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Investigation of Azole Resistance Involving cyp51A and cyp51B Genes in Clinical Aspergillus flavus Isolates
Dhoha Ghorbel1, Imen Amouri1, Nahed Khemekhem1
11Fungi and Parasitic Molecular Biology Laboratory, School of Medicine, University of Sfax, Sfax, Tunisia.
Abstract:
This study aimed to investigate azole resistance mechanisms in Aspergillus flavus, which involve cyp51A and cyp51B genes. Real-time Reverse Transcriptase qPCR method was applied to determine the overexpression of cyp51A and cyp51B genes for 34 A. flavus isolates. PCR sequencing of these two genes was used to detect the presence of gene mutations. Susceptibility test found sensitivity to voriconazole (VOR) in all strains. 14.7% and 8.8% of isolates were resistant to itraconazole (IT) and posaconazole (POS), respectively, with a cross-resistance in 5.8%. For the double resistant isolates (IT/POS), the expression of cyp51A was up to 17-fold higher. PCR sequencing showed the presence of 2 mutations in cyp51A: a synonymous point mutation (P61P) in eight isolates, which did not affect the structure of CYP51A protein, and another non synonymous mutation (G206L) for only the TN-33 strain (cross IT/POS resistance) causing an amino acid change in the protein sequence. However, we noted in cyp51B the presence of the only non-synonymous mutation (L177G) causing a change in amino acids in the protein sequence for the TN-31 strain, which exhibits IT/POS cross-resistance. A short single intron of 67 bp was identified in the cyp51A gene, whereas three short introns of 54, 53, and 160 bp were identified in the cyp51B gene. According to the models provided by PatchDock software, the presence of non-synonymous mutations did not affect the interaction of CYP51A and CYP51B proteins with antifungals. In our study, the overexpression of the cyp51A and cyp51B genes is the primary mechanism responsible for resistance in A. flavus collection. Nevertheless, other resistance mechanisms can be involved.
Insights
Azole resistance in Aspergillus flavus is primarily driven by overexpression of the cyp51A and cyp51B genes, not mutations. This finding is crucial for understanding and combating antifungal resistance in clinical settings.
Area of Science:
- Medical Mycology
- Antifungal Resistance Mechanisms
- Molecular Biology
Background:
- Azole antifungals are crucial for treating invasive fungal infections.
- Aspergillus flavus poses a significant threat, with emerging resistance complicating treatment.
- Understanding resistance mechanisms is vital for effective therapeutic strategies.
Purpose of the Study:
- To investigate the roles of cyp51A and cyp51B genes in azole resistance in Aspergillus flavus.
- To identify specific mutations and gene expression levels associated with resistance.
- To elucidate the primary mechanisms of azole resistance in A. flavus isolates.
Main Methods:
- Real-time Reverse Transcriptase qPCR to quantify cyp51A and cyp51B gene expression.
- PCR sequencing to detect mutations in cyp51A and cyp51B genes.
- Antifungal susceptibility testing for voriconazole, itraconazole, and posaconazole.
Main Results:
- All isolates remained sensitive to voriconazole.
- Resistance to itraconazole (14.7%) and posaconazole (8.8%) was observed, with cross-resistance in 5.8%.
- Overexpression of cyp51A (up to 17-fold) was noted in double-resistant isolates; specific mutations were identified but did not impact protein-antifungal interactions, suggesting overexpression is the key resistance mechanism.
Conclusions:
- Overexpression of cyp51A and cyp51B genes is the main mechanism of azole resistance in this A. flavus collection.
- Identified mutations in cyp51A and cyp51B did not appear to directly cause resistance.
- Further research into other potential resistance mechanisms is warranted.
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