Mubarak City for Scientific Research and Technology Applications MuCSAT

New Borg El Arab, Egypt

Mubarak City for Scientific Research and Technology Applications MuCSAT

New Borg El Arab, Egypt
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Salem M.L.,Medical University of South Carolina | Salem M.L.,Tanta University | EL-Demellawy M.,Mubarak City for Scientific Research and Technology Applications MuCSAT | El-Azm A.R.A.,Tanta University
Cellular Immunology | Year: 2010

Hepatitis C virus (HCV) infection is a major public health concern with approximately 3% of the world's population is infected, posing social, economical and health burden. Less than 20% of the infected individuals clear the virus during the acute infection, while the rest develop chronic infection. The treatment of choice for HCV infection is pegylated interferon-α (IFN-α) in combination with ribavarin. Despite the cost and side effects of this treatment regimen, many patients fail this therapy and develop persistent HCV infection, leading to cirrhosis and hepatocellular carcinoma. Although the mechanisms underlying the failure to resolve HCV infection are poorly understood, the incapability of patients to develop effective anti-HCV immunity is a potential cause. We hypothesize that the dysfunctional anti-HCV immunity is due to the emergence of immunosuppressive cells coinciding with a decrease in the stimulatory dendritic cells (DCs) and natural killer (NK) cells. We further hypothesize that applying agents that can correct the imbalance between the immunosuppressive cells and stimulatory cells can results in resolution of chronic HCV. In this review article, we will discuss potential approaches, focusing on the use of Toll-like receptor agonists, to block the suppressive effects of the regulatory cells and restore the stimulatory effects of DCs and NK cells. © 2010 Elsevier Inc.

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