrodynamic injection of the HBV-I97L molecular clone into mice, as indicated by other researchers, and the high rate of undetectable HBsAg and HBV DNA and the high annual reduction of these markers in HBV-I97L-infected patients in our clinical observation. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L;I97L;I97L 60;218;391 64;222;395 S 319 324 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. To date, this amino acid substitution, I97L, has been investigated in vitro. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 39 43 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. We reasoned that the production of immature particles is associated with lower infectivity of HBV-I97L and assessed the step of the HBV life cycle affected by this substitution. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 98 102 34352407 Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure. Yuan et al analyzed the cell culture-generated HBV-I97L virus by density gradient and demonstrated that this virus mainly contains a SS HBV DNA genome, even in the enveloped virion in the HBsAg-rich fraction, although the HBV-wt virus in the same fraction predominantly contains a RC HBV DNA genome. 2021 Cellular and molecular gastroenterology and hepatology Discussion HBV I97L 51 55 S 188 193 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. Among them, some mutations, such as D614G and N501Y of SARS-CoV-2, T350G of HBV, and C659T of HVP-16, have been proved to play an important role in the viruses, indicating the reliability and effectiveness of AutoVEM2. 2021 Computational and structural biotechnology journal Discussion HBV C659T 85 90 34512928 AutoVEM2: A flexible automated tool to analyze candidate key mutations and epidemic trends for virus. For HBV, the C659T mutation, which causes A331V mutation on S gene, is reported to be associated with increasing the efficiency of HBV replication. 2021 Computational and structural biotechnology journal Discussion HBV C659T;A331V 13;42 18;47 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. However, neither the mutants (P5T and L60V) nor wt HBc-CLPs with bound peptides show Phe-97 is in "conformation 2" suggesting that flipping of Phe-97 is dispensable for conformational changes at the tips of the spikes. 2021 Viruses Discussion HBV P5T;L60V 30;38 33;42 C 51 54 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. It is hard to reconcile how a pocket factor that is mimicked by TX100 could act as maturation signal considering that we do not see any major differences in the structural mode of binding in naturally occurring mutants (F97L, P5T and L60V) with different secretion phenotypes. 2021 Viruses Discussion HBV P5T;F97L;L60V 226;220;234 229;224;238 34834922 Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97. This mobile part is delineated by residues Gly-63 in helix 3 and Gly-94 in helix 4 and changes its conformation upon binding of certain peptides or in some mutants such as Y132A-HBc or D78S-HBc. 2021 Viruses Discussion HBV Y132A;D78S 172;185 177;189 C;C 178;190 181;193 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In our study, the massively glycosylated (W3S) and glycosylation-deficient (N146G) HBV replicated normally, but the virion seemed to be stacked in the cells. 2021 Viruses Discussion HBV W3S;N146G 42;76 45;81 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. In this W3S mutant, eight mutations in the RT domain were found, some of which were associated with massive glycosylation and silent antigenicity, but none of these have been reported as drug-resistant mutants (Figure 1B). 2021 Viruses Discussion HBV W3S 8 11 RT 43 45 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. The results confirmed that the patterns of particle formation were similar between the wild type and W3S, and thus massive glycosylation itself did not affect HBV particle formation (Figure 3A,B), though more sample required to show the profile of W3S particles and secretion of W3S HBsAg, i.e., the mature virion, was tremendously affected (Figure 2) and so was the non-glycosylated mutant W3S (N146G). 2021 Viruses Discussion HBV W3S;W3S;W3S;W3S;N146G 101;248;279;391;396 104;251;282;394;401 S 283 288 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. Though only a single N-linked glycosylation site at amino acid position 146 was present in both the wild-type and W3S HBsAg, the level of the glycosylated isoform was much higher in W3S compared to wild-type HBsAg, and two amino acids mutations in the HBs/RT region of W3S at P120K and T123D were responsible for this phenomenon as well as escape from HBs ELISA. 2021 Viruses Discussion HBV W3S;W3S;W3S;P120K;T123D 114;182;269;276;286 117;185;272;281;291 S;S;S;S;RT 252;352;118;208;256 255;355;123;213;258 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. To prove it, we tested the effect of entecavir (ETV) on the replication of W3S and found no resistance (data not shown). 2021 Viruses Discussion HBV W3S 75 78 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. To test particle formation of WT and W3S, cesium chloride (CsCl) density-gradient ultracentrifugation was conducted. 2021 Viruses Discussion HBV W3S 37 40 34835134 Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant. We tested whether accumulation of S proteins of W3S and W3S (N146G) in the cell caused ER-stress, but we found that they did not (data not shown). 2021 Viruses Discussion HBV W3S;W3S;N146G 48;56;61 51;59;66 S 34 35 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. A pre-S1 envelope mutation A119F, changing an alanine (A) to a phenylalanine (F), can erase the immature secretion phenotype of the mutant I97L and successfully restore the wild-type-like selective export of the mature genome. 