ArticleBlood advances2022
Platelet activation by SARS-CoV-2 implicates the release of active tissue factor by infected cells.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Antiplatelet therapy for patients with COVID-19: Systematic review and meta-analysis of observational studies and randomized controlled trials.Frontiers in medicine · 2022Pooled it
- Megakaryocytes Internalize and Are Activated by Immune Complexes.Circulation research · 2026Article
- In-depth serum proteomics atlas of COVID-19 defines a Severity-Resistance Index from a four-protein panel for disease severity and prognosis.Journal of translational medicine · 2026Article
- Evaluation of 3 commercial assays for the measurement of tissue factor activity in human plasma.Research and practice in thrombosis and haemostasis · 2026Article
- Megakaryocyte phenotyping in response to SARS-CoV-2 variants.Platelets · 2025Article
- Secretory phospholipase ACommunications biology · 2025Article
- Deficiency in platelet 12-lipoxygenase exacerbates inflammation and disease severity during SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The endothelial-immunothrombotic storm in viral sepsis: lessons from COVID-19.Frontiers in immunology · 2025Review
- Complex Pattern of Platelet Activation/Reactivity After SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
- Thymidine phosphorylase mediates SARS-CoV-2 spike protein enhanced thrombosis in K18-hACE2Thrombosis research · 2024Article
- Challenges with measuring tissue factor antigen and activity in human plasma.Blood vessels, thrombosis & hemostasis · 2024Review
- COVID-19 in the Initiation and Progression of Atherosclerosis: Pathophysiology During and Beyond the Acute Phase.JACC. Advances · 2024Review
- Preferential and sustained platelet activation in COVID-19 survivors with mental disorders.Scientific reports · 2024Article
- SARS-CoV-2 infection modifies the transcriptome of the megakaryocytes in the bone marrow.Blood advances · 2024Article
- Deciphering Abnormal Platelet Subpopulations in COVID-19, Sepsis and Systemic Lupus Erythematosus through Machine Learning and Single-Cell Transcriptomics.International journal of molecular sciences · 2024Article
- Dysregulated platelet function in patients with postacute sequelae of COVID-19.Vascular medicine (London, England) · 2024Article
- Beyond Borders of the Cell: How Extracellular Vesicles Shape COVID-19 for People with Cystic Fibrosis.International journal of molecular sciences · 2024Review
- Recombinant Rod Domain of Vimentin Reduces SARS-CoV-2 Viral Replication by Blocking Spike Protein-ACE2 Interactions.International journal of molecular sciences · 2024Article
- Does SARS-CoV-2 infect platelets?Frontiers in immunology · 2024Article
- Neutrophil Extracellular Traps in Tumors and Potential Use of Traditional Herbal Medicine Formulations for Its Regulation.International journal of nanomedicine · 2024Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 4 countries.
Funding
Abstract
Platelets are hyperactivated in coronavirus disease 2019 (COVID-19). However, the mechanisms promoting platelet activation by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are not well understood. This may be due to inherent challenges in discriminating the contribution of viral vs host components produced by infected cells. This is particularly true for enveloped viruses and extracellular vesicles (EVs), as they are concomitantly released during infection and share biophysical properties. To study this, we evaluated whether SARS-CoV-2 itself or components derived from SARS-CoV-2-infected human lung epithelial cells could activate isolated platelets from healthy donors. Activation was measured by the surface expression of P-selectin and the activated conformation of integrin αIIbβ3, degranulation, aggregation under flow conditions, and the release of EVs. We find that neither SARS-CoV-2 nor purified spike activates platelets. In contrast, tissue factor (TF) produced by infected cells was highly potent at activating platelets. This required trace amounts of plasma containing the coagulation factors FX, FII, and FVII. Robust platelet activation involved thrombin and the activation of protease-activated receptor (PAR)-1 and -4 expressed by platelets. Virions and EVs were identified by electron microscopy. Through size-exclusion chromatography, TF activity was found to be associated with a virus or EVs, which were indistinguishable. Increased TF messenger RNA (mRNA) expression and activity were also found in lungs in a murine model of COVID-19 and plasma of severe COVID-19 patients, respectively. In summary, TF activity from SARS-CoV-2-infected cells activates thrombin, which signals to PARs on platelets. Blockade of molecules in this pathway may interfere with platelet activation and the coagulation characteristic of COVID-19.
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