Method: All sequences with completely replaced mt were further determined based on an HBV-drug resistance interpretation online tool of Max Planck Institute for Informatics for classical mt, e.g., rtL180M, rtA181V/T, rtT184G/L, rtA194T, rtS202I/G, rtM204I/V, rtN236T, and rtM250I/V, and based on updated references for nonclassical/putative mt, e.g., V207I/M/L,
Prevalence of Potential Resistance Related Variants Among Chinese Chronic Hepatitis B Patients Not Receiving Nucleos(T)ide Analogues.
Abstract: Primary and secondary DR variants were found in 7.3% (15/206) of patients, including rtL80I/V, rtI169T
Result: Primary and/or secondary DR variants were found in 7.3% (15/206) of patients, and included rtL80I/V, rtI169T, rtV173L, rtL180M, rtA181T/V, rtM204I/V, and rtN236T.
Table: A181V/T
Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi.
PMID: 32887289
2020
International journal of molecular sciences
Abstract: Some of these mutants introduce premature stop codons in the overlapping surface (s) gene, including rtA181T/sW172*, which has been shown to enhance oncogenicity.
Discussion: Previously, we identified rtA181T/sW172* in HCC patients, either 3TC-treated or -naive.
An antiviral drug-resistant mutant of hepatitis B virus with high replication capacity in association with a large in-frame deletion in the preS1 region of viral surface gene.
Abstract: Mutation(s) in the polymerase gene responsible for ADV resistance included rtA181T (all clones) and rtN236T (four clones).
Abstract: The rtA181T mutation caused the W172* nonsense mutation in the overlapping S gene.
Mutational characterization of HBV reverse transcriptase gene and the genotype-phenotype correlation of antiviral resistance among Chinese chronic hepatitis B patients.
Abstract: rtV191I and rtA181T/V were the only resistance mutations identified as genotype-specific mutation.
Result: After scrutinizing the frequency of mutations within these sites, only two NA-r mutations, ntG700A (rtV191I, P = 0.014) and ntC671T (rtA181T/V, P = 0.048) from treatment-naive and post-treatment samples, respectively, were identified as genotype-specific mutations (Figure 3(C-D)).
Result: Five AA sites identified with the significantly elevated entropy levels were rtL180M, rt PMID: 33381105
2020
Frontiers in microbiology
Method: According to the most recent clinical practice guidelines of the European Association for the Study of the Liver, the following amino acid substitution profiles for HBV
Result: Overall, rtL180M, rtA181T/V, rtT184G/S, rtS202G/I, rtM204I, rtM204V, rtN236T, and rtM250V were more frequently detected in genotypes A (13.9%), C (0.8%), D (0.1%), H (3.8%), G (25%), A (13.1%), B (0.7%), and C (0.1%), respectively.
[Determination of reverse transcriptase inhibitor nucleoside analogue resistance profile in pretreatment phase of patients with viral hepatitis B].
Abstract: Primary drug resistance mutations such as rtI169T, rtA181T/V, rtT184A/C/F/G/I/L/M/S, rtA194T, rtS202C/G/I, rtM204I/V/S, rtN236T, rt M250I/L/V and rtV173L were not detected in any of the patient samples.
Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy.
PMID: 30906435
2019
Experimental and therapeutic medicine
Introduction: ADV-resistance has been associated with the rtN236T mutation in the D domain and/or the rtA181V/T mutation in the B domain.
Discussion: rtA181T was detected in one patient in the RS group.
Discussion: Similar to previous studies, the present study suggested that truncation mutations (rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182*)
Molecular cloning and phenotypic analysis of drug-resistance mutants with relevant S-region variants of HBV for a patient during 189-month anti-HBV treatment.
Discussion: It has been suggested rt181 mutation (rtA181 T/V) is involved in a shared pathway for resistance of sev
Discussion: Unlike rtA181 T mutation which may cause sW172stop and non-stop (sW172S, sW172L) mutations and the stop mutation will delete an HLA-A2-restricted s172-180 (env335-343) epitope of cytotoxic T lymphocytes (CTL) the rtA181C mutation only caused sW172C mutation in this study without deleting the CTL epitope.
HBV mutation literature information.
PMID: 
2020
Diagnostics (Basel, Switzerland)
Browser Board
Co-occurred Entities
Filtrator
ViMRT