Journal
CELL RESEARCH
Volume 16, Issue 2, Pages 141-147Publisher
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/sj.cr.7310019
Keywords
interferon; toll-like receptor; RIG-1; MAVS; mitochondria; NF-kappa B; IRF
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Funding
- NIAID NIH HHS [R01-AI60919] Funding Source: Medline
- NIGMS NIH HHS [R01-GM63692] Funding Source: Medline
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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 endosorne through endocytosis. The TLR pathway induces interferon production through several signaling proteins that ultimately lead to the activation of the transcription factors NF-kappa B, 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-kappa B 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.
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