AI Article Synopsis
- SARS-CoV-2, the virus causing COVID-19, affects the body by interacting with host-cell receptors via its spike protein (S protein).
- The study reveals that the S protein triggers significant changes in platelets, which can lead to their permanent activation, a factor contributing to coagulopathies in COVID-19 patients.
- Researchers found that the S protein binds to specific platelet integrins that induce filopodia formation, suggesting that these interactions play a role in the disease's severity and blood clotting complications.
Article Abstract
SARS-CoV-2 is a novel coronavirus responsible for the COVID-19 pandemic. Its high pathogenicity is due to SARS-CoV-2 spike protein (S protein) contacting host-cell receptors. A critical hallmark of COVID-19 is the occurrence of coagulopathies. Here, we report the direct observation of the interactions between S protein and platelets. Live imaging shows that the S protein triggers platelets to deform dynamically, in some cases, leading to their irreversible activation. Cellular cryo-electron tomography reveals dense decorations of S protein on the platelet surface, inducing filopodia formation. Hypothesizing that S protein binds to filopodia-inducing integrin receptors, we tested the binding to RGD motif-recognizing platelet integrins and find that S protein recognizes integrin αβ. Our results infer that the stochastic activation of platelets is due to weak interactions of S protein with integrin, which can attribute to the pathogenesis of COVID-19 and the occurrence of rare but severe coagulopathies.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9898865 | PMC |
| http://dx.doi.org/10.1038/s41467-023-36279-5 | DOI Listing |
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