Candida auris adhesins, specifically Als3, a key target to understand and mitigate.

The emergence of Candida auris, a multidrug-resistant fungal pathogen with unique heterogenic characteristics and clades, raised significant concerns globally, particularly in healthcare settings. C. auris pathogenicity resides in its adaptability and resilience, with the ability to form robust biofilms and adhere to host tissues and medical devices. Adhesins, particularly Als3, primarily mediate these processes. This review explores the variations in expression, copy numbers, and genetic modifications of Als3 in relation to different clades and environmental conditions. Furthermore, the role of Als3 in adhesion, biofilm formation, and invasion is discussed, in addition to its contribution to immune evasion and fungal virulence. Expression profiles of Als3 and copy numbers play important roles in fungal heterogeneity, aggregation, and pathogenicity, with high expression and copy numbers imposing significant effects. Gene mutation, transcriptional and translational controls of Als3, in addition to three-dimensional structure in C. auris, are areas of limited information. The potential of targeting Als3 for therapeutic interventions is also reviewed, including approaches such as the use of C. albicans Als3 vaccine, antibodies, natural ligands, and others, although research in this area is still limited. Future research directions should include in-depth investigation of Als3 structural and molecular differences, in addition to the discovery of target drugs.