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Journal article
Opinion: Inhibition of Blood-Brain Barrier Repair as a Mechanism in HIV-1 Disease
Frontiers in neuroscience, v 11, pp 228-228
26 Apr 2017
PMID: 28491017
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The blood-brain barrier (BBB) is a complex network of microvasculature, comprised primarily of brain microvascular endothelial cells (BMECs), astrocytes, and pericytes, which regulates cellular, macromolecule, and metabolite passage between the peripheral circulation and the central nervous system (CNS). Damage to the BBB has been linked to neurocognitive deficits sustained in multiple diseases, including stroke, Alzheimer's Disease, and numerous infections, including human immunodeficiency virus type 1 (HIV-1) (Krizanac-Bengez et al., 2004; Salmina et al., 2010; Logsdon et al., 2015). Although the development and deployment of anti-retroviral therapy (ART) has transformed HIV-1 infection from an acute terminal diagnosis to a chronic pharmaceutically-managed clinical condition (in the developed world), many clinical complications remain prevalent in HIV-1-infected patients, including the spectrum of neurocognitive deficits collectively termed HIV-1-associated neurocognitive disorders (HAND). While the current age of ART has decreased the occurrence of the more severe manifestations of neurocognitive impairment in patients, particularly with regards to the incidence of HIV-1-associated dementia (HAD), the overall prevalence of HAND has not subsided (Cysique et al., 2004; Robertson et al., 2007; Tozzi et al., 2007; Heaton et al., 2010, 2011; Cysique and Brew, 2011). In fact, it is currently estimated that nearly 50–70% of HIV-1-infected patients on a successful ART regimen experience some level of neurocognitive decline (Heaton et al., 2010, 2011, 2015; Simioni et al., 2010; Obermeit et al., 2017). Implicated in the development of HAND in patients is a combination of toxic viral proteins released into the CNS, a sustained host pro-inflammatory response in the CNS initiated by the virus, deregulated endogenous small molecule metabolism, detrimental metabolic byproducts associated with combination ART, as well as certain types of HIV-1 genetic variants that may cause some of these pathogenic processes (Krebs et al., 2000; Wang et al., 2006; Ferrucci et al., 2011, 2012; Strazza et al., 2011; Dahiya et al., 2013; Aiamkitsumrit et al., 2014; Gresele et al., 2014; Maubert et al., 2015; Dampier et al., 2017; James et al., 2016).
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Details
- Title
- Opinion: Inhibition of Blood-Brain Barrier Repair as a Mechanism in HIV-1 Disease
- Creators
- Monique E. Maubert - Drexel UniversityBrian Wigdahl - Drexel UniversityMichael R. Nonnemacher - Drexel University
- Publication Details
- Frontiers in neuroscience, v 11, pp 228-228
- Publisher
- Frontiers Media S.A
- Grant note
- NS089435 / National Institute of Neurological Disorders and Stroke MH092177; MH079785 / National Institute of Mental Health DA19807 / National Institute on Drug Abuse
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology
- Web of Science ID
- WOS:000406509600001
- Scopus ID
- 2-s2.0-85018412202
- Other Identifier
- 991019169107004721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences