Antibodies produced in response to COVID-19 may trigger blood clots
A study of the antibodies naturally produced to fight SARS-CoV-2’s spike protein was found to differ from the antibodies of healthy individuals, according to researchers at the University of Reading (Reading), UK. It may also be triggering an exaggerated platelet response, which could lead to fatal blood clots in patients with severe disease.
Platelets are small cells found in blood which form clots to stop or prevent bleeding – it is possible to reduce or stop platelets from overreaction by treating blood with medications that inhibit platelet function or immune responses. At present, a trial led by Imperial College London and Imperial College Healthcare NHS Trust — called MATIS — is underway testing different drugs in hospitals across the UK to see whether they will reduce serious clotting for patients with a severe COVID-19 infection.
Related: Antibodies against COVID-19 vary with vaccination vs natural infection
“Until now, we have only had assumptions about why platelets involved in clotting were being activated during COVID-19 infection,” said Professor Jon Gibbins, Director of the Institute for Cardiovascular and Metabolic Research at Reading.
“One way to think of what is happens is that the immune response that is designed to protect you from the infection in some cases, particularly in severely ill patients, actually causes more damage. In this case, the antibodies that are produced to stop COVID-19 from spreading trigger infected cells to induce platelet activity which causes clotting even though there is no wound that needs healing.
This new understanding of platelet cell biology provides both support and scientific validation for the MATIS clinical trial, as well as clues as to how unwanted blood clotting may be prevented.
Nichola Cooper, reader at Imperial College London and consultant haematologist at Imperial College Healthcare NHS Trust, supplemented: “Having been involved in early research around blood clotting related to inflammation, it occurred to me that the drugs we already use for other disorders could be easily accessible treatments for COVID-19. We are yet to see results from the MATIS trial so we do not yet know how these drugs will work in patients, but our hope is that we can both inhibit the inflammatory response and prevent severe disease and blood clots. It is exciting to see our collaboration with Reading backing our theory already and providing a solid scientific basis for clinical trials.”
