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Basic Characteristics of Mutations
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Mutation Site
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I253R |
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Mutation Site Sentence
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Three additional amino acid changes were observed outside B‐Cell and T‐cell epitopes (Table IV, Fig. 1). Also, nine polymorphic changes were identified in the HBsAg domain; L8H, C19S/F, L21W, Q30R, S31N, S34L, C76Y, I208T, and Y221C; and four in the RT domain; H13Y, N139H, I163V, and I253R (Figs. 1 and 2). |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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RT |
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Standardized Encoding Gene
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P
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Genotype/Subtype
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G;H |
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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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Hepatitis B, Chronic
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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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Y |
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Treatment
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- |
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Location
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Mexico |
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Literature Information
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PMID
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25732900
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Title
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New amino acid changes in drug resistance sites and HBsAg in hepatitis B virus genotype H
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Author
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Fernandez-Galindo DA,Sanchez-Avila F,Bobadilla-Morales L,Gomez-Quiroz P,Bueno-Topete M,Armendariz-Borunda J,Sanchez-Orozco LV
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Journal
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Journal of medical virology
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Journal Info
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2015 Jun;87(6):985-92
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Abstract
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Long-term treatment with retrotranscriptase (RT) inhibitors eventually leads to the development of drug resistance. Drug-related mutations occur naturally and these can be found in hepatitis B virus (HBV) carriers who have never received antiviral therapy. HBsAg are overlapped with RT domain, thus nucleot(s)ide analogues (NAs) resistance mutations and naturally-occurring mutations can cause amino acid changes in the HBsAg. Twenty-two patients with chronic hepatitis B were enrolled; three of them were previously treated with NAs and 19 were NAs-naive treated. HBV reverse transcriptase region was sequenced; genotyping and analysis of missense mutations were performed in both RT domain and HBsAg. There was predominance of genotype H. Drug mutations were present in 18.2% of patients. Classical lamivudine resistance mutations (rtM204V/rtL180M) were present in one naive-treatment patient infected with genotype G. New amino acid changes were identified in drug resistance sites in HBV strains from patients infected with genotype H; rtQ215E was present in two naive-NAs treatment patients and rtI169M was identified in a patient previously treated with lamivudine. Mutations at sites rt169, rt204, and rt215 resulted in the Y161C, I195M, and C206W mutations at HBsAg. Also, new amino acid changes were identified in B-cell and T-cell epitopes and were more frequent in HBsAg compared to RT domain. In conclusion, new amino acid changes at antiviral resistance sites, B-cell and T-cell epitopes in HBV genotype H were identified in Mexican patients.
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Sequence Data
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-
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