生物
仙台病毒
核糖核酸
病毒
病毒学
干扰素
病毒复制
RNA病毒
先天免疫系统
RNA依赖性RNA聚合酶
核糖核酸酶P
非编码RNA
RNA编辑
亚基因组mRNA
钻机-I
引导RNA
基因
环状RNA
长非编码RNA
抄写(语言学)
遗传学
免疫系统
作者
Jan Rehwinkel,Choon Ping Tan,Delphine Goubau,Oliver Schulz,Andreas Pichlmair,Katja Bier,Nicole C. Robb,Frank T. Vreede,William Barclay,Ervin Fodor,Caetano Reis e Sousa
出处
期刊:Cell
[Elsevier]
日期:2010-02-01
卷期号:140 (3): 397-408
被引量:494
标识
DOI:10.1016/j.cell.2010.01.020
摘要
RIG-I is a key mediator of antiviral immunity, able to couple detection of infection by RNA viruses to the induction of interferons. Natural RIG-I stimulatory RNAs have variously been proposed to correspond to virus genomes, virus replication intermediates, viral transcripts, or self-RNA cleaved by RNase L. However, the relative contribution of each of these RNA species to RIG-I activation and interferon induction in virus-infected cells is not known. Here, we use three approaches to identify physiological RIG-I agonists in cells infected with influenza A virus or Sendai virus. We show that RIG-I agonists are exclusively generated by the process of virus replication and correspond to full-length virus genomes. Therefore, nongenomic viral transcripts, short replication intermediates, and cleaved self-RNA do not contribute substantially to interferon induction in cells infected with these negative strand RNA viruses. Rather, single-stranded RNA viral genomes bearing 5′-triphosphates constitute the natural RIG-I agonists that trigger cell-intrinsic innate immune responses during infection.
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