Peripheral Expression of CXCL10 Gene in Chronic Hepatitis C Patients Treated with Sofosbuvir, Daclatasvir, and Ribavirin

Hepatitis C virus (HCV) causes persistent infection and invades host's innate and adaptive immune systems. During the eradication of this pathogen, the components of immune system may cause bystander damage to host, which might be even worse than the viral pathogenesis. Thus, the therapy should not only eliminate primary virus infection but also improve the inflammatory immune responses. The breakthrough of interferon free direct acting antiviral (DAA) drugs has provided the opportunity to unravel the association of HCV with immune response. This study aimed to examine the expression level of C-X-C motif chemokine ligand 10 (CXCL10) in the Peripheral blood mononuclear cells (PBMCs) of HCV infected patients treated with DAAs + Ribavirin. In this study we analyzed the expression levels ofCXCL10mRNA in the 90 chronic HCV patients using quantitative PCR (qPCR) prior, after, and during therapy with sofosbuvir/ribavirin (SOF+RBV) and sofosbuvir/daclatasvir/ribavirin (SOF+DCV+RBV), and further, the results were analyzed relative to treatment response. Significantly elevatedCXCL10mRNA was seen in naive patients having higher viral load (P = 0.005) and those suffering from hepatocellular carcinoma (P = 0.006). HCV patients had remarkable decline inCXCL10level after 4, 12, and 24 weeks of therapy with DAAs. An approximate one-fold decrease was observed in patients who attained sustained virological response compared to untreated patients (P< 0.0001). Comparing the 2 regimens, the reduction in peripheralCXCL10expression was more pronounced in patients undergoing SOF+DCV+RBV therapy. The current study implicitly shows the role ofCXCL10as an indicator of disruption of host-virus equilibrium and consequent pathogenesis of HCV during successful antiviral therapy. Furthermore, the drop inCXCL10level after HCV viral clearance might reflect the DAA-induced alleviation in the extrahepatic manifestation of this infection.