ABSTRACT
Fungal infections still represent an important clinical problem. Infections caused by fungi range from relatively mild superfi cial lesions to severe (and frequently life threatening) systemic diseases. The similarity of the fungus to the mammalian host cell (both eukaryotic) has complicated the development of antifungal antibiotics and treatment of fungal diseases rely
on a limited number of antifungals. Resistance to some of them (mainly azoles) further complicates the therapy. Understanding the mechanisms that fungi use to cause disease is therefore an important line of research to reveal novel therapeutic approaches. Research on clinical relevant fungi has been lagged historically due to limited molecular genetics. Candida albicans, the most important fungal pathogen accordingly to the incidence of diseases that it causes, is diploid and lacks natural plasmids; sexual recombination has only been recently recognized and its genetic manipulation has been a bottleneck to understand the mechanisms of pathogenesis (De Backer et al. 2000). The situation with other important pathogenic fungi like Cryptococcus neoformans, Aspergillus spp., Histoplasma capsulatum and non-albicans spp. is rather similar. However, in the last years, several tools have been developed: gene disruption schemes, more effi cient transformation protocols and genetic markers are now available. The analyses of the role of individual genes in key infectious processes of these fungi are now feasible. In addition, the availability of their genomes has been also essential in basic research.