2021 Journal of biomedical science Discussion HBV A119F;I97L 27;139 32;143 PreS1 2 17 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. As a side note, it is worth mentioning here that neither envelope W196L nor W196S could support HDV virion secretion. 2021 Journal of biomedical science Discussion HBV W196L;W196S 66;76 71;81 S 57 65 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. However, we were intrigued that the same polymerase mutant YIDD with a different envelope mutation W196L, displayed an even stronger signal of virion-associated DNA, at least in this in vitro HuH-7 cell culture setting. 2021 Journal of biomedical science Discussion HBV W196L 99 104 S;P;P 81;41;59 89;51;63 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. If CYL-II is nothing but a small loop without any important structure and function, it is unclear why only W196P and M198P had a phenotypic effect on virion secretion, but not M197P. 2021 Journal of biomedical science Discussion HBV W196P;M198P;M197P 107;117;176 112;122;181 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. In our study, we noted that the polymerase YIDD mutant with a W196S envelope mutation has no apparent defect in HBV virion secretion. 2021 Journal of biomedical science Discussion HBV W196S 62 67 S;P;P 68;32;43 76;42;47 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. Naturally occurring core mutants I97L (isoleucine to leucine) or F97L (phenylalanine to leucine), exhibited a so-called "immature secretion" phenotype, which allows excessive secretion of virions containing an immature genome. 2021 Journal of biomedical science Discussion HBV I97L;F97L 33;65 37;69 C 20 24 34852809 A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion. The enhanced virion secretion of mutant W196L provides another evidence that the small loop of the small envelope protein could be engaged in productive core-envelope interaction and virion morphogenesis. 2021 Journal of biomedical science Discussion HBV W196L 40 45 C;S;S 153;158;99 157;166;113 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. All these results suggested that E2G/A induce the HBsAg intracellular accumulation, which might be related to its secretion impairment. 2021 Frontiers in microbiology Discussion HBV E2G;E2A 33;33 38;38 S 50 55 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Another interesting novel finding from the present study was that N-terminal signal peptides were exclusively detected in S proteins with secretion-defective mutants mentioned previously (E2G/A) (Supplementary Figure 2). 2021 Frontiers in microbiology Discussion HBV E2G;E2A 188;188 193;193 S 122 123 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. extracellular) and why pHBV1.3C-E2D could rather promote HBsAg secretion. 2021 Frontiers in microbiology Discussion HBV E2D 32 35 S 57 62 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. First of all, further studies will be needed to elucidate the different mechanisms of OBI genotype B and genotype C caused by E2G. 2021 Frontiers in microbiology Discussion HBV E2G 126 129 Occult Hepatitis B 86 89 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Functional analysis showed that nearly all of the E2 mutations could significantly decrease extracellular and intracellular HBsAg level (except E2G in genotype B with increased intracellular HBsAg level) (p < 0.05) (Figures 1A,B), which could partly explain the lack of HBsAg detection that characterized the occult HBV carriage in vivo. 2021 Frontiers in microbiology Discussion HBV E2G 144 147 S;S;S 124;191;270 129;196;275 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. However, in genotype C, E2G could lead to a very significant HBsAg decrease both extracellularly (0.5% vs. 2021 Frontiers in microbiology Discussion HBV E2G 24 27 S 61 66 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. However, in this study, S proteins with secretion-defective mutations (E2G/A) lead to a signal peptide cleavage between amino acid positions 27 and 28 (Supplementary Figure 2). 2021 Frontiers in microbiology Discussion HBV E2G;E2A 71;71 76;76 S 24 25 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. In addition, pHBV1.3C-E2D could promote HBsAg secretion relatively (Figure 1B), whereas the fluorescence density of its transfected cells (median, 0.023 IOD/pixel) was not significantly lower (p > 0.05) (Figure 3B), which may be due to its weak effect on promoting HBsAg secretion. 2021 Frontiers in microbiology Discussion HBV E2D 22 25 S;S 40;265 45;270 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. In the present study, beside the S protein mutation E2G in OBI genotype B we previously reported, a significantly more frequent E2G mutation was also identified in 13.3% of OBI genotype C strains (p < 0.05). 2021 Frontiers in microbiology Discussion HBV E2G;E2G 52;128 55;131 S 33 34 Occult Hepatitis B;Occult Hepatitis B 59;173 62;176 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Interestingly, a considerable difference was found in the effect of E2G on the expression of intracellular and extracellular HBsAg between genotypes B and C (Figures 1A,B). 2021 Frontiers in microbiology Discussion HBV E2G 68 71 S 125 130 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Meanwhile, other kinds of E2 mutations (E2A/V/D) were observed in 1.1-7.8% of OBI strains (p > 0.05) (Table 1). 