The hepatitis C virus (HCV) is a single-stranded enveloped RNA virus, belonging to the Hepacivirus genus within the Flaviviridae family. HCV infection has become a major worldwide health problem because it causes a chronic hepatitis leading to hepatocarcinoma (HCC) and to non-Hodgkins B-cell lymphoma (NHL). The absence of a reliable experimental model, which mimics the physiological effect of HCV infection in human subjects, hampered the analysis of the mechanisms by which HCV leads to cancer. Nevertheless, both in vitro expression systems and in vivo transgenic mice studies suggest that HCV persistent infection in the host is able to induce neoplastic transformation. The oncogenic properties of HCV are often related to the ability of HCV-encoded proteins to interfere with cell signaling through the interaction with different molecules involved in the control of cell proliferation, apoptosis and interferon (IFN)-signaling pathways. The present systematic review will mainly focus on the HCV proteins dependent pathogenetic effects on the most important regulatory proteins of cell homeostasis. Since poor efficacy of the current therapy, studying the mechanisms underlying HCV-induced cell transformation and immune evasion will help researchers to identify new therapeutic targets, which may be useful in the near future to develop more effective and better-tolerated therapies, capable of impairing or reversing the progression of HCV-related tumors.
Keywords: HCV, HCC, HCV-related NHL, IFN, treatment, gene therapy
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