ArticleJournal of virology2019
Contemporary Circulating Enterovirus D68 Strains Infect and Undergo Retrograde Axonal Transport in Spinal Motor Neurons Independent of Sialic Acid.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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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.
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.
Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- Article
- Decoding the complex receptor landscape of enterovirus D68.PLoS pathogens · 2026Review
- Non-polio enterovirus infection and electrophysiological changes in human iPSC-derived neural networks.EBioMedicine · 2026Article
- Enterovirus D68 receptor usage: from static attachment to dynamic entry.Journal of virology · 2026Review
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Elucidating the role of human skeletal muscles in the pathogenesis of enterovirus D68 infection.Life science alliance · 2025Article
- Review
- Non-polio enteroviruses compromise the electrophysiology of a human iPSC-derived neural network.bioRxiv : the preprint server for biology · 2025Article
- Sialic Acid-Containing Glycolipids Extend the Receptor Repertoire of Enterovirus-D68.ACS infectious diseases · 2025Article
- MFSD6 is an entry receptor for enterovirus D68.Nature · 2025Article
- Article
- Insights Into Enterovirus D68 Immunology: Unraveling the Mysteries of Host-Pathogen Interactions.Immunity, inflammation and disease · 2025Review
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- VP1 is the primary determinant of neuropathogenesis in a mouse model of enterovirus D68 acute flaccid myelitis.Journal of virology · 2024Article
- Human B cells and dendritic cells are susceptible and permissive to enterovirus D68 infection.mSphere · 2024Article
- SARS-CoV-2 and oncolytic EV-D68-encoded proteases differentially regulate pyroptosis.Journal of virology · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Article
- Pathogenesis of enterovirus infection in central nervous system.Biosafety and health · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Enterovirus D68 (EV-D68) is an emerging virus that has been identified as a cause of recent outbreaks of acute flaccid myelitis (AFM), a poliomyelitis-like spinal cord syndrome that can result in permanent paralysis and disability. In experimental mouse models, EV-D68 spreads to, infects, and kills spinal motor neurons following infection by various routes of inoculation. The topography of virus-induced motor neuron loss correlates with the pattern of paralysis. The mechanism(s) by which EV-D68 spreads to target motor neurons remains unclear. We sought to determine the capacity of EV-D68 to spread by the neuronal route and to determine the role of known EV-D68 receptors, sialic acid and intracellular adhesion molecule 5 (ICAM-5), in neuronal infection. To do this, we utilized a microfluidic chamber culture system in which human induced pluripotent stem cell (iPSC) motor neuron cell bodies and axons can be compartmentalized for independent experimental manipulation. We found that EV-D68 can infect motor neurons via their distal axons and spread by retrograde axonal transport to the neuronal cell bodies. Virus was not released from the axons via anterograde axonal transport after infection of the cell bodies. Prototypic strains of EV-D68 depended on sialic acid for axonal infection and transport, while contemporary circulating strains isolated during the 2014 EV-D68 outbreak did not. The pattern of infection did not correspond with the ICAM-5 distribution and expression in either human tissue, the mouse model, or the iPSC motor neurons.
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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.