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).
Successful rescue therapy with tenofovir in a patient with hepatic decompensation and adefovir resistant HBV mutant.
Conclusion: Sequencing of the HBV polymerase revealed two common lamivudine resistant mutations - rtL180M and rtM204V.
Conclusion: Two adefovir resistant mutations, rtA181T and rtN236T, were detected, whereas previous lamivudine resistant mutations, rtL180M and rtM204V, were absent.
Discussion: reported recently decreased in vitro susceptibility to both tenofovir and adefovir of two HBV resistant mutants (N236T adefovir and
Inhibition of hepatitis B virus (HBV) replication by pyrimidines bearing an acyclic moiety: effect on wild-type and mutant HBV.
PMID: 16539393
2006
Journal of medicinal chemistry
Abstract: These compounds were also found to retain sensitivity against lamivudine-resistant HBV containing a single mutation (M204I) and double mutations (L180M/M204V).
Characteristics of drug resistant HBV in an international collaborative study of HIV-HBV-infected individuals on extended lamivudine therapy.
Abstract: The triple polymerase mutant (rtL173V, rtL180M, rtM204V), which behaves as a vaccine escape mutant in vitro, occurred in 17% of viraemic patients.
HBV mutation literature information.
PMID: 
2007
Journal of clinical microbiology
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