He says this theory of infection explains some things that doctors have been trying to puzzle out.

For example, certain conditions like high blood pressure, diabetes, and heart disease stress the endothelium. It’s no surprise, then, that people who have these conditions are also the ones who get the sickest when they catch COVID-19.

It also helps to explain why patients have such low oxygen in their blood, but their lungs may not be as stiff as they typically are in patients who have respiratory distress with pneumonia.

Mehra explains that one consequence of endotheliitis is that blood vessels can’t constrict the way they normally would. Typically, when a part of the lung becomes damaged, tiny blood vessels in that area close off so that blood will flow to a part of the lung that’s still working, where it can collect oxygen. This system protects the body from a sudden drop in oxygen, and it appears to break down in patients with severe COVID-19 infections. Mehra believes the infection of the endothelium is to blame.

The bottom line, he says, is that clotting is a feature of the COVID-19 syndrome. When it becomes a big problem, the disease is advanced and very severe. For that reason, treating the resulting blood clots probably won’t work.

He believes something worth trying might be to give patients drugs to support the endothelium, like ACE inhibitors and statins, along with anti-inflammatory drugs to tackle the cytokine storm, early in the course of the disease, but more research is needed to know for sure.

If COVID-19 is really an endothelial infection, Mehra thinks that also helps to explain why ventilators aren’t helping more patients. A study of 5,700 patients hospitalized with COVID-19 in New York City found that while just 12% needed a ventilator to help them breathe, 88% of those patients died.

“It’s not acting like influenza or other bacteria pneumonia where you get inflammation in the lungs and fluid buildup and very stiff lungs. That doesn’t seem to be the case, at least early on,” Poor says.