Platelet-activating antibodies against platelet factor 4 (PF4) cause highly prothrombotic disorders with reduced platelet counts. In heparin-induced thrombocytopenia (HIT), these antibodies bind PF4-heparin complexes, causing heparin-dependent platelet activation. Less common autoimmune and spontaneous HIT variants that are triggered by heparin and nonpharmacologic polyanions, respectively, have atypical clinical features and antibodies with additional heparin-independent platelet-activating properties. Vaccine-induced immune thrombocytopenia and thrombosis (VITT) antibodies directly target PF4. Initially, VITT was linked to adenoviral vector-based coronavirus disease 2019 vaccines, but in rare cases, an immune thrombocytopenia and thrombosis disorder that is clinically nearly identical to VITT can be caused by infection resulting from natural exposure to viruses, especially adenovirus. In persons with the
Warkentin et al. (Mon,) studied this question.