Evidence map›Paper›PMID 20642316›Full record

ArticleJournal of neurovirology2010

Mutations in the spike glycoprotein of human coronavirus OC43 modulate disease in BALB/c mice from encephalitis to flaccid paralysis and demyelination.

Hélène Jacomy, Julien R St-Jean, Elodie Brison, Gabriel Marceau, Marc Desforges, Pierre J Talbot

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 48 citations in OpenAlex.

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  8. Post-genomic platform for development of oligonucleotide vaccines against RNA viruses: diamond cuts diamond.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  9. Review
  10. Olfactory Bulb and Amygdala Gene Expression Changes in Subjects Dying with COVID-19.medRxiv : the preprint server for health sciences · 2021
    Article
  11. A Review of Neurological Involvement in Patients with SARS-CoV-2 Infection.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Review
  12. Article
  13. Purinergic Signaling of ATP in COVID-19 Associated Guillain-Barré Syndrome.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Review
  14. Mapping of SARS-CoV-2 Brain Invasion and Histopathology in COVID-19 Disease.medRxiv : the preprint server for health sciences · 2021
    Article
  15. Presentations and mechanisms of CNS disorders related to COVID-19.Neurology(R) neuroimmunology & neuroinflammation · 2021
    Review
  16. Review
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  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hélène JacomyLaboratory of Neuroimmunovirology, INRS-Institute Armand-Frappier, Laval, Québec, Canada.
Julien R St-Jean
Elodie Brison
Gabriel Marceau
Marc Desforges
Pierre J Talbot
Institut National de la Recherche Scientifique · CA

Funding

Canadian Institutes of Health Research MT-9203
6 · The paper itself

Abstract

The etiology of most neurodegenerative diseases of the central nervous system remains unknown and likely involves a combination of genetic susceptibility and environmental triggering factors. Given that exposure to numerous infectious pathogens occurs during childhood, and that some viral infections can lead to neurodegeneration and demyelination, it is conceivable that some viruses may act as triggering factors in neuropathogenesis. We have previously shown that the prototype OC43 strain of the common cold-associated human respiratory coronavirus has the capacity to infect human neuronal and glial cells and does persist in human brains. Moreover, it has neuroinvasive properties in susceptible BALB/c mice, where it leads to a chronic encephalitis with accompanying disabilities. Here, we show that mutations in the viral spike glycoprotein, reproducibly acquired during viral persistence in human neural cell cultures, led to a drastically modified virus-induced neuropathology in BALB/c mice, characterized by flaccid paralysis and demyelination. Even though infection by both mutated and wild-type viruses led to neuroinflammation, the modified neuropathogenesis induced by the mutated virus was associated with increased viral spread and significantly more CD4+ and CD8+ T-lymphocyte infiltration into the central nervous system, as well as significantly increased levels of the proinflammatory cytokine interleukin (IL)-6 and the chemokine CCL2 (monocyte chemoattractant protein [MCP]-1). Moreover, recombinant virus harboring the S glycoprotein mutations retained its neurotropism, productively infecting neurons. Therefore, interaction of a human respiratory coronavirus with the central nervous system may modulate virus and host factors resulting in a modified neuropathogenesis in genetically susceptible individuals.

Indexed as

MutationAnimalsCoronavirus InfectionsCoronavirus OC43, HumanDemyelinating DiseasesEncephalitis, ViralHumansImmunohistochemistryMembrane GlycoproteinsMiceMice, Inbred BALB CParaplegiaSpike Glycoprotein, CoronavirusViral Envelope ProteinsMembrane GlycoproteinsSpike Glycoprotein, CoronavirusViral Envelope Proteins

Identifiers

PMID20642316
PMCPMC7095228
OpenAlexW2123770562

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.