HCVs constitute a genus within the Flaviviridae, with closest homology to the hepatitis G and GB viruses, and Pestiviruses. The positive-stranded RNA genome encodes at least nine proteins. Core, El, and E2 constitute the structural proteins; NS2, NS3, NS4A, NS4B, NS5A, and NS5B are nonstructural (NS) proteins. HCV isolates display high levels of sequence heterogeneity allowing classification into at least 11 types and 90 subtypes (1). HCV infection of the human liver is often clinically benign, with mild icterus in the acute phase, the disease may even go unnoticed in some cases of acute resolving hepatitis C. In the majority (>70%) of cases, however, HCV infection leads to chronic persistent or active infection, often with complications of liver cirrhosis and auto-immune disorders. Hepatocellular carcinoma may occur after about 20-35 yr (2); sometimes even without the intermediate phase of cirrhosis. No prophylaxis is available today and treatment with interferon-alpha (IFN-α) only leads to long-term resolution in about 4-36% of treated cases, depending on the HCV genotype (1).