title: Antiviral innate immunity and stress granule responses.
abstract: Viral infection triggers the activation of antiviral innate immune responses in mammalian cells. Viral RNA in the cytoplasm activates signaling pathways that result in the production of interferons (IFNs) and IFN-stimulated genes. Some viral infections have been shown to induce cytoplasmic granular aggregates similar to the dynamic ribonucleoprotein aggregates termed stress granules (SGs), suggesting that these viruses may utilize this stress response for their own benefit. By contrast, some viruses actively inhibit SG formation, suggesting an antiviral function for these structures. We review here the relationship between different viral infections and SG formation. We examine the evidence for antiviral functions for SGs and highlight important areas of inquiry towards understanding cellular stress responses to viral infection.
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Onomoto
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan.
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Yoneyama
authors.affiliation: University of British Columbia (UBC) James Hogg Research Center, Providence Heart and Lung Institute, St. Paul's Hospital and Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Fung
authors.affiliation: Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan; Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8507, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Kato
authors.affiliation: Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan; Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8507, Japan. Electronic address: tfujita@virus.kyoto-u.ac.jp.
authors.forename: Takashi
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000818:Animals; D003594:Cytoplasmic Granules / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000235:genetics / Q000378:metabolism*; D066263:Protein Aggregation, Pathological; D012367:RNA, Viral / Q000276:immunology; D012261:Ribonucleoproteins / Q000378:metabolism*; D015398:Signal Transduction; D013312:Stress, Physiological / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology*
chemical_list: D012367:RNA, Viral; D012261:Ribonucleoproteins; D007372:Interferons
keywords: dsRNA; innate immunity; interferon; shut-off; stress granules; virus infection