Speaker: Bernhard Hube
Host: Alexander Weber (CMFI)
Geo- und Umweltforschungszentrum (GUZ)
The fungus Candida albicans is both, a commensal and an opportunistic pathogen. The adaptation of this fungus to the human host is the result of an ancient, mostly commensal, relationship and has led to the development of distinct fungal strategies to survive and proliferate in diverse host niches.
For its transition to a pathogenic phase in the host, it relies on attachment to, invasion into, and damage of epithelial cells. Adhesion is mediated by fungal surface proteins and stimulates hyphae production and expression of hypha-associated genes. These filaments are not only more adhesive, but also more invasive than yeast cells. Invasion is accompanied by epithelial damage, however, it does not necessarily cause damage per se. In fact, it has become clear that most of the damage is due to a hypha-associated polyprotein containing the first peptide toxin identified in a human pathogenic fungus.
On the other hand, the host has adapted and evolved mechanisms to prevent invasion and infection by any type of microbes, including C. albicans. This co-evolution scenario has not only led to the emergence of distinct microbial virulence factors, but also to “avirulence factors” (well known in the plant pathology field) or “immune modulators” (in the field of human immunology), which, once expressed by the microbial pathogen, are recognized by the host and trigger microbial clearance via immune responses.
In C. albicans, we found examples of proteins which contribute to both offence and defence, and which are thus both virulence and avirulence factors.