Hepatitis C virus: molecular biology and genetic variability

Hepatitis C virus (HCV) is the main etiological factor of post-transfusiona l and sporadic non-A, non-B hepatitis. This viral infection is characterise d by an extremely high rate (60% to 80%) of chronic carrier state developme nt, associated with a low grade, yet persisting, viral multiplication [1-5] . Among HCV chronically infected patients, the severity of the liver lesion varies markedly, ranging from very mild chronic hepatitis to cirrhosis and hepatocellular carcinoma (HCC). Several studies have, however, noted the h igh rate of cirrhosis (around 20%) and HCC after long-term evolution (10 to 30 years) [6-9]. However, detailed analysis of the natural course of HCV i nfection is not available [10]. It is also still debated whether or not acu te HCV infection, by itself, can induce fulminant hepatitis (FH): HCV-relat ed FH have been indeed reported in Japan [11] and Taiwan [12] while, among cases identified in France and United States, HCV was always associated to HBV infections [13-15]. The pathogenetic mechanisms of HCV infection are poorly known; in particula r the respective importance of the viral and host factors is still unclear. This review will focus on an update on HCV biology and the potential clini cal impact of HCV genetic variability.