4.2 Article

The relationship between HLA-G and viral loads in non-responder HCV-infected patients after combined therapy with IFN-α2α and ribavirin

Journal

HUMAN IMMUNOLOGY
Volume 76, Issue 2-3, Pages 181-186

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2014.12.012

Keywords

HLA-G; IFN-alpha 2 alpha; Ribavirin; Responder and non-responder patients; IL-10

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Funding

  1. Digestive Disease Research Institute of Tehran University, Tehran, Iran

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Hepatitis C disease is a virus mediated infection causing major health problem worldwide. Conversions of immune surveillance play an important role in response to virus clearance. Immune modulating molecules such as HLA-G and IL-10 that convert immune response toward Th2 may play a role to inhibit response from combined therapy with IFN-alpha 2 alpha and ribavirin. The objective of this study was to investigate the expression of HLA-G and IL-10 in responder and non-responder HCV positive patients. In this study, characteristics of the virus and 48 responder and non-responder patients in response to the combined therapy with IFN-alpha 2 alpha and ribavirin were analyzed. The expression levels of HLA-G and IL-10 were conducted using real-time PCR. Also, soluble HLA-G in both groups of patients and healthy individuals were determined by enzyme-linked immunosorbent assay. According to the obtained data, HCV 1 a was the predominant genotype in responder and non-responder patients. Expression levels of HLA-G and IL-10 in non-responder group was significantly more than responder and control groups (P < 0.001). Additionally, expression levels of HLA-G and IL-10 were remarkably higher compared to healthy individuals at the beginning of treatment. Soluble HLA-G in non-responder patients was noticeably increased in comparison to responder patients after treatment (P < 0.05). These findings suggest that elevation of HLA-G and IL-10 in HCV infected patients may play an important role in response to combined therapy with IFN-alpha 2 alpha and ribavirin. (C) 2014 Published by Elsevier Inc. on behalf of American Society for Histocompatibility and Immunogenetics.

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