2021 Frontiers in microbiology Discussion HBV E2A;E2V;E2D 40;40;40 47;47;47 Occult Hepatitis B 78 81 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Meanwhile, the fluorescence density of pHBV1.3B-E2G/A and pHBV1.3C-E2A was significantly higher than that of genotype-matched pHBV1.3B/C (Figure 3) (p < 0.0001), and the staining pattern of E2G/A mutated HBsAg (Figure 2) is consistent with that of HBsAg intracellular accumulation reported previously. 2021 Frontiers in microbiology Discussion HBV E2G;E2A;E2A;E2G;E2A 48;48;67;190;190 53;53;70;195;195 S;S 204;248 209;253 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Of note is that the significantly lower fluorescence density in pHBV1.3B-E2V/D-transfected cells (Figure 3A) might relate to the decrease of intracellular HBsAg without relative intracellular accumulation (Figure 1A and Supplementary Table 2). 2021 Frontiers in microbiology Discussion HBV E2V;E2D 73;73 78;78 S 155 160 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. On the other hand, the relative intracellular HBsAg of E2G/A were significantly increased than extracellular (110.7-338.3% vs. 2021 Frontiers in microbiology Discussion HBV E2G;E2A 55;55 60;60 S 46 51 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Our previous reports and the present analyses (Figures 1A,B, 2, 3) demonstrated that E2G in OBI genotype B could cause HBsAg intracellular accumulation and HBsAg secretion decrease (p < 0.05). 2021 Frontiers in microbiology Discussion HBV E2G 85 88 S;S 119;156 124;161 Occult Hepatitis B 92 95 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. Second, it remains unclear why the extent of HBsAg secretion impairment caused by E2G/A varies greatly (110.7-338.3% vs. 2021 Frontiers in microbiology Discussion HBV E2G;E2A 82;82 87;87 S 45 50 34867835 E2 Site Mutations in S Protein Strongly Affect Hepatitis B Surface Antigen Detection in the Occult Hepatitis B Virus. These results suggest that there are great differences in the underlying mechanism of OBI caused by E2G between genotype B and genotype C. 2021 Frontiers in microbiology Discussion HBV E2G 100 103 Occult Hepatitis B 86 89 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. A meta-analysis data also resported that C1653T is associated with an increased risk of HCC. 2022 PloS one Discussion HBV C1653T 41 47 Hepatocellular carcinoma 88 91 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. In the present study eight different (P90F, K91W/R, V92A/P, L93P, H94-, K95S, R96C, T97A) substitutions and deletion mutations were found in this region that may affect the viral replication and cell cycle and might play a role in the development of the advanced form of liver disease. 2022 PloS one Discussion HBV P90F;K91W;K91R;V92A;V92P;L93P;K95S;R96C;T97A 38;44;44;52;52;60;72;78;84 42;50;50;58;58;64;76;82;88 Liver disease 271 284 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. In this study, two mutations were found in the HNF1 Site (K118E/I and D119N) which were more prevalent in HCC (37%) patients as compared to LC (14.2%) and CH (12%). 2022 PloS one Discussion HBV K118E;K118I;D119N 58;58;70 65;65;75 Hepatocellular carcinoma;Chronic Hepatitis B;Liver cirrhosis 106;155;140 109;157;142 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Likewise, three mutations T97A, L100G, and S101F were reported in the HNF4 site which were more prevalent in HCC groups (12.5%, 50%, and 62% respectively) as compared to other two groups. 2022 PloS one Discussion HBV T97A;L100G;S101F 26;32;43 30;37;48 Hepatocellular carcinoma 109 112 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Moreover, double combinational mutation (K118E/I, D119N) within regulatory elements of Enh-II has been shown to affect the replication of HBcAg in situ and can manifest liver disease. 2022 PloS one Discussion HBV K118E;K118I;D119N 41;41;50 48;48;55 C 138 143 Liver disease 169 182 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Overall, twelve non-reported mutations were also identified (P90F, V92W/R, R96C, T97A, S104I/W, E109A/Y, D107R, A110S/K, Y111E, F112L, and D114G). 2022 PloS one Discussion HBV P90F;V92W;V92R;R96C;T97A;S104I;S104W;E109A;E109Y;D107R;A110S;A110K;Y111E;F112L;D114G 61;67;67;75;81;87;87;96;96;105;112;112;121;128;139 65;73;73;79;85;94;94;103;103;110;119;119;126;133;144 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. Substitution mutation S101F was detected in a considerable number of samples (N = 37) and found highest in HCC patients (62%) followed by LC patients (57%). 2022 PloS one Discussion HBV S101F 22 27 Hepatocellular carcinoma;Liver cirrhosis 107;138 110;140 34982798 Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases. The substitution mutation T106N/I associated with HCC was found in 43.75% of HCC and 28.52% ofLC patients of this study. 2022 PloS one Discussion HBV T106N;T106I 26;26 33;33 Hepatocellular carcinoma;Hepatocellular carcinoma 50;77 53;80 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. As demonstrated by Mello et al., Y100C alone may not affect HBsAg production, secretion or HBsAg affinity by commercial serological assays, as for our samples. 2022 Scientific reports Discussion HBV Y100C 33 38 S;S 60;91 65;96 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. In addition, L109R/V mutations were present in 2/10 samples and have been related to HBV vaccine escape and virus evasion to the host immune system. 2022 Scientific reports Discussion HBV L109R;L109V 13;13 20;20 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Overall, Y100C was the most frequent substitution, being present in 6/10 sequenced samples. 2022 Scientific reports Discussion HBV Y100C 9 14 35102169 Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Regarding resistance mutations, the double rtM204V/I-rtL180M mutation in polymerase gene (to lamivudine, telbivudine and entecavir:partial) was observed in both serum and DBS samples from an HIV-treated patient. 