HBV mutation literature information.


  rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome.
 PMID: 33803998       2021       Microorganisms
Abstract: We also found that there are a total of 19 signature single nucleotide polymorphisms (SNPs), of which 2 and 17 nonsynonymous mutation types were specific to rt269L and rt269I, respectively: Of these, most are HBeAg negative infections (preC-W28*, X-V5M and V131I), lowered HBV DNA or virion production (C-I97F/L, rtM204I/V) or preexisting nucleot(s)ide analog resistance (NAr) (rtN139K/H, rtM204I/V and


  Entecavir resistance in a patient with treatment-naive HBV: A case report.
 PMID: 33903819       2021       Molecular and clinical oncology
Discussion: There were 8 mutations in the RT region, rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V and rtM309K that were significantly associated with the progression of HCC in treatment-naive patients.


  Potential resistant mutations within HBV reverse transcriptase sequences in nucleos(t)ide analogues-experienced patients with hepatitis B virus infection.
 PMID: 31147594       2019       Scientific reports
Result: In case three, multiple mutation patterns were observed from L180M + M204V + I224V + N238H to L180M + M204V + T184S + I224V + N238H under LAM and ADV combined therapy, which developed resistance to ETV.
Result: In this study, non-classical mutations were observed in 29 patients who suffering from virological breakthrough and without classical mutations (Table 4) at 9 sites (V191I, V207I/M, S213T, E218D, F221Y, I224V, L229V<


  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
Abstract: Eight mutations in RT (rtL80I, rtD134N, rtN139K/T/H, rtY141F, rtM204I/V, rtF221Y, rtI224V, and rtM309K) are significantly associated with HCC progression.
Method: Of note, the following four putative or pretreatment mutations found in treatment naive patients, rt PMID: 26825915       2016       Medicine
Abstract: In addition to the common substitutions, unknown amino acid substitutions, such as rtL145 M/S, rtF151Y/L, rtR153Q, rtI224 V, rtN248H, rtS223A, rtS256C, need to be further verified.
Result: However, several other variants fluctuated at relatively high levels (ranging from 3.56% to 7.89%), including rtN248H, rtS223A,  PMID: 27602500       2016       Oncotarget
Result: The frequencies of the rtI224V, rtS223A, rtD134E mutations slowly increased after 4 year of treatment.
Result: The frequency of the rtI224V mutation increased slowly.
Result: The frequency of the rtI224V mutation was always high (70-80%) (Figure 8B).


  Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection.
 PMID: 26457811       2015       PloS one
Result: Amino acid substitutions in mother include T16I, R41S, V44A,N53S, H55R, W58R, N76D, S81T, V103I, G107E, N121I, I122L, N123D, Q125K, H126Y, N134D, N139H, N139Q, Y158H, I163V, F178L, S185N, V207M


  Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma.
 PMID: 24788140       2014       PloS one
Result: A799G and T1055A are missense mutations resulting in aa substitutions of I224V and M309K, and A987G is a synonymous mutation.
Table: I224V
Discussion: A799G and T1055A are missense mutations that cause rtI224V and rtM309K aa substitutions, respectively, in RT.


  Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population.
 PMID: 23409946       2013       Virology journal
Introduction: Pretreatment mutations (such as T38A, Y124H, D134E, N139K/H, I224V, and R242A) were defined as amino acid substitutions that have been reported among NA-naive patients but their relationships with antiviral resistance development have not been clarified yet.
Table: I224V


  Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues.
 PMID: 19302908       2009       Clinical therapeutics
Abstract: We also detected several polymorphic sites,including rtF221Y, rtS223A, rtI224V, rtN238H, rtL267Q, and rtQ271M, during the sequential treatment.



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