Abstract
In the last years, the clinical relevance of fungal diseases has gained importance because of an increasing population of immunocompromised hosts, such as patients who have undergone transplants, patients with various types of leukemia, and people infected with HIV. Although some virulence factors are of obvious importance, pathogenicity cannot be considered an inherent characteristic of fungi.1 Fungi seem to have a complex relationship with the vertebrate immune system, mainly due to some prominent features: among these, the ability of dimorphic fungi to exist in different forms and to reversibly switch from one to the other in infection. Although association between morphogenesis and virulence has long been presumed for fungi that are human pathogens2, no molecular data unambiguously establish a role for fungal morphogenesis as a virulence factor. What fungal morphogenesis implicates through antigenic variability, phenotypic switching, and dimorphic transition is the existence of a multitude of recognition and effector mechanisms to oppose fungal infectivity at the different body sites.
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Zelante, T. et al. (2007). Receptors and Pathways in Innate Antifungal Immunity. In: Katsikis, P.D., Schoenberger, S.P., Pulendran, B. (eds) Crossroads between Innate and Adaptive Immunity. Advances in Experimental Medicine and Biology, vol 590. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-34814-8_15
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