Intracellular innate immune cascades and interferon defenses that control hepatitis C virus

J Interferon Cytokine Res. 2009 Sep;29(9):489-98. doi: 10.1089/jir.2009.0063.

Abstract

Hepatitis C virus (HCV) is a global public health problem that mediates a persistent infection in nearly 200 million people. HCV is efficient in establishing chronicity due in part to the inefficiency of the host immune system in controlling and counteracting HCV-mediated evasion strategies. HCV persistence is linked to the ability of the virus to suppress the RIG-I pathway and interferon production from infected hepatocytes, thus evading innate immune defenses within the infected cell. This review describes the virus and host processes that regulate the RIG-I pathway during HCV infection. An understanding of these HCV-host interactions could lead to more effective therapies for HCV designed to reactivate the host immune response following HCV infection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Enzyme Inhibitors / immunology
  • Enzyme Inhibitors / metabolism*
  • Gene Expression Regulation
  • Hepacivirus / pathogenicity
  • Hepacivirus / physiology*
  • Hepatitis C / genetics
  • Hepatitis C / immunology*
  • Hepatitis C / metabolism
  • Hepatitis C / virology*
  • Humans
  • Immunity, Innate*
  • Interferons / immunology*
  • Intracellular Space / immunology
  • Intracellular Space / metabolism
  • Receptors, Retinoic Acid / antagonists & inhibitors
  • Receptors, Retinoic Acid / immunology
  • Signal Transduction / immunology
  • Viral Proteins / immunology
  • Viral Proteins / metabolism*
  • Virulence

Substances

  • Enzyme Inhibitors
  • PLAAT4 protein, human
  • Receptors, Retinoic Acid
  • Viral Proteins
  • Interferons