PubMed Journals: Cell Res

  Source:		PMID: 16474426
  Download:	https://www.nature.com/articles/7310019.pdf

    		Cell Res. 2006 Feb;16(2):141-7.
			Antiviral innate immunity pathways.

			Seth RB(1), Sun L, Chen ZJ.

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

			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.

			DOI: 10.1038/sj.cr.7310019 PMID: 16474426
			[Indexed for MEDLINE]

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