Dionna W. WIlliams, PhD

Dionna W. WIlliams, PhD

Instructor

Edward D. Miller Research Building
733 N. Broadway
Room 849

410-955-9770

Education

BS
MS
PhD
Certificate in Health Disparities & Health Inequalities
Hofstra University, Hempstead NY
Albert Einstein College of Medicine, Bronx NY
Albert Einstein College of Medicine, Bronx NY
Johns Hopkins Bloomberg School of Public Health
 
2009
2011
2014
2018

 

About

Dr. Dionna Williams is an Instructor in the Departments of Molecular and Comparative Pathobiology and Clinical Pharmacology at The Johns Hopkins School of Medicine with expertise in neuroscience, immunology, and pharmacology. Her research interests are in the neuropathogenesis of HIV, regulatory mechanisms of neuroimmune signaling, drug delivery to the central nervous system, and immunologic and pharmacologic contributors to health disparities.

She received her undergraduate degree cum laude from Hofstra University, where she studied biochemistry. She earned a master’s degree with distinction and a doctorate in biomedical science from the Albert Einstein College of Medicine. As a doctoral candidate, she received the UNCF/Merck Graduate Science Research Dissertation Fellowship and support from the Mount Sinai Institute for NeuroAIDS Disparities. Dr. Williams pursed her postdoctoral fellowship at Johns Hopkins to perform immunology, pharmacology, and health disparities research. While a postdoctoral fellow, Dr. Williams earned a certificate in health disparities and health inequalities from the Johns Hopkins Bloomberg School of Public Health. During the tenure of her postdoctoral fellowship, Dr. Williams was awarded the K99/R00 Pathway to Independence Award from the National Institutes of Health and the Johns Hopkins Provost’s Postdoctoral Fellowship. Additionally, she received support from the Translational Research in NeuroAIDS and Mental Health Center and the National Institutes of Health Loan Repayment Program.

Current Research

Central nervous system efficacy of HIV antiretroviral therapy
Antiretroviral therapy (ART) is a highly effective combination of drugs that reduces plasma viral loads to near undetectable levels. However, ART does not always quell virus to the same extent in other areas of the body. This is particularly true for the brain, which is separated from peripheral blood flow by the blood-brain barrier (BBB). As a result, low-level, ongoing HIV replication can occur within the brain, establishing the central nervous system as an anatomic viral reservoir.

The goal of this project is to identify the effects of ART on the BBB, characterize the mechanisms by which ART enters into the brain, and determine the spatiotemporal localization of ART within the brain parenchyma. In addition, the contribution of substance abuse and pharmacogenetic polymorphisms to ART extravasation and efficacy in the brain will be examined as potential contributors to HIV cognitive disparities among racial/ethnic minority populations.

Arrestin-mediated modulation of neuroinflammation
Neuroinflammation is a hallmark of neurologic disorders that exists to restore brain homeostasis during pathologic states. However, neuroinflammation may persist chronically, where it exacerbates rather than dampens disease. Therefore, appropriate regulatory mechanisms must exist to maintain the delicate balance between beneficial and deleterious neuroinflammatory responses. While best characterized for their roles in G protein-coupled receptor signaling and recycling, b-arrestins also serve as important regulators of the immune response.

The goal of this project is to evaluate the tissue- and cell-specific contribution of the two b-arrestin isoforms (arrestin 2 and arrestin 3) to inflammatory processes in the context of viral infection and substance abuse. Additionally, isoform specific contributions to signal transduction pathways, cellular migration, cytokine and chemokine production, and antiviral immune responses will be determined.

If you are interested in learning more about the work we do or would like to inquire about positions available within the lab, please contact Dr. Williams at dwill201@jhmi.edu.

 

Selected Publications

  1. Veenstra M, Williams DW, Calderon TM, Anastos K, Morgello S, Berman JW. Frontline Science: CXCR7 mediates CD14+CD16+ monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS. Journal of leukocyte biology. 2017; 102(5):1173-1185.

  2. Calderon TM, Williams DW, Lopez L, Eugenin EA, Cheney L, Gaskill PJ, Veenstra M, Anastos K, Morgello S, Berman JW. Dopamine Increases CD14+CD16+ Monocyte Transmigration across the Blood Brain Barrier: Implications for Substance Abuse and HIV Neuropathogenesis. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology. 2017; 12(2):353-370.

  3. Dickens AM, Tovar-Y-Romo LB, Yoo SW, Trout AL, Bae M, Kanmogne M, Megra B, Williams DW, Witwer KW, Gacias M, Tabatadze N, Cole RN, Casaccia P, Berman JW, Anthony DC, Haughey NJ. Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions. Science signaling. 2017; 10(473).

  4. Williams DW, Engle EL, Shirk EN, Queen SE, Gama L, Mankowski JL, Zink MC, Clements JE. Splenic Damage during SIV Infection: Role of T-Cell Depletion and Macrophage Polarization and Infection. The American journal of pathology. 2016; 186(8):2068-2087.

  5. McFarren A, Lopez L, Williams DW, Veenstra M, Bryan RA, Goldsmith A, Morgenstern A, Bruchertseifer F, Zolla-Pazner S, Gorny MK, Eugenin EA, Berman JW, Dadachova E. A fully human antibody to gp41 selectively eliminates HIV-infected cells that transmigrated across a model human blood brain barrier. AIDS (London, England). 2016; 30(4):563-72. NIHMSID: NIHMS743014

Link to my Pubmed bibliography:
https://www.ncbi.nlm.nih.gov/sites/myncbi/dionna.williams.1/bibliography/48569979/public/?sort=date&direction=descending