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Candida albicans is a fungal pathogen that lives in both commensal and opportunistic lifestyles within the human host. Fungal metabolism has long been thought to play a role in virulence, while the nutrient sources used by human pathogenic fungus in vivo remain obscure. A significant factor of disease progression is the interaction between C. albicans and the innate immune system. C. albicans has a complicated response to phagocytosis, which is like carbon deprivation. This shows that in vivo, nutritional deficiency is a substantial stressor. The mechanisms of Carbon and nitrogen catabolite repressions (CCR, NCR) are crucial for virulence as they utilize favored carbon and nitrogen sources respectively in a host niche-dependent manner. The findings of various studies demonstrate linkages between carbon metabolic regulations, pathogenicity, and Snf1 (sucrose-nonfermenting 1), a conserved regulator of nutrient stress response. It also links Mig1 (Multicopy Inhibitor of GAL) and Mig2 to the C. albicans glucose restraint pathway. Carbon utilization abnormalities in mutants lacking the ICL1 (Isocitrate lyase 1), a glyoxylate enzyme are likewise more severe than expected. These findings show that C. albicans' regulation of alternative carbon metabolism differs dramatically from that of other fungi. C. albicans regularly encounters nitrogen deficiency and carbon-poor environments throughout its development in the host, and the ability to effectively use a variety of non-fermentable carbon and nitrogen sources is a virulence determinant. The knowledge obtained from these studies could be useful for developing effective therapeutic strategies for the control of fungal diseases.
Sahoo et al. (2024) studied this question.