A marked increase in the number of patients with AIDS and other immuno-compromise in recent years has resulted in the emergence of fungi as predominant human pathogens all over the world. The Candida spp. are the leading cause of disseminated fungal infections in neonates (premature infants), immuno-compromised patients, diabetic and post-operative patients.  Although C. albicans is still the major culprit, an increase in the Candida infections due to the non-albicans species of Candida such as C. glabrata has been observed in the recent decade. C. glabrata is a haploid, pathogenic yeast and is very closely related to the model yeast Saccharomyces cerevisiae. However, unlike S. cerevisiae, C. glabrata is an opportunistic pathogen and can cause infections ranging from superficial mucosal to invasive, life-threatening systemic infections. Long term goals of our laboratory are aimed towards the better understanding of the pathogenesis of C. glabrata. Our immediate interests lie mainly in two different areas of C. glabrata biology. The first involves the study of host-pathogen interactions using mammalian cell line J774A.1 and the second is to understand the intrinsic resistance of C. glabrata to fluconazole.

C. glabrata-macrophage interactions: 
To study the molecular interactions of C. glabrata with macrophages which constitute the first line of host defense against this pathogenic yeast, we are using an in-vitro system comprised of murine macrophage like cell line J774A.1. One of the current projects involves the identification and characterization of the factors that are required for survival in-vivo using a combination of mutant screens, transcriptional profiling analysis and cell biology approaches.

Fluconazole resistance in C. glabrata: 
The second aspect of our research involves the study of fluconazole resistance in C. glabrata. A major clinical challenge in treating C. glabrata infections is the innate resistance of this yeast to fluconazole which is the most commonly used anti-fungal drug. One of the first step towards developing new combinatorial drugs is the better understanding of C. glabrata's response to fluconazole. To gain insights into the intrinsic resistance of C. glabrata, another project in the lab is focused on a genome-wide screen for mutants with altered fluconazole susceptibility profiles using a high-throughput strategy whereby pools of 96 mutants will be screened at once.