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.
Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies.
Abstract: Clinical prognosis-related genetic variations such as nucleotide mutation T1762/A1764 (27.93%), A2189C (12.85%), G1613A (8.94%), T1753C (8.38%), T53C (4.47%) T3098C (1.68%) and PreS deletion (2.23%) were detected in CD recombinants.
Table:
Table: A1516C
Table: A1762T
Table: A1984G
Table: A2075G
Table: A2189C
Table: A3057G
Table: A3108G
Table: A942T
Table: C129T
In silico Analysis of Genetic Diversity of Human Hepatitis B Virus in Southeast Asia, Australia and New Zealand.
Abstract: The three HBV variants identified most frequently were p.V5L, c.1896G>A and double mutation c.1762A>T/c.1764G>A, while genotypes B and C had the widest range of mutation types.
Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection.
Abstract: Through application of deep whole-genome sequencing we typed the isolate as genotype-D1, and identified several minority variants including G1764A and G1986A substitutions in the pre-core promoter and pre-core regions, which support CHB-AR rather than AHB.
Table: A128V
Table: A1762T
Table: C1766T/T
Table: C1799G
Table: G145R
Table: G1764A
Table: G1896A
Table: G1899A
Prolyl Isomerase Pin1 Regulates the Stability of Hepatitis B Virus Core Protein.
PMID: 32083080
2020
Frontiers in cell and developmental biology
Result: Although above Phos-tag analysis indicated that S162 is the major site of the Pin1-binding phosphorylation site (Figure 1B), we found that a single site-directed mutant (S162A) still interacted with Pin1 with relatively lower binding activity.
Result: Amounts of HBV DNA and HBcAg, but not HBeAg devoid of Pin1-binding site, were significantly reduced in the case of the T160A/S162A virus relative to the WT virus (Figures 6D-F).
Result: Cells expressing either HA-tagged WT HBc or the T160A/S162A mutant were processed for the immunoblot analysis with anti-pHBc or anti-HA antibody.
Result: Cycloheximide analysis demonstrated that the HBc-
A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro.
Abstract: These NLGSs are located in the major hydrophilic region of HBsAg (known to be the target of antibodies) and resulted from the single mutation T115N, T117N, T123N, N114ins, and from the triple mutant S113N+T131N+M133T.
Discussion: Considering the N-linked glycosylation sites observed in our study, recent studies have shown that the mutational profile T131N+M133T reduces HBsAg antigenicity and fails to induce anti-HBs response without altering HBV replicative capacity.
Discussion: Furthermore, another study has shown that the N-linked glycosylation site
[The prevalence clinically significant virus mutations among patients with chronic viral hepatitis B.]
Abstract: Another 12.5% of the isolates are characterized by mutations that are independently associated with the liver cirrhosis and hepatocellular carcinoma development, including 21, 24, 27 nucleotides deletions in the Pre-S2 region and the S11F mutation in the PreCore region.
Entecavir-resistant hepatitis B virus decreases surface antigenicity: A full genome and functional characterization.
Abstract: Additionally, the ETV resistance mutations rtT184A/L, rtS202G and rtM250V were found among three patients.
Abstract: More importantly, the rtI169T mutation in the RT domain, led to the sF161L mutation in the overlapping S gene, which decreased in surface antigenicity.
Abstract: RESULTS: The rtL180M + rtM204V mutations were common among all the clones analysed.
Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection.
Abstract: E2G might cause HBsAg secretion impairment that results in intracellular accumulation and a decrease in HBsAg secretion.
Abstract: Five of the ten mutations (E2G, D144E, G145R, V168A and S174N) strongly decreased extracellular HBsAg level (P < .05) in the transfection system.
Abstract: Hence, ten mutations were associated with genotype B occult HBV infection; E2G and V168A were novel mutations which we confirmed significantly affect HBsAg detection.
Abstract: Notably, the E2G
Molecular characterization of hepatitis B virus isolated from Black South African cancer patients, with and without hepatocellular carcinoma.
Abstract: The following mutations were significantly more frequent in HCC cases than in controls (p < 0.05): in the BCP/PC 1753C/G (22.5% vs. 0%), 1764A (69.4% vs. 38.1%), and T64C (51.5% vs. 20%) in the preS2, which results in a F22L substitution.
HBV mutation literature information.
PMID: 
2020
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