Interaction of hepatitis C virus with the type I interferon system.
Hepatitis C virus (HCV) needs to tightly manipulate host defences in order to establish infection. The innate immune response slows down viral replication by activating cytokines such as the type I interferons (IFN-alpha/beta), which trigger the synthesis of antiviral proteins and modulate the adaptive immune system. HCV has therefore developed a number of countermeasures to stay ahead of the IFN system. Here, I will attempt to summarize the current state of research regarding IFN responses against HCV and the viral escape strategies. Particular emphasis will be put on the newly discovered mechanisms HCV employs to avoid the induction of IFN in infected cells.
Weber
Friedemann
F
Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Freiburg D-79008, Germany. friedemann.weber@uniklinik-freiburg.de
D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000276:immunology / Q000821:virology*; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007370:Interferon Type I / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology