HBV mutation literature information.


  Global prevalence and phylogeny of hepatitis B virus (HBV) drug and vaccine resistance mutations.
 PMID: 33893696       2021       Journal of viral hepatitis
Discussion: For example, RAMs in HBV reverse transcriptase, A181T/V, M204I and M204V, cause corresponding changes in the overlapping region of HBsAg (W172 stop, W196S/L/Stop and I195M, respectively).


  A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion.
 PMID: 34852809       2021       Journal of biomedical science
Figure: A Polymerase mutants YIDD created corre
Figure: B No apparent defect in virion secretion was detected in two polymerase YIDD mutants containing envelope mutations W196L and W196S, respectively.
Discussion: As a side note, it is worth mentioning here that neither envelope W196L nor W196S could support HDV virion secretion.


  A recombinant human immunoglobulin with coherent avidity to hepatitis B virus surface antigens of various viral genotypes and clinical mutants.
 PMID: 32790777       2020       PloS one
Result: Because the entire S gene is embedded within the viral polymerase gene, some viral polymerase mutations that confer drug resistance can cause amino acid sequence changes in HBsAg; major ones include E164D, W172L, L173F, I195M and W196L/S/V.


  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
Introduction: rtM204I is a common 3TC-resistant mutation emerging in antiviral therapy, and may result in truncation or missense mutations on the overlapping surface gene (sW196*/S/L).
Discussion: As for rtM204I/sW196* (YIDDst in this study), a mutant less commonly encountered than rtM204I/sW196S/L (* 8.2%, L 76.4%, S 10.2%, and L/S 5.1%) in 3TC or Telbivudine-experienced patients, we proved that YIDDst-transfected cells presented a transformation and tumorigenesis potential.


  Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia.
 PMID: 32915862       2020       PloS one
Abstract: Resistance mutations included rtL80I, rtV173L, rtL180M, rtM204I/V and the overlapping sE164D, sW182*, s
Discussion: Lamivudine resistance mutations detected in the RT region resulted in sE164D, sI195M, and sW196L/S changes in the surface gene.


  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
Result: In the present study, the most prevalent mutations were those in the S region (sP120Q, sQ129R, sT131I, sM133I, sG145R, sY161F/H, sI195M/T, sW196S/L, sW199C/L and sM213I/T; Table III).


  Characterization and Clinical Significance of Natural Variability in Hepatitis B Virus Reverse Transcriptase in Treatment-Naive Chinese Patients by Sanger Sequencing and Next-Generation Sequencing.
 PMID: 31189581       2019       Journal of clinical microbiology
Introduction: For instance, I195M in the S protein (sI195M) and sW196S can produce rtM204I and rtL180M/rtM204I in RT, which could confer resistance to LMV.


  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: RT mutations rtN139K/T/H and rtM204I/V also cause simultaneous mutations in the overlapped HBsAg coding sequence ( Method: The mutations rtA181T/V, rtM204I, and rtM204V also cause the simultaneous HBsAg mutations, sW172 stop, sW196S/L/Stop, and sI195M, respectively (Table 1).


  Amino acid similarities and divergences in the small surface proteins of genotype C hepatitis B viruses between nucleos(t)ide analogue-naive and lamivudine-treated patients with chronic hepatitis B.
 PMID: 24316031       2014       Antiviral research
Abstract: With little influence on immune escape-associated mutation frequencies within 'a' determinant, LMV-monotherapy significantly induced classical LMVr-associated mirror changes sE164D/rtV173L, sI195M/rtM204V and sW196L/S/rtM204I, as well as non-classical ones sG44E/rtS53N, sT47K/A/rt


  Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants.
 PMID: 24053482       2013       Virology journal
Result: Similarly, the differences in avidity (as determined by the slope of the curve) was indistinguishable between the sT118M mutant and sT118M-rtM204V (sT118M- sW196S) mutant for all five assays, suggesting that drug-resistant YMDD mutants caused a negligib
Figure: rtM204V (sW196S) mutation also reduced the recognition of sG145R HBsAg in ELISA kits WT and BN.



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