id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-001834-6xf4o3oy	Sung, Pil Soo	Interferon Response in Hepatitis C Virus (HCV) Infection: Lessons from Cell Culture Systems of HCV Infection	2015-10-07		.txt	text/plain	4039	230	44	In HCV-infected cells, viral RNA is sensed by retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5) in the cytoplasm and Toll-like receptor 3 (TLR3) in the endosome, which leads to downstream signaling that results in the induction of type III and I IFNs and other inflammatory cytokines [28, [36] [37] [38] [39] . Intracellular signals from RIG-I, MDA-5, and TLR3 are transmitted via mitochondrial antiviral signaling protein (MAVS) and Toll/IL-1 receptor domain-containing adaptor inducing IFN- (TRIF), respectively, which leads to the interferon regulatory factor-3 (IRF-3)-dependent induction of IFNs and NF-κB activation in HCV-infected cells [38, 39] . IFN-s activate the same JAK-STAT pathway as type I IFNs [48] [49] [50] , thereby inducing a similar set of ISGs. Although the exact source of IFN-s in HCV-infected liver remains to be clarified, it seems that the production of IFN-s by HCV-infected hepatocytes results in the expression of ISGs, presumably through autocrine and/or paracrine signaling via the IFN-λ receptor [28, [44] [45] [46] . HCV infection induces a unique hepatic innate immune response associated with robust production of type III interferons	./cache/cord-001834-6xf4o3oy.txt	./txt/cord-001834-6xf4o3oy.txt