Evidence map›Paper›PMID 41243963›Full record

ArticleThe Journal of clinical investigation2025

P selectin promotes SARS-CoV-2 interactions with platelets and the endothelium.

Cesar L Moreno, Fernanda Vs Castanheira, Alberto Ospina Stella, Felicity Chung, Anupriya Aggarwal, Alexander J Cole, Lipin Loo, Alexander Dupuy, Yvonne X Kong, Lejla Hagimola and 15 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

25 authors.

Cesar L MorenoDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.
Fernanda Vs CastanheiraSnyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
Alberto Ospina StellaKirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Felicity ChungDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.
Anupriya AggarwalKirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Alexander J ColeCentenary Institute and Faculty of Medicine and Health.
Lipin LooDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.
Alexander DupuyHaematology Research Lab, Heart Research Institute, and.
Yvonne X KongHaematology Research Lab, Heart Research Institute, and.
Lejla HagimolaHaematology Research Lab, Heart Research Institute, and.
Jemma FenwickHaematology Research Lab, Heart Research Institute, and.
Paul R ColemanHaematology Research Lab, Heart Research Institute, and.
Rebecca CarrDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.
Tian Y DuDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.
Tim IsonKirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Michelle NewtonKirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Maxwell P Bui-MarinosSnyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
Scott B CohenCell Biology Unit, Children's Medical Research Institute, Faculty of Medicine and Health, The University of Sydney, Westmead, New South Wales, Australia.
Jennifer A CorcoranSnyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
Daniel HesselsonCentenary Institute and Faculty of Medicine and Health.
Jennifer R GambleVascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia.
Freda H PassamHaematology Research Lab, Heart Research Institute, and.
Stuart G TurvilleKirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Paul KubesSnyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
G Gregory NeelyDr. John and Anne Chong Lab for Functional Genomics, Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, New South Wales, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The physiology of SARS-CoV-2 virus/host interactions is not well understood. To better understand host/virus interactions, we performed a CRISPR activation screen to identify host genes that confer resistance to authentic SARS-CoV-2. This highlighted 34 new candidate genes that may alter the course of infection. We validated that 7 of these genes can suppress authentic SARS-CoV-2 infection, including the innate immune receptor P selectin, which increases SARS-CoV-2 spike-dependent binding to cells, while protecting from infection. P selectin also promotes binding to SARS-CoV-2 variants, SARS-CoV-1, and Middle East respiratory syndrome spike proteins, suggesting a general role for P selectin in highly pathogenic coronavirus infections. Importantly, P selectin protein expression driven by synthetic mRNA can block SARS-CoV-2 infection. Naturally, P selectin is expressed on platelets, and we show that it promotes spike-mediated platelet aggregation. P selectin is also expressed on the endothelium, where SARS-CoV-2 spike interactions are also P selectin dependent. In vivo, SARS-CoV-2 uses P selectin to home to capillary beds where the virus interacts with platelets and endothelium, and blocking this interaction can clear vascular-associated pulmonary SARS-CoV-2.

Indexed as

Blood PlateletsCOVID-19Endothelium, VascularP-SelectinSARS-CoV-2AnimalsHumansMiceSpike Glycoprotein, CoronavirusP-SelectinSELP protein, humanSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2CoagulationCOVID-19Endothelial cellsInfectious diseasePlateletsVirology

Identifiers

PMID41243963
PMCPMC12618076

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.