ArticleJournal of virology2011
Glutamate excitotoxicity is involved in the induction of paralysis in mice after infection by a human coronavirus with a single point mutation in its spike protein.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Respiratory Syndrome Coronavirus Infections: Possible Mechanisms of Neurological Implications-A Systematic Review.Frontiers in neurology · 2020Pooled it
- Expression of spike and hemagglutinin-esterase proteins is necessary to recover infectious recombinant bovine coronavirus.Journal of virology · 2025Article
- The kinase RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during central nervous system viral infection.Immunity · 2025Article
- Ceftriaxone attenuates Poly I:C-induced neuroinflammationFrontiers in cellular neuroscience · 2025Article
- Rapid generation and characterization of recombinant HCoV-OC43-VR1558 infectious clones expressing reporter Renilla luciferase.Biosafety and health · 2024Article
- Utilizing HCoV-OC43 to better understand the neurological impact of COVID-19.Brain, behavior, & immunity - health · 2024Article
- RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during CNS viral infection.bioRxiv : the preprint server for biology · 2024Article
- Multiple sclerosis and COVID-19: a bidirectional Mendelian randomization study.Frontiers in immunology · 2024Article
- Structural proteins of human coronaviruses: what makes them different?Frontiers in cellular and infection microbiology · 2024Review
- COVID-19 vaccination and the risk of autoimmune diseases: a Mendelian randomization study.Frontiers in public health · 2024Article
- A suitable model to investigate acute neurological consequences of coronavirus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Differential effects of SARS-CoV-2 variants on central nervous system cells and blood-brain barrier functions.Journal of neuroinflammation · 2023Article
- Article
- Shared genetics and causal associations between COVID-19 and multiple sclerosis.Journal of medical virology · 2023Article
- Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023Review
- Acute Cerebellar Inflammation and Related Ataxia: Mechanisms and Pathophysiology.Brain sciences · 2022Review
- A Mouse-Adapted Model of HCoV-OC43 and Its Usage to the Evaluation of Antiviral Drugs.Frontiers in microbiology · 2022Article
- Biological and Psychological Factors Determining Neuropsychiatric Outcomes in COVID-19.Current psychiatry reports · 2021Review
- Neurological complications of COVID-19: from pathophysiology to rehabilitation. An overview.Acta bio-medica : Atenei Parmensis · 2021Article
- Guillain-Barré Syndrome Associated with SARS-CoV-2 Infection: A Case Report.European journal of translational myology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human coronaviruses (HCoV) are recognized respiratory pathogens, and some strains, including HCoV-OC43, can infect human neuronal and glial cells of the central nervous system (CNS) and activate neuroinflammatory mechanisms. Moreover, HCoV-OC43 is neuroinvasive, neurotropic, and neurovirulent in susceptible mice, where it induces chronic encephalitis. Herein, we show that a single point mutation in the viral spike (S) glycoprotein (Y241H), acquired during viral persistence in human neural cells, led to a hind-limb paralytic disease in infected mice. Inhibition of glutamate excitotoxicity using a 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propranoic acid (AMPA) receptor antagonist (GYKI-52466) improved clinical scores related to the paralysis and motor disabilities in S mutant virus-infected mice, as well as protected the CNS from neuronal dysfunctions, as illustrated by restoration of the phosphorylation state of neurofilaments. Expression of the glial glutamate transporter GLT-1, responsible for glutamate homeostasis, was downregulated following infection, and GYKI-52466 also significantly restored its steady-state expression level. Finally, GYKI-52466 treatment of S mutant virus-infected mice led to reduced microglial activation, which may lead to improvement in the regulation of CNS glutamate homeostasis. Taken together, our results strongly suggest an involvement of excitotoxicity in the paralysis-associated neuropathology induced by an HCoV-OC43 mutant which harbors a single point mutation in its spike protein that is acquired upon persistent virus infection.
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Registered trials
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.