1Abstract: 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."
In vivo dynamics and pathogenicity of wild-type and resistant Hepatitis B virus during long-term lamivudine monotherapy - a clinical note.
Abstract: Nineteen weeks later, the virus exhibited additional resistance-associated mutations (L528M and I552V).
Abstract: Significant genotypic resistance was detectable after 68 weeks, indicated by a substitution of isoleucine for methionine at residue 552 (M552I).
Hepatitis B virus X gene variability in French-born patients with chronic hepatitis and hepatocellular carcinoma.
1Abstract: 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."
Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance.
Abstract: Breakthrough viremia was not associated with the single L528M mutation.
Abstract: 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.
Abstract: 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 PMID: 11050059
2000
Hepatology (Baltimore, Md.)
Abstract: Determination of viral genotype, precore mutants, and polymerase gene mutants (L528M, M552V, M552I) was performed using the research version of Lipa-HBV.
Characterization of novel human hepatoma cell lines with stable hepatitis B virus secretion for evaluating new compounds against lamivudine- and penciclovir-resistant virus.
PMID: 11083647
2000
Antimicrobial agents and chemotherapy
Abstract: 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.
"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."
1Abstract: 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."
Sequence variations of precore/core and precore promoter regions of hepatitis B virus in patients with or without viral reactivation during cytotoxic chemotherapy.
Abstract: 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.
Abstract: 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).
Intra-familial evidence of horizontal transmission of hepatitis B virus surface antigen mutant G145R.
Abstract: CONCLUSIONS: The G145R mutant could be transmitted horizontally among family members, and this could occur in the presence of high levels of anti-HBs.
Abstract: Improvement of detection system for the G145R and other HBsAg mutant will be needed for their effective control.
Abstract: In addition, liver damage was seen in one G145R carrier infant.
Abstract: In families 2 and 3, the G145R mutant detected previously in child 1 was detected in the father.
Abstract: METHODS: Serum samples from family members of 10 vaccinated infants who carried this G145R mutant were collected.
Abstract: OBJECTIVES: To provide intra-familial evidence on the horizontal transmission
Analysis of HBs antigen negative variant of hepatitis B virus: unique substitutions, Glu129 to Asp and Gly145 to Ala in the surface antigen gene.
Abstract: 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.
Abstract: 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.
Abstract: 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).
HBV mutation literature information.
PMID: 
2000
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