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pubmed-article:20138932pubmed:dateCreated2010-3-19lld:pubmed
pubmed-article:20138932pubmed:abstractTextAPOBEC3 proteins function as part of innate antiviral immunity and induce G to A hypermutation in retroviruses and hepatitis B virus (HBV) genomes. Whether APOBEC3 proteins affect viruses that replicate without a reverse transcription step is unknown. TT virus (TTV), known to present in serum of healthy individuals and HBV carriers, has a single-stranded circular DNA genome and replicates without reverse transcription. In this study, we examined 67 blood samples obtained from healthy individuals and HBV carriers and observed G to A hypermutation of genomes of TTV in both healthy individuals and HBV carriers. During ALT flare-up in HBV carriers, G to A hypermutation of HBV increased, but TTV genomes significantly decreased in number and hypermutated TTV genomes became undetectable. Our results show that hypermutated TTV exist in healthy individuals and HBV carriers and that TTV genomes were susceptible to immune reaction directed to HBV by interacting with APOBEC3 proteins.lld:pubmed
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pubmed-article:20138932pubmed:copyrightInfo(c) 2010 Elsevier B.V. All rights reserved.lld:pubmed
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pubmed-article:20138932pubmed:volume149lld:pubmed
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pubmed-article:20138932pubmed:pagination211-6lld:pubmed
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pubmed-article:20138932pubmed:year2010lld:pubmed
pubmed-article:20138932pubmed:articleTitleG to A hypermutation of TT virus.lld:pubmed
pubmed-article:20138932pubmed:affiliationDepartment of Medicine and Molecular Science, Division of Frontier Medical Science, Programs for Biomedical Research, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.lld:pubmed
pubmed-article:20138932pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20138932pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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