Abstract: However, this patient experienced virological breakthrough under TDF with a HBV strain bearing rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I combined mutations without rtA194T mutation.
Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen.
Abstract: RESULTS: Ten novel RT-mutations (rtN53T-rtS78T-rtS85F-rtS135T-rtA181I-rtA200V-rtK212Q-rtL229V/F-rtM309K) correlated with specific NUC-treatments and classical drug-resistance mutations on divergent evolutionary pathways.
Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients.
Discussion: In the longitudinal study of the patient sequentially treated with LMV, ADV, and ETV monotherapies, the blind SD-based algorithm ranked the 7 NA resistance-related aa substitutions previously detected by routine analysis (rtL180M, rtM204V, rtS202G, rtV207I, rtA181T, rtV173L and rtI169T) as the most variable, and 5 additional NA resistance substitutions (rtV191I, rt
Long-term monitoring drug resistance by ultra-deep pyrosequencing in a chronic hepatitis B virus (HBV)-infected patient exposed to several unsuccessful therapy schemes.
Abstract: Both mutations were statistically associated with rtA200V and rtV207I, respectively.
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.
Conclusion: These rtA200V and rtI253V variants remained present during entecavir therapy, and were also detected in samples sequenced after breakthrough during entecavir therapy.
Discussion: The role of the rtA200V and rtI253V mutations found during lamivudine therapy is not clear.
Four-year study of lamivudine and adefovir combination therapy in lamivudine-resistant hepatitis B patients: influence of hepatitis B virus genotype and resistance mutation pattern.
Abstract: An rtA200V mutation was present in the majority of HBV clones, in addition to the 3TC-resistant mutations of rtL180M+M204V.
Abstract: In vitro analysis showed that the rtA200V mutation recovered the impaired replication capacity of the clone with the rtL180M+M204V mutations and induced resistance to ADV.
Abstract: Moreover, rtT184S and rtS202C, which are known entecavir-resistant mutations, emerged in some rtL180M
Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
Method: We also analyzed the mutations that have been reported to possibly contribute to resistance at 10 additional positions: L82M, V84M,
Result: For these mutations, a significant association with L-nucleosides was present for L82M, A200V and Q215S and an association with ANPs was present for S85A (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01).
Result: Supporting these associations were the findings that each of the viruses with L82M or A200V had one or more established L-nucleoside mutation (L180M and/or M204IV) and that each of the viruses with S85A had the ANP mutation N236T.
[Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients].
Abstract: Other resistant substitutions included rtL80V/I, rtT184S, and rtA200V, and combined mutation of triple resistant substitutions was detected in HBV RT region of 5 patients by direct sequencing.
HBV mutation literature information.
PMID: 
2014
Journal of clinical virology
Browser Board
Co-occurred Entities
Filtrator
ViMRT