prophetoffacts wrote: "My family and in laws all got it on a cruise. For those under 60 it was literally a cough cold symptoms."
Seems like just another respiratory infection for many. Unfortunately, COVID is a vascular disease. It infects and damages blood vessels. This can open up longer term risks of heart disease, heart attack, and stroke, etc. It is not an infection you want.
----------- In a study published this summer, Li and an international team of researchers compared the lung tissues of people who died from COVID-19 with those who died from influenza.
They found stark differences: The lung tissues of COVID-19 patients had nine times as many tiny blood clots ("microthrombi'') compared with those of the influenza patients, 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 says. "We found blood vessels are blocked and blood clots are forming because of that lining damage."
It's already known that the coronavirus breaks into cells by way of a specific receptor, called ACE2, which is found all over the body. 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 says one theory is that the virus directly attacks endothelial cells. Lab experiments have shown that the coronavirus can infect engineered human endothelial cells.
It's also possible the problems begin elsewhere, and the endothelial cells sustain collateral damage along the way as the immune system reacts — and sometimes overreacts — to the invading virus.
Endothelial cells have a slew of important jobs; these include preventing clotting, controlling blood pressure, regulating oxidative stress and fending off pathogens. And Li says 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 Spain, skin biopsies of distinctive red lesions on toes, known as chilblains, found viral particles in the endothelial cells, leading the authors to conclude that "endothelial damage induced by the virus could be the key mechanism."
Could the lining of our blood vessels be a common denominator?
With a surface area larger than a football field, the endothelium helps maintain a delicate balance in the bloodstream. These cells are essentially the "gatekeeper" to the bloodstream.
"The endothelium has developed a distant early warning system to alert the body to get ready for an invasion if there's trouble brewing," says Peter Libby, a cardiologist at Brigham and Women's Hospital and research scientist at Harvard Medical School.
When that happens, endothelial cells change the way they function, he says. But that process can also go too far.
"The very functions that help us maintain health and fight off invaders, when they run out of control, then it can actually make the disease worse," Libby says.
In that case, the endothelial cells turn against their host and start to promote clotting and high blood pressure.
"In COVID-19 patients, we have both of these markers of dysfunction," says Gaetano Santulli, a cardiologist and researcher at the Albert Einstein College of Medicine in New York City.
The novel coronavirus triggers a condition seen in other cardiovascular diseases called endothelial dysfunction. Santulli, who wrote about this idea in the spring, says that may be the "cornerstone" of organ dysfunction in COVID-19 patients.
"The common denominator in all of these COVID-19 patients is endothelial dysfunction," he says. "It's like the virus knows where to go and knows how to attack these cells."