MOLECULAR DETERMINANTS OF ANTIFUNGAL RESISTANCE IN CANDIDA AURIS

Candida auris is known for its strains resistant to multiple antifungal agents, prompting research into the molecular mechanisms underlying this resistance. This review aims to summarize key findings from recent studies. A comprehensive search of online databases and relevant websites was conducted. The analysis reveals that most C. auris strains exhibit high resistance to fluconazole, moderate resistance to amphotericin B, and lower resistance to 5-fluorocytosine and caspofungin. Amphotericin B resistance in C. auris has been linked to the overexpression of mutated ERG genes, resulting in reduced ergosterol levels. Resistance to fluconazole is largely attributed to mutations in the ERG11 gene, an increased number of ERG11 gene copies, and overexpression of efflux pumps. For 5-fluorocytosine, resistance is hypothesized to stem from mutations in the FCY2, FCY1, and FUR1 genes. Caspofungin resistance is associated with mutations in the FKS1 gene. Moreover, resistance to each antifungal appears to be closely related to the clade type of the C. auris strain.