Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

SARS-CoV-2 Omicron variant spike protein maintains the ability to bind and activate human platelets: Comparison with the wild-type.

Scientific reports - 9 Apr 2026

Kusudo Eriko, Kawamoto Shuji, Matsumoto Tsuguhiro, Egi Moritoki

Abstract excerpt

Ongoing mutations in the SARS-CoV-2 spike protein contribute to the persistence of COVID-19. While the wild-type (WT) spike protein enhances platelet activity, the effects of the Omicron variant remain unclear. This study compared the effects of WT and Omicron spike proteins on platelet function in 10 healthy participants. We evaluated spike protein binding, P-selectin (platelet activation marker) expression, and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenosine Diphosphate
Share to Blood Platelets

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to COVID-19

Share to P-Selectin

Share to Platelet Activation

Share to Platelet Aggregation

Share to SARS-CoV-2

Share to Spike Glycoprotein, Coronavirus

Source

Open in PubMed Open full text

Identifiers

PMID: 41957450
DOI: 10.1038/s41598-026-46081-0
PMCID: PMC13223238

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SARS-CoV-2 Omicron variant spike protein maintains the ability to bind and activate human platelets: Comparison with the wild-type.PMID 41957450Read ↗

P-Selectin promotes SARS-CoV-2 interactions with platelets and the endotheliumSemantic proximity Read ↗

Alterations in platelet proteome signature and impaired platelet integrin α <sub>IIb</sub> β <sub>3</sub> activation in patients with COVID-19Semantic proximity Read ↗

SARS-CoV-2 Spike protein activates TMEM16F-mediated platelet pro-coagulant activitySemantic proximity Read ↗

New Consensus pattern in Spike CoV-2: potential implications in coagulation process and cell–cell fusionSemantic proximity Read ↗

SARS-CoV-2 Spike protein promotes vWF secretion and thrombosis via endothelial cytoskeleton-associated protein 4 (CKAP4)Semantic proximity Read ↗

SARS-CoV-2 infection is associated with a pro-thrombotic platelet phenotype.Semantic proximity Read ↗

SARS-CoV-2 spike protein activates NOX2-p66SHC axis via inhibiting SLAMF8 to promote thrombogenesisSemantic proximity Read ↗

COVID-19 induces a hyperactive phenotype in circulating plateletsSemantic proximity Read ↗

Comprehensive phenotyping of human platelets by single‐cell cytometrySemantic proximity Read ↗

The spike protein of SARS-CoV-2 induces endothelial inflammation through integrin α5β1 and NF-κBSemantic proximity Read ↗

COVID-19 induces a hyperactive phenotype in circulating platelets.Semantic proximity Read ↗

Bystander effect of SARS-CoV-2 spike protein on human monocytic THP-1 cell activation and initiation of prothrombogenic stimulus representing severe COVID-19Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.