Coronavirus and blood clots

Scientists are scratching their heads over the problem of blood clots in a coronavirus infection, and how this may determine who lives and who dies of the disease

Blood clots are a frequent, deadly complication of COVID-19, with studies predicting about 20-30% of patients with a serious infection developing these at some point. It is not certain why these clots arise, but hospitalised patients with COVID-19 are statistically more likely to encounter this problem than with any other infection. The presence of these blood clots also correlates with a poor prognosis.  

Researchers have looked into the possible mechanisms which result in the formation of these clots, and have found a few which could be responsible, or may not be. It is very much a mystery, why otherwise healthy, young people infected with COVID-19 are dying of strokes rather than pneumonia, and why critically ill coronavirus patients specifically, have elevated levels of a protein fragment, called D-dimer, in their blood.

D-dimer is a small protein fragment which has broken away from a larger protein net, called a fibrin mesh. This mesh is the scaffold on which blood clots form, therefore when blood clots are broken down in a process known as fibrinolysis (“the breaking of fibrin”) it is released into the blood stream. Since coronavirus patients have a higher level of this protein in their blood, it indicates they also have an abnormally large amount of blood clots throughout their body.

And they can be literally anywhere in the body. Researchers have found tiny clots in the smallest of blood vessels, including the brain. Scientists in New York City carefully examined lung and skin samples from COVID-19 patients and found that a significant proportion of the capillaries, the smallest blood vessels in the body, were completely blocked with clots.

Whilst in some cases these blood clots may be directly responsible for the death of a patient, in others, they contribute to lung tissue death which is sparked by pneumonia. In all pneumonia infections, regardless of additional COVID-19 exposure, fluid builds up in the alveoli of the lungs, the sites of oxygen exchange. In someone with a severe COVID-19 infection, the resulting pneumonia is fuelled by the accumulation of blood clots in capillaries surrounding these alveoli, which blocks the movement of oxygenated blood and restricts oxygen exchange further.

Scientists know that COVID-19 uses a specific receptor, known as ACE2 to enter lung cells. The endothelial cells which line blood vessels also express this receptor, so researchers are predicting that the virus is exploiting the receptor here. There is evidence to support this, as researchers from Zurich have observed the virus within endothelial cells inside kidneys. The virus damages the cells, which makes the walls of blood vessels bumpy and rough, triggering the release of proteins which stimulate the formation of blood clots.

Another possibility is that the virus is influencing the immune system, which results in a huge surge of chemicals to trigger inflammation and ultimately coagulation; the process of blood clot formation. The virus has also been found to activate the complement cascade, a series of protein-protein interactions which enhance the production of endothelial ‘tissue factor’, a critical initiator of coagulation.

Of course, it may be that these severely-ill patients are at a higher risk of blood clots anyway – they may be overweight, elderly or have high blood pressure. But since younger people have been affected by this issue, it may not be this clear-cut.

These blood clots are certainly something different, with blood thinners having absolutely no effect on their formation, and clot-busters having a hard time breaking them apart. Researchers are adding the development of potent drugs to combat this problem onto their never-ending list of potential COVID-19 therapies to tackle the virus from an angle different to a vaccine or ventilation therapy.


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