| Literature DB >> 28636969 |
Yang Qiu1, Yanpeng Xu2, Yao Zhang3, Hui Zhou4, Yong-Qiang Deng2, Xiao-Feng Li2, Meng Miao4, Qiang Zhang5, Bo Zhong5, Yuanyang Hu5, Fu-Chun Zhang6, Ligang Wu3, Cheng-Feng Qin7, Xi Zhou8.
Abstract
RNA interference (RNAi) functions as a potent antiviral immunity in plants and invertebrates; however, whether RNAi plays antiviral roles in mammals remains unclear. Here, using human enterovirus 71 (HEV71) as a model, we showed HEV71 3A protein as an authentic viral suppressor of RNAi during viral infection. When the 3A-mediated RNAi suppression was impaired, the mutant HEV71 readily triggered the production of abundant HEV71-derived small RNAs with canonical siRNA properties in cells and mice. These virus-derived siRNAs were produced from viral dsRNA replicative intermediates in a Dicer-dependent manner and loaded into AGO, and they were fully active in degrading cognate viral RNAs. Recombinant HEV71 deficient in 3A-mediated RNAi suppression was significantly restricted in human somatic cells and mice, whereas Dicer deficiency rescued HEV71 infection independently of type I interferon response. Thus, RNAi can function as an antiviral immunity, which is induced and suppressed by a human virus, in mammals.Entities:
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Year: 2017 PMID： 28636969 DOI： 10.1016/j.immuni.2017.05.006
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745