Send to

Choose Destination
See comment in PubMed Commons below
World J Gastroenterol. 2007 May 7;13(17):2446-54.

The interferon inducing pathways and the hepatitis C virus.

Author information

Hepacivirus Unit, Department of Virology, Pasteur Institute, 28 rue du Dr Roux, 75724 Paris Cedex 15, France.


The innate immune response is triggered by a variety of pathogens, including viruses, and requires rapid induction of type I interferons (IFN), such as IFNbeta and IFNalpha. IFN induction occurs when specific pathogen motifs bind to specific cellular receptors. In non-professional immune, virally-infected cells, IFN induction is essentially initiated after the binding of dsRNA structures to TLR3 receptors or to intracytosolic RNA helicases, such as RIG-I/MDA5. This leads to the recruitment of specific adaptors, such as TRIF for TLR3 and the mitochondrial-associated IPS-1/VISA/MAVS/CARDIF adapter protein for the RNA helicases, and the ultimate recruitment of kinases, such as MAPKs, the canonical IKK complex and the TBK1/IKKepsilon kinases, which activate the transcription factors ATF-2/c-jun, NF-kappaB and IRF3, respectively. The coordinated action of these transcription factors leads to induction of IFN and of pro-inflammatory cytokines and to the establishment of the innate immune response. HCV can cleave both the adapters TRIF and IPS-1/VISA/MAVS/CARDIF through the action of its NS3/4A protease. This provokes abrogation of the induction of the IFN and cytokine pathways and favours viral propagation and presumably HCV chronic infection.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons


    Supplemental Content

    Full text links

    Icon for Baishideng Publishing Group Inc. Icon for PubMed Central
    Loading ...
    Support Center