Cited by 281interferon and immune responsesNeuroinflammation and Neurodegeneration MechanismsBarrier Structure and Function Studies

Illuminating viral infections in the nervous system

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McGavern, Dorian B., Kang, Silvia S.·2011·Nature Reviews Immunology

Abstract

Viral infections are a major cause of human disease. Although most viruses replicate in peripheral tissues, some have developed unique strategies to move into the nervous system, where they establish acute or persistent infections. Viral infections in the central nervous system (CNS) can alter homeostasis, induce neurological dysfunction and result in serious, potentially life-threatening inflammatory diseases. This Review focuses on the strategies used by neurotropic viruses to cross the barrier systems of the CNS and on how the immune system detects and responds to viral infections in the CNS. A special emphasis is placed on immune surveillance of persistent and latent viral infections and on recent insights gained from imaging both protective and pathogenic antiviral immune responses.

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  • Viral infections in general downregulate TJ proteins and promote chemokine production and vascular cell adhesion molecule 1 (VCAM-1) expression in brain endothelial cells, thereby weakening the BBB and facilitating entry into the brain.

    “Viral infections in general downregulate TJ proteins and promote chemokine production and vascular cell adhesion molecule 1 (VCAM-1) expression in brain endothelial cells, thereby weakening the BBB and facilitating entry into the brain (5, 212, 399, 613).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [399]

    The “Crossing the vascular endothelium” section reports that, in many cases, viral infection of brain endothelial cell lines in vitro increases chemokine production and VCAM1 expression and alters tight-junction proteins. It says these changes have the potential to increase permeability and permit viral entry; it does not establish that viral infections generally downregulate tight-junction proteins or necessarily weaken the BBB. (LLM, conf=0.87)

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Research works printed but not linked: 2

  1. [6]Tyler KL Emerging viral infections of the central nervous system: part 1 Arch Neurol 66 939 948 2009 19667214 PMC2873855
  2. [99]Brockhaus J Moller T Kettenmann H Phagocytozing ameboid microglial cells studied in a mouse corpus callosum slice preparation Glia 16 81 90 1996 8787776

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Authors
McGavern, D. B., & Kang, S. S.
Affiliations
National Institutes of Health (US)
Corresponding author
McGavern, Dorian B.
Venue
Nature Reviews Immunology
Published
2011-04-21
Volume
11
Issue
5
Pages
318-329
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2059369279
Cited by
281
References
119
Citations by year
2026: 11 · 2025: 11 · 2024: 16 · 2023: 22 · 2022: 27 · 2021: 27 · 2020: 28 · 2019: 13 · 2018: 15 · 2017: 17 · 2016: 20 · 2015: 17 · 2014: 12 · 2013: 24 · 2012: 17
FWCI
1.61
Type
journal article
Language
en
Open access
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (NS 061447-01, F32NS061447, ZIANS003111)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Keywords
neurotropic viruses, viral persistence, viral latency, antiviral immunity, immune surveillance, neuroinflammation, viral neuroinfection
MeSH terms
Animals, Blood-Brain Barrier, Capillary Permeability, Central Nervous System, Endothelium, Vascular, Humans, Viruses, Virus Latency, Peripheral Nervous System, Central Nervous System Viral Diseases, Blood-Nerve Barrier, Virus Internalization

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