Hepatitis C and evasion of the interferon system: a PKR paradigm.
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.
Esteban
Mariano
M
Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología, CSIC, Madrid, Spain.
D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism / Q000821:virology; D006801:Humans; D050835:Interferon Regulatory Factors / Q000235:genetics / Q000378:metabolism*; D007370:Interferon Type I / Q000378:metabolism; D010766:Phosphorylation; D019892:eIF-2 Kinase / Q000235:genetics / Q000378:metabolism*
D050835:Interferon Regulatory Factors; D007370:Interferon Type I; D019892:eIF-2 Kinase