The role of Intercellular Adhesion Molecule Type-5 (ICAM-5) in the systemic inflammation during HIV infection Priyanka Saminathan1, Jennetta W. Hammond2, Patrick Miller-Rhodes2, Shao Ming Lu2, Harris A.Gelbard1,2 1Department of Microbiology, Immunology and Virology, University of Rochester, Rochester, New York; 2Center for Neural Development and Diseases, University of Rochester, Rochester, New York
Despite treatment with combined Anti-Retroviral Therapy (cART), HIV-infected individuals have increased risk of neurological complications that are collectively termed as NeuroAIDS. HIV-Associated Neurocognitive Disorders (HAND) is one such disorder that can severely debilitate brain functions. Low-level Tat production, inflammation, viral persistence, potential drug toxicity and systemic inflammation all contribute to HAND. A recent study discusses the possibility of using serum level of soluble neuron-specific Intercellular Adhesion Molecule Type - 5 (sICAM-5) as a biomarker for HAND. Neuronal ICAM-5, a dendritic surface molecule that is known to be cleaved through Matrix Metalloproteinase (MMP) activity has been shown to interact with Lymphocyte Function Associated antigen - 1 (LFA-1). We posit that Tat-mediated increase due to MMP activity contributes to monocyte activation and augments inflammation in the CNS. Our preliminary data suggests Tat-mediated loss of ICAM-5 in inflamed sections of CNS. Further, we were also able to observe activation of human monocytes treated with recombinant soluble ICAM-5. We believe future experiments that will analyze serum level sICAM-5, systemic inflammation and monocyte activation in the HIV-infected humanized mouse model will not only evaluate sICAM-5 as a biomarker for HAND but also highlight a novel mechanism of neuroinflammation influenced systemic inflammation.
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