The 'Amoeboid Predator-Fungal Animal Virulence' Hypothesis.

Autor: Casadevall A; Department of Molecular Microbiology and Immunology, Johns Hopkins School of Public Health, Baltimore, MD 21205, USA. Acasade1@jhu.edu., Fu MS; Department of Molecular Microbiology and Immunology, Johns Hopkins School of Public Health, Baltimore, MD 21205, USA. sarahfu52@gmail.com., Guimaraes AJ; Department of Microbiology and Parasitology, Biomedical Institute, Fluminense Federal University, Niterói, Rio de Janeiro 24020-141, Brazil. allanguimaraes@id.uff.br., Albuquerque P; Faculty of Ceilandia, University of Brasilia, Brasilia DF 70904-970, Brazil. pattycherie@gmail.com.
Jazyk: angličtina
Zdroj: Journal of fungi (Basel, Switzerland) [J Fungi (Basel)] 2019 Jan 21; Vol. 5 (1). Date of Electronic Publication: 2019 Jan 21.
DOI: 10.3390/jof5010010
Abstrakt: The observation that some aspects of amoeba-fungal interactions resemble animal phagocytic cell-fungal interactions, together with the finding that amoeba passage can enhance the virulence of some pathogenic fungi, has stimulated interest in the amoeba as a model system for the study of fungal virulence. Amoeba provide a relatively easy and cheap model system where multiple variables can be controlled for the study of fungi-protozoal (amoeba) interactions. Consequently, there have been significant efforts to study fungal⁻amoeba interactions in the laboratory, which have already provided new insights into the origin of fungal virulence as well as suggested new avenues for experimentation. In this essay we review the available literature, which highlights the varied nature of amoeba-fungal interactions and suggests some unsolved questions that are potential areas for future investigation. Overall, results from multiple independent groups support the 'amoeboid predator⁻fungal animal virulence hypothesis', which posits that fungal cell predation by amoeba can select for traits that also function during animal infection to promote their survival and thus contribute to virulence.
Databáze: MEDLINE