A study by investigators at the Stanford University School of Medicine and other institutions has turned up immunological deviations and lapses that appear to spell the difference between severe and mild cases of COVID-19.
That difference may stem from how our evolutionarily ancient innate immune system responds to SARS-CoV-2, the virus that causes the disease. Found in all creatures from fruit flies to humans, the innate immune system rapidly senses viruses and other pathogens. As soon as it does, it launches an immediate though somewhat indiscriminate attack on them. It also mobilizes more precisely targeted, but slower-to-get-moving, “sharpshooter” cells belonging to a different branch of the body’s pathogen-defense forces, the adaptive immune system.
Researchers analyzed the immune response in 76 people with COVID-19 and in 69 healthy people. They found enhanced levels of molecules that promote inflammation in the blood of severely ill COVID-19 patients. Three of the molecules they identified have been shown to be associated with lung inflammation in other diseases but had not been shown previously in COVID-19 infections.
The scientists also found elevated levels of bacterial debris, such as bacterial DNA and cell-wall materials, in the blood of those COVID-19 patients with severe cases. The more debris, the sicker the patient — and the more pro-inflammatory substances circulating in his or her blood. The findings suggest that in cases of severe COVID-19, bacterial products ordinarily present only in places such as the gut, lungs and throat may make their way into the bloodstream, kick-starting enhanced inflammation that is conveyed to all points via the circulatory system.
But the study also revealed, paradoxically, that the worse the case of COVID-19, the less effective certain cells of the innate immune system were in responding to the disease. Instead of being aroused by material from viruses and bacteria, these normally vigilant cells remained functionally sluggish.