2022 Scientific reports Discussion HBV M204V;M204I;L180M 45;45;55 52;52;60 P;RT;RT 73;43;53 83;45;55 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. As a result, artificial replicon with rtL180M and rtM204V mutations showed BFV resistance, proving that BFV resistance appears when rtL180M and/or rtM204V mutations are existed. 2022 Biomedicines Discussion HBV L180M;M204V;L180M;M204V 40;52;134;149 45;57;139;154 RT;RT;RT;RT 38;50;132;147 40;52;134;149 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Based on RT-qPCR data, the rtM204V mutant IC50 value for BFV was more than 50 microM, meaning that it could induces resistance to BFV per se. 2022 Biomedicines Discussion HBV M204V 29 34 RT;RT 9;27 11;29 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Besides, as shown in Table 4, the IC50 value of the rtL180M mutant was more than 5 times than that of WT rendering partial-resistant to BFV. 2022 Biomedicines Discussion HBV L180M 54 59 RT 52 54 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. But it may become a dominant species when combined with rtL180M mutation in vivo because of enhanced replication capability. 2022 Biomedicines Discussion HBV L180M 58 63 RT 56 58 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. Even in drug naive patient, the rtL180M and rtM204V might be selected as dominant mutant after long time treatment with BSV. 2022 Biomedicines Discussion HBV L180M;M204V 34;46 39;51 RT;RT 32;44 34;46 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. However, combining PCR and Southern blot data, BFV resistance efficiently appeared only when rtL180M and rtM204V mutations exist together. 2022 Biomedicines Discussion HBV L180M;M204V 95;107 100;112 RT;RT 93;105 95;107 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. In addition, rtL180M is a representative mutation that shows resistance to various NAs. 2022 Biomedicines Discussion HBV L180M 15 20 RT 13 15 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. In in vitro experiments, rtM204V exhibited low replication capacity thus it is unlikely for rtL180M and rtM204V mutations to become a dominant variant itself. 2022 Biomedicines Discussion HBV M204V;L180M;M204V 27;94;106 32;99;111 RT;RT;RT 25;92;104 27;94;106 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. In line with our data (Figure 4a), the rtL180M and rtM204V substitutions have been reported in previous studies as ETV and LMV resistant mutations. 2022 Biomedicines Discussion HBV L180M;M204V 41;53 46;58 RT;RT 39;51 41;53 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. In this study, the proportion of patients with L180M and M204V mutant HBV was 93.4% and 65.6% respectively. 2022 Biomedicines Discussion HBV L180M;M204V 47;57 52;62 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. On the other hand, rtL180M itself seems to be resistant to BFV as shown in Figure 3c, but there was stronger resistance to BFV in MV clone containing rtL180M and rtM204V simultaneously. 2022 Biomedicines Discussion HBV L180M;L180M;M204V 21;152;164 26;157;169 RT;RT;RT 19;150;162 21;152;164 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. The mechanism of BSV resistance in patient who was positive for rtL180M and rtM204V mutations is not clear. 2022 Biomedicines Discussion HBV L180M;M204V 66;78 71;83 RT;RT 64;76 66;78 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. The rtL180M and rtM204V mutations may have been occurred gradually while taking ETV as the first line anti-HBV agent. 2022 Biomedicines Discussion HBV L180M;M204V 6;18 11;23 RT;RT 4;16 6;18 35203489 Identification and Characterization of Besifovir-Resistant Hepatitis B Virus Isolated from a Chronic Hepatitis B Patient. This assay is relative not sensitive compared to our cloning and sequencing analysis, and cannot discriminate whether the two rtM204V and rtM204I mutations are separately or simultaneously exist in the same HBV genome. 2022 Biomedicines Discussion HBV M204V;M204I 128;140 133;145 RT;RT 126;138 128;140 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. As such, a vaccine containing both wild-type and the G145R mutant HBsAg can also confer immunity to both types of the virus. 2022 Vaccines Discussion HBV G145R 53 58 S 66 71 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. At the same time, the inability of HBsAg with the G145R mutation to enhance the expression of CD86 on B cells may indicate a lack of a compensatory mechanism in this escape mutant. 2022 Vaccines Discussion HBV G145R 50 55 S 35 40 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Comparative studies of sera from people who were vaccinated with monovalent vaccines and those recovered from HBV infection have demonstrated that only sera of the recovered patients contained highly active antibodies against both the G145R mutant HBsAg and wild-type HBsAg. 2022 Vaccines Discussion HBV G145R 235 240 S;S 248;268 253;273 HBV infections 110 123 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Evaluation of cytokine production by PBMC from healthy donors in response to stimulation with wild-type or G145R mutant rHBsAg also revealed differences between the two antigens. 2022 Vaccines Discussion HBV G145R 107 112 S 120 126 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Given the reduced immunogenicity of the G145R HBsAg mutant, the mutant spread is likely contained primarily by the cellular immune response. 2022 Vaccines Discussion HBV G145R 40 45 S 46 51 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. However, under conditions of additional stimulation of PBMC with PHA, HBsAg with the G145R mutation, in contrast to wild-type HBsAg, suppressed PHA-induced expression of CD69 on B cells, NK cells, and CD8+ T cells, i.e., the activated state of these cells. 