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Hepatitis C virus (HCV)--a review molecular biology of the virus, immunodiagnostics, genomic heterogeneity and the role of virus in hepatocellular carcinoma.

Hepatitis C virus (HCV), an RNA and a hepatotropic virus, is the leading cause of viral hepatitis worldwide. Infection with this virus causes a repertoire of liver diseases that include acute hepatitis, chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC), in addition to a number of extra-hepatic manifestations such as lichen planus, oral cancer, etc. At present, patients infected with this virus are treated with interferon either alone or in combination with ribavirin, a guanosine-like nucleoside analog. However, response to this treatment has been rather disappointing. For about a decade, lack of an alternative animal model other than chimpanzee, and an efficient cell culture system that could support long-term replication of the virus, hampered research on HCV. Despite this, a significant amount of information with regard to the molecular biology of the virus is available using bacterial cloning-expression systems, and based on computer predictions and analysis. Recent discovery of a cellular receptor to which the virus binds, identification of efficient cell culture/cell-free systems, HCV replicons and the development of a chimeric mouse model, provide a platform to verify the existing knowledge about this virus in the coming years. Additionally these developments aid the researchers in identifying novel therapeutic agents, apart from allowing us to reassess the efficiency of the currently available therapeutics. Presented in this article are a review of existing information with regard to the molecular biology of the virus, immunodiagnostic assays, genomic heterogeneity and the role of the virus in hepatocellular carcinoma. Likely therapeutic strategies other than those currently available are also introduced.