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Human Leukocyte Antigen Class II (HLA-II) Alleles and Interf | 17085
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International Research Journal of Microbiology

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Human Leukocyte Antigen Class II (HLA-II) Alleles and Interferon Response in HCV Chronically Infected Egyptian Patients

Abstract

Olfat M Hendy, Elhamy Abd Elmonean, Maha Allam, Mohamed A Rady, Helmy M El Shazly, Maha Sabawy, El Sayed Tharwa

Interferon (IFN) therapy of hepatitis C virus (HCV) comprises a high economic burden in developing countries. However, depending upon variations in their human leukocyte antigen (HLA), some patients do not respond well. This study aimed to determine association between HLA class II polymorphisms, HCV infection and disease outcome. HLA alleles were evaluated in 56 chronic HCV (CHC) infected patients and 30 healthy volunteers as a control group. HLA was typed by polymerase chain reaction-sequence specific primer (PCR-SSP) procedure for HLA-DRB and DQB alleles from peripheral blood. The frequency of HLA DRB1*07 allele was significantly higher in CHC patients (35.7%) than healthy controls (13.3%). But, other HLA DRB1 alleles were not significantly different. The HLA DQB1*02 allele frequency was significantly increased in CHC patients (55.4%) compared to controls (30%), while other HLA DQB1 alleles showed no significant difference. Only 26 (46.4 %) of CHC patients showed a sustained virological response to combined ribavirin and peg interferon (IFN) therapy, whereas 30 (53.6 %) did not. The viral clearance is mainly associated with HLA DRB1*01, DQB1*03 and DQB1*05 alleles, while DRB1*7, and DQB1*02 alleles were associated with viral persistence. These data support the role of HLA class II alleles in immune response to HCV and the associations of HLA class II with HCV persistence or clearance will be beneficial in deciding the therapeutic regimen. Therefore, recognition of HLA racial differences is likely important in studying HCV outcome and avoid bearing costs of ineffective treatment. Future studies in this regard with larger number of HCV patients are recommended.

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