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Basic Characteristics of Mutations
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Mutation Site
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M204I |
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Mutation Site Sentence
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Trans-Complementation of HBV rtM204I mutant replication by HBV wild-type polymerase |
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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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- |
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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 Virus Infection
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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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Lamivudine(LAM) |
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Location
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- |
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Literature Information
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PMID
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19383566
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Title
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trans-Complementation of HBV rtM204I mutant replication by HBV wild-type polymerase
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Author
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Heipertz RA Jr,Starkey JL,Miller TG,Hu J,Isom HC
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Journal
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Virology
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Journal Info
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2009 May 25;388(1):57-67
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Abstract
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The function of the hepatitis B virus (HBV) wild-type (WT) polymerase (pol) expressed alone or in the context of the intact genome when interacting with HBV rtM204I in HepG2 cells was compared. We show that WT pol expression from a packaging-defective RNA can complement defective rtM204I pol activity resulting in increased levels of HBV replicative intermediates (RI). Analysis of the genetically marked genomes showed that this restoration resulted from trans-complementation, rather than recombination. In contrast, we demonstrate that enhanced levels of total HBV RI observed when cells were cotransduced with both WT and rtM204I baculoviruses were predominantly WT RI. In this case, WT pol was produced from a full-length pregenomic RNA (pgRNA). We conclude that the WT pol has the capacity to trans-complement the replication defect of rtM204I; however, when expressed from an authentic pgRNA, as in a mixed infection, pol may not trans-complement efficiently.
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Sequence Data
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-
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