Whether it’s rashes on the toes or blood clots in the brain, the widespread ravages of COVID-19 have increasingly led researchers to focus on how the novel coronavirus sabotages blood vessels.
Scientists have homed in on the vascular system — the body’s network of arteries, veins and capillaries, stretching more than 60,000 miles — to understand this wide-ranging disease. Some of the earliest insights came from studying the aftermath of the most serious infections. Those reveal that the virus warps a critical piece of our vascular infrastructure: the single layer of cells lining the inside of every blood vessel, known as the endothelial cells or simply the endothelium.
In a study published this summer, Dr. William Li, a vascular biologist, and an international team compared the lung tissues of people who died of COVID-19 with those of people who died of influenza. The lung tissues of the COVID-19 victims had nine times as many tiny blood clots (“microthrombi”) as those of the influenza victims, and the coronavirus-infected lungs also exhibited “severe endothelial injury.”
“The surprise was that this respiratory virus makes a beeline for the cells lining blood vessels, filling them up like a gumball machine and shredding the cell from the inside out,” Li said.
It’s known that the coronavirus breaks into cells by way of a specific receptor, called ACE2. But scientists are still trying to understand how the virus sets off a cascade of events that cause so much destruction to blood vessels. Li said one theory is that the virus directly attacks endothelial cells.
It’s also possible the problems begin elsewhere, and the endothelial cells sustain collateral damage along the way.
Endothelial cells have a slew of important jobs, including preventing clotting, controlling blood pressure, regulating oxidative stress and fending off pathogens. And Li said uncovering how the virus jeopardizes the endothelium may link many of COVID-19’s complications: “the effects in the brain, the blood clots in the lung and elsewhere in the legs, the COVID toe, the problem with the kidneys and even the heart.”
In that case, the endothelial cells start to promote clotting and high blood pressure.
“The common denominator in all of these COVID-19 patients is endothelial dysfunction,” said Dr. Gaetano Santulli, a cardiologist and researcher at the Albert Einstein College of Medicine.
“It’s like the virus knows where to go and knows how to attack these cells.”