Hepatitis C Virus (HCV) is a RNA virus that lacks the retroviral properties of surviving in infected hosts by integration into cellular DNA, nevertheless it is capable to cause chronic infection and disease in 30-70% infected individuals. Genetic heterogeneity appears to play a major role for HCV persistence in the infected host. HCV infection is asymptomatic in the great majority of individuals and only about 10% of them present signs or symptoms of liver disease. Hepatitis type C appears clinically indistinguishable from the other forms of viral hepatitis. Chronic HCV infection is associated with a wide spectrum of liver disease ranging from asymptomatic carriage to severe forms of chronic hepatitis, cirrhosis and hepatocellular carcinoma. Using currently available assays we can not easily distinguish patients with chronic HCV hepatitis from HCV carriers with HCV unrelated liver disease. Specific markers of HCV induced liver disease are also required for a differential diagnosis of viral from autoimmune hepatitis in patients with coincidence of serum anti-HCV and autoantibodies. Alpha-interferon is capable to induce a persistent remission of chronic hepatitis in about 25% of treated patients. A significant amelioration of liver histology is also seen in patients with temporary remissions. Patients infected with genotype I HCVs and high viremia levels are less likely to respond to common therapy schedules (3-6 MIU i.m. thrice weekly for 6-12 months). In patients undergoing antiviral therapy, monitoring anti-HCV and HCV-RNA by quantitative assays represents the best tool to predict response that invariably occurs in patients who maintain undetectable serum HCV-RNA and/or show decreasing anti-HCV serum titres. In conclusion detection of HCV markers can help to understand the peculiar pathogenicity of HCV