期刊
CELL
卷 140, 期 3, 页码 397-U143出版社
CELL PRESS
DOI: 10.1016/j.cell.2010.01.020
关键词
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资金
- FEBS
- Human Frontier Science Program
- Baxter and Alma Ricard Foundation
- Biotechnology and Biological Sciences Research Council
- MRC
- Wellcome Trust
- European Union (FLUINNATE)
- Cancer Research UK
- MRC [G0700848] Funding Source: UKRI
- Medical Research Council [G0700848] Funding Source: researchfish
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 50-triphosphates constitute the natural RIG-I agonists that trigger cell-intrinsic innate immune responses during infection.
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