Abstract
Recurrent vulvovaginal candidiasis (RVVC) is a common, refractory fungal infection affectingwomen, primarily caused by Candida albicans. The interplay among fungal virulence factors, biofilm formation, and antifungal resistance is crucial in the pathogenesis of RVVC. This study compared 50 Candida albicans isolates from RVVC patients and 50 from asymptomatic vaginal colonizers. Antifungal susceptibility testing was performed using the broth microdilution method. Biofilm formation was assessed via crystal violet staining, and the expression levels of virulence factor hydrolases (SAP, PL, Lip) and cell wall protein genes (ALS1, ALS3, HWP1) were analyzed using phenotypic assays and quantitative real-time PCR (qRT-PCR). Pearson correlation analysis was used to evaluate the relationships among these parameters and antifungal resistance. RVVC isolates exhibited significantly higher MICs for fluconazole, voriconazole, and itraconazole. Biofilm formation ability and the expression levels of SAP, PL, Lip, ALS1, ALS3, and HWP1 were also significantly higher in RVVC isolates. A moderate correlation was observed between antifungal drug MIC values and biofilm OD, while a weak correlation existed between MIC values and ALS/HWP1 gene expression. Notably, hydrolase expression showed no significant correlation with resistance. Candida albicans from RVVC patients demonstrated enhanced biofilm formation, virulence factor expression, and antifungal resistance. Biofilm-mediated drug tolerance may be a key mechanism underlying the refractoriness of RVVC. Targeting biofilm formation and virulence factor genes may offer novel strategies for managing RVVC.