A. Characterization of molecular mechanisms that
contribute to HSV-1 invasion into skin or mucosa
Our longterm goal is to understand how HSV-1 penetrates into the epithelium in vivo and initiates infection. The current knowledge of HSV-1 entry reflects that the virus is able to use a variety of entry modes at least in cell culture. The variety of strategies may in turn indicate that HSV-1 is highly flexible to adapt to differences of the target cell. The challenge will be to demonstrate whether these different entry modes play a role in natural target cells such as epidermal keratinocytes and dermal fibroblasts. To reach its receptors and initiate infection, the virus has to invade tissue and to overcome the protective barrier provided by mucosa and skin. We aim to understand which physical barriers, signalling pathways and receptors are involved in the viral entry process. We established a protocol for ex vivo infection of epidermal sheets that allows studying viral entry into the epidermis of mouse models as well as of human mucosa.
B. Actin rearrangement during early AcMNPV infection: the role of viral Arif 1
AcMNPV-infection of insect cells leads to extensive changes of the actin cytoskeleton. We have identified actin rearrangement-inducing factor 1 (Arif-1) as an early viral gene product that is involved in the remodeling of the actin cytoskeleton early during infection. Our further studies aim to elucidate the mode of action of Arif-1, and the role of Arif-1-induced actin rearrangement during the infection cycle.
March 30, 2016
Institute for Biochemistry II,
Joseph-Stelzmann-Strasse 52, D50931 Cologne
Suggestions and wishes: Gudrun Konertz