Toll-Like Receptor 7 rs179008/Gln11Leu Gene Variants in Chronic Hepatitis C Virus Infection

: Authors

 Eva Askar, Giuliano Ramadori, and Sabine Mihm*
Department of Gastroenterology and Endocrinology, University Medical Center, Georg-August-University,
Goettingen, Germany 

 :Abstract

; "> Chronic infection caused by hepatitis C virus (HCV), an enveloped single-stranded RNA (ssRNA) virus [Chooet al., 1989], develops in 70–80% of patients [Schwabe et al., 2006]. Patients are at a high risk of developing severe disease as liver cirrhosis and hepatocellular carcinoma [Schwabe et al., 2006]. Toll-like receptors (TLRs) play a critical role in the innate immune sensing of the invasion of pathogenic microorganisms [Akira andTakeda, 2004]. Alpha interferon (IFN-a) is an important antiviral cytokine produced principally by plasmacytoid dentritic cells (pDCs), which circulate in the blood at low frequency and even lower in chronic hepatitis C [Kantoet al., 2004], through the stimulation of TLR7 and TLR9 
[Hornung et al., 2005; Ito et al., 2005]. TLR7 senses unmethylated viral ssRNA [Diebold et al., 2004; Heil et al., 2004]. The expression of TLR7 in humans is mainly confined to the endosome–lysosome membrane of pDCs (including hepatic pDCs), hepatic natural killer cells [Seki and Brenner, 2008], and B lymphocytes [Hornung et al., 2002]. When the virus or virus-infected apoptotic cells are taken up by phagocytes, viral RNA is released in the highly acidified phagolysosome by degradation enzymes, leading to ssRNA release and recognition by TLR7. Upon TLR7 stimulation, a complex cascade is formed, starting with myeloid differentiation factor 88 (MyD88) and ending with the production of  "> Hepatitis C virus (HCV) infection affects an estimated 3% of the world’s population 

 

 

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