Abstract: 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.
Abstract: 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.
Current aspects of hepatitis B surface antigen mutants in Singapore.
Abstract: These vaccine-escape HBsAg mutants display a predominance of the Gly145-to-Arg145 mutation in the antigenic 'a' determinant.
Association of mutations in the core promoter and precore region of hepatitis virus with fulminant and severe acute hepatitis in Japan.
PMID: 9870800
1998
Journal of gastroenterology and hepatology
Abstract: 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.
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.
Abstract: 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).
Abstract: 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.
Abstract: This mutation results in a Met-to-Val substitution at amino acid 539 of the polymerase.
Abstract: 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-res
Hepatitis B virus genomic sequence in the circulation of hepatocellular carcinoma patients: comparative analysis of 40 full-length isolates.
Abstract: 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.
Nucleic acid sequence analysis of the precore region of hepatitis B virus from sera of southern African black adult carriers of the virus.
Abstract: 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.
Infectivity and pathogenicity in chimpanzees of a surface gene mutant of hepatitis B virus that emerged in a vaccinated infant.
PMID: 9041321
1997
The Journal of infectious diseases
Abstract: 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.
Genotype F prevails in HBV infected patients of hispanic origin in Central America and may carry the precore stop mutant.
Abstract: 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.
Detection of hepatitis B surface gene mutation in carrier children with or without immunoprophylaxis at birth.
PMID: 9237708
1997
The Journal of infectious diseases
Abstract: A precore mutant (G to A) at nucleotide 1896 was detected in sera from 11 carriers without vaccination.
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.
PMID: 9267007
1997
The Journal of general virology
Abstract: 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.
HBV mutation literature information.
PMID: 
1998
Hepatology (Baltimore, Md.)
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