A new study has shed light on how deadly blood clots develop in some people who have received certain types of COVID-19 vaccination.
Researchers from the University of Birmingham have identified a mechanism by which blood clots develop, in the syndrome known as Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT).
Past studies show that antibodies are produced by people with VITT, which attach to a protein called Platelet factor 4 (PF4). This effect creates a sizeable grouping of molecules referred to as an immune complex.
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This immune complex triggers clotting and inflammation by platelets and immune system cells. Until now, the precise role of PF4 in this process was not known.
In the University of Birmingham study, researchers studied the blood of healthy donors alongside the serum and plasma from people with VITT.
For the first time, the team discovered how the PF4 protein has a key role in the triggering of platelets and blood clotting. The key finding was that the action of PF4 attaching to a certain receptor (c-Mpl) on the surface of platelets activated the production of the cells which cause clotting.
Senior author Dr Pip Nicolson, Associate Clinical Professor in Cardiovascular Medicine at the University of Birmingham, said: “The major advances seen in vaccine development during the global Covid-19 pandemic were thrown into sharp relief following the tragic, rare cases of vaccine-induced immune thrombosis.
“While there were alternative vaccines available to continue to provide protection against the coronavirus in some countries around the world, understanding the mechanisms behind these cases is critical to ensuring that the technology for delivering vaccines can be used with confidence in the future.”
The research, which was funded by the National Institute for Health and Care Research and the British Heart Foundation, could pave the way for new medication to prevent this type of deadly clotting. For instance, modifications could be made to drugs used in the treatment of bone marrow cancers to protect patients with VITT against blood clotting.
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Co-lead author Dr Richard Buka, Research Fellow in the Institute of Cardiovascular Sciences at the University of Birmingham, said: “As well as identifying a new way in which platelets are being activated in a potentially deadly manner in VITT, our research has also been able to find how this mechanism may lead to new drugs to protect against blood clots in VITT and blood clots in general.”
Co-lead author Dr Samantha Montague, also a Research Fellow in the Institute of Cardiovascular Sciences at the University of Birmingham, added: “It is gratifying that we have been able to identify a new, important biological mechanism through trying to thoroughly understand a new disease. This work helps us to understand more fundamental things about how blood clots form and may also be relevant in other related diseases that are more common.
“Our ongoing research funded by the British Heart Foundation is looking at how we can identify patients who may develop VITT, with a view that future vaccine programmes around the world can be delivered while understanding and managing the potential risk for those few at greatest risk.”
Read the study in Blood Journal.
