ArticleNature microbiology2024
Acquired amphotericin B resistance leads to fitness trade-offs that can be mitigated by compensatory evolution in Candida auris.
Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed.
- Pathogenicity and virulence ofVirulence · 2026Review
- Micafungin microevolution inVirulence · 2026Article
- Genome architecture drives antifungal resistance in Candida auris.Nature communications · 2026Article
- Natural Product-Inspired Antifungal Drugs Introduced for Human Use from 1872 to August 2026.Antibiotics (Basel, Switzerland) · 2026Review
- Antimicrobial Peptides as Eco-Innovative Therapeutics to Overcome Antifungal Pressure-Induced Resistance in Candida Infections.Current microbiology · 2026Review
- Beyond intrinsic resistance: novel insights into the emergence and management of resistance acquired in Candida auris upon antifungal exposure.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- In vitro evaluation of Curcuma longa extract for antifungal, antibiofilm, and synergistic activity against Candida spp.Scientific reports · 2026Article
- Article
- Micafungin exposure drives multidrug resistance inbioRxiv : the preprint server for biology · 2026Article
- Urosepsis by multidrug-resistantmBio · 2026Article
- Emerging evidence for a multitude of mechanisms and factors that determine amphotericin B resistance in pathogenic fungi.Cell surface (Amsterdam, Netherlands) · 2026Review
- Peroxin Pex8 couples stress responses, antifungal tolerance, and virulence regulation inAntimicrobial agents and chemotherapy · 2026Article
- EneA of Aspergillus fumigatus is a regulator of secondary metabolism and enhances nscA expression in presence of polyenes and Streptomyces.Scientific reports · 2026Article
- Uncovering actionable trade-offs of antifungal resistance in a yeast pathogen.Molecular systems biology · 2026Article
- Deciphering the multidrug resistance paradigm inAntimicrobial agents and chemotherapy · 2026Review
- Visible Photosensitizing Disinfectant Spray for Combating Multidrug-ResistantExploration (Beijing, China) · 2026Article
- Review
- The emerging pathogen Candida auris: host interactions and disease drivers.Journal of biomedical science · 2026Review
- EditingBiomolecules · 2026Review
- Candida auris Testing by the Antimicrobial Resistance Laboratory Network, United States, 2022-2023.Emerging infectious diseases · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida auris is a growing concern due to its resistance to antifungal drugs, particularly amphotericin B (AMB), detected in 30 to 60% of clinical isolates. However, the mechanisms of AMB resistance remain poorly understood. Here we investigated 441 in vitro- and in vivo-evolved C. auris lineages from 4 AMB-susceptible clinical strains of different clades. Genetic and sterol analyses revealed four major types of sterol alterations as a result of clinically rare variations in sterol biosynthesis genes ERG6, NCP1, ERG11, ERG3, HMG1, ERG10 and ERG12. In addition, aneuploidies in chromosomes 4 and 6 emerged during resistance evolution. Fitness trade-off phenotyping and mathematical modelling identified diverse strain- and mechanism-dependent fitness trade-offs. Variation in CDC25 rescued fitness trade-offs, thereby increasing the infection capacity. This possibly contributed to therapy-induced acquired AMB resistance in the clinic. Our findings highlight sterol-modulating mechanisms and fitness trade-off compensation as risks for AMB treatment failure in clinical settings.
Indexed as
Identifiers
39567662What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.