Evolution of antifungal-drug resistance: mechanisms and pathogen fitness
Abstract
Like other microorganisms, fungi exist in populations that are adaptable. Under the selection imposed by antifungal drugs, drug-sensitive fungal pathogens frequently evolve resistance. Although the molecular mechanisms of resistance are well-characterized, there are few measurements of the impact of these mechanisms on pathogen fitness in different environments. To predict resistance before a new drug is prescribed in the clinic, the full spectrum of potential resistance mutations and the interactions among combinations of divergent mechanisms can be determined in evolution experiments. In the search for new strategies to manage drug resistance, measuring the limits of adaptation might reveal methods for trapping fungal pathogens in evolutionary dead ends.
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In C. albicans, two major classes of efflux pumps modulate drug exportation: the ATP-binding cassette transporter superfamily (including CDR1 and CDR2) and the major facilitator class (including MDR1).
“In C. albicans, two major classes of efflux pumps modulate drug exportation: the ATP-binding cassette transporter superfamily (including CDR1 and CDR2) and the major facilitator class (including MDR1) (4, 33, 156).”
From <i>Candida albicans</i> Biofilms and Human Disease (2015) · cites this paper as [4]
It is widely believed that antifungal drugs with new mechanisms of action are needed.
“and it is widely believed that antifungal drugs with new mechanisms of action are needed (4, 18, 79).”
From <i>Candida albicans</i> Biofilms and Human Disease (2015) · cites this paper as [4]
Current antifungal drugs have only two specific targets: ergosterol biosynthesis and 1,3-β-D-glucan synthesis.
“Current antifungal drugs have only two specific targets (ergosterol biosynthesis and 1,3-β-D-glucan synthesis)”
From <i>Candida albicans</i> Biofilms and Human Disease (2015) · cites this paper as [4]
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References 63 · Cited by 375
- Authors
- Anderson, J. B.
- Affiliations
- University of Toronto (CA)
- Corresponding author
- Anderson, James B.
- ORCID
- Anderson, James B.
- Venue
- Nature Reviews Microbiology
- Published
- 2005-06-10
- Volume
- 3
- Issue
- 7
- Pages
- 547-556
- ISSN
- 1740-1526 (ISSN-L)
- 1740-1534
- OpenAlex
- W1979749196
- Cited by
- 375
- References
- 63
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 14 · 2023: 19 · 2022: 8 · 2021: 32 · 2020: 24 · 2019: 22 · 2018: 20 · 2017: 22 · 2016: 19 · 2015: 24 · 2014: 22 · 2013: 23 · 2012: 22
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Keywords
- antifungal resistance, fungal pathogens, pathogen fitness, resistance mechanisms, resistance mutations, drug resistance evolution, evolutionary dead ends, resistance management, fitness cost of resistance
- MeSH terms
- Antifungal Agents, Candida albicans, Epistasis, Genetic, Biological Evolution, Forecasting, Fungi, Humans, Microbial Sensitivity Tests, Mutation, Saccharomyces cerevisiae, Virulence, Drug Resistance, Fungal
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