Hepatitis C and evasion of the interferon system: a PKR paradigm

Cell Host Microbe. 2009 Dec 17;6(6):495-7. doi: 10.1016/j.chom.2009.11.009.

Abstract

Hepatitis C virus (HCV) is resistant to the antiviral cytokine type I interferon, representing a major clinical problem. Garaigorta and Chisari (2009) reveal that HCV uses the activation of the ds-RNA-dependent protein kinase R, which phosphorylates and inhibits the translation initiation factor eIF-2 alpha, to block translation of interferon-stimulated genes.

Publication types

  • Comment

MeSH terms

  • Hepacivirus / physiology*
  • Hepatitis C / enzymology*
  • Hepatitis C / genetics
  • Hepatitis C / metabolism
  • Hepatitis C / virology
  • Humans
  • Interferon Regulatory Factors / genetics
  • Interferon Regulatory Factors / metabolism*
  • Interferon Type I / metabolism
  • Phosphorylation
  • eIF-2 Kinase / genetics
  • eIF-2 Kinase / metabolism*

Substances

  • Interferon Regulatory Factors
  • Interferon Type I
  • eIF-2 Kinase