Abstract: RESULTS: Forty out of the 120 patients were found to have one or two point mutations associated with drug resistance, including 17 with L180M and M204V/I mutations (42.5%), 10 with M204V/I mutation (25%), 8 with N236T mutation (20%), 3 with L180M mutation (7.5%), and 1 with both A181V/T and N236T mutations (2.5%), and 1 with A181V/T mutation(2.5%).
Convergence and coevolution of hepatitis B virus drug resistance.
Introduction: Other mutations that have been reported to be associated with lamivudine resistance include rtA181V/T and several secondary RT mutations, for example, rtV173L and rtL180M.
Result: 1) harboured additional substitution rtA181T that also confers decreased susceptibility to lamivudine and adefovir.
Discussion: HBV resistance to lamivudine is considered to be primarily associated with point mutations, such as rtM204I/V and rtA181V/T (ref.).
Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing.
Abstract: In the patients with viral rebound and ADV genotypic resistance, 19 (25.7%) showed rtA181V/T/S + rtN236T substitutions.
Abstract: Multiple logistic regression analysis showed that the rtN236T and time resistant strains occurred during ADV-treatment were statistically significant for influencing rtA181 variation types (P = 0.007 and P = 0.024, respectively), and the occurrence of rtA181T was found to be significantly earlier than rtA181V.
Abstract: Seventy-six patients (47.2%) were found to carry the rt
Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome.
Abstract: In the overlapping surface region, NA-resistant substitutions caused selection of stop codons in a significant percentage of sequences both at pre-treatment and during sequential treatment; the rtA181T substitution, related to sW172stop, predominated during treatment with lamivudine and adefovir.
Abstract: On linkage analysis of the RT region studied, NA-resistant HBV variants (except for rtA181T) were present in combinations of amino acid substitutions that increased in complexity after viral breakthrough to entecavir, at which time the combined variant rtL180M-S202G-M2
In vitro inhibition of HBV replication by a novel compound, GLS4, and its efficacy against adefovir-dipivoxil-resistant HBV mutations.
Abstract: To determine the antiviral activity of GLS4 against adefovir dipivoxil (ADV)-resistant HBV mutants, HepG2 cells transiently transfected with PUC-HBV1.2 plasmids that contained one of three major ADV-resistant mutations (rtA181T, rtA181V and rtN236T) were treated with GLS4.
Hepatitis B virus gene mutations in liver diseases: a report from New Delhi.
Abstract: 17.9% patients with cirrhosis and 24.6% hepatocellular carcinoma cases were ADV-resistant with rtA181T/V mutations in the S-gene.
Discussion: A large percentage of the cases with rtA181T mutations developed SW172stop mutations.
Discussion: Drug resistant mutations to ADV have been reported mainly in the HBV polymerase domain D rtN236T or the domain B rtA181V/T, whereas a domain D rtN236T mutation does n
Case report: management and HBV sequencing in a patient co-infected with HBV and HIV failing tenofovir.
Abstract: No known mutations, such as rtA181T/V associated with rtN236T or A194T that are associated with reduced susceptibility or resistance to tenofovir were detected.
Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients.
Abstract: METHODS: In 10 HBV-monoinfected patients (9 male, mean age 47 +-11 [range 27-67] years, 6 hepatitis B e antigen-positive) with virological breakthrough during ADV treatment associated with the mutations rtN236T and/or rtA181T/V, HBV polymerase gene variants were studied during up to 24 months of consecutive monotherapy with TDF by population sequencing, line probe assay and clonal analysis.
Abstract: To assess the clinical relevance of this cross-resistance, we studied the evolution of HBV polymerase gene variants in patients with genotypic resistance against ADV (rtN236T and/or rt<
HBV mutation literature information.
PMID: 
2012
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