Lois L. Hoyer
Professor, Pathobiology
Professional Interests: The main focus of my research is Candida albicans, a fungus that can exist in the human body as a commensal and, when presented with the correct opportunity, cause a variety of disease conditions. Two main forms of candidiasis are superficial and disseminated disease. Superficial (mucocutaneous) disease, such as vaginal candidiasis, can occur in normally healthy individuals. It is estimated that 75% of all women will experience Candida vaginitis and that 5% of women suffer from a recurrent, acute form of the condition. Normally healthy people can also suffer from denture stomatitis (denture sore mouth), a condition that affects up to 65% of denture wearers. Superficial candidiasis also strikes immunocompromised individuals. One prime example is esophageal candidiasis, an initial clinical sign associated with AIDS. Development of disseminated candidiasis typically requires a severe immunodeficiency. Once disseminated through the bloodstream, C. albicans can affect a variety of organs and tissues and may be fatal.
Our major research effort investigates the function of cell-surface glycoproteins encoded by the C. albicans ALS (agglutinin-like sequence) gene family. Adhesive function has been demonstrated for some Als proteins. Other possible roles for Als proteins include cell size homeostasis, maintenance of cell wall structure, or signal transduction. We have investigated the ALS family at the level of gene expression in cultured cells, disease models, and clinical specimens. Regardless of the source of the specimen, some ALS genes exhibit large increases and decreases in transcriptional activity, while others are relatively quiet. We constructed C. albicans als/als mutant strains and found that some exhibit decreased adhesion to host cells while others, unexpectedly, show increased adhesion. Our current studies include efforts to explain these observations at the molecular level. We are also raising a specific monoclonal antibody against each Als protein and to study the dynamics of the proteins on the C. albicans cell surface. These studies have conclusively ruled out some hypotheses for Als family function including the idea that the family functions in phase variation. The collection of monoclonal antibodies is being used to address larger questions in C. albicans morphology and pathogenesis. Experimental approaches to our studies utilize molecular and biochemical techniques, in vitro and animal disease models, and analysis of human clinical specimens.
Selected Publications:
Hoyer, LL, CB Green, S-H Oh and X Zhao. 2008. Discovering the secrets of the Candida albicans agglutinin-like sequence (ALS) gene family—a sticky pursuit. Medical Mycology 46:1-15.
Zhao, X, S-H Oh, R Jajko, DJ Diekema, MA Pfaller, C Pujol, DR Soll and LL Hoyer. 2007. Analysis of ALS5 and ALS6 allelic variability in a geographically diverse collection of Candida albicans isolates. Fungal Genetics and Biology 44:1298-1309.
Zhao, X, S-H Oh, and LL Hoyer. 2007. Unequal contribution of ALS9 alleles to adhesion between Candida albicans and human vascular endothelial cells. Microbiology 153:2342-2350.
Zhao, X, S-H Oh and LL Hoyer. 2007. Deletion of ALS5, ALS6 or ALS7 increases adhesion of Candida albicans to human vascular endothelial and buccal epithelial cells. Medical Mycology 45:429-434.
Zhao X, K Daniels, CB Green, S-H Oh, DR Soll and LL Hoyer. 2006. Candida albicans Als3p is required for wild-type biofilm formation on silicone elastomer surfaces. Microbiology 152:2287-2299.
Cheng G, KM Yeater and LL Hoyer. 2006. Cellular and molecular biology of Candida albicans estrogen response. Eukaryotic Cell 5:180-191.
