الفهرس 
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Abstract
Hepatitis C virus (HCV) infection is one of the major causes of chronic liver disease worldwide. The pathogenesis of HCV infection remains largely unclear, but it seems very possible that it is directly related to a strong interplay between the host immune responses and the ability of the virus to evade them. Recently, pegylated interferon (PEG-IFN) in combination with ribavirin has become the standard of care for the treatment of chronic HCV infection. Nevertheless, only 50–60% of treated patients achieve a sustained virologic response and current treatment is expensive with many adverse effects. Searching for surrogate predictors of treatment response has thus drawn great attention.
It is generally believed that genetic background of the host plays an important role in both susceptibility to chronic hepatitis C infection and responsiveness to antiviral therapy in HCV-infected patients. However, the mechanisms remain largely unknown. Given previous reports of the role of IL10 variants in both HCV therapy and clearance, it is sought to evaluate the role of genetic variants at this gene.
The IL-10 level differs widely between individuals probably due to polymorphisms in the promoter region of IL-10 gene and three frequent point mutations -1082(G/A),-819(C/T), and -592(C/A). The -1082(G), -819(C) and -592(C) alleles were associated with higher IL-10 production (probably in both monocytes and T-cells).
The aim of the current study is to throw some light on the role of IL-10 gene polymorphisms in HCV infected children, and whether it can determine the response to combination therapy with (PEG-IFN) and ribavirin, so that it could serve as a predictor for response to combined HCV therapy.
The study was conducted on 40 subjects divided into two groups: 23 responders to anti-viral therapy and 17 were non-responders.
Concerning the genotype of the studied groups; the group of responders included 47.8% homozygous wild (G/G), 34.8% heterozygous (G/A) and 17.4% homozygous mutant (A/A). In the group of non-responders 23.5 % were homozygous wild (G/G), 64.7% heterozygous (G/A) and only 11.8% were homozygous mutant (A/A).
The frequencies of the C and A alleles in SNP -592 C/A were as follows: In the group of responders 13% were homozygous wild (C/C), 47.8% heterozygous (C/A) and 39.1% homozygous mutant (A/A). In the group of non-responders 5.9% were homozygous wild (C/C), 52.9% heterozygous (C/A) and only 41.7 % homozygous mutant (A/A).
There was no significant association between polymorphisms in the IL-10 (-1082 and -592) gene or cytokine haplotype and either severity of hepatitis or response to therapy.
Although the effects of the cytokine polymorphisms identified in various studies have been proven to be important in determining viral outcomes, this only accounts for a small factor among enormously complicated immune mechanisms. Thus, other genes, acting alone or interacting with other genetic determinants and environmental factors, need to be identified to understand the differences in the host response to this virus.
Since this study failed to demonstrate a relationship between major IL-10 promoter gene polymorphisms and antiviral responsiveness, it is recommended that this work should be carried out on a wider scale in order to confirm or refute this finding.