Abstract

HCV infection has shown to be strongly linked to the development of hepatocellular carcinoma in epidemiological studies. However, the mechanism of carcinogenesis by HCV is poorly understood. Unlike other human oncogenic viruses, HCV is a typical RNA virus, and thus there is no integration of the viral genome or a piece of the genome into host chromosomes. Moreover, trans-acting transcriptional factors which are coded by other human oncogenic viruses and required primarily for virus replication and often involved in cell immortalization, may not be coded by HCV. Although regeneration of hepatocytes in an HCV-infected liver may be of primary importance in driving hepatocytes to the malignant stage, an additional unknown carcinogenic function of HCV may also exist. For this reason, clarification of the molecular mechanism of virus replication in hepatocytes should be emphasized.

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