In the last five to 10 years, scientists have begun to understand that platelets play a role in promoting unwanted clotting and inflammation in other diseases such as HIV, psoriasis, lupus, and rheumatoid arthritis. These tiny round blood cells serve one major purpose: to stop bleeding by binding to a damaged blood vessel and forming a clot. With that in mind, Jeffrey Berger, director of the New York University Centre for the Prevention of Cardiovascular Disease, and a team of researchers set out to investigate what role the platelets might play in COVID-19.

In a study published in "Science Advances", the researchers showed that the virus can enter the bone marrow cells that make platelets. The infected cell then alters the genetic material in the platelets so that they become more active and give off protein signals that make the lining of the blood vessels sticky and inflamed. This makes the vessels prone to developing clots that can spread throughout the body.

Scientists also learnt that the virus weakens connections in the tissue that lines blood vessels, making them leaky instead of sealing them up, as you might expect when clots are present.

Leaky vessels allow blood and other chemicals in the body to spill into places they’re not supposed to go — including the air sacs of the lungs and the tissues of other organs. That can have a cascade of downstream effects, from the flooded lungs seen in many severe COVID-19 cases to complications of the liver, kidneys, and, of course, the heart.