Circulating brain-derived extracellular vesicles expressing neuroinflammatory markers are associated with HIV-related neurocognitive impairment

• DOI: 10.3389/fimmu.2022.1033712
• Publication Date: 2022-12-19T05:13:37Z
• Authors: Erika G. Marques ...; Jocelyn S. Liu; Scott A. Bowler; Leila B. Giron; Michelle L. D’Antoni; Cecilia M. Shikuma; Mohamed Abdel-Mohsen; Lishomwa C. Ndhlovu; Philip J. Norris
• Keywords: CD16; Neurocognitive; CD63

Background Neurocognitive impairment remains prevalent in people with HIV (PWH) despite long term virological suppression by antiretroviral therapy (ART) regimens. Systemic and neuro-inflammatory processes are suggested to contribute the complex pathology leading cognitive this population, yet underlying mechanisms remain unresolved. Extracellular vesicles (EVs) play a central role intracellular communication have emerged as key modulators of immunological inflammatory responses. In report, we examined impact EVs PWH experiencing deficits determine their relevance associated neuropathology. Methods EV phenotypes were measured plasma samples from 108 either (CI, n=92) or normal cognition (NC, n=16) flow cytometry. Matched cerebrospinal fluid (CSF)-derived similarly profiled subgroup 84 individuals who underwent lumbar puncture. Peripheral blood mononuclear cells assayed cytometry measure monocyte frequencies subset 32 individuals. Results Plasma-EVs expressing CD14, CD16, CD192, C195, GFAP significantly higher HIV-infected compared cognition. Increased CSF-EVs CD200 found group group. Frequencies patrolling monocytes correlated plasma-EVs CD66b, MCSF, MAP2, GFAP. CD195 expression on positively CD41a, CD62P, CD63. Expression CD163 CD200. Finally, CD192 total CD200, Conclusions activation neuronal markers impairment, suggesting that distinct subsets may serve novel biomarkers injury infection. Further circulating platelet levels linked indicating potential interaction pathogenesis HIV-related impairment.