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Related Experiment Videos

[Azole resistance in Candida spp].

Hiroshi Kakeya1, Taiga Miyazaki, Yoshitsugu Miyazaki

  • 1Division of Molecular and Clinical Microbiology, Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan.

Nihon Ishinkin Gakkai Zasshi = Japanese Journal of Medical Mycology
|May 16, 2003
PubMed
Summary

Azole resistance in Candida spp. is a growing concern. Mutations in the ERG11 gene, specifically Y132H and I471T, and ERG3 gene deletions contribute to azole resistance in HIV patients.

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Area of Science:

  • Mycology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Azole-resistant Candida species pose a significant challenge in treating recurrent oropharyngeal candidiasis, particularly in HIV-infected individuals.
  • Mechanisms of azole resistance include reduced drug accumulation via efflux transporters and alterations in the target enzyme Erg11p.
  • Understanding these resistance mechanisms is crucial for developing effective treatment strategies.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying azole resistance in Candida albicans.
  • To identify specific mutations in the ERG11 gene contributing to azole resistance.
  • To explore the role of the ERG3 gene in azole susceptibility.

Main Methods:

  • Sequencing of the ERG11 gene in an azole-resistant Candida albicans strain.

Related Experiment Videos

  • Site-directed mutagenesis to introduce specific ERG11 substitutions (Y132H, I471T) in an azole-susceptible strain.
  • Gene deletion of ERG3 in Candida albicans.
  • Sterol analysis of wild-type and mutant strains.

    • Main Results:

    • Two amino acid substitutions, Y132H and I471T, were identified in the ERG11 gene of an azole-resistant strain.
    • Introduction of Darlington ERG11 into an azole-susceptible strain conferred a modest increase in azole resistance.
    • The I471T substitution alone conferred azole resistance, which was enhanced when combined with Y132H.
    • Deletion of the ERG3 gene resulted in reduced azole susceptibility and altered sterol profiles.

    Conclusions:

    • Mutations in the ERG11 gene, particularly I471T, are significant contributors to azole resistance in Candida albicans.
    • Alterations in the sterol biosynthetic pathway, such as ERG3 deletion, also play a role in modulating azole susceptibility.
    • These findings provide insights into the genetic basis of azole resistance and potential targets for therapeutic intervention.