2013 Fiscal Year Final Research Report
Antiviral factor AID/APOBECs and Hepatitis B virus-related hepatocellular carcinogenesis
| Project/Area Number |
23790780
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Keywords | ウイルス / がん |
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| Research Abstract |
Recent studies have revealed that AID/APOBEC cytidine deaminase family members can induce C-to-U hypermutation on viral genome and restrict replication of various types of virus including HBV. Uracil residues in DNA are removed by base excision repair (BER) enzyme, uracil DNA glycosylase (UNG) when cytidine deamination is occurred in host genome.Here, we investigated whether uracil residues were removed by UNG from HBV and DHBV DNAs using in vitro cell culture system. When UNG activity was inhibited by the expression of UNG inhibitory protein (UGI), the APOBEC3G-mediated hypermutation of HBV nucleocapsid DNA was enhanced. The enhanced hypermutation by APOBEC3G and UGI was also observed in DHBV cccDNA, which was more frequent than in nucleocapsid DNA. We also found that overexpression of chicken AID caused hypermutation and reduction of DHBV cccDNA levels. These results indicate that UNG excises uracils from viral genome deaminated by AID/APOBEC protein during or after cccDNA formation.
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[Journal Article] Interleukin-1 and tumor necrosis factor-alpha trigger restriction of hepatitis B virus infection via a cytidine deaminase AID2013
Author(s)
Watashi K, Liang G, Iwamoto M, Marusawa H, Uchida N, Daito T, Kitamura K, Muramatsu M, Ohashi H, Kiyohara T, Suzuki R, Li J, Tong S, Tanaka Y, Murata K, Aizaki H, Wakita T
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Journal Title
J Biol Chem
Volume: 288 (44)
Pages: 31715-31727
DOI
Peer Reviewed
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