Abstract: Resistance mutations included rtL80I, rtV173L, rtL180M, rtM204I/V and the overlapping sE164D, sW182*, sI195M and sW196LS variants.
Result: Amino acid changes including rtL80I, rtV173L, rtL180M,
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: 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.
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 i
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 Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease.
PMID: 30406036
2018
Frontiers in cellular and infection microbiology
Introduction: The pre-S2 mutation F141L and the pre-S1 mutation W182*, leading to the premature termination of HBsAg, are reportedly associated with more severe HBV infection (Mun et al.,; Lee et al.,).
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.
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.
HBV mutation literature information.
PMID: 
2020
PloS one
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