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.
2'-Fluoro-6'-methylene carbocyclic adenosine and its phosphoramidate prodrug: A novel anti-HBV agent, active against drug-resistant HBV mutants.
Abstract: In vitro, these molecules have demonstrated significant activity against LMV/entecavir (ETV) triple mutants (L180M + S202G + M204V).
Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation.
Abstract: 3.69-fold in half maximal effective concentration of wild-type strain); rtA181T/sW172L + rtS202G + rtM204V strain exhibited higher HBV DNA production and entecavir resistance fold than that of rtA181T/sW172* + rtS202G + rtM204V strain (50.98% vs.
Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression.
PMID: 29713126
2018
World journal of gastroenterology
Method: Our literature based pooled incidence data showed that of primary drug resistance mutations, M204I/V is the most frequently encountered in treatment-naive patients (5.89%), which was far more than the pooled mutation rate of rtA181T/V, rtS202C/G/I and rtN236T (incidence: 1.16%, 0.85% and 0.81%, respectively).
Table: S202C/G
Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis.
Result: Clonal analysis of the isolate with the rtA181C substitution from Pt23 identified the ETVr S202G substitution in the HBV RT population not observed by direct sequencing of the PCR amplicon (Supporting Table S5).
Result: Phenotypic analysis of the remaining 12 of 15 identified novel emergent substitutions indicated a reduced susceptibility to ETV (>758-fold greater than WT; Table 2) due to the presence of high-level ETVr HBV RT substitutions rtT184L, rtT184A, rtS202G, or rtM250V (Table 2).
Table: PMID: 28303969
2017
Scientific reports
Result: Among these, sT114S, sA194V and sW196L corresponded to rtF/H122L, rtS202G and rtM204V respectively.
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,
Comparison of Detection Rate and Mutational Pattern of Drug-Resistant Mutations Between a Large Cohort of Genotype B and Genotype C Hepatitis B Virus-Infected Patients in North China.
PMID: 27792585
2017
Microbial drug resistance (Larchmont, N.Y.)
Abstract: For entecavir-resistant mutations, HBV/C-infected patients had a higher detection rate of rtM204 V/I+T184 substitution or S202G/C (3.66% vs.
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: M204I, N236T and L180M+M204V+V173L/S202G were the most common substitutions for l-nucleoside (3TC and LdT), ADV and ETV genotypic resistant phenotypes, respectively.
Selection of the highly replicative and partially multidrug resistant rtS78T HBV polymerase mutation during TDF-ETV combination therapy.
3Introduction: The molecular explanation is that ETV resistance usually requires the LAM-resistant ""YMDD mutation(s)"" (rtM204V/I +-L180M) plus an additional ETV 'signature' substitution in the B domain (rtI169T or rtS184G), C domain (rtS202G/I), or E domain (rtM250V)."
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, rtA194T, rtS202C/G/I, rtM204I/V, rtN236T and rtM250I/L/V) and secondary substitutions at 3 codons in RT<
HBV mutation literature information.
PMID: 
2018
PloS one
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