Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity

Exposure to hepatitis C virus (HCV) usually results in persistent infection that often develops into chronic liver disease. Interferon-alpha (IFN) treatment comprises the foundation of current approved therapy for chronic HCV infection but is limited in overall efficacy. IFN is a major effector of i...

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Main Authors: Helene Minyi Liu, Michael Gale
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:Gastroenterology Research and Practice
Online Access:http://dx.doi.org/10.1155/2010/548390
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author Helene Minyi Liu
Michael Gale
author_facet Helene Minyi Liu
Michael Gale
author_sort Helene Minyi Liu
collection DOAJ
description Exposure to hepatitis C virus (HCV) usually results in persistent infection that often develops into chronic liver disease. Interferon-alpha (IFN) treatment comprises the foundation of current approved therapy for chronic HCV infection but is limited in overall efficacy. IFN is a major effector of innate antiviral immunity and is naturally produced in response to viral infection when viral pathogen-associated molecular patterns (PAMPs) are recognized as nonself and are bound by cellular pathogen recognition receptors (PRRs), including Toll-like receptors (TLRs) and the RIG-I-like receptors (RLRs). Within hepatocytes, RIG-I is a major PRR of HCV infection wherein PAMP interactions serve to trigger intracellular signaling cascades in the infected hepatocyte to drive IFN production and the expression of interferon-stimulated genes (ISGs). ISGs function to limit virus replication, modulate the immune system, and to suppress virus spread. However, studies of HCV-host interactions have revealed several mechanisms of innate immune regulation and evasion that feature virus control of PRR signaling and regulation of hepatic innate immune programs that may provide a molecular basis for viral persistence.
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spelling doaj-art-11247bf381fc4c769686435b558a53a92025-02-03T01:12:10ZengWileyGastroenterology Research and Practice1687-61211687-630X2010-01-01201010.1155/2010/548390548390Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate ImmunityHelene Minyi Liu0Michael Gale1Department of Immunology, School of Medicine, University of Washington, Seattle, WA 98195-7650, USADepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98195-7650, USAExposure to hepatitis C virus (HCV) usually results in persistent infection that often develops into chronic liver disease. Interferon-alpha (IFN) treatment comprises the foundation of current approved therapy for chronic HCV infection but is limited in overall efficacy. IFN is a major effector of innate antiviral immunity and is naturally produced in response to viral infection when viral pathogen-associated molecular patterns (PAMPs) are recognized as nonself and are bound by cellular pathogen recognition receptors (PRRs), including Toll-like receptors (TLRs) and the RIG-I-like receptors (RLRs). Within hepatocytes, RIG-I is a major PRR of HCV infection wherein PAMP interactions serve to trigger intracellular signaling cascades in the infected hepatocyte to drive IFN production and the expression of interferon-stimulated genes (ISGs). ISGs function to limit virus replication, modulate the immune system, and to suppress virus spread. However, studies of HCV-host interactions have revealed several mechanisms of innate immune regulation and evasion that feature virus control of PRR signaling and regulation of hepatic innate immune programs that may provide a molecular basis for viral persistence.http://dx.doi.org/10.1155/2010/548390
spellingShingle Helene Minyi Liu
Michael Gale
Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
Gastroenterology Research and Practice
title Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
title_full Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
title_fullStr Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
title_full_unstemmed Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
title_short Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity
title_sort hepatitis c virus evasion from rig i dependent hepatic innate immunity
url http://dx.doi.org/10.1155/2010/548390
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