[Hepatitis C virus infection and hepatocarcinogenesis].

It is evidenced that both HBV and HCV infections may cause chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). HCV is considered as an oncogen virus. The mechanism of carcinogenesis in case of the two distinct viruses shows a number of common and different features. HCC usually develops in stage of liver cirrhosis caused by chronic inflammation of many years or decades. In contrast to HBC, HCV will not be incorporated into the genome of hepatocytes. It induces throughout different mechanisms the development of cancer cells, which will proliferate out of control. Before the discovery of HCV, the connection of non-A non-B (NANB) hepatitis and liver cancer has yet been observed. The subsequent epidemiological studies confirmed this association. A number of publications prove that HCC may develop without cirrhosis in HCV infected patients. The exact mechanism is not known, but data indicate that some proteins of the virus may induce oncogenic process. Differences were found in HCV core gene between HCC patients with and without cirrhosis. It is postulated that the virus evolves its oncogenic effect via endoplasmic and oxidative stress, further on by activation of different oncogenic signal pathways. Recent publications indicate the role of virus induced insulin resistance. Besides the virus determined factors, the host reaction, the deficient tumor cell eliminating capacity may also have a role in the development of liver carcinoma. Monitoring of HCV infected patients for HCC is an important clinical issue. Most relevant is the regular ultrasound cheek up. Serum alpha fetoprotein level is elevated only in a smaller proportion of the patients. The treatment protocol of HCV induced HCC does not differ from the others developed in non-HCV liver diseases.