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School of Medicine
Dionna Whitney Williams, Ph.D.
Instructor of Molecular and Comparative Pathobiology
Research Interests: HIV; Central nervous system drug delivery; Neuroimmunology; Substance abuse
- Instructor of Molecular and Comparative Pathobiology
Departments / Divisions
- B.Sc., Hofstra University (New York) (2009)
- Ph.D., Albert Einstein College of Medicine of Yeshiva University (Bronx) (New York) (2014)
Research & Publications
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, beta-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 beta-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.