Cited by 128Infectious Encephalopathies and EncephalitisAnimal Virus Infections StudiesLong-Term Effects of COVID-19

Vacuolating encephalitis in mice infected by human coronavirus OC43

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Jacomy, Hélène, Talbot, Pierre J·2003·Virology

Abstract

Involvement of viruses in human neurodegenerative diseases and the underlying pathologic mechanisms remain generally unclear. Human respiratory coronaviruses (HCoV) can infect neural cells, persist in human brain, and activate myelin-reactive T cells. As a means of understanding the human infection, we characterized in vivo the neurotropic and neuroinvasive properties of HCoV-OC43 through the development of an experimental animal model. Virus inoculation of 21-day postnatal C57BL/6 and BALB/c mice led to a generalized infection of the whole CNS, demonstrating HCoV-OC43 neuroinvasiveness and neurovirulence. This acute infection targeted neurons, which underwent vacuolation and degeneration while infected regions presented strong microglial reactivity and inflammatory reactions. Damage to the CNS was not immunologically mediated and microglial reactivity was instead a consequence of direct virus-mediated neuronal injury. Although this acute encephalitis appears generally similar to that induced by murine coronaviruses, an important difference rests in the prominent spongiform-like degeneration that could trigger neuropathology in surviving animals.

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  • SARS-CoV, MERS-CoV, and HCoV-OCR43 were able to invade the murine CNS using the transcribrial route, infecting olfactory sensory neurons of the nasal cavity and passing to other neural cells, indicating that SARS-CoV-2 could use the same mechanism.

    “In fact, SARS-CoV, MERS-CoV, and HCoV-OCR43 were able to invade the murine CNS using the transcribrial route, infecting olfactory sensory neurons of nasal cavity, and passing to other neural cells, indicating that SARS-CoV-2 could use the same mechanism [24, 35–37].”

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  1. McIntosh K. Fields B.N. Knipe D.M. Virology third ed 1996 Raven Press New York 1095 1103

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Authors
Jacomy, H., & Talbot, P. J.
Affiliations
Institut National de la Recherche Scientifique (CA)
Corresponding author
Talbot, Pierre J
Venue
Virology
Publisher
Elsevier BV
Published
2003-10
Volume
315
Issue
1
Pages
20-33
ISSN
0042-6822 (ISSN-L)
OpenAlex
W1999566808
Cited by
128
References
84
Citations by year
2025: 2 · 2024: 3 · 2023: 9 · 2022: 8 · 2021: 23 · 2020: 40 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 1
FWCI
1.94
Type
journal article
Language
en
Open access
Locations
  • Virology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Canadian Institutes of Health Research
  • Institute of Infection and Immunity
Topics
  • Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
  • Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
  • Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
Keywords
HCoV-OC43, neuroinvasion, neurotropism, neurovirulence, encephalitis, neuronal vacuolation, neurodegeneration, microglial activation, neuroinflammation, neuropathology, murine coronavirus, animal models, neurodegenerative diseases
MeSH terms
Animals, Brain, Disease Models, Animal, Humans, Immunohistochemistry, Inflammation, Mice, Inbred BALB C, Mice, Inbred C57BL, Microscopy, Electron, Spinal Cord, Vacuoles, Virulence, Coronavirus Infections, Encephalitis, Viral, Coronavirus OC43, Human, Mice

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