Interleukin‐10 promoter polymorphisms in hepatitis C patients with and without Schistosoma mansoni co‐infection

Background/Aim: Interleukin (IL-10) plays a major role in chronic hepatitis C virus (HCV) disease pathogenesis, in particular in Schistosoma mansoni (S. mansoni) co-infected patients. Given that interindividual variations in IL-10 production are influenced by functional polymorphisms in the IL-10 gene promoter, we determined the frequencies of common (−1082, −819 and −592) IL-10 promoter polymorphisms in chronic HCV patients with and without S. mansoni co-infection and healthy controls, and investigated their association with the degree of histological activity index (HAI) and response to interferon–ribavirin therapy. Methods: Genomic DNA from 99 patients and 62 healthy controls, born in the same geographical hyperendemic area, was studied by the polymerase chain reaction, followed by restriction enzyme digestion. Sera were assessed for S. mansoni antibodies. Results: The frequencies of IL-10 polymorphisms at positions −1082, −819 and −592 from the transcription start site were comparable between HCV patients and controls, as well as between HCV mono-infected and either S. mansoni co-infected patients or controls. The grade of inflammation and the stage of fibrosis showed no association with IL-10 polymorphisms. The frequencies of S. mansoni co-infection and IL-10 genotypes/haplotypes were insignificantly different between non-responders and responders to combination therapy. No effect of other factors like age, gender, HAI group scores and serum alanine aminotransferase and aspartate aminotransferase levels was observed on response to therapy in our patients. Conclusion: Our findings suggest that common IL-10 (−1082, −819 and −592) genotypes/haplotypes do not influence the degree of HAI and response to combination therapy or susceptibility to HCV infection with and without S. mansoni co-infection.