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Basic Characteristics of Mutations
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Mutation Site
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G1896A |
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Mutation Site Sentence
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Variants in the precore (G1896A) and core promoter (A1762T, G1764A) regions of hepatitis B virus (HBV) may be related to serum HBV DNA levels and severity of liver disease. |
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Mutation Level
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Nucleotide level |
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Mutation Type
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Nonsense mutation |
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Gene/Protein/Region
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PreC |
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Standardized Encoding Gene
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C
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Genotype/Subtype
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- |
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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 Diseases
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Immune
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- |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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- |
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Location
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US |
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Literature Information
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PMID
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12939588
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Title
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Prevalence of HBV precore/core promoter variants in the United States
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Author
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Chu CJ,Keeffe EB,Han SH,Perrillo RP,Min AD,Soldevila-Pico C,Carey W,Brown RS Jr,Luketic VA,Terrault N,Lok AS
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Journal
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Hepatology (Baltimore, Md.)
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Journal Info
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2003 Sep;38(3):619-28
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Abstract
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Variants in the precore (G(1896)A) and core promoter (A(1762)T, G(1764)A) regions of hepatitis B virus (HBV) may be related to serum HBV DNA levels and severity of liver disease. The aims of this nationwide study were to determine the prevalence of HBV precore/core promoter variants in the United States and the association between these variants and patient demographics, HBV genotypes, serum HBV DNA level, and severity of liver disease. A total of 694 consecutive chronic HBV-infected patients seen in 17 U.S. liver centers during a 1-year period were enrolled. Demographic, clinical, and laboratory data were collected. Sera were tested for HBV genotypes as well as precore and core promoter variants by line-probe assays. Quantitative HBV DNA levels were determined using Cobas Amplicor HBV Monitor kits. Precore and core promoter variants were found in 27% and 44% of patients with chronic HBV infection in the United States. Precore and core promoter variants were more common in hepatitis B e antigen (HBeAg)-negative than in HBeAg-positive patients (precore, 38% vs. 9%; core promoter, 51% vs. 36%; respectively, P <.001). The prevalence of these variants was related to ethnicity, place of birth, and HBV genotypes. Patients with core promoter variants were more likely to have hepatic decompensation. Precore and/or core promoter variants were associated with higher serum HBV DNA levels in HBeAg-negative but not in HBeAg-positive patients. In conclusion, HBV precore and core promoter variants are not rare in the United States. Physicians should be aware of the existence of HBV precore and core promoter variants and the clinical condition of ""HBeAg-negative chronic hepatitis.
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Sequence Data
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-
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