"Introduction
... Here, we investigated whether SARS-CoV-2 S contributes to endothelial and epithelial barrier dysfunction in vitro and vascular leak in vivo...
Discussion
Our study reveals the capacity and mechanism by which SARS-CoV-2 S mediates barrier dysfunction in epithelial and endothelial cells in vitro and vascular leak in vivo, thus suggesting that S [spike] alone can mediate barrier dysfunction independently from viral infection. Our work indicates that levels of S observed in clinical samples from COVID-19 patients are sufficient to mediate barrier dysfunction (2.5 μg/ml). Our findings suggest that, in addition to functioning in viral entry, S interactions with GAGs and integrins induce vascular leak via activation of the TGF-β pathway. Further, our study offers a mechanistic explanation for the overproduction of TGF-β during COVID-19, which has been correlated with disease severity."
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