TLR3 Gene Polymorphisms and Liver Disease Manifestations in Chronic Hepatitis C


: Authors

 "> <Eva Askar,1 Rusudan Bregadze,1 Jasmin Mertens,1 Stefan Schweyer,2 Albert Rosenberger,3
Giuliano Ramadori,1 and Sabine Mihm1*
1Department of Gastroenterology and Endocrinology, University Medical Center, Georg-August-Universita ¨t,
Go ¨ttingen, Germany
2Department of Pathology, University Medical Center, Georg-August-Universita ¨t, Go¨ttingen, Germany
3Department of Genetic Epidemiology, University Medical Center, Georg-August-Universita¨t, Go¨ttingen, Germany

Published in

 Journal of Medical Virology 81:1204–1211 (2009)


 Hepatitis C virus (HCV) is an enveloped singlestranded plus-sense RNA virus that causes acute and often chronic hepatitis [Choo et al., 1989]. Currently, an estimated 3% of the   world’s population—about  210 million people—is infected with HCV [Shepard et al., 2005]. The natural outcome of infection ranges from silent to self-limited to chronic [Micallef et al., 2006]. The natural course of chronic disease is also highly variable and ranges from asymptomatic to mild disease to cirrhosis and hepatocellular carcinoma (HCC) and  HCV-related co-diseases [Seeff, 2002]. The complete pattern of host responses to HCV infection is still unclear. However, the HCV genome encodes regions of extensive  secondary double-stranded RNA (dsRNA) structure, and the viral replication cycle includes dsRNA as an intermediate; both entities are assumed bto be sensed by pattern recognition receptors (PRRs) during infection [Gale and Foy, 2005]. PRRs comprise membrane Toll-like receptors (TLRs), bwhich are either expressed on the cell surface or onendosomal–lysosomal membranes, and cytosolic receptors such as nucleotide-binding oligomerization domain  (NOD)-like receptors and the RNA-helicase family [reviewed in Akira et al., 2006; Takeuchi and Akira , 2007; Seki and Brenner, 2008]. Viral dsRNA is a ligand of TLR3 which is expressed within the endosomal compartment of conventional  dendritic cells (cDCs)  [Alexopoulou et al., 2001; Matsumoto et al., 2004]. Upon phagocytosis of infectious material and signaling through TLR3, DCs become activated.


single nucleotide polymorphism (SNP); hepatitis C virus (HCV); Toll-like receptor (TLR); HCV genotypes; T-976A; L412F

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