Abstract: Complex mutational patterns characterized by the co-presence of rtM204V/I-rtA181T/V (impairing the efficacy of all anti-HBV drugs) were detected in four patients (2.7%) with virological rebound.
Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients.
Abstract: An additional five patients developed entecavir genotypic resistance, with prior occurrence of lamivudine-resistant mutation (L180 M +- M204 V/I).
Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B.
Abstract: In patient 5, M204V/I was detected in 1% and 2% of clones, respectively.
Introduction: The main mutation associated with LAM resistance is rtM204I/V.
Discussion: Pre-existing LAM-resistance mutation, rtM204V/I, was found in 3% (3/100) of clones in patient 5, whereas rtL180M mutation was detected in 1% (1/100) of clones in patient 1 and 2.
Discussion: The finding that more diverse HBV quasispecies was identified in LAM-failure patients than in LAM-responding patients and that the frequency of pre-existing M204V/I substitution was not different between two groups suggests that degree of overall viral quasispecies rather than M204
Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen.
Abstract: Furthermore, the HBsAg-mutation sP217L, silent in RT, significantly correlated with M204V/I-related virological-breakthrough and increased HBsAg-quantification in cell-lysate.
Lamivudine-resistant HBV strain rtM204V/I in acute hepatitis B.
Abstract: A plasma sample obtained at the first observation was tested for HBV mutants in the polymerase region by direct sequencing; the antiviral drug-resistant rtM204V/I mutations, the most frequent HBV mutants in Italy, were also sought by the more sensitive allele-specific polymerase chain reaction (PCR).
Abstract: AIMS: To detect HBV rtM204V/I lamivudine-resistant strains in serum of patients with acute hepatitis B and to assess their biological and clinical significance.
Abstract: CONCLUSI
Abstract: Compared with those with the HBV wild strain, patients with rtM204V/I more frequently showed severe acute hepatitis B (36.4% vs 8.7%; p < 0.05) and lower values of serum HBV DNA (1.77 x 10(6) +- 4.76 x 10(6) vs.
Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients.
Abstract: CONCLUSIONS: Long-term clevudine monotherapy is effective for suppression of serum HBV DNA level and normalization of serum alanine amino transaminase levels, but associated with occurrence of rtM204I mutation.
Abstract: The rtM204I mutation in HBV polymerase was predominantly detected.
Result: Of 24 cases with the rtM204I mutation, three had co-dominant rtM204I and rtL180M mutations.
Result: One patient had a mixed pattern of rtM204I/V and rt PMID: 23892239
2013
Journal of acquired immune deficiency syndromes (1999)
Abstract: HBV pol sequencing demonstrated M204I (n = 3) and N236T (n = 1) resistance-associated mutations in 4 of 8 (50%) lamivudine-treated participants and none in tenofovir-treated participants.
Dynamics of hepatitis B virus resistance substitutions correlates with virological response in lamivudine-refractory patients with entecavir rescue monotherapy.
Abstract: LMV-resistant mutations (rtL180M and/or rtM204VI) were detected in 9 patients before ETV treatment and not in another 5 patients before and after the treatment.
[Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year].
Abstract: In five of nine samples primary and compensatory multiple mutations (L180M + M204I in one sample, L80I + L180M + M204I in two samples, L80I/V + M204I in one sample) and primary single mutations associated with LVD resistance (M204I/V) in four samples were detected by Inno-Lipa HBV DRv2.
Abstract: Multiple mutations that comprise L180M + M204I in four and L180M + M204V in one sample and single mutations (M204I) in three samples were identified by SEQ.