Oxidative Stress Response in Patients Infected by Diverse Hepatitis C Virus Genotypes

BACKGROUND: The molecular mechanism of hepatitis C-virus (HCV) genome-specific pathogenesis remains unclear. Oxidative stress is an important pathophysiological mechanism in chronic HCV infection, but its relation to HCV genotypes has not been thoroughly examined. OBJECTIVES: In the present case-control study, the effect of diverse HCV genotypes on oxidative status changes was investigated. PATIENTS AND METHODS: From 310 patients examined by enzyme immunoassay and PCR, 160 patients with positive results for HCV with previously determined genotypes were chosen. For the control group, 160 first time blood donors referred to the Regional Blood Transfusion organization of the West Azerbaijan province, northwestern Iran were selected. Oxidative stress markers such as total antioxidant status (TAS), serum levels of reduced (GSH) and oxidized (GSSG) glutathione, Gamma-glutamyl transferase (GGT) and malondialdehyde (MDA) were evaluated in patients infected with diverse HCV genotypes and those in the control group. RESULTS: In the patient and control groups, the mean ± SE of TAS, GSH, GSSG, GGT and MDA were 1.04 ± 0.35 vs. 2.68 ± 0.77, 1.25 ± 0.37 vs. 3.12 ± 0.58, 0.20 ± 0.05 vs. 0.08 ± 0.04, 26.82 ± 5.62 vs 8.28 ± 2.03 and 2.56 ± 0.60 vs. 0.93 ± 0.34. All markers had statistical difference between the two groups (P <0.05). Obvious differences were found in oxidant/antioxidant balance among diverse HCV genotypes with an ascending trend in antioxidant levels among patients infected with genotypes 1a/b, 4, 2a/c, 2b, 3a and healthy controls and a vice versa trend in measures of oxidative markers except for malondialdehyde with a variable pattern. CONCLUSIONS: More serious disease in HCV genetic subtype 1a/1b might be associated with more severe oxidative stress. Milder damage in subtypes 4, 2a/c, 2b and 3a could be related to lower oxidative response, respectively. A combination of antiviral and antioxidative therapies may enhance the overall response rate of patients with HCV infection, especially with more destructive genotypes.