Our organism is constantly bombarded with countless pathogens, yet we are relatively healthy. This is partially due our immune system, which recognises and destroys most invaders with only few of them escaping and causing illness. The pathogenicity of viruses is determined by virus-host interactions that occur at two sites: (1) cellular proteins sense incoming viruses and either trigger alarm signals or are directly involved in destruction of bugs and (2) viral gene products perturb the initiation or the execution of the immune response.

My lab is generally interested in the interaction of viral structures (proteins and nucleic acids) with host factors and the relevance for antiviral immunity. We further want to understand and gain mechanistic insights in changes on transcriptome and proteome level following viral infection. The research is based on mass spectrometric analysis or other unbiased screening approaches and extends to very focused hypothesis-driven in depth validation strategies that include the testing of interactions on molecular basis, in vitro cell culture assays and in vivo models using genetically modified animals.

We are also working on the function of viral open reading frames (vORFs) that function as modulators of the immune system. Such vORFs are partially responsible for the pathogenicity of viruses. We recently finished a large-scale mass spectrometry based survey (nicknamed “the Inhibitome”) identifying approximately 600 cellular interactors of viral immune modulators (iVIMs). We are now complementing this survey to assess the functional consequences for antiviral immunity of selected individual proteins.

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