2022 Vaccines Discussion HBV G145R 85 90 S;S 70;126 75;131 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast to wild-type rHBsAg, stimulation of PBMC with rHBsAg with the G145R mutation induced significant production of IL-2. 2022 Vaccines Discussion HBV G145R 74 79 S;S 25;58 31;64 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, the mutant G145R HBsAg, which enhanced PHA-induced IL-2 production, does not appear to be able to inhibit the phosphorylation of JNK-1/2 and c-Jun kinases. 2022 Vaccines Discussion HBV G145R 24 29 S 30 35 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In contrast, there was a small cumulative effect in the presence of the G145R rHBsAg mutant. 2022 Vaccines Discussion HBV G145R 72 77 S 78 84 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. In response to stimulation with wild-type rHBsAg or the rHBsAg G145R mutant, PBMC produced IFN-gamma, TNF-alpha, and IL-10; however, the effect of the rHBsAg mutant was significantly weaker compared to wild-type HBsAg. 2022 Vaccines Discussion HBV G145R 63 68 S;S;S;S 212;42;56;151 217;48;62;157 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Overall, the major differences between the immunopotentiation effects of wild-type and G145R mutant HBsAg emphasize the importance of including mutant HBsAg in the composition of a multivalent vaccine. 2022 Vaccines Discussion HBV G145R 87 92 S;S 100;151 105;156 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Since the G145R mutant can persist as minor subpopulations and can coexist with wild-type HBV, it is likely that patients that recovered from HBV may develop antibodies to both viruses simultaneously. 2022 Vaccines Discussion HBV G145R 10 15 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The current study demonstrated for the first time, using the preculturing model, a major difference in phenotypic and cytokine responses to HBsAg with the G145R mutation compared with wild-type HBsAg in PBMC from healthy donors. 2022 Vaccines Discussion HBV G145R 155 160 S;S 140;194 145;199 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The development of a primary immune response to the G145R HBsAg mutant, which escapes recognition by neutralizing antibodies, may partly explain the epidemiological situation regarding the mutant spread. 2022 Vaccines Discussion HBV G145R 52 57 S 58 63 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The experiments have shown that simultaneous immunization of animals with three recombinant HBsAg variants, including, in addition to the G145R mutant, wild-type ad and ay HBsAg immobilized on aluminum hydroxide, elicited the production of antibodies that recognized natural wild-type and G145R mutant-type viral particles. 2022 Vaccines Discussion HBV G145R;G145R 138;289 143;294 S;S 92;172 97;177 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The lack of a direct effect of wild-type HBsAg on CD40 and CD279, observed under different experimental conditions, as well as a similar inertness of the escape G145R mutant, seem to demonstrate general properties characteristic of HBV. 2022 Vaccines Discussion HBV G145R 161 166 S 41 46 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. The level of antibodies to the G145R mutant antigen in sheep was higher than in the mouse model. 2022 Vaccines Discussion HBV G145R 31 36 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. This suggests that HBsAg with the G145R mutation can inhibit signaling pathways associated with CD69 expression, which promotes immunosuppression and is utilized by the HBV G145R escape mutant for persistence and spread. 2022 Vaccines Discussion HBV G145R;G145R 34;173 39;178 S 19 24 35214692 Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro. Yet, the patients' sera varied considerably in the level of specific antibodies to the G145R mutant HBsAg. 2022 Vaccines Discussion HBV G145R 87 92 S 100 105 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. This result is consistent with a previous study demonstrating that the HBx with A1762T/G1764A (K130M/V131I) mutation (the same as M1-HBx in our study) had a stronger tumorigenic effect than its WT counterpart in a SB mouse model. 2022 Frontiers in oncology Discussion HBV G1764A;V131I;A1762T;K130M 87;101;80;95 93;106;86;100 X;X 71;133 74;136 35223517 The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma. We provide evidence supporting the oncogenic function of T1674G+T1753C+A1762T/G1764A (M2) and C1653T+T1674G+A1762T/G1764A (M3) combo mutations. 2022 Frontiers in oncology Discussion HBV G1764A;G1764A;T1753C;A1762T;T1674G;A1762T;T1674G;C1653T 78;115;64;71;57;108;101;94 84;121;70;77;63;114;107;100 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Moreover, the BCP A1762T and G1764A mutations are reported in association with HBV genotypes C and D. 2022 PloS one Discussion HBV A1762T;G1764A 18;29 24;35 BCP 14 17 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Nevertheless, P120T and G145R mutations associated with failure of HBsAg detection were not found in this sample. 2022 PloS one Discussion HBV P120T;G145R 14;24 19;29 S 67 72 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Notably, the sample with G1896A mutation was HBeAg negative. 2022 PloS one Discussion HBV G1896A 25 31 C 45 50 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. Of these, the pre-C mutation (G1896A) eliminates HBeAg expression at the translational level, whereas BCP mutations (G1764A) decrease HBeAg expression at the transcriptional level. 