Author/Editor		Coer, Andrej; Pižem, Jože; Luzar, Boštjan; Ferlan-Marolt, Vera
Title		Proliferative processes, cell cycle deregulation and apoptosis in viral hepatitis
Type		članek
Source		In: Ferlan-Marolt V, Luzar B, editors. Viral hepatitis. Proceedings of the 35th memorial meeting to professor Janez Plečnik with international participation; 2004 Dec 2-3; Ljubljana. Ljubljana: Faculty of medicine, Institute of pathology,
Publication year		2004
Volume		str. 87-92
Language		eng
Abstract		Hepatitis B virus (HBV) and hepatitis C virus (HCV) are typical non-cytopatic viruses that can induce tissue damage of variable severity by stimulating a protective immune response that can simultaneously cause damage and protection, by eliminating the intracellular virus through the destruction of virus infected cells. In hepatitis, virus infection apoptosis of the hepatocytes represents a host defence mechanism against viral infections in which an infected cell prevents viral replication and spread by dying. HBV and HCV replication is cell cycle dependent, supporting the concept of reduced virus replication in proliferative hepatocytes and viral elimination during cell regeneration. Increased hepatocyte proliferative activity is a well-established risk factor for cancer development. Among other environmental factors, hepatitis viruses should be listed in the etiology of hepatocellular carcinoma (HCC). Direct integration of HBV viral sequences into the host genome increases genomic instability, which does not occur in HCV infection. However, viral proteins may directly play a significant role in increased hepatocyte proliferation and induction of carcinogenesis by both viruses.
Descriptors		HEPATITIS, VIRAL, HUMAN APOPTOSIS CELL DIVISION LIVER NEOPLASMS CARCINOMA, HEPATOCELLULAR