Virus replication depends on the help of the infected host. For their multiplication viruses misuse components of the host cell and evade or even shut off cellular defense mechanisms. We are interested in identification of new interaction partners of viral components in animal and human cells. Furthermore, we want to discover new cellular signaling pathways, which are altered or exploited by viruses for their own purpose.  Especially, we focus on the interaction of retro- and influenza viruses with cellular factors in the late phase of viral replication. Another aspect of our research has been the improvement of so-called minicircle expression vectors. This novel type of vector supports our investigations and is characterized by high-level expression, the lack of a bacterial backbone, as well the ability for stable, episomal replication.

Understanding the interplay of viral proteins and cellular interfaces and defining new cellular targets for therapy are central aims of our research. The acquired knowledge then can serve for development of antiviral therapies or the improvement of vaccine- or viral vector production.

To date, we demonstrated that caveolin-1, a multifunctional membrane protein, influences the propagation of retroviruses as well as human influenza A viruses. Interestingly, interaction of these viruses, which belong to different viral families, evokes distinct, but different mechanisms suggesting that cav-1 exerts different functions in the life cycle of these viruses. The characterization of the participating late events in virus synthesis and the elucidation of affected cellular signaling pathways is part of current research. The results will gain valuable hints for putative targets for developing antiviral strategies.

Further information and details for bachelor and master thesis can be received from Dr. Manfred Wirth

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