2022 PloS one Discussion HBV G1896A;G1764A 30;117 36;123 BCP;C;C;Precore 102;49;134;14 105;54;139;19 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. P120T and G145R mutations in the S gene are associated with low responses to HBV vaccination and immunoglobulin therapy as well as failures of diagnostic tests. 2022 PloS one Discussion HBV P120T;G145R 0;10 5;15 S 33 34 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. The G1896A mutation causes the conversion of TGG TAG (Trp Stop codon) at codon 28 of the pre-C gene and the suppression of HBeAg expression. 2022 PloS one Discussion HBV G1896A 4 10 C;Precore 125;91 130;96 35271684 Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran. The pre-C G1896A mutation is frequently found in HBV genotypes B, D, and E. 2022 PloS one Discussion HBV G1896A 10 16 Precore 4 9 35359734 Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy. The S gene sequencing in August 2021 revealed that mutations were detected at three amino acid sites (S143T, D144G, and G145R), while HBsAg was positive, which could be due to wild-type accounting for a large proportion at the time. 2022 Frontiers in microbiology Discussion HBV S143T;D144G;G145R 102;109;120 107;114;125 S;S 134;4 139;5 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. cE64D was previously reported to reduce T-cell proliferation in vitro and correlated to HBV-associated liver disease progression. 2022 BMC pediatrics Discussion HBV E64D 0 5 C 0 1 Liver disease 103 116 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. In fact, in addition to the immune escape mutations, two lesser-known LAM resistance mutations (rtS256G and rtM267L) developed (Table 1), which were previously identified in LAM-failed CHB patients. 2022 BMC pediatrics Discussion HBV S256G;M267L 98;110 103;115 RT;RT 96;108 98;110 Chronic Hepatitis B 185 188 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. Moreover, the HBV sequence clustered with sequences of the southwest African origin (Angola, Namibia, and DRC), which have unique mutations of T57I in the s gene and V30L in the x gene. 2022 BMC pediatrics Discussion HBV T57I;V30L 143;166 147;170 S;X 155;178 156;179 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. preS1N97K is located within the overlapping B-cell /T-cell epitope region, which is frequently mutated in HBV from CHB patients. 2022 BMC pediatrics Discussion HBV N97K 5 10 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. sP52L is inside the HLA class I-restricted epitope of the HBsAg. 2022 BMC pediatrics Discussion HBV P52L 0 5 S;S 58;0 63;1 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. The cL100I mutation is found within the overlapping CD4+ T- and CD8+ T-cell epitope of core gene. 2022 BMC pediatrics Discussion HBV L100I 4 10 C;C 4;87 5;91 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. Three mutations, namely xV30L, xD36G, and xA47T mapped to the B-cell epitope of HBx protein (residue 29-48). 2022 BMC pediatrics Discussion HBV V30L;D36G;A47T 24;31;42 29;36;47 X;X;X;X 80;24;31;42 83;25;32;43 35361141 Molecular characterization of hepatitis B virus (HBV) isolated from a pediatric case of acute lymphoid leukemia, with a delayed response to antiviral treatment: a case report. Thus, the preS2T7I can affect the hydrophilicity and reduce antigenicity. 2022 BMC pediatrics Discussion HBV T7I 15 18 PreS2 10 15 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2008) had also reported W4P/R and other changes at codons 7, 81 on the PreS1, and at codon 68 on the S region related to HCC. 2022 PloS one Discussion HBV W4P;W4R 25;25 30;30 PreS1;S 72;102 77;103 Hepatocellular carcinoma 122 125 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2017) (N38E 71.9%, N38K 71.1%, A60V/E 100% on the PreS1 region, L126T/S 77% on the PreS2 and N3S 27.4% on the S region), from Kim et al. 2022 PloS one Discussion HBV N3S;N38E;N38K;A60V;A60E;L126T;L126S 94;8;20;32;32;65;65 97;12;24;38;38;72;72 PreS1;PreS2;S 51;84;111 56;89;112 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2017) had stated that P203Q and the combination of P203R and S210R hampered the HBsAg secretion and increased cellular proliferation. 2022 PloS one Discussion HBV P203Q;P203R;S210R 23;52;62 28;57;67 S 81 86 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2018) (K122R 69.3% on the S region compared to 8.9% R122K in our study). 2022 PloS one Discussion HBV K122R;R122K 8;53 13;58 S 27 28 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. (2019) had previously found the higher rate of P120T/S in HCC with cirrhosis group. 2022 PloS one Discussion HBV P120T;P120S 47;47 54;54 Hepatocellular carcinoma;Liver cirrhosis 58;67 61;76 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Contrarily, frequent amino acid replacements in our study were detected at the widely known structural and functional sequences such as N51Y/T/S/Q (30.4%), V68T/S/I (44.9%) on the S promoter; T/N87S/T/P (46.2%) on the HSP 70 (heat shock protein) and T125S/N/P (30.8%) on the NBS region. 2022 PloS one Discussion HBV T87S;T87T;T87P;N87S;N87T;N87P;N51Y;N51T;N51S;N51Q;V68T;V68S;V68I;T125S;T125N;T125P 192;192;192;192;192;192;136;136;136;136;156;156;156;250;250;250 202;202;202;202;202;202;146;146;146;146;164;164;164;259;259;259 S promoter 180 190 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. had detected 2 PreS mutations (W4R and A60V) and more other PreS amino acid replacements at codon 5, 30, 35, 5, 54, 77, I84, 98, 102, 118, 123 and 124. 2022 PloS one Discussion HBV W4R;A60V 31;39 34;43 PreS;PreS 15;60 19;64 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Inversely, we detected higher rates of S point-mutations as L21S (29.1%), S53L (37.7%), A184V/G (39.3%), S204R/N (10%) and S210K/N/R/S (39.3%), and also on the "a" determinant (39.7% cases with mutation, compared to 7% from Hudu's group. 