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Molecular analysis of cyp51 from fluconazole-resistant Candida albicans strains

J Löffler1, S L Kelly, H Hebart

  • 1Medizinische Klinik, Abt. II, Universität Tübingen, Germany.

Insights

Fluconazole resistance in Candida albicans may stem from mutations in the target enzyme, sterol 14 alpha-demethylase (cyp51). DNA sequencing identified several new mutations in resistant strains, aiding in the development of diagnostic tests for this fungal infection.

Area of Science:

  • Medical Mycology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Fluconazole is a key antifungal medication targeting sterol 14 alpha-demethylase (CYP51).
  • Candida albicans can develop resistance to fluconazole, posing a significant clinical challenge.
  • Altered target enzyme sites are a suspected mechanism for fluconazole resistance.

Purpose of the Study:

  • To investigate the role of target site alteration in fluconazole resistance in Candida albicans.
  • To identify specific mutations in the cyp51 gene associated with fluconazole resistance.

Main Methods:

  • DNA sequencing of the cyp51 gene in fluconazole-resistant and sensitive Candida albicans isolates.
  • Analysis of point mutations and their correlation with resistance phenotypes.
  • Utilizing molecular modeling to assess the impact of mutations on enzyme function.

Main Results:

  • Multiple point mutations were identified in the cyp51 gene of fluconazole-resistant isolates, absent in sensitive strains.
  • Specific mutations included F105L, E266D, K287R, G448G, G450E, G464S, and V488I.
  • Sequence-specific primers were developed to detect resistance-associated polymorphisms.

Conclusions:

  • Target site modification via cyp51 mutations is a likely mechanism of fluconazole resistance in Candida albicans.
  • Identified mutations provide insights into enzyme-drug interactions and resistance mechanisms.
  • Diagnostic tests based on these polymorphisms can aid in managing fluconazole-resistant infections.

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