RANTES, TNF-α, oxidative stress, and hematological abnormalities in hepatitis C virus infection.

Background Chronic infection with hepatitis C virus (HCV) is associated with failures of T-cell–mediated immune clearance and with abnormal B-cell growth and activation. Hepatitis C virus infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. After a viral infection, multiple proinflammatory mediators contribute to recruitment of immune cells to the liver and to the generation of an antiviral immune response. Recent publications mark chemokines and their receptors as key players in leukocyte recirculation through the inflamed liver. Materials and Methods The present study involved 75 male subjects, divided into 2 groups: group 1 (n = 30), control group; group 2 (n = 45), patients with chronic HCV. For all subjects, the following investigations were performed: estimation of the levels of bilirubin, albumin, prothrombin concentration, glycosylated hemoglobin, creatinine, α-fetoprotein, HCV RNA, and activities of alanine and aspartate transaminases as well as alkaline phosphatase. In addition, regulated on activation normal T cell expressed and secreted (RANTES), tumor necrosis factor alpha, malondialdehyde (MDA) and nitric oxide (NO) were assessed. Plasma HCV-RNA concentration (viral load) was determined by real-time polymerase chain reaction (PCR) StepOne system using Applied Biosystem. Complete blood picture was assayed using Abbott Cell-Dyn 3700 hematology analyzer. Results There were significant increases of the levels of RANTES, tumor necrosis factor alpha, MDA, and NO in HCV-infected patients compared with the control group ( P Conclusion The data support the concept of chemokines (RANTES) as mediators of liver cell injury in HCV infection. In addition, MDA and NO levels might be used as monitoring markers for oxidative stress in hepatitis C infection.