Morphogenesis in Paracoccidioides brasiliensis

Abstract

Paracoccidioidomycosis (PCM) is a deep systemic mycosis originally described in 1908 caused by the ascomycete Paracoccidioides brasiliensis, a thermodimorphic fungal pathogen. The disease is autochthonous to Latin America and areas of higher incidence occur in countries such as Brazil, Argentina, Colombia, and Venezuela. Inside the mammalian host, PCM is characterized by a granulomatous inflammation that invades conjunctival tissue or viscera. P. brasiliensis grows as yeast in cultures incubated at 37°C or inside the host and in a filamentous saprophytic form at low temperatures (26°C) or in the environmental niches. The relative temperature-dependent simplistic mechanisms whereby P. brasiliensis orchestrates its developmental program for switching morphological forms have been under intense scrutiny for several decades, and although major advances have been achieved, much remains to be uncovered for the identification of new virulence determinants and therapeutical targets, and for the comprehension of the pathophysiology of this fungus. Although recent studies have begun to identify genes and overall pathways required for the thermodimorphic process and pathogenicity, master regulators mediating morphogenesis, virulence, and the mycelium-to-yeast transition are still not recognized. Transcriptional profiling studies have highlighted the importance of differential expression genes in the mycelial and yeast phases of P. brasiliensis and have analyzed putative genes involved in virulence and morphogenesis based on evidences from other dimorphic fungi or pathways involved in virulence traits. Here, we consider the current information obtained at the transcriptional level in P. brasiliensis as the basis for an update of the main pathways involved in the virulence and pathogenicity of this fungus, and the experimental possibilities generated by the newly released genomic sequences that will drive the forthcoming years of systematic research of P. brasiliensis. © 2012 Springer-Verlag Berlin Heidelberg.