Platelet-activating Antibodies Are Associated with Increased Platelet Degranulation and Thromboinflammation in Hospitalized COVID-19 Patients.

---

Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B234
Abstract ID: 5490

Presenting Author:
Nathan Witman , Graduate Student at Med. Col. of Wisconsin, Versiti Blood Res. Inst.

Abstract:

Severe COVID-19 is characterized by systemic inflammation, respiratory failure, dysregulated coagulation, and thrombosis. In this study, we investigated whether patients with severe COVID-19 develop platelet-activating antibodies similar to those in patients with heparin-induced thrombocytopenia (HIT), a condition associated with prothrombotic autoreactive antibodies. To test this, we modified the P-selectin expression assay (PEA) to test COVID-19 patient plasma for platelet-activating antibodies. We revealed that 41% of hospitalized COVID-19 patients developed antibodies capable of activating platelets from healthy donors. Importantly, the development of platelet-activating antibodies is independent of heparin exposure, unlike in HIT patients. Additionally, we observed an increase in the levels of platelet α-granule contents in the plasma of COVID-19 patients who had developed platelet-activating antibodies compared to those who had not, indicating that these antibodies were functional in vivo. Furthermore, we observed the levels of platelet-activating antibodies to be negatively correlated with O₂ saturation and positively correlated with ferritin, fibrinogen, and C-reactive protein, all of which are associated with increased thrombotic risk. These data indicate that hospitalized COVID-19 patients develop antibodies that can activate platelets and may be associated with increased disease severity and a higher risk of thrombosis during COVID-19 infection.