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Basic Characteristics of Mutations
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Mutation Site
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G1764A |
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Mutation Site Sentence
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The frequencies of HBV mutations (A1762T/G1764A, G1896A, C2063A, A2131C, and C2304A) are summarized in Table 1. |
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Mutation Level
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Nucleotide level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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BCP |
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Standardized Encoding Gene
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Genotype/Subtype
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B;C |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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Liver Cirrhosis
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Immune
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Y |
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Target Gene
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CD274
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Clinical and Epidemiological Correlations
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Clinical Information
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Y |
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Treatment
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- |
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Location
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China |
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Literature Information
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PMID
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32860707
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Title
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Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion
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Author
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Wu JF,Chang KC,Ni YH,Hsu HY,Chang MH
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Journal
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The Journal of infectious diseases
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Journal Info
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2021 Apr 23;223(8):1381-1389
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Abstract
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BACKGROUND: We investigated the relationships among the percentage of hepatitis B virus (HBV) mutations and liver fibrosis after hepatitis B e antigen (HBeAg) seroconversion. METHODS: We quantified the percentage of HBV mutants by pyrosequencing using serum samples obtained at inflammatory phase and after HBeAg seroconversion in 160 initially HBeAg-positive chronic HBV-infected patients. The relationships between antiviral agents, percentages of HBV mutations, and liver stiffness measurements (LSMs) were analyzed. RESULTS: We demonstrated that the percentages of A1762T/G1764A mutation are significantly higher in subjects with an LSM >7 kPa than in those with an LSM =7 kPa after HBeAg seroconversion. Hepatitis B e antigen seroconversion age is positively correlated with the percentages of A1762T/G1764A mutation at inflammatory phase before HBeAg seroconversion. Subjects who underwent interferon, entecavir, or tenofovir disoproxil fumarate therapy before HBeAg seroconversion possessed a lower percentage of A1762T/G1764A mutation after HBeAg seroconversion. The percentage of A1762T/G1764A >/=20% after HBeAg seroconversion was predictive of an LSM >7 kPa (hazard ratio = 6.37, P = .001). The presence of A1762T/G1764A led to downregulated messenger ribonucleic acid and protein levels of programmed-death ligand-1 (PD-L1) in hepatocytes. CONCLUSIONS: The percentage of A1762T/G1764A mutations after HBeAg seroconversion was associated with liver fibrosis. The A1762T/G1764A mutation may evoke hepatic inflammation by suppressing PD-L1 in hepatocytes.
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Sequence Data
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-
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