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APOBEC3 deaminases induce hypermutation in human papillomavirus 16 DNA upon beta interferon stimulation
http://hdl.handle.net/2297/36486
http://hdl.handle.net/2297/36486d3910e38-f699-4149-833b-1f554fc718e5
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-KITAMURA-K-1308.pdf (555.3 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | APOBEC3 deaminases induce hypermutation in human papillomavirus 16 DNA upon beta interferon stimulation | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Wang, Zhe
× Wang, Zhe× Wakae, Kousho× Kitamura, Kouichi× Aoyama, Satoru× Liu, Guangyan× Koura, Miki× Monjurul, Ahasan M.× Kukimoto, Iwao× Muramatsu, Masamichi |
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| 書誌情報 |
Journal of Virology 巻 88, 号 2, p. 1308-1317, 発行日 2014-01-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0022-538X | |||||
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| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00708779 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1128/JVI.03091-13 | |||||
| 出版者 | ||||||
| 出版者 | American Society for Microbiology | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Apolipoprotein B mRNA-editing catalytic polypeptide 3 (APOBEC3) proteins are interferon (IFN)-inducible antiviral factors that counteract various viruses such as hepatitis B virus (HBV) and human immunodeficiency virus type 1 (HIV-1) by inducing cytidine (C)-to-uracil (U) mutations in viral DNA and inhibiting reverse transcription. However, whether APOBEC3 proteins (A3s) can hypermutate human papillomavirus (HPV) viral DNA and exhibit antiviral activity in human keratinocyte remains unknown. Here we examined the involvement of A3s in the HPV life cycle using cervical keratinocyte W12 cells, which are derived from low-grade lesions and retain episomal HPV16 genomes in their nuclei. We focused on the viral E2 gene as a potential target for A3-mediated hypermutation because this gene is frequently found as a boundary sequence in integrated viral DNA. Treatment of W12 cells with beta interferon (IFN-ß) increased expression levels of A3s such as A3A, A3F, and A3G and induced C-to-U conversions in the E2 gene in a manner depending on inhibition of uracil DNA glycosylase. Exogenous expression of A3A and A3G also induced E2 hypermutation in W12 cells. IFN-ß-induced hypermutation was blocked by transfection of small interfering RNAs against A3G (and modestly by those against A3A). However, the HPV16 episome level was not affected by overexpression of A3A and A3G in W12 cells. This study demonstrates that endogenous A3s upregulated by IFN-ß induce E2 hypermutation of HPV16 in cervical keratinocytes, and a pathogenic consequence of E2 hypermutation is discussed. © 2014, American Society for Microbiology. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
