A group of researchers are now questioning whether COVID-19 is primarily a respiratory illness, as is widely believed.
Instead, they suggest, full-blown COVID-19 is a disease of the vascular system that preys on weakness in our blood vessels.
Does this matter in practical terms? In terms of targeting treatments in the early stage of the disease, yes it does.
But don’t we catch it from coughing and sneezing?
It’s accepted that we catch the COVID-19 via viral droplets that enter the nose, mouth or eyes, and that it presents initially as an upper respiratory tract infection. In many to most cases, the virus appears to be defeated by the body’s immune system.
What has mystified doctors is the catastrophic second phase where patients – especially those with diabetes, cardio-vascular disease and obesity – develop a profound inflammatory response, often in the form of pneumonia.
From the start of the pandemic, so many people were dying of pneumonia, and at at an overwhelming rate, that COVID-19 was thought to be a classic respiratory disease.
Then it was found that young people were suffering blood clots and fatal strokes. Inflammation was found not only in the lungs, but in the kidneys, heart, liver, bowel and even the fingertips and toes in various patients.
Suddenly, the disease seemed deeply mysterious and even more threatening. However, when taken together, all of these symptoms pointed to an impeded blood flow.
So what is really going on?
“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” said Dr Mandeep Mehra, medical director of the Brigham and Women’s Hospital Heart and Vascular Center, in a widely-reported statement.
In a paper published in April, Dr Mehra and his associates found that the SARS-CoV-2 virus can directly infect and inflame the endothelial cells that line the inside of blood vessels. Damage to these cells – that play a protective role to the body – was found in all major organs.
What happens with these endothelial cells, when they become infected, appears to be the key to understanding the real nature of the disease. It is also key to that deadly second phase.
Endothelial cells form a single cell layer along the walls of all blood vessels, also lining the chambers of the heart and the lymphatic vessels, and play multiple protective roles.
The entire collection of endothelial cells – known as the endothelium – is considered to be an organ in its own right. Taken together, it weighs about a kilo, the same as the liver.
The main function of endothelial cells is to provide a barrier between the blood and the rest of the body tissues. It’s a bit like the doorman at a nightclub – in this case deciding what substances to let into the bloodstream and what to keep out.
When substances – chemicals, nutrition and white blood cells – are permitted to cross this selectively permeable layer, the endothelium then further directs them to where they are needed.
The role of the endothelium as a door-keeper is critical around the brain, restricting the passage of large molecules, toxic substances, and bacteria into the brain tissue while allowing necessary molecules like oxygen, enzymes, and hormones to go through.
But it also has a complex role in responding to pathogens – causing the sites of infection to become inflamed and hot – and to blood-clotting.
On the one hand, it makes proteins that prevent blood clotting from happening inside the blood vessel – and thereby blocking it – but also enables blood clotting at the source of bleeding.
Once infected with COVID-19, the endothelium goes awry, forfeits its ability as a guardian, and works against the body.
And this explains why the virus has so successfully invaded and damaged people from head to toe.