الفهرس 
Hepatitis C VirusOnly 14 pages are availabe for public view
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Abstract
Hepatitis C virus (HCV) is the most prevalent liver disease in the world. The World Health Organization considers Hepatitis C an epidemic. An estimated 150-200 million people worldwide are infected with hepatitis C. The high genetic variability of HCV contributes to the chronicity of hepatitis C.
The elimination or persistence of HCV infection depends on the balance between the effectiveness, specificity and rapidity of the innate and adaptive immune responses, as well as on the HCV replication rate.
Natural killer (NK) cells are key players in immune responses to viruses. They can kill virus-infected cells via perforin release and induction of apoptosis and can provide early bursts of cytokines, such as interferon-g (IFN-g), that have direct antiviral effects and can activate cytotoxic and helper T (Th) lymphocyte responses. NK cells are activated and regulated by signals through a variety of stimulatory and inhibitory receptors (NKRs). NK cells can be divided into two subsets, dim and bright, according to CD56 surface density expression.
Some T cells also express NKRs and mediate functions of both T cells and NK cells. NK cells and NKR+ T cells make up ~13% of the lymphocyte pool in human blood and 50% in liver. The phenotypes and/or functional activities of various populations of these cells have been reported to be impaired in patients with chronic HCV infection. Furthermore, HCV has evolved mechanisms by which it can inhibit the responses of NK cells and possibly NKR+ T cells.
In this study we aimed to estimate different cell populations including total T cells, CD56+T cells, total NK including both CD56 dim and bright population with their CD16 expression using flowcytometry in different clinical outcomes of HCV infection.