Method: Additionally, some of above BALB/c nude mice were also given TGFbeta1(Peprotech, UK) at the dose of 2 ng/ml 20 g via tail vein injection to clarify whether TGF-beta/Smad pathway was involved in the tumorigenicity of HBV-rtA181T/sW172* mutant.
Method: The first part was to investigate and compare the tumorigenesis of different overlapping S gene mutation (sW172L and sW172*) on rtA181T mutant strain in vitro and in vivo.
Discussion: And this finding is also consistent with the clinical increased risk of developing HCC in PMID: 29315352
2018
PloS one
Method: As previously described, we used the Mutation Reporter Tool (MRT) software (http://hvdr.bioinf.wits.ac.za/mrt/) to look for HBV resistance-associated mutations (RAMs) in the Polymerase catalytic domain represented by major RAMs (A181T/V/S, A194T, M204V/I/S and N236T) and compensatory RAMs (I169T, V173L, L180M, S202G/I and M250V.
Evolution of drug-resistant mutations in HBV genomes in patients with treatment failure during the past seven years (2010-2016).
Abstract: Among the primary NA-resistant mutations, rtM204I (13.44%, 545/4055) occurred more frequently, followed by rtM204V, rtN236T, rtA181T, and rtA181V.
Abstract: Frequencies of rtL180M and rtA181T/V increased gradually in the past seven years, to which we should pay more attention.
Stop codons in the hepatitis B surface proteins are enriched during antiviral therapy and are associated with host cell apoptosis.
Abstract: Cell lines were transfected with infectious HBV clones encoding surface stop codons rtM204I/sW196*, rtA181T/sW172*, rtV191I/sW182*, and a panel of substitutions in the surface proteins.
Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA.
Introduction: reported that the rtA181T/sW172stop (sW172*) variant had a secretory defect and exerted a dominant negative effect on wild-type (WT) HBV virion secretion.
Analysis of the prevalence of drug-resistant hepatitis B virus in patients with antiviral therapy failure in a Chinese tertiary referral liver centre (2010-2014).
PMID: 28017671
2017
Journal of global antimicrobial resistance
Abstract: and genotype C isolates had a significantly higher A181V/T incidence than genotype B (54.9% vs.
HBV quasispecies composition in Lamivudine-failed chronic hepatitis B patients and its influence on virological response to Tenofovir-based rescue therapy.
Result: Direct sequencing of the PCR amplified RT domain of HBV/D from 16 LMV-failed patients demonstrated the presence of well-known LMV resistance mutations, rtM204V/I, rtL180M, rtS202G, rtL80I and rtA181T, either singly or in combinations.
Result: In the remaining 4 (25%) patients, the multi-drug resistant mutation rtA181T was identified.
Result: The rtA181T variant was detected in 10-40% of the HBV clones from four LMV-failed patients while the clo
Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer.
Discussion: The W172* mutation is associated with resistance to nucleos(t)ide analogues and secondary to substitution in the reverse trancriptase (RT) domain of the P protein (rtA181T/ sW172*).
HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining.
Introduction: According to several clinical practice guidelines and authoritative reviews, NUCr substitutions can be classified into two categories: primary NUCr substitutions at 8 codons (rtI169T, rtA181T/V, rtT184A/C/F/G/I/L/M/S,
Discussion: This suggests that these atypical substitutions might not play important roles in the emergence of NUCr as compared to rtA181T/V, rtS202C/G/I, rtM204I/V and rtM250I/L/V.
Genotyping of HBV and tracking of resistance mutations in treatment-naive patients with chronic hepatitis B.
HBV mutation literature information.
PMID: 
2018
Virology journal
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