Neural effects of inflammation, cardiovascular disease, and HIV: Parallel, perpendicular, or progressive?

• Type of Material: Article
• Authors: C. L. Nemeth, Emory University; M. Bekhbat, Emory University; Gretchen Neigh, Emory University
• Language: English
• Date: 2015-08-27
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2014 IBRO.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.neuroscience.2014.09.016
• Title of Journal or Parent Work: Neuroscience
• ISSN: 0306-4522
• Volume: 302
• Start Page: 165
• End Page: 173
• Grant/Funding Information: G.N.N. and M.B. partially supported by CNIHR Grant R24-AI067039-06; G.N.N. and C.L.N. supported by American Heart Association Predoctoral Fellowship.
• Keywords: RISK-FACTORS; CEREBROVASCULAR-DISEASE; ANTIRETROVIRAL THERAPY; Neurosciences; Life Sciences & Biomedicine; Science & Technology; AIDS; immune; CARDIOPULMONARY-RESUSCITATION; cardiovascular; HIV; ENDOTHELIAL PROGENITOR CELLS; ALZHEIMERS-DISEASE; INFECTED PATIENTS; Neurosciences & Neurology; cerebrovascular; COGNITIVE IMPAIRMENT; inflammation; AMERICAN-HEART-ASSOCIATION; ANXIETY-LIKE BEHAVIOR
• Research Categories: Biology, Physiology; Health Sciences, Mental Health; Biology, Neuroscience

Abstract

The pervasive reach of the inflammatory system is evidenced by its involvement in numerous disease states. Cardiovascular disease, marked by high levels of circulating inflammatory mediators, affects an estimated 83.6 million Americans. Similarly, human immunodeficiency virus (HIV) produces a paradoxical state of generalized immune activity despite widespread immunosuppression, and affects 35 million people worldwide. Patients living with HIV (PLWH) suffer from inflammatory conditions, including cardiovascular disease (CVD), at a rate exceeding the general population. In this combined disease state, immune mechanisms that are common to both CVD and HIV may interact to generate a progressive condition that contributes to the exacerbated pathogenesis of the other to the net effect of damage to the brain. In this review, we will outline inflammatory cell mediators that promote cardiovascular risk factors and disease initiation and detail how HIV-related proteins may accelerate this process. Finally, we examine the extent to which these comorbid conditions act as parallel, perpendicular, or progressive sequela of events to generate a neurodegenerative environment, and consider potential strategies that can be implemented to reduce the burden of CVD and inflammation in PLWH.