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).


  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.
 PMID: 32840739       2020       Virus genes
Abstract: The rtA181T mutation caused the W172* nonsense mutation in the overlapping S gene.


  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.
Introduction: We investigated four such mutants (sL15*, sL21*, sW156*, and sW172*) in our 3TC-experienced HCC cases for their nearby locations to the transactivity-on-region, and proved sL15*,  PMID: 30866789       2019       Emerging microbes & infections
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.


  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.
 PMID: 30882363       2019       Antiviral therapy
Abstract: Interestingly, the rtA181T-causative sW172stop to sW172non-stop mutation transition was observed at HBV DNA fluctuations.


  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: Furthermore, three out of five stop codons in the S region (sS34*, sW74*, sW172*, sW182*, sW196*) were identified in the RT region; the stop codons have been associated with NAs resistance, also affected the HBsAg reading frame (rtA181T/sW172*, rtV191I/sW182* and


  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
Table: W172stop


  Complementation of Wild-Type and Drug-Resistant Hepatitis B Virus Genomes to Maintain Viral Replication and Rescue Virion Production under Nucleos(t)ide Analogs.
 PMID: 31218588       2019       Virologica Sinica
Abstract: In the present study, HBV genomes with frequently detected reverse transcriptase (RT)/surface truncation MTs, rtA181T/sW172*, rtV191I/sW182* and rtM204I/sW196*, were phenotypically characterized alone or together with their WT counterparts in different ratios by transient transfection in the absence or presence of NAs.


  The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response.
 PMID: 31249567       2019       Frontiers in microbiology
Introduction: Recently, it was shown that HBsAg truncated mutants such as sW172*, sW182*, and sW199* occurred in patients both with and without antiviral treatment.
Introduction: Similarly, it was also shown that HBV WT rescued the replication and secretion of variants such as sW172*, sW182*, and sC69*.
Discussion: showed that sW172* mutant could be rescued by WT for secretion.


  Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure.
 PMID: 31527514       2019       Viruses
Method: In addition, two more variants were used as controls, the SHB D144E which could be found in both groups and the SHB W172*, and its impact on HBsAg secretion has been already described before.
Method: In detail, a Strep-tag HBsAg genotype D was cloned in the pEXPR-IBA 44 (iba-lifesciences) Vector and was subsequently used as a template to generate the HBsAg mutants, D144E, W172* and L216*.
Result: A similar pattern was observed for the W172* mutant.



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