Antiviral innate immunity pathways

Cell Res. 2006 Feb;16(2):141-7. doi: 10.1038/


Recent studies have uncovered two signaling pathways that activate the host innate immunity against viral infection. One of the pathways utilizes members of the Toll-like receptor (TLR) family to detect viruses that enter the endosome through endocytosis. The TLR pathway induces interferon production through several signaling proteins that ultimately lead to the activation of the transcription factors NF-kappaB, IRF3 and IRF7. The other antiviral pathway uses the RNA helicase RIG-I as the receptor for intracellular viral double-stranded RNA. RIG-I activates NF-kappaB and IRFs through the recently identified adaptor protein MAVS, a CARD domain containing protein that resides in the mitochondrial membrane. MAVS is essential for antiviral innate immunity, but it also serves as a target of Hepatitis C virus (HCV), which employs a viral protease to cleave MAVS off the mitochondria, thereby allowing HCV to escape the host immune system.

Publication types

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

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / metabolism
  • Immunity, Innate / physiology*
  • Interferon Type I / genetics
  • Interferon Type I / metabolism
  • Models, Biological
  • Signal Transduction / physiology*
  • Toll-Like Receptors / metabolism
  • Viruses / genetics
  • Viruses / immunology
  • Viruses / pathogenicity*


  • Adaptor Proteins, Signal Transducing
  • Interferon Type I
  • Toll-Like Receptors
  • VISA protein, mouse
  • Ddx58 protein, mouse
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases