Research group Dynamics of early viral infection and the innate antiviral response

Infection-associated cancer can be caused by so-called oncogenes introduced directly by the pathogen (e.g. the E6/E7 genes of the papilloma virus), but in any case a persistent/chronic infection is essential for cancer development. Even in the complete absence of classical oncogenes, the long-term presence of pathogens and pathogen components can induce a persistent inflammatory response in the infected organ, ultimately promoting "passive" carcinogenesis (reviewed in a mini-review by Scott A. Read and Marc W. Douglas).

Our research group focuses on viral infections and tries to understand why the innate viral defense, which almost every cell in the body is capable of, recognizes and controls some viruses well, but fails with others. This can lead to serious courses of infections (e.g. SARS-CoV-2 / COVID-19) or to virus persistence (e.g. hepatitis C virus / chronic hepatitis C). Our goal is to better understand which molecular mechanisms are responsible for this, both on the side of the virus, but especially on the side of the host cell. In the long term, a better understanding of the responsible processes can ideally be exploited therapeutically (or prophylactically) to prevent severe courses, or to counteract or break the chronification of an infection.

Another aspect of our work is the relationship between these antiviral defense mechanisms and the body's control of tumorigenesis. In recent years, increasing evidence has been found that these same antiviral signaling pathways are also centrally involved in the recognition of DNA damage, which in principle has the potential to "transform" a cell and turn it into a cancer cell. We are trying to understand how and under what circumstances the antiviral system leads to the elimination of the damaged cell before tumorigenesis occurs. Furthermore, we are trying to exploit this system to improve chemo- and radiotherapy of tumors.

For the study of cellular pathogen recognition and subsequent antiviral signaling pathways, we use a wide variety of model viruses and systems, such as Vesicular Stomatitis Virus (VSV), Rift Valley Fever Virus (RVFV), or virus-free stimulation of the antiviral defense program by transfection of ligand RNA or expression of constitutively active signaling molecules. Using molecular and cell biological, as well as biochemical methods, we investigate the signaling pathways leading to the induction of type I and III interferons, the proinflammatory system and, in certain cases, cell death. Increasing focus is currently being put on interactions between "professional" immune cells and "normal" tissue cells, as well as mechanisms of gene regulation at the single cell level.

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