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Updated: Oct 8, 2025
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
Platelets mediate inflammatory monocyte activation by SARS-CoV-2 spike protein
Tianyang Li1, Yang Yang1, Yongqi Li1
1Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
Abstract:
Infection with SARS-CoV-2, the causative agent of COVID-19, causes mild to moderate disease in most patients but carries a risk of morbidity and mortality. Seriously affected individuals manifest disorders of hemostasis and a cytokine storm, but it is not understood how these manifestations of severe COVID-19 are linked. Here, we showed that the SARS-CoV-2 spike protein engaged the CD42b receptor to activate platelets via 2 distinct signaling pathways and promoted platelet-monocyte communication through the engagement of P selectin/PGSL-1 and CD40L/CD40, which led to proinflammatory cytokine production by monocytes. These results explain why hypercoagulation, monocyte activation, and a cytokine storm are correlated in patients severely affected by COVID-19 and suggest a potential target for therapeutic intervention.
Insights
The SARS-CoV-2 spike protein activates platelets and promotes communication with monocytes, leading to inflammation. This explains hypercoagulation and cytokine storms in severe COVID-19, suggesting a therapeutic target.
Area of Science:
- Immunology
- Hematology
- Virology
Background:
- Severe COVID-19 is associated with hemostasis disorders and cytokine storms.
- The precise mechanisms linking these severe manifestations remain unclear.
Purpose of the Study:
- To elucidate the molecular mechanisms by which SARS-CoV-2 infection leads to severe COVID-19 pathology.
- To identify potential therapeutic targets for mitigating severe COVID-19 outcomes.
Main Methods:
- Investigated the interaction between SARS-CoV-2 spike protein and platelet receptor CD42b.
- Analyzed platelet-monocyte communication pathways involving P-selectin/PSGL-1 and CD40L/CD40.
- Assessed the impact on proinflammatory cytokine production by monocytes.
Main Results:
- SARS-CoV-2 spike protein activates platelets through CD42b via two distinct signaling pathways.
- Activated platelets promote monocyte activation and proinflammatory cytokine release.
- Established a link between platelet activation, monocyte communication, and cytokine storm in severe COVID-19.
Conclusions:
- The findings explain the correlation between hypercoagulation, monocyte activation, and cytokine storm in severe COVID-19.
- Targeting the identified spike protein-receptor interactions may offer a therapeutic strategy.
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