ArticleJournal of virology2013
Enterovirus 71 uses cell surface heparan sulfate glycosaminoglycan as an attachment receptor.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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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.
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Who cites it
128 citing papers in PubMed, 185 citations in OpenAlex.
- Physicochemical fingerprinting reveals convergent evolutionary determinants of enterovirus A71 neurovirulence through integrative machine learning and structural analysis.Virus research · 2026Article
- Intestinal Organoids as Models to Study Viruses: Current Application and Future Perspective.Journal of microbiology and biotechnology · 2026Review
- Advances in Antiviral Drug Development Targeting Enteroviruses: From Viral Proteins to Host Factors.Viruses · 2026Review
- Mutation of the highly conserved amino acids in the N-terminal region of the EV-A71 VP1 protein impairs viral RNA release during virus entry.Microbiology spectrum · 2026Article
- Meta-analysis of functional genomics studies reveals conserved cellular pathways required by viruses of pandemic concern.Access microbiology · 2026Article
- Molecular mechanisms of receptor recognition and antibody neutralization of coxsackievirus A6.Nature communications · 2025Article
- Antiviral candidates for enterovirus 71: targeting viral proteome and stage-specific lifecycle interventions.Virology journal · 2025Review
- Review
- Plasminogen deficiency reduces disease severity and immune responses in enterovirus A71-infected mice.Microbiology spectrum · 2025Article
- Platelet factor 4-derived C15 peptide broadly inhibits enteroviruses by disrupting viral attachment.Journal of virology · 2025Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Screening of Insertion Sites and Tags on EV-A71 VP1 Protein for Recombinant Virus Construction.Viruses · 2025Article
- Novel virulence determinants in VP1 regulate the assembly of enterovirus-A71.Journal of virology · 2024Article
- Construction of an infectious clone for enterovirus A89 and mutagenesis analysis of viral infection and cell binding.Microbiology spectrum · 2024Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Enterovirus A71 does not meet the uncoating receptor SCARB2 at the cell surface.PLoS pathogens · 2024Article
- Review
- Neutralizing antibody landscape of the non-polio Enteroviruses and future strategy.Frontiers in immunology · 2024Review
- Pteropine orthoreoviruses use cell surface heparan sulphate as an attachment receptor.Emerging microbes & infections · 2023Article
- Experimental animal models for development of human enterovirus vaccine.Clinical and experimental vaccine research · 2023Review
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV-71) infections are usually associated with mild hand, foot, and mouth disease in young children but have been reported to cause severe neurological complications with high mortality rates. To date, four EV-71 receptors have been identified, but inhibition of these receptors by antagonists did not completely abolish EV-71 infection, implying that there is an as yet undiscovered receptor(s). Since EV-71 has a wide range of tissue tropisms, we hypothesize that EV-71 infections may be facilitated by using receptors that are widely expressed in all cell types, such as heparan sulfate. In this study, heparin, polysulfated dextran sulfate, and suramin were found to significantly prevent EV-71 infection. Heparin inhibited infection by all the EV-71 strains tested, including those with a single-passage history. Neutralization of the cell surface anionic charge by polycationic poly-d-lysine and blockage of heparan sulfate by an anti-heparan sulfate peptide also inhibited EV-71 infection. Interference with heparan sulfate biosynthesis either by sodium chlorate treatment or through transient knockdown of N-deacetylase/N-sulfotransferase-1 and exostosin-1 expression reduced EV-71 infection in RD cells. Enzymatic removal of cell surface heparan sulfate by heparinase I/II/III inhibited EV-71 infection. Furthermore, the level of EV-71 attachment to CHO cell lines that are variably deficient in cell surface glycosaminoglycans was significantly lower than that to wild-type CHO cells. Direct binding of EV-71 particles to heparin-Sepharose columns under physiological salt conditions was demonstrated. We conclude that EV-71 infection requires initial binding to heparan sulfate as an attachment receptor.
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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.