2022 PloS one Discussion HBV S210K;S210N;S210R;S210S;L21S;S53L;A184V;A184G;S204R;S204N 123;123;123;123;60;74;88;88;105;105 134;134;134;134;64;78;95;95;112;112 S 39 40 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. On the contrary, three remaining mutations had only been detected on small numbers of cases with especially high ORs and wide 95% confidential intervals including 3 cases of W4P/R/Y (preS1), OR 11.56 (1.99-67.05); 4 cases of S174N (S), OR 29.73 (2.12-417.07); and 8 cases of P203R (S), OR 8.45 (1.43-50.06) (Table 6). 2022 PloS one Discussion HBV W4P;W4R;W4Y;S174N;P203R 174;174;174;225;275 181;181;181;230;280 PreS1;S;S 183;232;282 188;233;283 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Only F141V/L/I had the higher distribution in the HCC group (18.4% vs 9.6%, p = 0.08) (Table 3). 2022 PloS one Discussion HBV F141V;F141L;F141I 5;5;5 14;14;14 Hepatocellular carcinoma 50 53 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Our finding seemed compatible with a report from Mun et al., who had found that F141L mutation strain increased the risk of HCC in HBV genotype C infected subjects. 2022 PloS one Discussion HBV F141L 80 85 Hepatocellular carcinoma 124 127 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Outside of the MHR region we also detected higher rates of other 3 S mutations T47A/E/V/K, S174N (in the HLA II region) and P203S (in the HLA II region, the C-terminal domain) in the HCC group (Table 4). 2022 PloS one Discussion HBV T47A;T47E;T47V;T47K;S174N;P203S 79;79;79;79;91;124 89;89;89;89;96;129 S 67 68 Hepatocellular carcinoma 183 186 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. Regarding to the OR values of mutations on the final multivariable analysis, 2 S mutations including 23 cases of T47A/E/V/K (S) and 21 cases of P120S/T (S) had revealed three folds increase in HCC risk associated with reasonable confidential intervals. 2022 PloS one Discussion HBV T47A;T47E;T47V;T47K;P120T;P120S 113;113;113;113;144;144 123;123;123;123;151;151 S;S;S 79;125;153 80;126;154 Hepatocellular carcinoma 193 196 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. S174N (S) for instance had been observed in our study with the highest OR and relative high PPV, NPV and specificity (75%, 81.1% and 99.5%, respectively) but its sensitivity was only 6.1% (S3 Table). 2022 PloS one Discussion HBV S174N 0 5 S 7 8 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The correlation of the C-terminus P203Q (17.4% vs 1.0%, p = 0.004), S210R (34.8% vs 3.8%, p<0.001) and of their combination with HCC had been reported in genotype A and D CHB patients. 2022 PloS one Discussion HBV P203Q;S210R 34;68 39;73 Hepatocellular carcinoma;Chronic Hepatitis B 129;171 132;174 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The final findings had recognized 5 mutations (W4P/R/Y on the PreS1 region and T47A/E/V/K, P120S/T, S174N, P203R on the S region) that significantly related to HCC. 2022 PloS one Discussion HBV T47A;T47E;T47V;T47K;W4P;W4R;W4Y;P120T;P120S;S174N;P203R 79;79;79;79;47;47;47;91;91;100;107 89;89;89;89;54;54;54;98;98;105;112 PreS1;S 62;120 67;121 Hepatocellular carcinoma 160 163 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. The findings that related to the first 3 mutations that were in agreement with other published papers, except the P203R which had not been well reported. 2022 PloS one Discussion HBV P203R 114 119 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. They had also proved the enhanced cell cycling effects of F141L-expression cell lines through the doubling frequencies of colony-forming versus the wild types. 2022 PloS one Discussion HBV F141L 58 63 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. They were W4P/R/Y and S5L/T (p = 0.055) on the NTCP region; A90T/S/G on the HSP70 region and L108V/I on the S promoter and B cell epitopes (Table 2). 2022 PloS one Discussion HBV A90T;A90S;A90G;W4P;W4R;W4Y;S5L;S5T;L108V;L108I 60;60;60;10;10;10;22;22;93;93 68;68;68;17;17;17;27;27;100;100 S promoter 108 118 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. We also found a significant higher distribution of cases with mutation on the MHR region (p = 0.009) in the HCC group, especially a higher rate of P120S/T. 2022 PloS one Discussion HBV P120S;P120T 147;147 154;154 Hepatocellular carcinoma 108 111 35390033 Mutations in the HBV PreS/S gene related to hepatocellular carcinoma in Vietnamese chronic HBV-infected patients. We found mutations as Y100C/F, P120S/T, R122K, I126T/N/S, S132P, M133T/S/L/I, G145R (the vaccine escape mutant, 2%), Y200F/W and Y206H/F/C as same as that were reported from other studies (Hudu et al. 2022 PloS one Discussion HBV M133T;Y206H;Y206F;Y206C;Y100F;P120T;Y100C;P120S;R122K;I126T;I126N;I126S;S132P;M133S;M133L;M133I;G145R;Y200F;Y200W 65;129;129;129;22;31;22;31;40;47;47;47;58;65;65;65;78;117;117 76;138;138;138;29;38;29;38;45;56;56;56;63;76;76;76;83;124;124 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. found that HBc L60V variation was associated with higher viral loads, necroinflammation of the liver, and probably a poor prognosis. 2022 Clinical and experimental hepatology Discussion HBV L60V 15 19 C 11 14 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. However, in spite of their prevalence, our data showed that E80Q/D, E113D/Q, S181P/R and Q182K/*Stop variations were not statistically significantly different among the groups. 