Abstract
Hepatitis C virus (HCV), the etiologic agent of chronic non-A, non-B hepatitis,is a 9.4 kb positive strand RNA virus classified within the Flaviviridae family.1 The RNA genome of HCV encodes a single precursor polyprotein of 3011 amino acids, which is cleaved by host and viral proteases into a series of structural and non-structural proteins as reviewed elsewhere (Figure 1). (reviewed in reference 2) Although HCV gene products have not been definitively identified in infected hosts, they have been successfully expressed via genetic engineering.3,4 The HCV structural proteins (core and envelope) are thought to circulate in the blood of infected individuals as virion components, while the non-structural proteins (NS2-NS5) are thought to function as regulatory enzymes (e.g., protease, helicase, RNA replicase) during the intracellular phase of the viral life cycle.
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Gretch, D.R., Polyak, S.J., Willson, R.A., Carithers, R.L. (1996). Treatment of Chronic Hepatitis C Virus Infection: A Clinical and Virological Perspective. In: Mills, J., Volberding, P.A., Corey, L. (eds) Antiviral Chemotherapy 4. Advances in Experimental Medicine and Biology, vol 394. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9209-6_20
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