ArticleBioscience reports2021
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19.
Article in Bioscience reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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.
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.
Who cites it
116 citing papers in PubMed, 186 citations in OpenAlex.
- Beyond correlation and causation: epistemic caution, anomalous findings, and COVID-19 vaccine safety.Philosophy, ethics, and humanities in medicine : PEHM · 2026Review
- Spike protein and fibrin(ogen) interactions.Blood advances · 2026Article
- Bioinformatic assessment of the potential amyloidogenicity of the human and evolutionarily more ancient proteomes.The Biochemical journal · 2026Article
- Surface cues shape procoagulant properties of amyloidogenic microclots.Cell death & disease · 2026Review
- Assessing the Health and Functionality of the Microcirculation Using Thermal Imaging.Journal of biophotonics · 2026Review
- Current status and future perspectives on the mechanistic and pathophysiological understanding of long COVID.Communications medicine · 2026Article
- SARS-CoV-2 spike protein can bind fibrin(ogen), but does not alter plasma fibrin formation, clot structure, or lysis.Blood advances · 2026Article
- Gut metabolite TMAO and its structural analogs bind to fibrinogen thereby enhancing clot formation: a rationale for atherosclerosis risk.Scientific reports · 2026Article
- Clinical relevance of circulating blood microaggregates and reactivation of Epstein Barr Virus in long-term Post-CoVID syndrome patients.Scientific reports · 2026Article
- A novel metacyte metafer classifier for platelet morphology using long COVID as a model.Journal of thrombosis and thrombolysis · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Uncovering the hidden biology of fibrinaloid microclot complexes in complex, inflammatory diseases.QRB discovery · 2026Review
- Proteomic signatures of COVID-19 Post-Vaccination/Post-Infection Syndrome (PV/PIS): insights into immune dysregulation and coagulopathy.Frontiers in cellular and infection microbiology · 2026Article
- Robust antibody and T cell responses tracked longitudinally in patients with long COVID.The Journal of general virology · 2025Article
- Review
- AmyloGram reveals amyloidogenic potential in stroke thrombus proteomes.The Biochemical journal · 2025Article
- Unique Features and Collateral Immune Effects of mRNA-LNP COVID-19 Vaccines: Plausible Mechanisms of Adverse Events and Complications.Pharmaceutics · 2025Review
- Viral persistence in long COVID: Research advances and treatment strategies.Infectious diseases & immunity · 2025Review
- COVID-19-induced thrombotic microangiopathy in patients with multiple myeloma receiving carfilzomib treatment.International journal of hematology · 2025Article
- Multisystem Endothelial Inflammation: A Key Driver of Adverse Events Following mRNA-Containing COVID-19 Vaccines.Vaccines · 2025Review
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, the cause of coronavirus disease 2019 (COVID-19), is characterized by unprecedented clinical pathologies. One of the most important pathologies, is hypercoagulation and microclots in the lungs of patients. Here we study the effect of isolated SARS-CoV-2 spike protein S1 subunit as potential inflammagen sui generis. Using scanning electron and fluorescence microscopy as well as mass spectrometry, we investigate the potential of this inflammagen to interact with platelets and fibrin(ogen) directly to cause blood hypercoagulation. Using platelet-poor plasma (PPP), we show that spike protein may interfere with blood flow. Mass spectrometry also showed that when spike protein S1 is added to healthy PPP, it results in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin. These proteins were substantially resistant to trypsinization, in the presence of spike protein S1. Here we suggest that, in part, the presence of spike protein in circulation may contribute to the hypercoagulation in COVID-19 positive patients and may cause substantial impairment of fibrinolysis. Such lytic impairment may result in the persistent large microclots we have noted here and previously in plasma samples of COVID-19 patients. This observation may have important clinical relevance in the treatment of hypercoagulability in COVID-19 patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.