Evidence map›Paper›PMID 11773370›Full record

ArticleJournal of virology2002

Soluble receptor potentiates receptor-independent infection by murine coronavirus.

Fumihiro Taguchi, Shutoku Matsuyama

Abstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Tectonic conformational changes of a coronavirus spike glycoprotein promote membrane fusion.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  6. Article
  7. Article
  8. Coronavirus Spike Protein and Tropism Changes.Advances in virus research · 2016
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Coronavirus pathogenesis.Advances in virus research · 2011
    Review
  14. Pathogenesis of murine coronavirus in the central nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  15. Cytopathy of an infiltrating monocyte lineage during the early phase of infection with murinecoronavirus in the brain.Neuropathology : official journal of the Japanese Society of Neuropathology · 2010
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors.

Fumihiro TaguchiNational Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo 187-8502, Japan. taguchi@ncnp.go.jp
Shutoku Matsuyama

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mouse hepatitis virus (MHV) infection spreads from MHV-infected DBT cells, which express the MHV receptor CEACAM1 (MHVR), to BHK cells, which are devoid of the receptor, by intercellular membrane fusion (MHVR-independent fusion). This mode of infection is a property of wild-type (wt) JHMV cl-2 virus but is not seen in cultures infected with the mutant virus JHMV srr7. In this study, we show that soluble MHVR (soMHVR) potentiates MHVR-independent fusion in JHMV srr7-infected cultures. Thus, in the presence of soMHVR, JHMV srr7-infected DBT cells overlaid onto BHK cells induce BHK cell syncytia and the spread of JHMV srr7 infection. This does not occur in the absence of soMHVR. soMHVR also enhanced wt virus MHVR-independent fusion. These effects were dependent on the concentration of soMHVR in the culture and were specifically blocked by the anti-MHVR monoclonal antibody CC1. Together with these observations, direct binding of soMHVR to the virus spike (S) glycoprotein as revealed by coimmunoprecipitation demonstrated that the effect is mediated by the binding of soMHVR to the S protein. Furthermore, fusion of BHK cells expressing the JHMV srr7 S protein was also induced by soMHVR. These results indicated that the binding of soMHVR to the S protein expressed on the DBT cell surface potentiates the fusion of MHV-infected DBT cells with nonpermissive BHK cells. We conclude that the binding of soMHVR to the S protein converts the S protein to a fusion-active form competent to mediate cell-cell fusion, in a fashion similar to the fusion of virus and cell membranes.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDCarcinoembryonic AntigenCell Adhesion MoleculesCell LineCricetinaeGlycoproteinsMembrane FusionMembrane GlycoproteinsMiceMurine hepatitis virusReceptors, VirusRecombinant Fusion ProteinsSolubilitySpike Glycoprotein, CoronavirusAntibodies, MonoclonalAntigens, CDCarcinoembryonic AntigenCD66 antigensCeacam1 protein, mouseCell Adhesion MoleculesGlycoproteinsMembrane GlycoproteinsReceptors, VirusRecombinant Fusion ProteinsSpike Glycoprotein, Coronavirusspike glycoprotein, SARS-CoVspike protein, mouse hepatitis virusViral Envelope Proteins

Identifiers

PMID11773370
PMCPMC135807

What OpenQuestion holds

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Registered trials

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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.