Submission Date

7-24-2015

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Jennifer King

Comments

Presented during the 17th Annual Summer Fellows Symposium, July 24, 2015 at Ursinus College.

Project Description

Anti-retroviral therapy (ART) has been successful in increasing the survival rate of patients infected with HIV, but the incidence of moderate cognitive impairment experienced by patients remains high. Researchers have attributed the occurrence of HIV-Associated Neurocognitive Disorders (HAND) to the persistence of latent HIV in resting T cells and macrophages, as well as chronic inflammation. Previous research has shown that as HIV invasion of the brain occurs, neurons are damaged indirectly despite their inability to be infected with the HIV virus. Local microglia and peripheral leukocytes, such as macrophages, collaborate to eliminate the virus by producing neurotoxic chemokines such as CXCL10, potentially creating a toxic environment leading to this indirect neuronal damage. Phagocytic activity of macrophages has been shown to be altered when exposed to HIV in vitro but the true cause for these changes is unknown. Therefore, we hypothesize that pro-inflammatory chemokines released from macrophages/microglia co-incubated with the HIV-1 Tat protein play a role in the functional activity of macrophages thereby damaging nearby neurons. The overall goal of the project is to explore the effect of the HIV-1 Tat protein on BV-2 microglial cells’ function in vitro. Microglial function will be evaluated by performing a phagocytosis assay with fluorescent latex beads on both BV-2 and Cos-7 cells with and without exposure to HIV Tat. The phagocytic activity will be quantified by measuring the fluorescence of the beads engulfed. Our results will give us further insight into the indirect factors that may play a role in neuronal death in HAND.

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