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).
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: The rtM204I/sW196* transformants, compared with the control or wild type, showed enhanced transactivation activities for c-fos, increased cell proliferation, decreased apoptosis, more anchorage-independent
Abstract: The rtM204I/sW196* preS/S truncation may endorse the cell transformation and tumorigenesis ability via altered host gene expressions, including MGST2, HIF1A, and TGFbi.
Abstract: The oncogenicity of another drug-resistant mutant, rtM204I/sW196*, has not been studied.
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
Complementation of Wild-Type and Drug-Resistant Hepatitis B Virus Genomes to Maintain Viral Replication and Rescue Virion Production under Nucleos(t)ide Analogs.
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.
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 (sT131N/P and sI195M, or sW196S/L/Stop).
Method: The mutations rtA181T/V, rtM204I, and rtM204V also cause the simultaneous HBsAg mutations,
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.
Abstract: The most cytopathic variant was rtM204I/sW196*.
Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia.
Discussion: Similar mutations induced by antiviral treatment resulting in a truncated protein have been reported in other studies, such as W196* (31 amino acid deletion) and W172* (55 amino acid deletion).
Nucleos(t)ide analogues causes HBV S gene mutations and carcinogenesis.
PMID: 27919846
2016
Hepatobiliary & pancreatic diseases international
1Abstract: DATA SOURCES: PubMed and Web of Science were searched using terms: ""hepatitis B virus"", ""HBV drug resistance mutation"", ""HBV surface protein"", ""HBV truncation"", ""hepatocellular carcinoma"", ""rtA181T/sW172*"", ""rtM204I/sW196*"", ""rtV191I/sW182*"", and relevant articles published in English in the past decades were reviewed."
Abstract: RESULTS: The rtA181T/s
Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma.
Discussion: Among the 11 HBV S gene truncation mutants we have identified (sL15*, sL21*, sS61*, sC69*, sL95*, sW156*, sW163*, sW172*, sW182*, sW196*, and sL216*) in HBV-related PMID: 22314422
2012
Journal of hepatology
Abstract: As expected, mutants harboring a sW196Stop mutation in the surface gene did not express small envelope proteins.
HBV mutation literature information.
PMID: 
2021
Journal of viral hepatitis
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