Invasive candidiasis, the most frequent healthcare associated invasive fungal infection, is commonly caused by Candida albicans. However, in recent years other antifungal-resistant Candida species – namely C. glabrata and C. auris – have emerged as a serious matter of concern. Much of our understanding of the mechanisms regulating antifungal resistance and tolerance relies on studies utilising C. albicans, C. glabrata, and the model yeast Saccharomyces cerevisiae. ‘Omics studies have been used to describe alterations in metabolic, genomic and transcriptomic expression profiles upon antifungal treatment of fungal cells. The physiological changes identified by these approaches could significantly affect fungal fitness in the host and survival during antifungal challenge, as well as provide further understanding of clinical resistance. Thus, this review aims to comparatively address ‘omics data for C. albicans, C. glabrata, and S. cerevisiae published from 2000 to 2021 to identify what these technologies can tell us regarding cellular responses to antifungal therapy. We will also highlight possible effects on pathogen survival and identify future avenues for antifungal research.
We are grateful to P. David Rogers for permission to review datasets from Kelly Caudle‘s thesis. We wish to acknowledge our friends and colleagues in the Aberdeen Fungal Group and Edward Wallace (University of Edinburgh) for their comments on this manuscript. Finally, we wish to apologize to any colleagues whose work we have left out due to space constraints.
G.F. Ribeiro: PhD studentship from University of Aberdeen.
E. Denes: PhD studentship from BBSRC Eastbio doctoral training programme.
H. Heaney is supported by The Academy of Medical Sciences (SBF006\1128).
D.S. Childers has financial support from Carnegie Trust (RIG009286), The Royal Society (RGS\R2\202409) and The Academy of Medical Sciences (SBF006\1128).
All: This work was supported by the University of Aberdeen.
- Candida albicans
- Candida glabrata
- Saccharomyces cerevisiae