The study, which was published in The Lancet in April, demonstrates that endothelial cells — that is, cells which form the barrier between blood vessels and organ tissues and control the transmission of fluids between the two — are involved in various health problems associated with the coronavirus. They observed this in multiple patients with COVID-19. One patient, a 71-year-old man who had had a kidney transplant, died of multisystem organ failure after being diagnosed with COVID-19, and a subsequent analysis of his transplanted kidney found that viral inclusion structures were in his endothelial cells. They also found inflammatory cells associated with endothelial cells in his heart, small bowel and lungs.
A second patient, a 58-year-old obese woman with diabetes and arterial hypertension, suffered multi-organ failure and eventually died of a cardiac arrest. According to the authors of the Lancet article, they discovered "lymphocytic endotheliitis in lung, heart, kidney, and liver as well as liver cell necrosis."
As the researchers write, "the development "of this disease seems to be that it utilizes the ACE2 receptors as an entry way to a range of cells causing destruction.. . . This explains why the disease has such a variety of presentations and makes it potentially more dangerous," they continue. ACE2 receptors refers to a specific protein that allows coronavirus to infect human cells.
Georges Benjamin, Executive Director of the American Public Health Association, expressed optimism about the report, telling Salon by email that "the study has major potential implications for understanding and treating the coronavirus, which often causes complications deemed unusual for strictly respiratory ailments."
Other medical professionals had similar outlooks.
"This paper describes evidence of microscopic damage and direct viral infection in blood vessels from multiple organs in three patients infected with SARS-CoV2," Russell Medford, Chairman of the Center for Global Health Innovation and Global Health Crisis Coordination Center, told Salon by email. "These findings are consistent with a growing body of scientific and clinical evidence that strongly suggests that the SARS-CoV2 virus can infect and damage multiple organs in addition to the lungs, such as the kidney, heart, intestines and liver, by targeting the endothelial cells that line the inner surface of their blood vessels."
William Li, MD, president of the Angiogenesis Foundation, told Medium that "all these Covid-associated complications were a mystery. We see blood clotting, we see kidney damage, we see inflammation of the heart, we see stroke, we see encephalitis [swelling of the brain],"
Mandeep Mehra, MD, medical director of the Brigham and Women's Hospital Heart and Vascular Center, had a similar observation, telling the publication that "a whole myriad of seemingly unconnected phenomena that you do not normally see with SARS or H1N1 or, frankly, most infectious diseases. If you start to put all of the data together that's emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels]."
Prior to this study, scientists were baffled as to why blood clots were a common symptom of the coronavirus. The clots alone were not what confused them, but also the fact that blood thinners did not seem to prevent them and people would die of strokes caused by brain blockages. As of last month, one report found that up to 30 percent of patients who are seriously ill with the coronavirus develop blood clots that become dangerous.