New Drug Target Emerges for a Dangerous Fungal Pathogen
Mansa Munshi, a PhD student in the genetics program within the Department of Molecular Genetics & Microbiology, in the laboratory with slides of C. neoformans, including ones without the Cer1 gene that are disabled.
STONY BROOK, N.Y., February 6, 2018 – Cryptococcus neoformans is a fungal pathogen usually affecting immunocompromised patients, particularly AIDS and organ transplant patients, and is one that can be lethal. Current treatments against cryptococcosis are often not effective. Now a team of researchers led by Stony Brook University scientists Mansa Munshi and Maurizio Del Poeta in the Department of Molecular Genetics & Microbiology, have discovered a novel gene that helps understand the mechanism of survival of this pathogen in various host conditions. Their finding, published in Cell Reports , may help pave the way for more effective and innovative treatments against cryptococcosis.
When C. neoformans survives in a host, disease results. In the paper, the team details how they uncovered that ceramides (a class of lipid molecules) play a role in the pathogenicity of C. neoformans. They identified a new gene within this process, called Cer1, which synthesizes ceremides. By targeting Cer1, pathogenicity in the host is altered.
Munshi and colleagues delete Cer1 from the pathogen, and a mutant form of C. neoformans is created that is completely disabled and unable to cause disease. These results have led the team to theorize that Cer1 may be a new drug target in the search for better treatments of cryptococcosis.
The research was supported in part by the National institutes of Health.
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Reporter Contact: Gregory Filiano