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Cited by 218Barrier Structure and Function StudiesHIV Research and TreatmentInfectious Diseases and Tuberculosis

Breaking down the barrier: The effects of HIV-1 on the blood–brain barrier

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Strazza, Marianne, Pirrone, Vanessa, Wigdahl, Brian, Nonnemacher, Michael R.·2011·Brain Research
DOI 10.1016/j.brainres.2011.05.015PMC PMC3139430
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Abstract

Human immunodeficiency virus type 1 (HIV-1) primarily infects CD4(+) T cells and cells of the monocyte-macrophage lineage, resulting in immunodeficiency in an infected patient. Along with this immune deficiency, HIV-1 has been linked to a number of neurological symptoms in the absence of opportunistic infections or other co-morbidities, suggesting that HIV-1 is able to cross the blood-brain barrier (BBB), enter the central nervous system (CNS), and cause neurocognitive impairment. HIV-1-infected monocyte-macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types. HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines. It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS. It is proposed in this review that the dysregulation of the BBB during and after neuroinvasion is a critical component of the neuropathogenic process and that dysregulation of this protective barrier is caused by a combination of viral and host factors including secreted viral proteins, components of the inflammatory process, the aging process, therapeutics, and drug or alcohol abuse.

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  • Blood-brain barrier disruption plays a major role in HIV-1-associated dementia development by allowing HIV-1-infected monocyte-macrophages to traverse the blood-brain barrier and enter the brain.

    “BBB disruption plays a major role in HAD development by allowing HIV1-infected monocyte-macrophages to traverse the BBB and enter the brain (562).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [562]

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Cited by

Sorted by citations

Authors
Strazza, M., Pirrone, V., Wigdahl, B., & Nonnemacher, M. R.
Affiliations
Drexel University (US)
Corresponding author
Nonnemacher, Michael R.
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2011-07
Volume
1399
Pages
96-115
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2011.05.015
PMC
PMC3139430
OpenAlex
W2047838688
Cited by
218
References
4
Citations by year
2026: 6 · 2025: 10 · 2024: 14 · 2023: 8 · 2022: 15 · 2021: 14 · 2020: 12 · 2019: 7 · 2018: 13 · 2017: 12 · 2016: 24 · 2015: 16 · 2014: 24 · 2013: 15 · 2012: 23
FWCI
1.89
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Neurological Disorders and Stroke (NS32092, NS46263)
  • National Institute of Drug Abuse (DA19807)
  • Department of Microbiology and Immunology
  • Institute for Molecular Medicine and Infectious Disease
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
  • Health Sciences › Medicine › Surgery › Infectious Diseases and Tuberculosis
Keywords
HIV-1, blood-brain barrier, neuroinvasion, HIV-associated neurocognitive disorders, monocyte/macrophage lineage, microglia, astrocytes, gp120, Tat, NEF, cytokines, chemokines, neuroinflammation, aging, antiretroviral therapy, drug abuse, alcohol abuse
MeSH terms
Animals, Blood-Brain Barrier, HIV, Humans, Macrophages, Models, Biological, HIV Infections

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