Hepatitis E virus–host interactions and the development of infection models

We are interested in understanding the fundamental mechanisms that govern hepatitis E virus (HEV) infection. Our work focuses on identifying host factors that enable viral entry and determining how these cellular signalling pathways influence the tropism of HEV. Using genetic, molecular biological and cell biological approaches, we aim to define the host determinants necessary for productive infection and to understand how HEV exploits the cellular machinery of its target cells. In parallel, we are developing new, physiologically relevant culture systems, including porcine models, to better reflect the natural biology of HEV infection and to provide new experimental platforms for investigating virus-host interactions.

Intrinsic immunity and interferon-stimulated genes as restriction factors for intracellular pathogens

We are investigating how the interferon system and its downstream effectors protect cells from infection and genomic instability. Our research aims to identify interferon-stimulated genes (ISGs) that restrict various intracellular pathogens and to define the molecular mechanisms underlying their antiviral and antibacterial activity. Current work analyses cellular defence mechanisms against HEV, processes that suppress the mobilisation of the endogenous retroelement LINE-1, and host factors that limit the intracellular replication of bacterial pathogens such as Salmonella enterica. By investigating these different biological systems, we aim to uncover fundamental principles of innate immunity and gain mechanistic insights into how cells recognise and control intracellular threats.