Evidence map›Paper›PMID 27795420›Full record

ArticleJournal of virology2017

Pivotal Role of Receptor-Interacting Protein Kinase 1 and Mixed Lineage Kinase Domain-Like in Neuronal Cell Death Induced by the Human Neuroinvasive Coronavirus OC43.

Mathieu Meessen-Pinard, Alain Le Coupanec, Marc Desforges, Pierre J Talbot

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 23% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Review
  6. Review
  7. Article
  8. Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
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  14. Neurological complications and infection mechanism of SARS-COV-2.Signal transduction and targeted therapy · 2021
    Review
  15. Article
  16. Review
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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

4 authors at 1 institution in 1 country.

Mathieu Meessen-PinardLaboratory of Neuroimmunovirology, INRS-Institut Armand-Frappier, Université du Québec, Laval, Québec, Canada.
Alain Le CoupanecLaboratory of Neuroimmunovirology, INRS-Institut Armand-Frappier, Université du Québec, Laval, Québec, Canada.
Marc DesforgesLaboratory of Neuroimmunovirology, INRS-Institut Armand-Frappier, Université du Québec, Laval, Québec, Canada pierre.talbot@iaf.inrs.ca marc.desforges@iaf.inrs.ca.
Pierre J TalbotLaboratory of Neuroimmunovirology, INRS-Institut Armand-Frappier, Université du Québec, Laval, Québec, Canada pierre.talbot@iaf.inrs.ca marc.desforges@iaf.inrs.ca.
Institut National de la Recherche Scientifique · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human coronaviruses (HCoV) are respiratory pathogens with neuroinvasive, neurotropic, and neurovirulent properties, highlighting the importance of studying the potential implication of these viruses in neurological diseases. The OC43 strain (HCoV-OC43) was reported to induce neuronal cell death, which may participate in neuropathogenesis. Here, we show that HCoV-OC43 harboring two point mutations in the spike glycoprotein (rOC/U IMPORTANCE: Because they are naturally neuroinvasive and neurotropic, human coronaviruses are suspected to participate in the development of neurological diseases. Given that the strain OC43 is neurovirulent in mice and induces neuronal cell death, we explored the neuronal response to infection by characterizing the activation of RCD. Our results revealed that classical apoptosis associated with the Bax protein does not play a significant role in HCoV-OC43-induced neuronal cell death and that RIP1 and MLKL, two cellular proteins usually associated with necroptosis (an RCD back-up system when apoptosis is not adequately induced), both play a pivotal role in the process. As necroptosis disrupts cellular membranes and allows the release of damage-associated molecular patterns (DAMP) and possibly induces the production of proinflammatory cytokines, it may represent a proinflammatory cell death mechanism that contributes to excessive neuroinflammation and neurodegeneration and eventually to neurological disorders after a coronavirus infection.

Indexed as

Host-Pathogen InteractionsAnimalsbcl-2-Associated X ProteinCell DeathCell LineCell Line, TumorCoronavirus InfectionsCoronavirus OC43, HumanEmbryo, MammalianFemaleGene Expression RegulationGTPase-Activating ProteinsHumansMiceMice, Inbred BALB CMutationBax protein, mousebcl-2-Associated X ProteinGTPase-Activating ProteinsMLKL protein, mouseProtein KinasesRalbp1 protein, mouseRNA, Small InterferingSpike Glycoprotein, Coronaviruscoronavirushuman coronavirushuman coronavirus OC43necroptosisregulated cell deathRIP

Identifiers

PMID27795420
PMCPMC5165216
OpenAlexW2536357747

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.