ArticleBlood advances2022
Platelet activation and partial desensitization are associated with viral xenophagy in patients with severe COVID-19.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting GPVI with glenzocimab in COVID-19 patients: Results from a randomized clinical trial.PloS one · 2024Trial
- Megakaryocyte phenotyping in response to SARS-CoV-2 variants.Platelets · 2025Article
- Immuno-haemostatic dysregulation in heart failure with preserved ejection fraction.ESC heart failure · 2025Article
- Longitudinal Metabolomics Reveals Metabolic Dysregulation Dynamics in Patients with Severe COVID-19.Metabolites · 2024Article
- Beyond basic characterization and omics: Immunomodulatory roles of platelet-derived extracellular vesicles unveiled by functional testing.Journal of extracellular vesicles · 2024Article
- Platelet Aggregation Alterations in Patients with Severe Viral Infection Treated at the Intensive Care Unit: Implications for Mortality Risk.Pathogens (Basel, Switzerland) · 2024Article
- COVID-19 in the Initiation and Progression of Atherosclerosis: Pathophysiology During and Beyond the Acute Phase.JACC. Advances · 2024Review
- SARS-CoV-2 infection modifies the transcriptome of the megakaryocytes in the bone marrow.Blood advances · 2024Article
- Molecular Modulators and Receptors of Selective Autophagy: Disease Implication and Identification Strategies.International journal of biological sciences · 2024Review
- COVID-19: Not a thrombotic disease but a thromboinflammatory disease.Upsala journal of medical sciences · 2024Review
- The Ways of the Virus: Interactions of Platelets and Red Blood Cells with SARS-CoV-2, and Their Potential Pathophysiological Significance in COVID-19.International journal of molecular sciences · 2023Review
- Breakthrough infections after COVID-19 vaccinations do not elicit platelet hyperactivation and are associated with high platelet-lymphocyte and low platelet-neutrophil aggregates.Research and practice in thrombosis and haemostasis · 2023Article
- Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023Article
- SARS-CoV-2 Omicron variant infection affects blood platelets, a comparative analysis with Delta variant.Frontiers in immunology · 2023Article
- The impact of platelets on pulmonary microcirculation throughout COVID-19 and its persistent activating factors.Frontiers in immunology · 2022Review
- Occurrence and role of lung megakaryocytes in infection and inflammation.Frontiers in immunology · 2022Review
- Platelet in thrombo-inflammation: Unraveling new therapeutic targets.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mild thrombocytopenia, changes in platelet gene expression, enhanced platelet functionality, and presence of platelet-rich thrombi in the lung have been associated with thromboinflammatory complications of patients with COVID-19. However, whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) gets internalized by platelets and directly alters their behavior and function in infected patients remains elusive. Here, we investigated platelet parameters and the presence of viral material in platelets from a prospective cohort of 29 patients with severe COVID-19 admitted to an intensive care unit. A combination of specific assays, tandem mass spectrometry, and flow cytometry indicated high levels of protein and lipid platelet activation markers in the plasma from patients with severe COVID-19 associated with an increase of proinflammatory cytokines and leukocyte-platelets interactions. Platelets were partly desensitized, as shown by a significant reduction of αIIbβ3 activation and granule secretion in response to stimulation and a decrease of surface GPVI, whereas plasma from patients with severe COVID-19 potentiated washed healthy platelet aggregation response. Transmission electron microscopy indicated the presence of SARS-CoV-2 particles in a significant fraction of platelets as confirmed by immunogold labeling and immunofluorescence imaging of Spike and nucleocapsid proteins. Compared with platelets from healthy donors or patients with bacterial sepsis, platelets from patients with severe COVID-19 exhibited enlarged intracellular vesicles and autophagolysosomes. They had large LC3-positive structures and increased levels of LC3II with a co-localization of LC3 and Spike, suggesting that platelets can digest SARS-CoV-2 material by xenophagy in critically ill patients. Altogether, these data show that during severe COVID-19, platelets get activated, become partly desensitized, and develop a selective autophagy response.
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