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PLoS One. 2012;7(8):e43031. doi: 10.1371/journal.pone.0043031. Epub 2012 Aug 13.

Critical role of an antiviral stress granule containing RIG-I and PKR in viral detection and innate immunity.

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  • 1Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.

Erratum in

  • PLoS One. 2013;8(4). doi:10.1371/annotation/14a6b875-ed9d-41ae-8ce6-52e8c5c7f85b.

Abstract

Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs) function as cytoplasmic sensors for viral RNA to initiate antiviral responses including type I interferon (IFN) production. It has been unclear how RIG-I encounters and senses viral RNA. To address this issue, we examined intracellular localization of RIG-I in response to viral infection using newly generated anti-RIG-I antibody. Immunohistochemical analysis revealed that RLRs localized in virus-induced granules containing stress granule (SG) markers together with viral RNA and antiviral proteins. Because of similarity in morphology and components, we termed these aggregates antiviral stress granules (avSGs). Influenza A virus (IAV) deficient in non-structural protein 1 (NS1) efficiently generated avSGs as well as IFN, however IAV encoding NS1 produced little. Inhibition of avSGs formation by removal of either the SG component or double-stranded RNA (dsRNA)-dependent protein kinase (PKR) resulted in diminished IFN production and concomitant enhancement of viral replication. Furthermore, we observed that transfection of dsRNA resulted in IFN production in an avSGs-dependent manner. These results strongly suggest that the avSG is the locus for non-self RNA sensing and the orchestration of multiple proteins is critical in the triggering of antiviral responses.

PMID:
22912779
[PubMed - indexed for MEDLINE]
PMCID:
PMC3418241
Free PMC Article

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