Our lab studies the interplay between viruses and the immune system. Our research contributes to the development of better antivirals and aims to understand the molecular basis of autoinflammatory diseases.

Viruses are obligate intracellular pathogens. In order to replicate they need to deliver their genomes, which are made of RNA or DNA, inside the host cell. Cells contain sensory proteins called nucleic acid receptors, which detect virally derived nucleic acids. Different types of nucleic acid receptors activate distinct antiviral defence mechanisms, which cooperate to clear the viral pathogen. Some receptors respond to infection by releasing antiviral molecules such as type I/III interferons, which prepare surrounding cells for the ensuing viral attack. Others, including the nucleic acid receptor ZBP1, instruct the infected cell to commit suicide thereby preventing viral dissemination. Our research focuses on the identification of the precise molecular mechanisms that activate nucleic acid receptors and how viruses fight back by blocking these processes.

In another aspect of our research we try to understand how nucleic acid receptors recognise viral nucleic acids and avoid contact with cellular RNA and DNA. Healthy uninfected cells are packed with RNA and DNA molecules, which make up our genetic material and contribute to normal cell function. Unwanted detection of these nucleic acids can result in the development of autoinflammatory diseases. We study the molecular processes that drive pathology through recognition of self-nucleic acids. In the future, this will enable us to selectively interfere with disease-causing mechanisms while leaving all other cellular processes untouched.