Prevalence of Molecular Mechanisms of Resistance to Azole Antifungal Agents in Candida albicans Strains Displaying High-Level Fluconazole Resistance Isolated from Human Immunodeficiency Virus-Infected Patients

Perea, Sofia; López-Ribot, José L.; Kirkpatrick, William R.; McAtee, Robert K.; Santillán, Rebecca A.; Martı́nez, Marcos; Calabrese, David; Sanglard, Dominique; Patterson, Thomas F.

doi:10.1128/aac.45.10.2676-2684.2001

Cited by 470Antifungal resistance and susceptibilityFungal Plant Pathogen ControlAntibiotic Resistance in Bacteria

Prevalence of Molecular Mechanisms of Resistance to Azole Antifungal Agents in Candida albicans Strains Displaying High-Level Fluconazole Resistance Isolated from Human Immunodeficiency Virus-Infected Patients

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Perea, Sofia, López-Ribot, José L., Kirkpatrick, William R., McAtee, Robert K., Santillán, Rebecca A., Martı́nez, Marcos, Calabrese, David, Sanglard, Dominique +1 more·2001·Antimicrobial Agents and Chemotherapy

DOI 10.1128/aac.45.10.2676-2684.2001PMC PMC90716

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Abstract

Molecular mechanisms of azole resistance in Candida albicans, including alterations in the target enzyme and increased efflux of drug, have been described, but the epidemiology of the resistance mechanisms has not been established. We have investigated the molecular mechanisms of resistance to azoles in C. albicans strains displaying high-level fluconazole resistance (MICs, > or =64 microg/ml) isolated from human immunodeficiency virus (HIV)-infected patients with oropharyngeal candidiasis. The levels of expression of genes encoding lanosterol 14alpha-demethylase (ERG11) and efflux transporters (MDR1 and CDR) implicated in azole resistance were monitored in matched sets of susceptible and resistant isolates. In addition, ERG11 genes were amplified by PCR, and their nucleotide sequences were determined in order to detect point mutations with a possible effect in the affinity for azoles. The analysis confirmed the multifactorial nature of azole resistance and the prevalence of these mechanisms of resistance in C. albicans clinical isolates exhibiting frank fluconazole resistance, with a predominance of overexpression of genes encoding efflux pumps, detected in 85% of all resistant isolates, being found. Alterations in the target enzyme, including functional amino acid substitutions and overexpression of the gene that encodes the enzyme, were detected in 65 and 35% of the isolates, respectively. Overall, multiple mechanisms of resistance were combined in 75% of the isolates displaying high-level fluconazole resistance. These results may help in the development of new strategies to overcome the problem of resistance as well as new treatments for this condition.

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Studies in clinical isolates have implicated multiple mechanisms in resistance, but have focused on large-scale aberrations or candidate genes, and do not comprehensively chart the genetic basis of adaptation.
“Studies in clinical isolates have implicated multiple mechanisms in resistance, but have focused on large-scale aberrations or candidate genes, and do not comprehensively chart the genetic basis of adaptation.”
From The evolution of drug resistance in clinical isolates of Candida albicans. (2015) · cites this paper as Perea et al., 2001
Overexpression of ERG11 contributes to decreased azole susceptibility through increased production of the azole target 14α-lanosterol demethylase.
“The overexpression of ERG11 had been shown to contribute to decreased azole susceptibility through increased production of the azole target 14α-lanosterol demethylase (Figure 1a).78 , 98 , 106 , 107”
From Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungusCandida albicans (2020) · cites this paper as [106]
In clinical and agricultural azole-resistant isolates, overexpression of sterol 14α-demethylase or azole efflux pumps are among the major causes for azole resistance.
“In clinical and agricultural azole-resistant isolates, overexpression of sterol 14α-demethylase or azole efflux pumps are among the major causes for azole resistance (White, 1997; Perea et al., 2001; Perea et al., 2002; Redding et al., 2003; Cools et al., 2013; Price et al., 2015).”
From Abnormal Ergosterol Biosynthesis Activates Transcriptional Responses to Antifungal Azoles (2018) · cites this paper as Perea et al., 2001

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Authors: Perea, S., López-Ribot, J. L., Kirkpatrick, W. R., McAtee, R. K., Santillán, R. A., Martı́nez, M., Calabrese, D., Sanglard, D., & Patterson, T. F.
Affiliations: The University of Texas at San Antonio Health Science Center (US)
Department of Medicine, Division of Infectious Diseases, The University of Texas Health Science Center at San Antonio,1 and
Centre Hospitalier Universitaire Vaudois (CH)
ORCID: Perea, Sofia
Sanglard, Dominique
Patterson, Thomas F.
Venue: Antimicrobial Agents and Chemotherapy
Publisher: American Society for Microbiology
Published: 2001-10
Volume: 45
Issue: 10
Pages: 2676-2684
ISSN: 0066-4804 (ISSN-L)
1098-6596
DOI: 10.1128/aac.45.10.2676-2684.2001
PMC: PMC90716
OpenAlex: W2147757952
Cited by: 470
References: 45
Citations by year: 2026: 7 · 2025: 13 · 2024: 17 · 2023: 12 · 2022: 14 · 2021: 14 · 2020: 13 · 2019: 30 · 2018: 14 · 2017: 21 · 2016: 18 · 2015: 28 · 2014: 28 · 2013: 24 · 2012: 20
FWCI: 17.24
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Antimicrobial Agents and Chemotherapy (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Funders: University of Texas Health Science Center at San Antonio
National Institute of Allergy and Infectious Diseases (1 R29 AI42401, R29AI042401)
National Institute of Dental and Craniofacial Research (5 R01 DE11381, 3 R01 DE11381-04A2S2, R01DE011381)
National Center for Research Resources (M01RR001346)
Topics: Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
Keywords: Candida albicans, azole resistance, fluconazole resistance, HIV infection, oropharyngeal candidiasis, ERG11, lanosterol 14α-demethylase, efflux pumps, MDR1, CDR, gene overexpression, point mutations, multidrug resistance, antifungal resistance mechanisms
MeSH terms: RUNX1 Translocation Partner 1 Protein, Antifungal Agents, Azoles, Candida albicans, Cytochrome P-450 Enzyme System, DNA-Binding Proteins, Drug Resistance, Microbial, Gene Frequency, Humans, Microbial Sensitivity Tests, Mutation, Oxidoreductases, Proto-Oncogene Proteins, Transcription Factors, HIV Infections, Fluconazole, ATP Binding Cassette Transporter, Subfamily B, Member 1, Sterol 14-Demethylase

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Prevalence of Molecular Mechanisms of Resistance to Azole Antifungal Agents in Candida albicans Strains Displaying High-Level Fluconazole Resistance Isolated from Human Immunodeficiency Virus-Infected Patients

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