Candida glabrata is a major cause of invasive candidiasis and is difficult to treat due to its intrinsic resistance to antifungal drugs and its ability to survive inside host immune cells. How this pathogen regulates its intracellular lifestyle and exit from macrophages remains poorly understood. We show that C. glabrata actively modulates its interaction with macrophages through the protein kinase Ksp1, which regulates mitochondrial dysfunction and the formation of respiration-deficient cells. These variants display enhanced resistance to two antifungal drugs and killing by phagocytes. Our findings suggest that prolonging the intramacrophage phase and generating stress-resistant variants are key components of C. glabrata’s survival strategy. Recognizing these processes has important implications for clinical diagnostics and the management of persistent and recurrent fungal infections.

Nature Reviews Microbiology - In this Review, Hube and colleagues overview the commensal and pathogenic lifestyles of Candida albicans, focusing on how the fungus transitions between these two...

In medicine, women constitute a large proportion of the workforce but remain underrepresented in senior positions. Scientific conferences, critical for career advancement, reflect these inequities, wi...

Author summary In this study, we set out to understand whether Candida albicans found in nature can be as dangerous as the strains collected from patients, and whether a diet high in sugar affects the...

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Author summary In this study, we set out to understand whether Candida albicans found in nature can be as dangerous as the strains collected from patients, and whether a diet high in sugar affects the...