Nevertheless, the phenotypical activation of platelets and endothelial cells that we observed following exposure to COVID-19 TPE plasma did not lead to the production of platelet or endothelial inflammatory factors such as sCD40l or IL-6, nor to any increase in endothelial permeability, which was comparable to that observed on exposure of the platelet-endothelial co-culture to COVID-19 control plasma. This evidence concerns the gene CD40LG and COVID-19.