Zinc-finger antiviral protein inhibits HIV-1 infection by selectively targeting multiply spliced viral mRNAs for degradation
文献类型：期刊论文
| 作者 | Zhu YP1,2; Chen GF1; Lv FX1; Wang XL1; Ji X1; Xu YH1; Sun J1; Wu L3; Zheng YT4; Gao GX[*]1 |
| 刊名 | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
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| 出版日期 | 2011 |
| 卷号 | 108期号:38页码:15834-15839 |
| 关键词 | retrovirus host restriction factor RNA degradation |
| 通讯作者 | gaogx@moon.ibp.ac.cn |
| 合作状况 | 其它 |
| 英文摘要 | The zinc-finger antiviral protein (ZAP) was originally identified as a host factor that inhibits the replication of Moloney murine leukemia virus. Here we report that ZAP inhibits HIV-1 infection by promoting the degradation of specific viral mRNAs. Overexpression of ZAP rendered cells resistant to HIV-1 infection in a ZAP expression level-dependent manner, whereas depletion of endogenous ZAP enhanced HIV-1 infection. Both human and rat ZAP inhibited the propagation of replication-competent HIV-1. ZAP specifically targeted the multiply spliced but not unspliced or singly spliced HIV-1 mRNAs for degradation. We provide evidence indicating that ZAP selectively recruits cellular poly(A)-specific ribonuclease (PARN) to shorten the poly(A) tail of target viral mRNA and recruits the RNA exosome to degrade the RNA body from the 3' end. In addition, ZAP recruits cellular decapping complex through its cofactor RNA helicase p72 to initiate degradation of the target viral mRNA from the 5' end. Depletion of each of these mRNA degradation enzymes reduced ZAP's activity. Our results indicate that ZAP inhibits HIV-1 by recruiting both the 5' and 3' mRNA degradation machinery to specifically promote the degradation of multiply spliced HIV-1 mRNAs. |
| 收录类别 | SCI |
| 资助信息 | This work was supported in part by National Science Foundation Grants 30530020 and 81028011, Ministry of Science and Technology 973 Program Grant 2006CB504302, and Ministry of Health of China Grant 2009ZX09501-029 (to G.G.); and by National Science Foundation Grant 30800053 and Ministry of Health of China Grant 2008ZX10001-002 (to G.C.). |
| 语种 | 英语 |
| 公开日期 | 2011-10-10 |
| 源URL | [http://159.226.149.42:8088/handle/353002/6815]  |
| 专题 | 昆明动物研究所_分子免疫药理学 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
| 作者单位 | 1.Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 2.Graduate School of the Chinese Academy of Sciences, Beijing 100049, China 3.Center for Retrovirus Research, Department of Veterinary Biosciences, Ohio State University, Columbus, OH 43210 4.Key Laboratory of Animal Models and Human Disease, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China |
| 推荐引用方式 GB/T 7714 | Zhu YP,Chen GF,Lv FX,et al. Zinc-finger antiviral protein inhibits HIV-1 infection by selectively targeting multiply spliced viral mRNAs for degradation[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,2011,108(38):15834-15839. |
| APA | Zhu YP.,Chen GF.,Lv FX.,Wang XL.,Ji X.,...&Gao GX[*].(2011).Zinc-finger antiviral protein inhibits HIV-1 infection by selectively targeting multiply spliced viral mRNAs for degradation.PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,108(38),15834-15839. |
| MLA | Zhu YP,et al."Zinc-finger antiviral protein inhibits HIV-1 infection by selectively targeting multiply spliced viral mRNAs for degradation".PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 108.38(2011):15834-15839. |
入库方式： OAI收割
来源：昆明动物研究所
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