Among the complications most attributed to Covid-19 is thrombosis. The formation of blood clots in the veins or arteries in the weeks following the coronavirus infection, impairing blood circulation, was one of the symptoms seen frequently among patients around the world. At the beginning of the pandemic, the phenomenon was even used to explain most deaths from the disease.
In a study published in Nature magazine last week, researchers from the Faculty of Medicine at Imperial College London, in the United Kingdom, claim to have discovered an explanation for the situation.
A “deregulation” in the function of monocytes, blood cells of the body’s defense system with important functions in detecting invaders and in activating the innate and adaptive immune response during viral infection, may be behind the formation of thrombi in some patients of the Covid-19.
To reach this conclusion, scientists examined the function of monocytes from patients with mild and moderate Covid-19 during the acute phase of the infection and compared it with the process in healthy individuals.
The blood defense cells of infected patients, which should protect them against the action of the virus, showed an altered expression of cell surface receptors and a dysfunctional metabolic profile, triggering a prothrombotic effect.
During a viral infection, circulating monocytes should infiltrate affected tissues, contributing to the elimination of pathogens and tissue regeneration.
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It is estimated that between 0.6 and 2 patients per 100,000 infected with the coronavirus have clot formation during infection, increasing the risk of thrombosis. With the Covid-19 vaccine, the chance of developing the problem decreases by up to 10 times.
Scientists hope the discovery can be used to advance the understanding of coronavirus infection and the development of treatments that reduce post-infection risks.
“These results identify a potential mechanism by which monocyte dysfunction may contribute to the COVID-19 study,” the study authors state in the paper.
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