A proposed mechanism for vaccine-induced thrombotic thrombocytopenia

What is this research about?

Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a new, rare clotting disorder associated with administration of adenoviral vector vaccines against COVID-19 (e.g., ChAdOx1 nCoV-19, AstraZeneca). VITT causes moderate to severe thrombocytopenia (low platelet levels) and thrombosis (formation of blood clots) that mimics the response observed in patients with heparin-induced thrombocytopenia (HIT).

HIT occurs when immunoglobulin G (IgG) antibodies recognize novel epitopes (antibody binding sites) exposed after heparin binds to a platelet protein called platelet factor 4 (PF4). The antibodies bound to the PF4-heparin complex form an immune complex which activates platelets (by binding to a platelet receptor called FcgRIIa) and promotes clot formation. One idea is that VITT has a similar pathophysiology to HIT but without dependence on heparin. This study aims to better understand the mechanism behind clot formation observed in VITT patients.

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