Researchers observed changes in platelet morphology, including elongated membranous protrusions rich in integrin αIIbβ3 and tetraspanin CD9, in patients with severe COVID-19 infection, sepsis, or bacterial infection.[1][2] These structures, called platelet-derived integrin- and tetraspanin-enriched tethers (PITTs), are formed during flow-induced activation of αIIbβ3 in in vitro conditions and in murine models of lung inflammation.[1] PITTs detach from the body of the platelet, adhere to endothelial cells and neutrophils, thereby stimulating inflammation and immune activation.[1][2] After PITTs were detached, platelets were left depleted of αIIbβ3, which reduced their ability to promote blood clotting.[1] In patients with sepsis, COVID-19, or severe infections, the formation of PITTs and loss of αIIbβ3 on platelets correlates with greater disease severity and adverse outcomes.[1][2] PITTs thus contribute to the intensification of vascular inflammation and the weakening of the adhesive function of platelets during severe infections.[1]