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World J Gastroenterol. Sep 28, 2007; 13(36): 4865-4872
Published online Sep 28, 2007. doi: 10.3748/wjg.v13.i36.4865
Hepatitis C virus infection and apoptosis
Richard Fischer, Thomas Baumert, Hubert E Blum
Richard Fischer, Hubert E Blum, Department of Internal Medicine II, University of Freiburg, Germany
Thomas Baumert, Inserm U748, Service d’Hépatogastro-entérologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France
Author contributions: All authors contributed equally to the work.
Correspondence to: Richard Fischer, MD, Department of Internal Medicine II, University of Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany.
Telephone: +49-761-2703403 Fax: +49-761-2703760
Received: June 26, 2007
Revised: July 2, 2007
Accepted: July 9, 2007
Published online: September 28, 2007

Apoptosis is central for the control and elimination of viral infections. In chronic hepatitis C virus (HCV) infection, enhanced hepatocyte apoptosis and upregulation of the death inducing ligands CD95/Fas, TRAIL and TNFα occur. Nevertheless, HCV infection persists in the majority of patients. The impact of apoptosis in chronic HCV infection is not well understood. It may be harmful by triggering liver fibrosis, or essential in interferon (IFN) induced HCV elimination. For virtually all HCV proteins, pro- and anti-apoptotic effects have been described, especially for the core and NS5A protein. To date, it is not known which HCV protein affects apoptosis in vivo and whether the infectious virions act pro- or anti-apoptotic. With the availability of an infectious tissue culture system, we now can address pathophysiologically relevant issues. This review focuses on the effect of HCV infection and different HCV proteins on apoptosis and of the corresponding signaling cascades.

Keywords: Hepatitis C, Spoptosis, TRAIL, CD95/Fas, TNFα, Perforin