Discussion: sW182* causes termination in the SHB gene, leading to intracellular accumulation of HBsAg protein; which may increase apoptosis of hepatocytes, potentially driving hepatocarcinogenesis.
Discussion: Selection of the sW182 stop codon (sW182*) arose from rtV191I.
Discussion: Though the diagnostic sensitivity of APRI to identify liver fibrosis is relatively low (reported to be around 47%), it is worth noting that this patient also harboured HBV mutations associated with severe liver disease including s<
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
Discussion: Other researchers also identified sW182* in HCC tissues, and demonstrated its enhanced tumorigenesis and migration ability in vitro.
Discussion: The downregulated TGFbi expression was revealed by cDNA microarray study of the sW182*-transfected cells due to the hypermethylation of its promoter.
Discussion: This finding coincided with that in the sW182* study by Jiang et al.
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
Conclusion: Downregulated TGFbi not only contributes to oncogenicity in sW196*-transfected cells, but also in other preS/S* (sW172* and sW182*) cells, suggesting a common oncogenic mechanism shared by the Discussion: C-terminal truncated surface gene mutations, including sW172*, sW182*, and sW196* in this study, coincidentally resulted in TGFbi downregulation in transfected-cells, which presented transforming characteristics and mouse xenograft tumorigenesis.
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Method: These AA sites were sE2, sL21, sR24, sT47, sI68, sC69*, sC76, sL95, sL98, sS117, sR122, sI126, sG145R, sV177, sW182*, sM198, sI218, and sV224.
A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1.
Abstract: Although the sW182* protein appeared not to be very stable in the cultured liver cells, we confirmed that the protein can be highly expressed and retained for a prolonged period of time in the hepatocytes in the mouse liver, indicating its stable nature in the physiological condition.
Abstract: Here, we expressed in a liver cell line Huh-7 a carboxy terminally truncated protein from a nonsense mutant of the LHBs gene, sW182* (stop codon at tryptophane-182).
Abstract: In the Huh-7 cells, the sW182* mutant downregulated tumor suppressors p53 and Smad4.
Abstract: On the other hand, we found that c-Jun activation domain-binding protein 1 (Jab1) physically interacts with the s
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*, s Discussion: Similar to previous studies, the present study suggested that truncation mutations (rtA181T/sW172*, rtM204I/sW196* and rtV191I/sW182*) occurred at the highest frequency.
The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response.
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: reported that sW182* mutant showed lower HBV DNA levels and existed preferentially in older patients.
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.
The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-beta/Smad signaling pathway.
Discussion: Lee et al.found that the percentage of S-phase cells increased in the presence of HBV rtV191I/sW182* as compared to that in the presence of wide-type HBV, and the possible mechanism may be associated with the down-regulation of p53 and p21 and up-regulation of Cyclin A and CDK4 gene expressions, which also could promote cells from G1 phase to S phase thus accelerating cell proliferation.
Discussion: has been reported that the presence of HBV rtV191I/sW182* mutant may induce cell canceration via inhibiting TGFBI expression and increasing CyclinD1expression.
Quasispecies variant of pre-S/S gene in HBV-related hepatocellular carcinoma with HBs antigen positive and occult infection.
Result: Differences in the major populations were attributed to the I126S/T, Y200F/S, and Y206C/H/S mutations, while those in the minor populations were attributed to the L21F/S, L42F/S, W182Stop, and L213F/I/T mutations.
HBV mutation literature information.
PMID: 
2020
PloS one
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