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

 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.

 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.

 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.

 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).

 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.