Detection of lamivudine- or adefovir-resistant hepatitis B virus mutations by a liquid array.
PMID: 21513743
2011
Journal of virological methods
Abstract: A novel polymerase chain reaction (PCR)-Luminex assay was developed for rapid, accurate, and high-throughput detection of the most important hepatitis B virus (HBV) variants, including those with reverse transcriptase (RT) domain L180M, M204I/V, A181T/V/S, I233V and N236T mutations associated with resistance to lamivudine (LAM) or adefovir (ADV).
Detection of hepatitis B virus variants in HBV monoinfected and HBV/HIV coinfected Iranian patients under lamivudine treatment.
Abstract: While no resistance mutation was detected in HBV/HIV coinfected cohort, LAM-resistance mutations (rtM204I/V in YMDD and rtL180M in FLLA polymerase motifs) were identified in 30% (9 out of 30) and 16.66% (5 out of 30) of HBV monoinfected patients (P<0.05).
HBV primary drug resistance in newly diagnosed HIV-HBV-coinfected individuals in Spain.
Abstract: Drug-resistant mutations in the HBV polymerase were found in four (5.5%) patients: two harboured rtL180M, one rtL80V and one rtV173L.
Large-scale survey of naturally occurring HBV polymerase mutations associated with anti-HBV drug resistance in untreated patients with chronic hepatitis B.
Abstract: HBV mutations associated with antiviral drug resistance were detected in 13 (5%) patients: three patients infected with HBV genotype C had the rtM204V + rtL180M mutations associated with lamivudine (LMV) resistance.
Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations.
Abstract: At the end of the 14-year follow up period, high viral loads were predominant, with viral strains harboring the lamivudine-resistance signature rtL180M+M204V.
Abstract: The L180M+M204V dominant mutant displayed strong lamivudine-resistance.
Discussion: In presence of the rtL180M and rtM204V as well as entecavir-associated mutations, the susceptibility to entecavir decreased dramatically as seen by an increase in inhibitory concentration 50% (IC50) values from 280 to over 1500 fold.
Discussion: The combination of the rtL180M+ rt
[Variants and quasispecies of reverse transcriptase region in polymerase gene of hepatitis B virus during lamivudine treatment].
PMID: 21789847
2011
Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: The rtL180M variant was found in association with the rtM204I/V variant, HBV variants and wild-type in YMDD motif all existed together in these two groups.
Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development.
Abstract: rtL80I/V-rtL180M-rtV173L), whilst most primary mutations (including rtM204V-rtA181T/V-rtI169T-rtA194T) are associated with low genetic barrier.
The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations.
Abstract: BACKGROUND: A recent study indicated that addition of the hepatitis B e antigen (HBeAg) precore (PC) or basal core promoter (BCP) mutations to wild-type HBV offset the reduced replication of the HBV polymerase rtA194T+-rtL180M+rtM204V mutations.
Abstract: METHODS: A plasmid containing a wild-type 1.3 genome length genotype D HBV laboratory strain was used as a parent for PC, BCP, rt
The main hepatitis B virus (HBV) mutants resistant to nucleoside analogs are susceptible in vitro to non-nucleoside inhibitors of HBV replication.
Abstract: Furthermore, the effect of a combination of either AT-61 or AT-130 with BAY41-4109, and the combination of these compounds with tenofovir was studied on wild type HBV as well as on a lamivudine and an adefovir-resistant mutant (rtL180M+M204V and rtN236T, respectively).
Abstract: HepG2 stable cell lines permanently expressing wild type (WT) HBV or the main HBV mutants resistant to lamivudine and/or adefovir (rtL180M+rtM204V, rtV173L+rtL180M+rtM204V,
Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B.
Abstract: During ADV and LAM treatment, one patient developed ADV plus LAM resistance mutations (rtI163V+rtL180M+rtA181V+rtN236T), in this case, HBV strains harbouring polymerase mutations did not develop LAM associated rtM204V/I primary mutation.
Abstract: In addition, ETV resistance mutations (rtL180M+rtT184A+rtS202G+rtM204V
HBV mutation literature information.
PMID: 
2011
Journal of virological methods
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