Expression of virulence factors inCandida albicans

Abstract

Virulence in the pathogenic yeast Candida albicans involves the interplay of many complex developmentally and environmentally regulated properties. Morphological and developmental changes such as the yeast–hyphae transition and switch phenotypes identified as colony morphologies result in the differential expression of a variety of cell properties that may include (i) secreted aspartyl proteinase (Sap) enzymatic activity that is now known to be the product of at least seven distinct genes, (ii) azole resistance that can be the result of altered expression of the target enzyme, lanosterol demethylase, or active efflux of azole drugs from the cells that may be facilitated by multidrug resistance genes (MDR genes), and (iii) a variety of Candida antigens that are recognized by patient antisera, including mannoproteins, glycolytic enzymes (especially enolase), heat shock proteins (especially Hsp90), and several Sap isoenzymes. As the details of these systems are elucidated, it becomes important to characterize the interactions between these factors that can lead to pathogenesis. The patterns of expression for genes associated with azole resistance, Sap activity, and potential antigens have been determined during the yeast–hyphae transition and between cell types in the white–opaque switch system of strain WO-1. The results suggest that genes involved in azole resistance and genes encoding potential antigens are not grossly affected by the yeast–hyphae transition or by switching between white and opaque colony morphologies. However, SAP gene expression is strictly controlled by these cell types. Key words: Candida, virulence, proteinase, azole, antigens, switch.