New research conducted by scientists from the University of Birmingham, with funding from the National Institute for Health and Care Research and the British Heart Foundation, has identified the mechanism behind the development of deadly blood clots in some patients after receiving certain COVID-19 vaccines. The study, published in the journal Blood, focuses on Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT), a condition where patients experience cases of clotting.
Previous studies have indicated that individuals with VITT produce antibodies that bind to a protein called Platelet factor 4 (PF4), leading to the formation of immune complexes. The activation of platelets and immune system cells subsequently triggers clotting and inflammation. However, the specific role of PF4 in this process was previously unknown.
In the recent study, the team analyzed blood samples from healthy donors as well as serum and plasma from VITT patients. For the first time, they discovered how PF4 directly activates platelets and results in thrombotic events. By binding to a receptor called c-Mpl on the surface of platelets, PF4 stimulates the production of small cells that are responsible for clotting.
Dr Pip Nicolson, senior author of the study and Associate Clinical Professor in Cardiovascular Medicine at the University of Birmingham, highlighted the importance of understanding the mechanisms behind these cases in order to ensure confidence in vaccine delivery technology for future use. Despite the availability of alternative vaccines in certain countries, comprehending the underlying reasons for vaccine-induced immune thrombosis is crucial.
Additionally, the research indicated that variations of a drug used to treat bone marrow cancers might be developed to protect VITT patients from clotting disasters. The team utilized ruxolitinib, a drug commonly prescribed for certain blood cancers, to inhibit the receptor triggered by PF4 after a vaccine-induced event. Although the current formulation of the drug is unsuitable for VITT patients, the study suggests that blocking the pathway through ruxolitinib slows down platelet aggregation, offering a potential solution to prevent blood clots in the future.
Dr Samantha Montague, co-lead author of the study and Research Fellow in the Institute of Cardiovascular Sciences at the University of Birmingham, expressed her satisfaction in uncovering a new biological mechanism through a thorough understanding of a novel disease. This discovery not only enhances understanding of blood clot formation but may also have relevance for other related, more common diseases.
Ongoing research supported by the British Heart Foundation is now focused on identifying individuals at risk of developing VITT. The goal is to enable future vaccine programs worldwide to be implemented while comprehensively managing and addressing the potential risks faced by those few who are most susceptible.
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1. Source: Coherent Market Insights, Public sources, Desk research
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