Abstract: rtL80I/V-rtL180M-rtV173L), whilst most primary mutations (including rtM204V-rtA181T/V-rtI169T-rtA194T) are associated with low genetic barrier.
Characterization of Hepatitis B virus polymerase mutations A194T and CYEI and tenofovir disoproxil fumarate or tenofovir alafenamide resistance.
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: CONCLUSIONS: PC or BCP mutations increased HBV DNA replication, offset the decreased replication by rtA194T alon
Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs.
Abstract: HBV reverse-transcriptase (RT) region was sequenced and analyzed for 20 mutations, confirmed by in vitro studies as associated with resistance to nucleos(t)ide HBV-RT inhibitors (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-
Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies.
Introduction: For example, studies demonstrated that the rtA194T mutation in the HBV genome led to a decrease in HBV replication capacity with TDF treatment; however, additional and more long-term data investigating the effects of TDF treatment on HBV resistance are needed .
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Method: In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V.
Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T
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, S85A, A194T, A200V, V214A, Q215S, I233V, P237H and NASH238TD.
Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B.
PMID: 20382061
2010
International journal of infectious diseases
Abstract: Interestingly, the treatment-naive patients had preexisting drug resistance mutations related to lamivudine (rtL180M+rtM204I), adefovir (rtA181V, rtQ215S, rtI233V), entecavir (intermediate susceptibility with rtL180M+rtM204IHBV variant), telbivudine (rtL180M+rtM204I), and tenofovir (rtA194T).
Naturally occurring amino-acid substitutions to nucleos(t)ide analogues in treatment naive Turkish patients with chronic hepatitis B.
Abstract: The rtA194T mutation in association with lamivudine resistance may confer resistance to TDF, although both in vivo and in vitro studies regarding this mutation demonstrate conflicting results.
Method: Another study reported of 5 HBV-infected patients also harboring the rtA194T mutation in association with LAM-resistance.
Method: In contrast, in a study by Delaney et al the rtA194T mutation, whether or not in combination with LAM-resistant mutations, did not confer resistance to TDF in vitro.
Method: In one patient a HBV subpopulation with mutations rtM204V, rtL180M, a
Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients.
PMID: 19301976
2009
The Journal of infectious diseases
Method: Established NRTI-resistance mutations included the following RT mutations: rtL80V/I, rtI169T, rtV173L, rtL180M, rtA181TV, rtT184S/A/I/L/F/G, rtA194T, rtS202G/I, rtM204V/I/S, rtN236T, and rt
ViMRT
HBV mutation literature information.
PMID: 
2011
Digestive and liver disease
