Submission Date


Document Type

Paper- Restricted to Campus Access



Faculty Mentor

Jennifer King


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

Project Description

For the majority of treated HIV+ individuals effective viral suppression attained through combination antiretroviral therapy (cART) has led to a notable decrease in the presence of moderate to severe HIV-Associated Neurocognitive Disorders (HAND). The rate of HAND remains high, even in individuals that are being treated with antiretroviral therapy. Cells in the brain, including macrophages, microglia and astrocytes, are infected with HIV that has crossed the blood-brain barrier (BBB). HIV and its’ proteins act on the BBB to decrease entry of anti-viral drugs, which allows the central nervous system to be a reservoir for HIV infection. HIV persists in the brain due to inflammation and the release of pro-inflammatory cytokines. This toxic environment has the potential to alter the cytoskeletal network of cells via signaling cascades, which could negatively impact microglia function. Cofilin is an actin-binding protein associated with cytoskeleton dynamics and is likely to assist in the control of the immune response in microglia. HIV patients who have neurocognitive disorders have a higher cofilin expression compared to HIV patients who do not have neurocognitive disorders. Therefore we hypothesize that HIV proteins lead to rearrangement of the macrophage cytoskeleton through the activation of cofilin and its kinase LIMK.The objective of this research is to quantify the protein expression of cofilin and LIMK in microglia cytoskeleton by conducting western blot analysis. Through this research we can better understand the impact that HIV proteins have on the function of brain microglia and how those changes can indirectly effect neurons.


Available to Ursinus community only.