Fungal virulence determinants at the interface between commensalism and infection

C. albicans displays a remarkable intraspecies diversity. Genetically distinct isolates differ in their interaction with the host. This project seeks to identify genetic determinants that differentiate virulent from avirulent commensal isolates. By combining phenotyping, transcriptomic and genomic profiling, and genetic approaches, we aim at unravelling novel virulence attributes of C. albicans.

This project also investigates how pathogenicity of C. albicans is modulated by the host immune status. It interrogates whether commensal isolates are fixed in an avirulent state, or whether, in an immunodeficient host environment, they are able to adopt virulence traits.

Malassezia is the dominant fungal component of the skin microbiome. It is however not only a commensal but is also implicated in common skin disorders such as dandruff and atopic dermatitis. Only a handful of virulence attributes of Malassezia have been identified so far. These include the secreted aspartyl protease 1 (Sap1), which promotes skin inflammation, and a mycovirus, which elicits a type I interferon response. In this project we seek to identify novel virulence factors of Malassezia that explain how the fungus contributes to and exacerbates some of the most common skin diseases, many of which progress chronically-recurrent and are difficult to treat. Better knowledge about the role of Malassezia in pathogenesis will likely reveal new targets for future therapeutic approaches.