Norma V. Solis

This study shows that fungal-induced immunosurveillance remodels the oral mucosal barrier via a non-canonical IL-22 receptor complex, enhancing resistance to Candida albicans colonization.

This study identifies a metabolic-epigenetic mechanism in oral epithelial cells that enhances protection against fungal infection through proline catabolism and mitochondrial function.

This study shows that Chr7 trisomy in Candida albicans affects colonization and virulence differently depending on strain background and homolog identity.

This study identifies sulfated glycosaminoglycans as targets of candidalysin, a virulence factor in C. albicans, and shows that blocking these interactions can protect epithelial cells from fungal damage.

This study shows how azole resistance in Candida albicans evolves through copy number variation followed by KSR1 loss of heterozygosity, resulting in a >500-fold resistance increase.

This study identifies ERG251 mutations that confer azole tolerance and pleiotropic effects on stress responses and filamentation in C. albicans.

The paper shows that trisomy of chromosomes 5 or 6 in Candida albicans during oropharyngeal infection leads to a commensal-like phenotype with reduced virulence.

This study shows that Candida albicans rapidly generates genotypic and phenotypic diversity in the mouse oral cavity, with higher mutation rates compared to in vitro conditions.