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Journal Article | Research Support, U.S. Gov't, P.H.S.

Avirulence of Candida albicans FAS2 mutants in a mouse model of systemic candidiasis.

X J Zhao, G E McElhaney-Feser, M J Sheridan, S E Broedel Jr, R L Cihlar
X J Zhao
Department of Microbiology and Immunology, Georgetown University, Washington, D.C. 20007, USA.
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G E McElhaney-Feser
Department of Microbiology and Immunology, Georgetown University, Washington, D.C. 20007, USA.
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M J Sheridan
Department of Microbiology and Immunology, Georgetown University, Washington, D.C. 20007, USA.
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S E Broedel Jr
Department of Microbiology and Immunology, Georgetown University, Washington, D.C. 20007, USA.
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R L Cihlar
Department of Microbiology and Immunology, Georgetown University, Washington, D.C. 20007, USA.
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ABSTRACT

Disruption of both alleles of the Candida albicans FAS2 gene abolishes the ability of the organism to establish infection in a murine model of systemic candidiasis. Within 72 h all mice inoculated with 10(6) CFU of the parental C. albicans strain had died. In contrast, all animals inoculated with the mutant strain CFD2 survived for the course of the experiment (21 days). Animals infected with either mutant strain CFD1 or CFD3, in which only one FAS2 allele was disrupted, also succumbed to infection, but mortality was not observed until 4 days postinfection and survivors remained for up to 20 days postinfection. The results demonstrate that FAS2 is required for successful C. albicans infection.

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Avirulence of Candida albicans FAS2 mutants in a mouse model of systemic candidiasis.
X J Zhao, G E McElhaney-Feser, M J Sheridan, S E Broedel Jr, R L Cihlar
Infection and Immunity Feb 1997, 65 (2) 829-832; DOI:

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Avirulence of Candida albicans FAS2 mutants in a mouse model of systemic candidiasis.
X J Zhao, G E McElhaney-Feser, M J Sheridan, S E Broedel Jr, R L Cihlar
Infection and Immunity Feb 1997, 65 (2) 829-832; DOI:
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