Lois L. Hoyer
Associate 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 cause disease in a variety of organs and tissues and can be fatal. Work in my laboratory includes investigations into Candida adherence and biofilm formation.
For the past several years, we have been investigating
the ALS (agglutinin-like sequence) gene family of Candida albicans.
The family includes eight genes that encode cell-surface glycoproteins,
some of which function in adhesion to host surfaces. Current projects
are aimed at understanding the comparative structure and function of
the Als proteins and at answering larger questions about the role of
gene families in Candida pathogenesis. Experimental approaches
include molecular and biochemical techniques, the use of in vitro and
animal disease models, and also analysis of human clinical specimens.
A full-genome microarray that we constructed as part of a collaborative
group is also used in our studies of Candida adherence.
In more recent collaborative work, we are studying the biology of formation
and antifungal drug resistance in Candida biofilms. Formation
of Candida biofilms on prosthetic devices is a significant
medical problem and often necessitates removal of the device. Using microarray
analysis, we have identified genes that are differentially expressed
at various timepoints during biofilm development. These
genes are being studied in more detail to understand their contribution
to biofilm formation and antifungal drug resistance.
Selected Publications:
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.
Green CB, S Manfra Marretta, G Cheng, FF Faddoul, EJ Ehrhart and LL Hoyer.
2006. RT-PCR analysis of Candida albicans ALS gene expression in a hyposalivatory
rat model of oral candidiasis and in HIV-positive human patients. Medical
Mycology 44:103-111.
Oh S-H, G Cheng, JA Nuessen, R Jajko, KM Yeater, X Zhao, C Pujol, DR Soll and LL Hoyer. 2005. Functional specificity of Candida albicans ALS3p proteins and clade specificity of ALS3 alleles discriminated by the number of copies of the tandem repeat sequence in the central domain. Microbiology 151:673-681.
Cheng G, K Wozniak, MA Wallig, PL Fidel Jr, SR Trupin and LL Hoyer. 2005. Comparison between Candida albicans ALS gene expression patterns in human clinical specimens and models of vaginal candidiasis. Infection and Immunity 73:1656-1663.
Zhao X, S-H Oh, G Cheng, CB Green, JA Nuessen, K Yeater, RP Leng, AJP Brown and LL Hoyer. 2004. ALS3 and ALS8 represent a single locus that encodes a Candida albicans adhesin; functional comparisons between Als3p and Als1p. Microbiology 150:2415-2428.
Hoyer LL. 2001. The ALS gene family
of Candida albicans. Trends Microbiol. 9:176-180.
