Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes.
PMID: 33562603
2021
International journal of molecular sciences
Discussion: Nevertheless, some recent studies have shown that rtS78T/sC69*, rtS106C/rtH126Y/rtD134E/rtL269I, and rtL180M/T184L/M204V/rtA200V are related to TDF resistance.
Analysis of HBsAg mutations in the 25 years after the implementation of the hepatitis B vaccination plan in China.
Abstract: HBV strains with internal stop codons of HBsAg (e.g., sC69*) and additional N-glycosylation (e.g., sG130N) mutations should be studied extensively to prevent them from becoming dominant circulating strains.
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.
Abstract: In addition, all the clones harbored another nonsense mutation in the S gene (C69*) and a 207nt in-frame deletion in the preS1 region.
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Introduction: Moreover, HBV rtL269I and rtS78 T/sC69stop mutations were respectively reported being associated with enhanced viral replication of LAMr mutants and insufficient response to ETV treatment.
Association of HBsAg mutation patterns with hepatitis B infection outcome: Asymptomatic carriers versus HCC/cirrhotic patients.
Abstract: A number of truncation-related mutations were higher in HCC/Cirrhotic group (P>0.001), albeit only C69* stop codon was statistically significant (P=0.003).
Abstract: CONCLUSION: The higher frequency of substitutions in MHR and immune epitopes at positions such as Y134 and P120 as well as stop codons such as C69* in HCC/cirrhotic group might candidate them as predictive factors for infection outcome.
The Effect of the Hepatitis B Virus Surface Protein Truncated sC69* Mutation on Viral Infectivity and the Host Innate Immune Response.
Abstract: Functional studies showed that sC69* mutant was associated with lower viral spread, but could be rescued by coexisting with the WT.
Abstract: Here, a mutant of sC69* in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69* was 4.37% (19/435), most of which coexisted with the WT (78.95%, 15/19), indicating mixed viral populations.
Abstract: Our data provide information that sC69* coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host.
Abstract: The lower immune response was not caused by the lower replication of <
The Effect of the Hepatitis B Virus Surface Protein Truncated sC69* Mutation on Viral Infectivity and the Host Innate Immune Response.
Abstract: All mutations simultaneously created a stop codon at sC69 (sC69*).
Abstract: The HBV DNA and RNA levels of the rtS78T/sC69* mutant were significantly increased compared to the wild-type; while the mutant had undetectable secreted and intracellular HBsAg, and its half maximal effectiv
Abstract: The data obtained in the present study suggested that the emergence of the rtS78T/sC69* mutation was not closely related to entecavir/tenofovir treatment and itself appeared insufficient to confer drug resistance unless it coexisted with signature drug-resistance mutations.
Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA.
Abstract: Some mutations (e.g., sE2G, sL21S, sR24K, sT47A/K, sC69stop (sC69*), sL95W, sL98V, and sG145R) negatively correlated with serum HBsAg levels.
Abstract: Virion secretion could be rescued for sE2G, sC
Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer.
Discussion: The G72* and Q121* nonsense mutations in the preS region could explain the lack of L protein expression and HBsAg negative phenotype of clones 12.1, 12.3, 8.3, and 8.4, while the C69* and S61* nonsense mutations in the S region were confirmed to abolish HBsAg production.
HBV mutation literature information.
PMID: 
2021
International journal of molecular sciences
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