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Summary
The yeast Candida albicans is a component of the human oro-gastrointestinal and genital microbiota where it can exist in a commensal state without causing pathological infection. Yet, it is one of the main fungal pathogens of humans, responsible for superficial infections as well as disseminated, often deadly, infections (1). As the focus of recent research has been on understanding what makes C. albicans such a harmful pathogen, we know little about the commensal state and whether the interaction of C. albicans with the healthy human host has some reciprocally beneficial (mutualistic) components. Exploring this aspect has been hampered, in part, by the observation that most laboratory animals (including mice) are not natural hosts of C. albicans, and persistence of C. albicans in the gastrointestinal (GI) tract of these animals requires antibiotic-induced dysregulation of the microbiota (dysbiosis). By contrast, when allowed to reach the bloodstream, C. albicans behaves as a highly virulent pathogen of mice. On page 589 of this issue, Tso et al. (2) report how they have taken advantage of this dichotomy in C. albicans–mouse interactions to evolve this fungal pathogen into a genuine commensal that protects the host from other pathogens and might pave the way to a universal vaccine.
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