REVIEW

Cell Research (2006)16: 141-147
© 2006 IBCB, SIBS, CAS All rights reserved 1001-0602/06 $ 30.00
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Anti-viral innate immunity pathways

Rashu B Seth¹, Lijun Sun¹, Zhijian J Chen¹

¹Howard Hughes Medical Institute, Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA

Correspondence: Zhijian J Chen Tel: 214-648-1145, Fax: 214-648-1675; E-mail: Zhijian.Chen@UTSouthwestern.edu

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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-κB, 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-κB 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.

Cell Research (2006) 16:141-147. doi:10.1038/sj.cr.7310019; published online 13 February 2006

Keywords: interferon, Toll-like receptor, RIG-I, MAVS, mitochondria, NF-κB, IRF