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Basic Characteristics of Mutations
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Mutation Site
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A1899G |
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Mutation Site Sentence
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A homogeneous population of a pre-core mutant strain harbouring the A1896G and A1899G affecting HBeAg expression was invariably found in the liver tissue, plasma and peripheral blood mononuclear cells despite active HBeAg secretion |
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Mutation Level
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Nucleotide level |
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Mutation Type
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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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D;F |
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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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HBV-HIV Coinfection
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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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- |
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Literature Information
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PMID
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19946588
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Title
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Virological pattern of hepatitis B infection in an HIV-positive man with fatal fulminant hepatitis B: a case report
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Author
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Bagaglio S,Albarello L,Biswas P,Uberti-Foppa C,Fortis C,Morsica G
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Journal
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Journal of medical case reports
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Journal Info
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2009 Nov 9;3:110
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Abstract
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INTRODUCTION: There seem to be no published data concerning the clinical impact of populations of hepatitis B virus (HBV) in the hepatic and extrahepatic compartments of HIV-infected people with severe acute hepatitis. CASE PRESENTATION: A 26-year-old Caucasian man presenting to our hospital with clinical symptoms suggesting acute hepatitis was found to have an acute hepatitis B profile upon admission. He developed fatal fulminant hepatitis and was found to be heavily immunocompromised due to HIV-1 infection. He had a high plasma HBV and HIV load, and analysis of the partial pre-S1/pre-S2 domain showed the presence of mixed infection with D and F genotypes. Analysis of the point mutations within this region revealed the presence of HBV strains with amino acid substitutions at the immunodominant epitopes involved in B or T cell recognition. A homogeneous population of a pre-core mutant strain harbouring the A1896G and A1899G affecting HBeAg expression was invariably found in the liver tissue, plasma and peripheral blood mononuclear cells despite active HBeAg secretion; it was the dominant strain in the liver only, and was characterised by the presence of two point mutations in the direct repeat 1 domain involved in HBV replication activity. Taken together, these mutations are indicative of a highly replicative virus capable of evading immune responses. CONCLUSION: This case report provides clinical evidence of a possible association between the rapid spread of highly replicative escape mutants and the development of fulminant hepatitis in a heavily immunocompromised patient. Virological surveillance of severe acute hepatitis B may be important in establishing an early treatment strategy involving antiviral drugs capable of preventing liver failure, especially in individuals for whom liver transplantation is not accepted as a standard indication.
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Sequence Data
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-
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