The role of the tyrosine kinase c-Src for
the replication
of the Hepatitis C Virus
In over 60% Hepatitis C Virus (HCV) develops chronic infection in its host and is a leading cause of chronic liver disease worldwide. Although the virus is targeted by the antiviral response of the host immune system, the high frequency of persistent infection indicates that HCV has evolved efficient mechanisms to interfere with the adaptive and innate immune response of the host and strategies to occupy and utilize host cell infrastructure. Apart from their role in the regulation of cell proliferation, c-Src, as well as the other members of the src family protein kinases (SFKs) are known to mediate intracellular signalling networks regulating metabolism, cytoskeletal alterations, differentiation, viability, adhesion and migration with in different cell lineages. Since Src-kinases are known to be a potential target for viral interference as demonstrated for e.g. the dengue virus (Chu and Yang, Proc. Natl. Acad. Sci. USA, 2007, 104, 3520–3525) and are involved in the replication of HIV (Saksela, Front. Biosci., 1997, 2, d606–d618) or the herpes simplex virus (Liang and Roizman, J. Virol., 2006, 80, 3349–3359), the question is whether c-Src plays a role for HCV replication.
1st supervisor: Prof. Dr. Johannes Bode
2nd supervisor: Prof. Dr. Hartmut Hengel
Institute:
Experimental Hepatology, Department of Gastroenterology, Hepatology and Infectiology, Heinrich Heine University Düsseldorf
Telephone: +49 (0)211 - 81 - 15639
E-mail: andreaspf@gmx.de |
