The Role of Autophagy in Interferon/Ribavirin Responders and Non-Responders with Hepatitis C Virus Infection

Abstract

Background: Hepatitis C virus (HCV) is a significant cause of chronic inflammatory liver diseases. Hepatitis C virus infection is a common disorder worldwide, which has become a significant public health concern. The survival of viruses in host cells is associated with their ability to engage in cellular mechanisms benefitted from. Objectives: This study aimed at evaluating the expression rate of Beclin 1, as a critical protein of autophagy, and its correlation with interferon-alpha (IFN-α) expression in both IFN-ribavirin responder and non-responder groups. Methods: In this study, a total of 40 samples of the peripheral blood mononuclear cells (PBMCs) were evaluated. Twenty samples were collected from the patients with chronic HCV as non-responders and 20 samples obtained from the patients considered as responders; all samples were collected in the "pretreatment period". The expression level of IFN-α and Beclin 1 mRNA was assessed by Taq-man real-time PCR. Results: The mean of HCV load was 4.2 × 106 ± 8.8 × 106 and 1.1 × 107 ± 9.1 × 106 in the responder and non-responder groups, respectively. The expression rate of IFN-α in the responder group was significantly higher, than the non-responders (P < 0.02), whereas the expression rate of the Beclin 1 gene was significantly lower in responders compared with non-responders (P < 0.02). Conclusions: In non-responders, the level of Beclin 1 expression and its correlation with IFN-α expression level, along with other genetic and physiological factors of the host, can be considered as influential factors involved in IFN-αexpression, as an antiviral agent.