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The ergosterol biosynthesis pathway, transporter genes, and azole resistance in Aspergillus fumigatus

M E da Silva Ferreira1, A L Colombo, I Paulsen

  • 1Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil.

Medical Mycology
|August 23, 2005
PubMed

Insights

Continuous triazole use drives antifungal resistance in Aspergillus fumigatus. Resistance mechanisms include target mutations and reduced drug accumulation due to efflux pumps.

Area of Science:

  • Mycology
  • Molecular Biology
  • Drug Resistance

Background:

  • Continuous triazole use leads to antifungal resistance.
  • Azole resistance in Aspergillus fumigatus is a growing clinical concern.
  • Azoles target the ergosterol biosynthesis pathway by inhibiting CYP51 (14-alpha-demethylase).

Purpose of the Study:

  • To investigate the mechanisms of azole resistance in Aspergillus fumigatus.
  • To understand the role of efflux transporters in reduced drug accumulation.
  • To compare gene duplication and transporter gene families in Aspergillus spp. versus other fungi.

Main Methods:

  • Analysis of azole-resistant clinical isolates and mutants of Aspergillus fumigatus.
  • Examination of the ergosterol biosynthesis pathway and associated gene duplications.
  • Comparative genomics of transporter genes (ABC and MFS) in Aspergillus spp. and other fungal species.

Main Results:

  • Azole resistance involves target site alterations and decreased intracellular accumulation.
  • Reduced accumulation is linked to overexpression of multidrug resistance (MDR) efflux transporters (ABC and MFS).
  • Aspergillus fumigatus has duplicated erg3 and erg11 genes; Aspergillus spp. possess proportionally more MFS and specific ABC transporter genes than other fungi.

Conclusions:

  • Fungal azole resistance is multifactorial, involving target modification and active efflux.
  • Overexpression of MDR transporters significantly contributes to azole resistance.
  • Aspergillus spp. exhibit unique genetic features, including gene duplications and expanded transporter families, potentially influencing drug resistance profiles.

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