Abstract: L180M/M204V mutations were identified during virological breakthrough.
In vitro drug susceptibility analysis of hepatitis B virus clinical quasispecies populations.
PMID: 17687019
2007
Journal of clinical microbiology
Abstract: 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.
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.
Abstract: 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.
Abstract: 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.
Abstract: The rt
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.
PMID: 17913933
2007
Journal of clinical microbiology
Abstract: 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).
Successful treatment of an entecavir-resistant hepatitis B virus variant.
Abstract: 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.
Abstract: 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
Efficacy of hepatitis B virus (HBV) vaccination in treating lamivudine-resistant HBV reactivation following hepatitis B surface antigen seroconversion.
Result: One (209-CW) displayed the double rtL180M-rtM204V lamivudine-resistance mutation and the other (043-N) showed an additional rtV173L mutation,
Table: M204V
Discussion: 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).
Selection of hepatitis B virus (HBV) vaccine escape mutants in HBV-infected and HBV/HIV-coinfected patients failing antiretroviral drugs with anti-HBV activity.
PMID: 18167643
2007
Journal of acquired immune deficiency syndromes (1999)
Abstract: 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.
Genotypic resistance to lamivudine among hepatitis B virus isolates in Mexico.
PMID: 16373428
2006
The Journal of antimicrobial chemotherapy
Abstract: 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.
Dynamics of hepatitis B virus resistance to lamivudine.
Abstract: 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).
HBV mutation literature information.
PMID: 
2007
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