Speakers: Zicheng Hu, Ph.D. (Assistant Professor, Bakar Computational Health Sciences Institute, Department of Microbiology and Immunology, University of California San Francisco)
Original Broadcast date: November 5, 2021
Over 40% of HIV patients experience neurological complications. The most severe form of neurological impairment due to HIV infection is HIV-associated dementia (HAD) that results in cognitive deficiency. Neurological damage can also occur when anti-retroviral therapy (ART) fails, enabling the virus to replicate freely in the brain and causing neural symptomatic escape (NSE). Here, Dr. Hu used the Olink® Explore platform to analyze proteins in the cerebrospinal fluid (CSF) of 315 HIV patients with and without ART treatment to determine, in part, which proteins are involved in HIV infection, neural damage, or both. His data show that HIV patients with HAD or NSE show high levels of immune activation markers. Moreover, proteins highly upregulated in HAD and NSE were identified, with HAD-associated proteins highly enriched in T cell activation pathways while NSE-associated proteins were highly enriched in macrophage-related processes and clearance of apoptotic cells. A comparison of data obtained with Olink® Explore and conventional enzyme-linked immunosorbent assay (ELISA) for a very important biomarker of neurological damage, neurofilament light chain (NFL), demonstrates a high correlation (r = 0.94) between the two immunoassays. His work has revealed proteins that are uniquely involved in HIV infection or neural damage, and suggest potential treatments for treating HIV-associated cerebrospinal damage by inhibiting myeloid cell activation.
The webinar covers the following points:
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