title: [Chronic hepatitis C virus infection attenuates host antiviral innate immune response].
abstract: The innate immune system is essential for controlling viral infection. Hepatitis C virus (HCV) is a causative agent of hepatocellular carcinoma. HCV evades host innate immune response and maintains persistent infection. RIG-I is a cytoplasmic viral RNA sensor and triggers the innate immune response. The Riplet ubiquitin ligase mediates K63-linked polyubiquitination of RIG-I, which is essential for RIG-I activation. Previous studies have shown that HCV NS3-4A protease cleaves RIG-I adaptor MAVS to escape host antiviral response. However, MAVS cleavage is supposed to be not sufficient for viral chronicity. Recently, we found that NS3-4A cleaves both MAVS and Riplet to attenuate RIG-I activation. These findings indicate that HCV NS3-4A cleaves several proteins to shut off antiviral innate immune response.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Oshiumi
authors.forename: Misako
authors.initials: M
authors.lastname: Matsumoto
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Seya
mesh_terms: D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000502:physiology; D019698:Hepatitis C, Chronic / Q000276:immunology*; D007113:Immunity, Innate / Q000502:physiology; D007372:Interferons / Q000096:biosynthesis; D011971:Receptors, Immunologic; D017361:Viral Nonstructural Proteins / Q000502:physiology; D012324:RNA-Dependent RNA Polymerase
chemical_list: D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases; D007372:Interferons; D011971:Receptors, Immunologic; D017361:Viral Nonstructural Proteins; C087036:NS-5 protein, hepatitis C virus; D012324:RNA-Dependent RNA Polymerase; C452820:RIGI protein, human