This may be the reason why COVID-19 has so many different symptoms

“I think we can see light at the end of the tunnel,” Pfizer Chairman and CEO Dr. Albert Bourla told CNBC in reference to recent vaccine trials. “I believe this is likely the most significant medical advance in the last 100 years if you count the impact this will have in public health, global economy.”

Many can identify with Dr. Bourla’s optimism right now, even if there are compelling reasons not to.

Reports of a promising vaccine have arrived alongside new data on COVID-19’s clinical pathology.

Although the disease funding our pandemic is primarily recognized as a respiratory and vascular one, the associated symptoms are wide-ranging.

Some affected populations have reported neuropathies, including the loss of taste and smell. While others have experienced delirium, skin discoloration, and hair thinning.

These outliers may in fact suggest that academicians didn’t have enough information to properly categorize COVID-19 until relatively recently.

Endothelial cells are responsible for exchanges between the bloodstream and surrounding tissues and they line every one of our blood vessels. In addition to reducing clotting, and regulating blood pressure, endothelial cells, commonly referred to as endothelium, help protect us from invading antigens.

During severe coronavirus infection, this lining endures considerable damage. Dr. William Li, a vascular biologist who contributed to a diagnostic COVID-19 study published in The New England Journal of Medicine believes the novel coronavirus may even attack endothelial cells directly.

“When the virus damages the inside of the blood vessel and shreds the lining, that’s like the ice after a hockey game,” Dr. Li, explained in a recent release. “You wind up with a situation that is really untenable for blood flow. 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. We found blood vessels are blocked and blood clots are forming because of that lining damage.”

To support his theory, Li and a team of researchers analyzed seven lungs during autopsies on patients who died from Covid-19 and compared them with seven lungs from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection alongside 10 age-matched, uninfected control lungs.

“Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19,” the authors wrote in the new paper.

“In patients who died from Covid-19–associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes.”

The increasingly frequent reports of neurodegeneration in the brain, blood clots in the lung and the legs, and the COVID toe and finger may be due to cumulative effects on our blood vessels.

Even if researchers are wrong about the novel coronavirus directly targeting endothelium, the cell lining clearly suffers as a result of serious manifestations of COVID-19. This development may in turn yield new promising therapeutics.

“Despite previous experience with SARS-CoV and early experience with SARS-CoV-2, the morphologic and molecular changes associated with these infections in the peripheral lung are not well documented,” the authors concluded. “The universality and clinical implications of our observations require further research to define.”