Induction and Evasion of Innate Antiviral Responses by Hepatitis C Virus
Open Access
- 1 July 2010
- journal article
- review article
- Published by Elsevier
- Vol. 285 (30) , 22741-22747
- https://doi.org/10.1074/jbc.r109.099556
Abstract
No abstract availableKeywords
This publication has 99 references indexed in Scilit:
- Double-stranded RNA-activated protein kinase inhibits hepatitis C virus replication but may be not essential in interferon treatmentLiver International, 2009
- Toll-Like Receptor 3 Mediates Establishment of an Antiviral State against Hepatitis C Virus in Hepatoma CellsJournal of Virology, 2009
- MAVS Dimer Is a Crucial Signaling Component of Innate Immunity and the Target of Hepatitis C Virus NS3/4A ProteaseJournal of Virology, 2009
- Antiviral Suppression vs Restoration of RIG-I Signaling by Hepatitis C Protease and Polymerase InhibitorsGastroenterology, 2008
- Hepatitis C Virus Nonstructural Protein 5A Modulates the Toll-Like Receptor-MyD88-Dependent Signaling Pathway in Macrophage Cell LinesJournal of Virology, 2007
- The Interferons: 50 Years after Their Discovery, There Is Much More to LearnJournal of Biological Chemistry, 2007
- Activation of anti-hepatitis C virus responses via Toll-like receptor 7Proceedings of the National Academy of Sciences, 2006
- Distinct Poly(I-C) and Virus-activated Signaling Pathways Leading to Interferon-β Production in HepatocytesJournal of Biological Chemistry, 2005
- Crystal structure of ATF-2/c-Jun and IRF-3 bound to the interferon-β enhancerThe EMBO Journal, 2004
- Mutations in the Nonstructural Protein 5a Gene and Response to Interferon in Patients with Chronic Hepatitis C Virus 1b InfectionNew England Journal of Medicine, 1996