The commensal-to-pathogen shift of the human pathogenic fungus Candida albicans

Fungal infections are often underestimated as a significant cause of mortality. Most pathogenic fungi originate from the environment, but one of the most common and important fungal pathogens, Candida albicans, lives as a commensal within the vast majority of humans. The adaptation of this fungus to the human host is the result of an ancient, mostly commensal relationship which has led to the development of distinct fungal strategies to survive and proliferate in diverse host niches. 
In its pathogenic phase, C. albicans relies on attachment to, invasion into, and damage of epithelial cells. The yeast-to-hypha transition is essential for these pathogenic events. Hyphae production is strongly linked to the expression of hypha-associated genes, a transcriptional pattern which represents a virulence program and anticipatory gene expression mechanisms. Filaments of C. albicans are more adhesive and more invasive than yeast cells. Invasion is accompanied by epithelial damage, however, it does not cause damage per se. In fact, most of the damage is due to the hypha-associated peptide toxin candidalysin, which is conserved among clinical isolates of C. albicans. 
However, considering that C. albicans is predominantly a commensal within a normal microbiota we asked which selective pressures are responsible for the conservation of such a critical toxin. Only recently, we discovered that hypha formation and the expression of candidalysin is also critical for commensal growth. This led us to propose that the adaptation to a commensal lifestyle of C. albicans has primed the fungus to be such a successful pathogen.