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 PMID: 15259898
2004
Antiviral therapy
Abstract: Although all patients responded to ADV in this clinical study, the serum HBV reduction was lower in the seven patients with the triple mutation (median -3.3 log copies/ml) compared to the patients who had only the rtL180M/M204V mutations (median -4.1 log copies/ml) at week 48 (P=0.04, Mann-Whitney test).
Abstract: For ADV and TDF, comparison of wild-type and lamivudine-resistant HBV IC50 (rtL180M-M204V) showed, respectively, 2.85-fold (from 0.07 to 0.2 microM) and 3.3-fold (from 0.06 to 0.2 microM) increases, indicating a mild decrease of both drug activities, in vitro.
Abstract: In a clinical study of ADV (Gilead 460i study), seven of the 35 patients carried HBV strains with the triple lamivudine resistance-associated amino-acid changes PMID: 15261293
2004
Bioorganic & medicinal chemistry letters
Abstract: Molecular modeling studies of adefovir diphosphate with the wild type and the mutant HBV polymerase-DNA complex demonstrated that the increase in adefovir sensitivity toward HBV polymerase mutants (rtL180M, rtM204V/I, rtL180M-M204V/I) is a result of increased van der Waals interaction and is supplemented by the decreased affinity of natural substrate toward the mutant HBV polymerase.
Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants.
Abstract: Resistance to LMV (rtM204I/rtL180M+rtM204V) was accompanied by a reduced replication efficacy as evidenced by reduced pregenomic RNA, encapsidated progeny DNA, polymerase activity, and virion release.
Abstract: Treatment of chronic HBV infection with lamivudine (LMV) often selects drug-resistant strains with single (rtM204I) or double (rtL180M+rtM204V) point mutations in the YMDD motif of HBV reverse transcr
HBV mutation literature information.
PMID: 
2005
Alimentary pharmacology & therapeutics
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