Paracoccidioidomycosis (PCM) is the most important systemic mycosis in Brazil, and it is widespread throughout Latin America. An estimated 10 million individuals are infected, with about 2% developing the disease. This mycosis has also been reported among patients with AIDS in Latin America. PCM presents several clinical forms, ranging from a localized and benign disease to a progressive and potentially lethal systemic infection. All patients from whom the fungus is isolated should be treated, and pulmonary fibrosis is still a common sequel, despite the availability of new antifungal drugs for therapy. The etiological agent of PCM is the pathogenic ascomycete fungus Paracoccidioides brasiliensis, which has a close relationship to other pathogenic fungi, such as Blastomyces dermatitidis and Histoplasma capsulatum. Paracoccidioides brasiliensis exists as a mycelium in the soil and as a yeast in the host. The unicellular hyphae and fungal propagules, or conidia, are uninucleate, while the yeasts are multinucleate. Information on genome size, chromosome organization, mechanisms that contribute to dimorphism, pathogenicity, and virulence are scarce. In addition, a strong variability among the fungus isolates has been reported, with genotypic differences showing some correlation with virulence, geographic distribution and susceptibility or resistance to drugs. Our group has been working for the last eight years in order to identify the differentially expressed genes in the dimorphism of P. brasiliensis and also to look for genes encoding proteins that are immunogenic in humans during infection. Several genes that are up-regulated in mycelial and yeast cells have been previously identified by proteome analysis, and by immunoscreening of cDNA libraries from mycelium and yeast cells, using patient’s sera.
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