title: Viral RNA detection by RIG-I-like receptors.
abstract: In higher vertebrates, recognition of the non-self signature of invading viruses by genome-encoded pattern recognition receptors initiates antiviral innate immunity. Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) detect viral RNA as a non-self pattern in the cytoplasm and activate downstream signaling. Detection of viral RNA also activates stress responses resulting in stress granule-like aggregates, which facilitate RLR-mediated antiviral immunity. Among the three RLR family members RIG-I and melanoma differentiation-associated gene 5 (MDA5) recognize distinct viral RNA species with differential molecular machinery and activate signaling through mitochondrial antiviral signaling (MAVS, also known as IPS-1/VISA/Cardif), which leads to the expression of cytokines including type I and III interferons (IFNs) to restrict viral propagation. In this review, we summarize recent knowledge regarding RNA recognition and signal transduction by RLRs and MAVS/IPS-1.
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8673, Japan. Electronic address: myoneyam@faculty.chiba-u.jp.
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Yoneyama
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, 1-8-1, Inohana, Chuo-ku, 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, 1-8-1, Inohana, Chuo-ku, Chiba 260-8673, Japan.
authors.forename: Michihiko
authors.initials: M
authors.lastname: Jogi
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8673, Japan.
authors.forename: Teppei
authors.initials: T
authors.lastname: Akaboshi
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; D053487:DEAD-box RNA Helicases / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D010766:Phosphorylation; D011485:Protein Binding; D012367:RNA, Viral / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction; D013312:Stress, Physiological; D025801:Ubiquitin / Q000378:metabolism
chemical_list: D012367:RNA, Viral; D025801:Ubiquitin; D053487:DEAD-box RNA Helicases