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UCLA: UCLA-Led Team Gets $8.4 Million NIH Grant To Probe Mysteries Of Valley Fever
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UCLA Newsroom
February 15, 2022
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Why do some people infected with Valley fever develop a potentially fatal form of the disease that ravages their body while most experience only mild symptoms or none at all? A team led by UCLA’s Dr. Manish Butte has been awarded an $8.4 million grant from the National Institute of Allergy and Infectious Diseases to study this and other questions related to genetic risk factors and immune responses to the disease, which occurs when people breathe in microscopic spores of the fungus Coccidioides that are present in soil. First identified in Argentina in the late 1800s, Valley fever today is seen in a geographic swath that stretches from South America through Central America and Mexico and into the American Southwest. While people with symptoms usually recover on their own or with the help of antifungal medication, those who develop a severe, or “disseminated,” form of the disease can become severely ill and die. “Everyone in the endemic areas is susceptible to this infection, but we have almost no ability to predict who will develop disseminated disease and lack an understanding of what part of their immune response fails to control the infection,” said Butte, the E. Richard Stiehm Professor of Pediatric Allergy, Immunology and Rheumatology at the David Geffen School of Medicine at UCLA. The five-year grant will establish a Conccidioidomycosis Collaborative Research Center at which researchers from UCLA and UC San Diego led by Butte will investigate innate and adaptive immune responses to Valley fever, the genomic basis for heightened susceptibility to the disease and the mechanisms that allow the fungus to evade the body’s immune system. Two similar centers, at UC San Francisco and the University of Texas, San Antonio, will study how the disease attacks the body and work to develop therapeutics and vaccines. Read the full news release.
This press release was produced by UCLA. The views expressed here are the author’s own.