2022 Clinical and experimental hepatology Discussion HBV Q182X;E80Q;E80D;E113D;E113Q;S181P;S181R;Q182K 89;60;60;68;68;77;77;89 96;66;66;75;75;84;84;100 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. In this regard, a meta-analysis study showed a significant correlation between G29D mutation and higher risk of HCC. 2022 Clinical and experimental hepatology Discussion HBV G29D 79 83 Hepatocellular carcinoma 112 115 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Instead, as a new finding, the prevalence of E40D/Q was significantly higher in the IC subjects than CA and C/HCC groups. 2022 Clinical and experimental hepatology Discussion HBV E40D;E40Q 45;45 51;51 Hepatocellular carcinoma 110 113 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. Our results also showed G29D precore mutation at the highest frequency in the C/HCC group among the groups, but the difference was not statistically significant. 2022 Clinical and experimental hepatology Discussion HBV G29D 24 28 Precore 29 36 Hepatocellular carcinoma 78 83 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. reported 6 core mutations (F24Y, E64D, E77Q, A80I/T/V, L116I, and E180A) related to the progression of the disease to cirrhosis and HCC. 2022 Clinical and experimental hepatology Discussion HBV A80I;A80T;A80V;F24Y;E64D;E77Q;L116I;E180A 45;45;45;27;33;39;55;66 53;53;53;31;37;43;60;71 C 11 15 Liver cirrhosis;Hepatocellular carcinoma 118;132 127;135 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. reported no significant correlation between W28* and higher susceptibility to HCC. 2022 Clinical and experimental hepatology Discussion HBV W28X 44 48 Hepatocellular carcinoma 78 81 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. reported that 31.8% (14/44) of patients had mutations in the precore region (G1896A). 2022 Clinical and experimental hepatology Discussion HBV G1896A 77 83 Precore 61 68 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The present study also demonstrated that the rates of F24Y, E64D, E77Q, L116I, and E180A mutations were higher in the C/HCC patients than the other groups; however, these differences were not statistically significant. 2022 Clinical and experimental hepatology Discussion HBV F24Y;E64D;E77Q;L116I;E180A 54;60;66;72;83 58;64;70;77;88 Hepatocellular carcinoma 118 123 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The result of our study showed that a precore point mutation, G1896A, that converts the tryptophan to a stop codon (W28*), was the most common variation in the patients, as detected in chronic HBV in Asia and the Mediterranean region. 2022 Clinical and experimental hepatology Discussion HBV G1896A;W28X 62;116 68;120 Precore 38 45 Chronic Hepatitis B 185 196 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. The substitution E180A which was not mapped in an epitope region was suggested to be significantly associated with disease progression by other strategies. 2022 Clinical and experimental hepatology Discussion HBV E180A 17 22 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. There were some variations such as E77Q, E113Q, S181P/H and Q182K/*Stop outside of the epitope regions which have previously been reported to accumulate with disease progression. 2022 Clinical and experimental hepatology Discussion HBV Q182X;E77Q;E113Q;S181P;S181H;Q182K 60;35;41;48;48;60 67;39;46;55;55;71 35415256 Precore/core mutations of hepatitis B virus genotype D arising in different states of infection. They also found that F24Y, E64D, and V91S/T mutations were located in the T-cell epitope regions, and E77Q, A80I/T/V, and L116I were located within the B-cell epitope regions. 2022 Clinical and experimental hepatology Discussion HBV F24Y;E64D;V91S;V91T;E77Q;A80I;A80T;A80V;L116I 21;27;37;37;102;108;108;108;122 25;31;43;43;106;116;116;116;127 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. A relatively high prevalence of the N236T mutation was recorded in the study patients, which is frequently associated with the A181T/V mutation, a combination that confers decreased efficacy of tenofovir in vitro and was linked to a delayed response to TDF/TAF in patients with high viral loads, or with the compensatory L80V mutation, reported to be associated with LAM and ADV resistance. 2022 Medicina (Kaunas, Lithuania) Discussion HBV N236T;A181T;A181V;L80V 36;127;127;321 41;134;134;325 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. For example, the A181T mutation, also common in this study's patients, was associated with a stop codon in the overlapping portion of the S gene that alters the virion, yet not the subviral particles' secretion. 2022 Medicina (Kaunas, Lithuania) Discussion HBV A181T 17 22 S 138 139 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. In our study, despite the frequent association of the primary resistance mutations M204V/I with the compensatory L180M, V173L, and L80V/I mutations, lamivudine-resistant HBV strains tend to be associated with lower viral loads compared to wild-type strains; further characterization of the viral strains, using Next-Generation Sequencing (NGS), might reveal the presence of other mutations that alter viral replication. 2022 Medicina (Kaunas, Lithuania) Discussion HBV M204I;M204V;L180M;V173L;L80V;L80I 83;83;113;120;131;131 90;90;118;125;137;137 35454370 Hepatitis B Virus Genotypes and Antiviral Resistance Mutations in Romanian HIV-HBV Co-Infected Patients. The most frequently LAM-associated mutations detected in this study were M204V and V173L, commonly reported worldwide across all genotypes, with a similar distribution in HBV genotype A and D infections, as dual (M204V + L180M) and triple mutations (V173L + L180M + M204V). 2022 Medicina (Kaunas, Lithuania) Discussion HBV M204V;V173L;M204V;L180M;V173L;L180M;M204V 73;83;213;221;250;258;266 78;88;218;226;255;263;271