Study explains why some get deathly ill from COVID-19, others don't

The findings signal that the main difference stems from how the patient's "evolutionarily ancient innate immune system" responds to a COVID-19 infection.

Medical workers in protective suits attend to novel coronavirus patients inside an isolated ward at a hospital in Wuhan, Hubei province, China February 6, 2020. Picture taken February 6, 2020 (photo credit: CHINA DAILY VIA REUTERS)
Medical workers in protective suits attend to novel coronavirus patients inside an isolated ward at a hospital in Wuhan, Hubei province, China February 6, 2020. Picture taken February 6, 2020
(photo credit: CHINA DAILY VIA REUTERS)
Stanford University researchers seem to have pinpointed the reasoning behind why some patients get deathly ill from COVID-19 infections and others don't.
A new study published in the online journal Science reveals immunological deviations and lapses within their sample, divergences that the researchers believe distinguish between severe and mild cases of the novel infection.
The findings signal that the main difference stems from how the patient's "evolutionarily ancient innate immune system" – responsible for sensing and extinguishing harmful viruses and pathogens – responds to a COVID-19 infection. 
“These findings reveal how the immune system goes awry during coronavirus infections, leading to severe disease, and point to potential therapeutic targets,” said senior author of the study Bali Pulendran, PhD, professor of pathology and of microbiology and immunology at the Stanford School of Medicine.
The study itself examined the immune responses of 76 people infected with coronavirus and 69 healthy individuals.
The researchers found that within severely ill COVID-19 cases, many of the patients possess "enhanced levels of molecules that promote inflammation." Three of these molecules have been proven to be associated with inflammatory lung diseases in addition to others, "but had not been shown previously in COVID-19 infections."
“These three molecules and their receptors could represent attractive therapeutic targets in combating COVID-19,” said Pulendran.
"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," Stanford University said in a statement.
"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," the university added.
Although ever-present in numbers within severe cases of COVID-19, the response time of these cells are delayed and their effectiveness in combating COVID-19 is under-par. These cells would normally respond rapidly and effectively to other viral compounds, sort of like the "first-responders" of the immune system.

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This led the researchers to ask: If the numbered presence of these molecules sets apart mild COVID-19 infections from severe ones and the bloodstream is not producing them on its own, where do they come from?
Pulendran believes they stem from tissues in other parts of the body, purportedly from the site of the infection – in this case, the patient's lungs.
“One of the great mysteries of COVID-19 infections has been that some people develop severe disease, while others seem to recover quickly,” Pulendran said. “Now we have some insights into why that happens.”