Candida albicans is a yeast-like fungal pathogen known to cause serious infections in immunocompromised patients. The incidence of disseminated candidiasis has increased in recent years because of a rise in the number of risk groups. A 500 % increase in the number of Candida sp. bloodstream infections were reported in the United States between 1980 and 1989 by the National Nosocomial Infections Surveillance System. 80% of AIDS patients suffer from oropharyngeal candidiasis at some time. Candida albicans occurs in two biotypes based on their ability to assimilate sucrose. C. albicans var. stellatoidea, the sucrose negative variant, is known to have reduced virulence in animal models compared to the sucrose positive strains. To understand the regulatory pathway of sucrose assimilation in C. albicans, we have focused our attention on the SNF1 gene which encodes a serine/threonine protein kinase essential for the removal of catabolic repression. In the previous year, we have attempted to disrupt both alleles and presented evidence that, unlike in Sacharomyces, the SNF1 gene is essential for the viability of C. albicans. We demonstrated that both alleles can only be disrupted under conditions that allow the simultaneous creation of a functional copy. Such a mutant maintained its ability to utilize sucrose but produced stellate colonies with extensive hyphal growth. Since hyphal formation in C. albicans has been considered to be an important virulence factor, we have compared virulence of the wild type and the heterozygote strains. Using a mouse model it was demonstrated that the virulence of this mutant and the wild type strain are similar, suggesting that hyphal growth itself is not a prominent virulence factor.
