Evidence map›Paper›PMID 32047128›Full record

ArticlemBio2020

Distinct Roles for Sialoside and Protein Receptors in Coronavirus Infection.

Enya Qing, Michael Hantak, Stanley Perlman, Tom Gallagher

Abstract read
In one paragraph

Article in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
–field-weighted citation impact
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

69 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Human coronavirus HKU1 neutralization by glycan receptor mimicry.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Variations inBiomolecules · 2023
    Article
  18. Article
  19. Teicoplanin derivatives block spike protein mediated viral entry as pan-SARS-CoV-2 inhibitors.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Article
  20. Review

9 more citing papers are in PubMed but not listed here.

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.

Enya QingDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois, USA.
Michael HantakDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois, USA.
Stanley PerlmanDepartment of Microbiology and Immunology, University of Iowa, Iowa City, Iowa, USA.ORCID 0000-0003-4213-2354
Tom GallagherDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois, USA tgallag@luc.edu.

Funding

SARS-CoV Proteins in Heterologous Viral InfectionP01AI060699 · NIAID · UNIVERSITY OF IOWA · PI PERLMAN, STANLEY · 2004 to 2021
$21.5M
6 · The paper itself

Abstract

Coronaviruses (CoVs) are common human and animal pathogens that can transmit zoonotically and cause severe respiratory disease syndromes. CoV infection requires spike proteins, which bind viruses to host cell receptors and catalyze virus-cell membrane fusion. Several CoV strains have spike proteins with two receptor-binding domains, an S1A that engages host sialic acids and an S1B that recognizes host transmembrane proteins. As this bivalent binding may enable broad zoonotic CoV infection, we aimed to identify roles for each receptor in distinct infection stages. Focusing on two betacoronaviruses, murine JHM-CoV and human Middle East respiratory syndrome coronavirus (MERS-CoV), we found that virus particle binding to cells was mediated by sialic acids; however, the transmembrane protein receptors were required for a subsequent virus infection. These results favored a two-step process in which viruses first adhere to sialic acids and then require subsequent engagement with protein receptors during infectious cell entry. However, sialic acids sufficiently facilitated the later stages of virus spread through cell-cell membrane fusion, without requiring protein receptors. This virus spread in the absence of the prototype protein receptors was increased by adaptive S1A mutations. Overall, these findings reveal roles for sialic acids in virus-cell binding, viral spike protein-directed cell-cell fusion, and resultant spread of CoV infections.

Indexed as

AnimalsCarcinoembryonic AntigenCoronavirus InfectionsDipeptidyl Peptidase 4HumansMembrane FusionMiceMiddle East Respiratory Syndrome CoronavirusMurine hepatitis virusMutationProtein BindingProtein Interaction Domains and MotifsReceptors, VirusSialic AcidsSpike Glycoprotein, CoronavirusVirus InternalizationCarcinoembryonic AntigenCeacam1 protein, mouseDipeptidyl Peptidase 4DPP4 protein, humanReceptors, VirusSialic AcidsSpike Glycoprotein, Coronaviruscoronavirusmembrane fusionsialic acidsvirus entryvirus glycoproteinsvirus receptors

Identifiers

PMID32047128
PMCPMC7018658

What OpenQuestion holds

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LicenceCC BY
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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.