The Fungal PathogenCandida albicans

Abstract

Research on Candida albicans is driven by the major questions regarding any infectious microbe. This chapter first introduces the medical problem and then animal models of infection and genetic tools for Candida albicans manipulation. It then focuses on three topics-morphogenesis, adherence, and azole drug resistance-that have long held the attention of our research community, in order to give the reader a sense of key questions and prospects for future study. There is a growing selection of minihost models. Models such as Drosophila melanogaster, Caenorhabditis elegans, and Galleria mellonella cannot recapitulate all of the complexity of mammalian infection, but they lend themselves to highthroughput screens that would be prohibitive for many reasons with mammalian hosts. The glycophosphatidylinositol (GPI) proteins of C. albicans are linked to the β-1,6 glucans, and for many, their expression can vary depending on morphology. A final thought is that natural selection has probably acted on C. albicans most strongly as a commensal. Its functional repertoire has likely evolved to avoid inflammation of host tissues and to support effective competition with its bacterial cohabitants. The true logic behind deployment of C. albicans virulence factors may be most apparent when they are viewed as commensalism factors.