Major Areas of Research
- Pathophysiology and treatment of neuroinflammatory syndromes in refractory fungal infections.
- Role of RNA biology in susceptibility to human fungal disease
- Granulocyte-monocyte colony stimulating factor (GMCSF) signaling in fungal susceptibility
- Fungal genetic studies of clinical outcome of Cryptococcus in AIDS and solid organ transplant recipients
- Genetic susceptibility to bloodstream infections by Candida albicans
- International Studies: Use of orally available amphotericin B lipid nano-crystals for treatment of HIV-associated cryptococcal meningitis (Uganda and Ethiopia)
The Translational Mycology Unit seeks to understand the role of host-pathogen genetics in the outcome of human fungal infections. We use an array of methods from fungal genetics, cell biology, immunology, and population genetics to key aspects of the host-pathogen interface that might facilitate personalized therapeutic interventions.
The laboratory currently focuses on the neurotropic pathogen Cryptococcus which is a major cause of mortality in AIDS as well as in solid-organ transplant recipients and previously healthy individuals. Candida albicans is a major cause of bloodstream infections in the United States.
Dr. Williamson received his M.D./Ph.D. from Boston University in 1987 and completed a residency in internal medicine at Georgetown University before coming to the National Institutes of Health (NIH) for a fellowship in infectious diseases. In 1995, after serving a short stint as chief medical officer, Lalmba Sudan, Dr. Williamson joined the faculty at the University of Illinois at Chicago as an assistant professor of medicine in the section of infectious diseases. After progressing to the rank of professor of medicine, pathology, microbiology, and immunology, Dr. Williamson then returned to NIH to head the Translational Mycology Unit in the Laboratory of Clinical Infectious Diseases.
Hammoud DA, Mahdi E, Panackal AA, Wakim P, Sheikh V, Sereti I, Bielakova B, Bennett JE, Williamson PR. 2017. Choroid Plexitis and Ependymitis by Magnetic Resonance Imaging are Biomarkers of Neuronal Damage and Inflammation in HIV-negative Cryptococcal Meningoencephalitis.(link is external) Sci Reports. 2017; 7: 9184.
Panackal AA, Rosen LB, Uzel G, Hu G, Adeyemo A, Ayele F, Lisco A, Diachok C, Kim JD, Shaw D, Sereti I, Stoddard J, Niemela J, Rosenzweig S, Bennett JE, Williamson PR. Susceptibility to cryptococcal meningoencephalitis associated with idiopathic CD4 lymphopenia and secondary germline or acquired defects.(link is external) Open Forum Infect Dis. 2017 Jun 7;4(2):ofx082. doi: 10.1093/ofid/ofx082
Panackal AA, Komori M, Kosa P, Khan P, Hammoud D, Rosen LB, Browne SK, Lin YC, Romm E, Ramaprasad C, Fries BC, Bennett JE, Bielekova B, Williamson PR. Spinal arachnoiditis as a complication of cryptococcal meningoencephalitis in non-HIV previously healthy adults.(link is external) Clin Infect Dis. 2017 Feb 1;64(3):275-283. doi: 10.1093/cid/ciw739.
Hu G, McQuiston T, Bernard A, Park YD, Qiu J, Vural A, Zhang N, Waterman SR, Blewett NH, Myers TG, Maraia RJ, Kehrl JH, Uzel G, Klionsky DJ, Williamson PR. A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.(link is external) Nat Cell Biol. 2015 July; 17(7):930-42.
Panackal AA, Wuest SC, Lin YC, Wu T, Zhang N, Kosa P, Komori M, Blake A, Browne SK, Rosen LB, Hagen F, Meis J, Levitz SM, Quezado M, Hammoud D, Bennett JE, Bielekova B, Williamson PR. Paradoxical Immune Responses in Non-HIVCryptococcal Meningitis(link is external)(link is external). PLoS Pathog. 2015 May 28;11(5):e1004884.
Hu G, Hacham M, Waterman SR, Panepinto J, Shin S, Liu X, Gibbons J, Valyi-Nagy T, Obara K, Jaffe HA, Ohsumi Y, Williamson PR. PI3K signaling of autophagy is required for starvation tolerance and virulence of Cryptococcus neoformans(link is external)(link is external). J Clin Invest. 2008 Mar;118(3):1186-97.
NIH researchers show that Cryptococcus infection progresses differently in healthy people compared to those with underlying infections like HIV. The work suggests that different therapies should be explored for healthy people who develop the disease.