Research

We are interested in the interplay between viruses and their hosts, with a special focus on intrinsic defense mechanisms. Viral infections rely on the efficient and specific manipulation of host cells by viruses. We use genetic approaches to identify the underlying host factors that viruses need to replicate. By employing a broad spectrum of methods from virology, cell biology, and biochemistry, we aim to characterize these virus-host relationships and ultimately help identify novel targets for antiviral therapies.

Additionally, we focus on cell-intrinsic immune responses that limit infection. Our cells are capable of sensing viruses as foreign and consequently produce interferons. These interferons act as alarm signals to surrounding cells, triggering the expression of a panel of antiviral factors known as interferon-stimulated genes (ISGs). These ISGs help control and restrict viral infections in various ways. We are interested in these factors and seek to understand how they contribute to controlling viral infections.

Selected current projects

Innate immune responses upon hepatitis E virus infection

The hepatitis E virus (HEV) is the most common cause of acute viral hepatitis in humans worldwide. Each year, an estimated 20 million HEV infections occur, leading to approximately 3.3 million cases of acute illness and 70,000 HEV-related deaths. So far, the underlying molecular mechanisms by which intrinsic immune mechanisms help control HEV infections remain elusive. We performed a gain-of-function screen and identified critical human ISGs with anti-HEV activity. By utilizing state-of-the-art virological, biochemical, and genetic techniques, we are currently unraveling the mechanisms of action of individual factors with a strong anti-HEV phenotype. The results of this project will not only contribute to understanding the role of ISGs in restricting HEV but also to fundamental aspects of HEV virology and mammalian innate immunity.

Restriction of retrotransposable elements by interferon-stimulated genes

Retrotransposons are jumping genes in our genome that can cause a number of age-related and neurological diseases such as amyotrophic lateral sclerosis. The cellular protein shiftless appears to be an important factor in controlling retrotransposon activity. In this project, we aim to uncover the molecular mechanism of shiftless and whether the factor can prevent the development of diseases. The results of the project may contribute to basic understanding of pathogenesis and to the development of new therapy and prevention strategies for neurological and age-related diseases.