Is THIS why Covid-19 causes strokes? The coronavirus causes ‘hyperactivity’ in blood-clotting cells

“Hyperactivity” in blood clotting cells may be the cause of strokes and heart attacks in Covid-19 patients, scientists say.

Experts from the University of Utah made the “significant” discovery by comparing the blood of 82 people, half of whom tested positive for the coronavirus.

Platelets, blood cells that clot, were much more active in samples from Covid-19 patients, according to the study.

In Petri dishes, platelets stick together faster, a process that leads to the formation of blood clots.

Inflammation caused by the virus is likely to cause the change, the scientists said.

The finding could have implications for the way doctors treat patients at risk for dangerous blood clots.

Up to 30 percent of hospital patients suffer from blood clots as a complication of the virus, studies show, but doctors are only beginning to understand why.

Platelets, blood cells that clot (stock), were hyperactive in the blood samples from Covid-19 patients at the University of Utah Hospital in Salt Lake City

Platelets, blood cells that clot (stock), were hyperactive in the blood samples from Covid-19 patients at the University of Utah Hospital in Salt Lake City

While the coronavirus is known to cause primarily respiratory failure in the worst cases, it does have some harmful effects on organs other than the lungs.

Thrombosis is when blood clots form in the blood vessels and veins, which can block the heart (causing a heart attack), brain (stroke), or lungs (pulmonary embolism).

A study published last week found that 62 percent of the 125 hospitalized Covid-19 patients in the UK experienced a stroke during their hospital stay.

Although the events are common in Covid-19 patients, the drivers are not yet clear.

But Dr. Robert Campbell, senior author of the latest study, said, “Our finding adds an important piece to the puzzle we call Covid-19.


One in three people who become seriously ill with coronavirus develop dangerous blood clots, which scientists say contribute to their deaths.

The clots can become deadly if they migrate to important organs, such as the lungs, and cut off their blood supply.

The blockages can cause heart attacks, strokes, organ failure and pulmonary embolism if they migrate to important organs.

While experts aren’t sure why the virus causes the blockages, there are three main theories:


The prevailing theory is that it is the result of an immune overreaction called a ‘cytokine storm’.

Cytokines are chemical signaling molecules that direct a healthy immune response.

They tell immune cells to attack viral molecules in the body.

But in some people, this reaction goes overdrive, and immune cells also start attacking healthy tissue, known as a cytokine storm.

If blood vessels become damaged, they can leak, lowering blood pressure and increasing the chance of clots.


Other scientists say the increase in strokes may be a byproduct of how COVID-19 enters the human body.

Professor Ian Jones, a virologist at the University of Reading, told MailOnline, “Covid binds to the enzyme ACE2 that is located on the surface of the cell.

“It just uses it as a way to bond, but it reduces the enzyme function of ACE2.

‘The consequence of this is an imbalance of the hormones Angiotensin I and Angiotensin II, which together regulate blood pressure.

“It could be related to the increase in reported strokes.”


Dr. Robert Bonow, a professor of cardiology at Northwestern University, said it may be the unique form of the coronavirus that causes blood clotting problems.

He said that the spikes of the virus, which snap to receptors in cells, can also attach to blood vessels.

Once docked on these blood vessel cells, the viral particles can damage both this and the heart muscle, Dr. Bowow says.

“We found that inflammation and systemic changes due to the infection affect the functioning of platelets, causing them to aggregate faster, which could explain why we see an increased number of blood clots in Covid patients.”

Dr. Campbell and colleagues looked at patients who were hospitalized at the University of Utah Hospital in Salt Lake City.

Seventeen of these patients were in ICU, including nine who were on respirators, according to the paper in Blood, a journal of the American Society of Hematology. About 17 percent of the Covid-19 patients died.

The team compared blood from these patients with samples from healthy individuals matched by age, gender, and race.

Using gene analysis, the researchers found that SARS-CoV-2, the virus that causes Covid-19, appeared to cause genetic changes in platelets.

They were more activated – that’s when the platelets change shape from a flat disc to a ball, with the ability to summon other platelets to stick together.

The study authors wrote, ‘SARS-CoV-2 induces robust gene expression and functional changes in platelets.

“We hypothesize that these changes may contribute to thrombotic events in Covid-19 patients.”

The virus was not found in the platelets themselves, suggesting that it causes changes indirectly through different routes.

One theory is that inflammation in the body in response to the virus causes a cascade of changes, including to platelets.

Dr. Bhanu Kanth Manne, one of the study authors, said the inflammation can affect megakaryocytes, the cells that produce platelets.

As a result, critical genetic changes are passed from megakaryocytes to the platelets, which in turn make them hyperactive.

Dr. Campbell said, “There are genetic processes we can focus on to prevent platelet changes.

“If we can figure out how Covid-19 interacts with megakaryocytes or platelets, we may be able to block that interaction and reduce a person’s risk of developing a blood clot.”

In laboratory studies, the scientists studied platelet aggregation, an important part of blood clot formation.

Platelet aggregation is when the platelets stick together to form a clump. This would put a hole in a wound to stop the bleeding.

Platelet aggregation was significantly increased in the blood of Covid-19 patients, compared to healthy donors in tests.

This was especially seen in patients at the ICU, suggesting that the more severe the disease, the greater the platelet hyperactivity.

Platelets from Covid-19 patients also showed greater adhesion – when they then adhere to blood vessel walls.

In addition to their traditional role in thrombosis, platelets mediate the most important aspects of inflammatory and immune processes.

The team noted that the changes in their activity significantly altered the interaction of platelets with the immune system.

This likely contributes to inflammation of the airways, which in turn can lead to more serious lung injuries.