05) (data not shown). Host genetic factors are

proposed to be governing the pathology of HCV disease progression or regression along with the viral and environmental factors. Interplay of HLA-restricted T lymphocytes, antibody-secreting B lymphocytes, natural killer cells and cytokines conditions the immune response to viral infections. Effective presentation of viral antigens to CD4+ T cells and CD8+ T cells by HLA Class II and Class I molecules, respectively, is the key regulation of optimum immune response against viral infection and further KPT 330 dictates viral clearance or persistence [20]. The results of the present study demonstrated that HLA-A11 is the only HLA click here Class I antigens that show statistical significant association with chronic HCV infection (P = 0.001, Pc = 0.021), suggesting that HLA-A11 antigen may be a susceptibility antigen for viral persistence and chronic liver disease in Egyptian patients infected with HCV. Although HLA-B12, HLA-B13, HLA-B17 and HLA-B40 were more frequent in patients (P = 0.02, P = 0.04, P = 0.04, P = 0.02, respectively) and HLA-A32 (P = 0.03) and HLA-B14 (P = 0.015) were more frequent in controls, the significance was lost after correction for multiple testing and no other HLA Class I antigens were

associated with chronic HCV infection in this

study. The associations between HLA Class I antigens and the outcome of HCV infection are extensively investigated in different ethnic populations such as Caucasian Americans and populations from Korea, Italy, Russia, Spain, Ireland, Saudi Arabia, Western India, Japan and Germany [21–37]. The earlier reported associations showed ethnic and geographical differences sometimes with contradictory results. While HLA-A11 is associated with HCV persistence in Ireland [14, 25] in agreement with the results of the present study, Tau-protein kinase HLA-A*1101 showed stronger association with viral clearance both in Caucasians and African Americans [29]. HLA-A32 in populations from Western India [27] and HLA-B14 in Italy [22] are associated with HCV infection in contrast to our findings. On other hand, several studies failed to demonstrate an association between the outcome of HCV infection and HLA Class I antigens [34–36]. In Egyptian, association was reported between HLA-A28, HLA-A29, HLA-B14 and HCV infection, and HLA-B50(21) with viral clearance in two cases of the studied sera [17]. HLA-A28 and HLA-29 were not detected in patients with HCV infection of the present study; in the same time, HLA-B14 shows a trend with protection (OR = 0.1) and not susceptibility.