Cytokines and hepatitis C virus replication

D. Moradpour, Michael FRESE, H. Heim, Otto Haller, Ralf Bartenschlager, H. E. Blum

Research output: A Conference proceeding or a Chapter in BookConference contribution


With an estimated 170 million chronically infected individuals, the hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC) worldwide. A protective vaccine does not exist to date and therapeutic options are still limited. At present, inferon-a (IFN-a) in combination with ribavirin is the treatment of choice for chronic hepatitis C. The mechanism of action of IFN-a is only partially understood and may involve both direct antiviral and immunomodulatory effects. Recently, the replicon system has allowed the investigation of the effect of IF-a and other cytokines on HCV RNA replication. In addition, data obtained in other experimental model systems indicate that HCV has evolved strategies to counteract the antiviral effect of IFN-a. Such mechanisms could contribute to the resistance to IFN-a therapy observed in many patients and may represent a general escape strategy of HCV contributing to viral persistence and pathogenesis. In the following, we will briefly review current concepts of the interaction between cytokines, primarily IFN-a, and HCV.
Original languageEnglish
Title of host publicationCytokines in liver injury and repair
Subtitle of host publicationproceedings of Falk Symposium No. 125
EditorsA. M. Gressner, P. C. Heinrich, S. Matern
Place of PublicationThe Netherlands
PublisherKluwer Academic Publishers
Number of pages16
ISBN (Electronic)9780792387756
ISBN (Print)0792387759
Publication statusPublished - 2002
EventCytokines in liver injury and repair: proceedings of Falk Symposium No. 125 - Hanover, Hanover, Germany
Duration: 30 Sept 20011 Oct 2001


ConferenceCytokines in liver injury and repair


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