Emergence of a novel mutation in the FLLA region of hepatitis B virus during lamivudine therapy.
PMID: 15980328
2005
Antimicrobial agents and chemotherapy
Abstract: The major mechanism of resistance has been attributed to the alteration in the YMDD motif of the HBV polymerase due to an amino acid change of rtM204 to V/I and an accompanying rtL180M conversion.
Response to long-term lamivudine treatment (up to 5 years) in patients with severe chronic hepatitis B, role of genotype and drug resistance.
Abstract: To investigate this in vitro, we generated novel stable cell lines expressing HBV encoding the four major patterns of lamivudine resistance mutations (rtL180M+rtM204V, rtV173L+rtL180M+rtM204V, rtM204I and rtL180M+ rtM204I).
Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis.
Abstract: RESULTS: 'Polymerase region': M204V/I variants were found in all group A patients, but in none of group B1 (P=0.0007) and in four of nine of group B2 (44%; P=0.02) patients.
Selection of hepatitis B virus polymerase mutations in HIV-coinfected patients treated with tenofovir.
Abstract: Phenotypic analyses revealed that constructs harbouring rtA194T combined with rtL180M and rtM204V displayed an over 10-fold increase in the IC50 for TDF compared with the wild type.
Hepatitis B virus DNA quantitation and detection of core promoter, precore and polymerase mutations in chronic hepatitis B: evaluation and clinical usefulness of three new commercial assays.
Abstract: affigene HBV mutant VL (positions G1764A, G1896A) and affigene HBV DE/3TC (positions rtL180M, rtM204V/I) were able to detect a low presence of mutants in a mixed population (wild type and mutant) compared to direct sequencing and Inno-LIPA HBV DR, which identified only the dominant population.
Heart transplantation in patients with chronic hepatitis B: clinical evolution, molecular analysis, and effect of treatment.
Abstract: Lamivudine treatment was initially effective in all patients; three patients during the second year of treatment developed lamivudine resistance-associated mutations (rt-L180M, rt-M204V) with severe disease reactivation, remitted after switch to adefovir treatment.
Clinical features of chronic hepatitis B patients with YMDD mutation after lamivudine therapy.
PMID: 16358376
2005
Journal of Zhejiang University. Science. B
Abstract: Four types of YMDD mutation were observed in this study, rtL180M/M204V mutation was the predominant type (26/63, 41.3%).
Abstract: Add-on adefovir therapy is effective in suppressing rtM204 I/V in both compensated and decompensated patients.
Abstract: However, HBV species with mutations in the tyrosine-methionine-aspartate-aspartate (YMDD) locus of the HBV RNA-dependent DNA polymerase (rtM204 I/V) conferring resistance to lamivudine may emerge after 9-10 months therapy.
Abstract: Serum alanine aminotransferase (ALT) elevation and HBV DNA rebound ( I log) occur in >90% of the patients with rtM204 I/V during continued lamivudine therapy.
No benefit to continue lamivudine therapy after emergence of YMDD mutations.
Abstract: AIM: To evaluate whether continuing lamivudine therapy after emergence of rt M 204 I/V is appropriate.
Abstract: BACKGROUND: Mutations in the sequence of the conserved tyrosine-methionine-aspartate-aspartate (YMDD) locus of the HBV RNA-dependent DNA polymerase (rt M 204 I/V) may develop after 6-9 months of lamivudine therapy.
Abstract: CONCLUSION: These results suggest that there is no benefit to continued lamivudine therapy after emergence of rt M 204 I/V.
Abstract: In addition, experiments have shown that the defective replication competency of rt
ViMRT
HBV mutation literature information.
PMID: 
2005
Antimicrobial agents and chemotherapy
