[Pre-Core mutation of HBV among 26 families with history of chronic HBV infection in Shenyang].
PMID: 12665929
2002
Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: CONCLUSIONS: The G to A mutation at nucleotide 1896 in the pre C gene of HBV DNA could be associated with persistent HBV infection.
Abstract: METHODS: The G to A mutation at nucleotide 1896 in the pre C gene of HBV DNA was detected by PCR-RFLP.
Abstract: 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%).
[The prevalence of hepatitis B virus precore mutant isolated from asymptomatic carriers in Guangxi].
PMID: 12667359
2002
Zhonghua liu xing bing xue za zhi
Abstract: Among samples with stopped mutation, 4 samples had mutation at nt1846 (A-->T), 2 samples at nt1862 (G-->T).
Abstract: Both mutation at nt1856 (C-->T) and nt1858 (T-->C) could be seen in sample 734.
Abstract: 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).
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.
PMID: 11076934
2001
The Journal of biological chemistry
Abstract: 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.
A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C. Japan HBV Genotype Research Group.
Abstract: 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.
Abstract: 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.
Vaccination of chronic hepatitis B virus carriers with preS2/S envelope protein is not associated with the emergence of envelope escape mutants.
PMID: 11161275
2001
The Journal of general virology
Abstract: Two mutations (T140S and P127L) diverged from subtype variations.
The polymerase L528M mutation cooperates with nucleotide binding-site mutations, increasing hepatitis B virus replication and drug resistance.
PMID: 11181644
2001
The Journal of clinical investigation
Abstract: 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.
Abstract: However, addition of the B-domain mutation L528M restored replication competence.
Abstract: 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.
Abstract: The replication competency of the single C-domain mutants M552I and M552V was markedly decreased compared
Nomenclature for antiviral-resistant human hepatitis B virus mutations in the polymerase region.
Abstract: 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).
Hepatitis B surface antigen variants in vaccinees, blood donors and an interferon-treated patient.
Abstract: One child had a double mutation (P142S and G145R) and the other a G145A substitution.
Abstract: 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).
Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC).
Abstract: 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.
Abstract: 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.
Abstract: 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 t
Cross-resistance testing of antihepadnaviral compounds using novel recombinant baculoviruses which encode drug-resistant strains of hepatitis B virus.
PMID: 11353615
2001
Antimicrobial agents and chemotherapy
Abstract: 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.
Abstract: 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.
HBV mutation literature information.
PMID: 
2002
Zhonghua shi yan he lin chuang bing du xue za zhi
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