Nature: Why does the AstraZeneca COVID-19 adenovirus vaccine cause blood clots?
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Nature: Why does the AstraZeneca COVID-19 adenovirus vaccine cause blood clots?
Nature: Why does the AstraZeneca COVID-19 adenovirus vaccine cause blood clots? Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare but serious adverse reaction that occurs after vaccination with the adenovirus vector COVID-19 vaccine, which can lead to low platelet counts (thrombocytopenia) and blood clots in arteries or veins .
Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a bit like heparin-induced thrombocytopenia (HIT). Previous studies have shown that both VITT and HIT are related to antibodies against platelet factor 4 (PF4). PF4 is a type that can bind to platelets. The protein is involved in blood clotting. However, the specific mechanism by which these antibodies cause VITT has not been clear.
On July 12, 2021, a research team from McMaster University in Canada published a research paper titled Antibody epitopes in vaccine-induced immune thrombotic thrombocytopenia in Nature.
The study explains how some of the antibodies induced by the COVID-19 vaccine may cause the rare symptom of vaccine-induced immune thrombotic thrombocytopenia (VITT).
The study found that the antibodies of five VITT patients who had been vaccinated with the AstraZeneca adenovirus COVID-19 vaccine would bind to a protein involved in blood coagulation, and the binding site was the same as the binding site of the anticoagulant heparin to the protein.
The research team analyzed the sera of five VITT patients (average age 44 years) who had received a dose of AstraZeneca adenovirus vaccine. The authors found that the antibodies obtained from the sera of these patients had the same binding sites as PF4 and heparin. After comparing it with the serum samples of 10 HIT patients, the authors found that the VITT antibody binds to PF4 more strongly.
The research team believes that the VITT antibody binds to PF4 to form immune complexes, which then activate platelets through the FcγRIIa receptor on the platelet surface, which may cause blood clotting, leading to thrombocytopenia and thrombosis. However, the author also pointed out that this may not be the only factor leading to thrombotic events in VITT patients. Other serum factors may also be involved in platelet activation.
(source:internet, reference only)
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