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Invasive candidiasis is among the most life-threatening infections in patients in intensive care units. Although  Candida albicans  is the leading cause of candidaemia, the incidence of  Candida parapsilosis  infections is also rising, particularly among the neonates. Due to differences in their biology, these species employ different antifungal resistance and virulence mechanisms and also induce dissimilar immune responses. Previously, it has been suggested that core virulence effecting transcription regulators could be attractive ligands for future antifungal drugs. Although the virulence regulatory mechanisms of  C. albicans  are well studied, less is known about similar mechanisms in  C. parapsilosis . In order to search for potential targets for future antifungal drugs against this species, we analyzed the fungal transcriptome during host-pathogen interaction using an  in vitro  infection model. Selected genes with high expression levels were further examined through their respective null mutant strains, under conditions that mimic the host environment or influence pathogenicity. As a result, we identified several mutants with relevant pathogenicity affecting phenotypes. During the study we highlight three potentially tractable signaling regulators that influence  C. parapsilosis  pathogenicity in distinct mechanisms. During infection,  CPAR2_100540  is responsible for nutrient acquisition,  CPAR2_200390  for cell wall assembly and morphology switching and  CPAR2_303700  for fungal viability.

Investigation of Candida parapsilosis virulence regulatory factors during host-pathogen interaction