Coronavirus May Cause Blood-Clotting Cells to Become 'Hyperreactive'

The COVID-19 coronavirus may cause cells which help blood to clot to become "hyperreactive," according to scientists who believe this may be why clotting is a problem for some patients.

Complications with blood clotting are common in COVID-19 patients and can cause organ failure and death, particular in those with underlying conditions such as obesity, diabetes, and high blood pressure, according to the authors of the paper published in the journal Blood.

To try to shed light on this phenomenon, the team collected the blood of 41 COVID-19 patients hospitalized at the University of Utah Health Sciences Center. Of the total, 41 percent were in the ICU, of which 53 percent were on a ventilator. The researchers compared the patients' blood with that of COVID-19-free people of the same age and gender.

The team focused on the participants' platelets, which help blood to clot but also play a role in our inflammatory and immune responses. They looked at the genetic material in the platelets, which is a reflection of how they were made by mother cells in the bone marrow, and also examined their ability to clot.

The researchers found that the virus appears to influence how platelets are made by changing gene expression. This suggests the virus can somehow communicate with bone marrow cells where they are made. The germ also seems to affect how blood clots in COVID-19 patients, making platelets "hyperreactive", or overly sensitive to stimuli, and more likely to cluster, stick together, and spread.

These changes may make patients more vulnerable to dangerous blood clotting, the team believes.

Cedric Ghevaert, who researches transfusion medicine at the University of Cambridge Stem Cell Institute and didn't work on the study, told Newsweek that neither the platelet mother cells in the bone marrow nor the platelets themselves express the receptor which the coronavirus uses to invade cells. Ghevaert was therefore surprised the virus was able to somehow communicate with these cells when they are a long way from the main site of the virus in the lungs and throat.

The findings were limited, according to Ghevaert, because the researchers didn't study the patients long-term.

"Does the platelet function come back to normal after the infection or are individual hospitalised simply because they are the most likely to get sick and their higher platelet reactivity is always a feature of their blood?" said Ghevaert. "That is a real important distinction which this paper does not make. If patients with a higher platelet reactivity are the most likely to be hospitalised it would be good to know."

It's also unclear if the increased reactivity is because of the virus itself or because the bug alters other cells, such as those that line the blood vessels, and can in turn activate platelets, he said.

Ghevaert went on that platelet hyperactivity is not unique to COVID-19 patients, and seen in flu patients, so the study "only gives a partial explanation as to why clotting is such a problem in COVID19 infections."

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A stock image shows a person giving blood samples. Getty