Steuerung der HCMV-Endothelzellinteraktion durch virale Gene

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Induction, maintenance and the disruption of homologous and heterologous cell interactions are hallmarks of endothelial cell (EC) function. To this purpose EC express specific adhesion molecules. Cytomegaloviruses, human cytomegalovirus (HCMV) and murine cytomegalovirus (MCMV) infect EC. How the CMV-EC-interaction is genetically orchestrated to the advantage of the virus, thereby causing chronic inflammation and induction of vascular disease is unknown. The genetic plasticity of the virus and a lack of a genetic approach has prevented the molecular analysis. We have pioneered complete cloning of herpesvirus genomes and have now succeeded in cloning an HCMV prototype for studies on EC CMV interactions. We wish to identify and to study HCMV genes responsible for EC tropism and for the exchange of virus material between EC cells, leukocytes and monocytes.