Stanford University researchers seem to have established the reasoning why some patients become terminally ill with COVID-19 infections and others do not. A new study published in the online journal Science reveals immunological abnormalities and decay within their sample, differing that researchers believe distinguishes between severe and mild cases of the new infection. The findings suggest that the main difference stems from how the patient’s evolutionary ancient immune system – responsible for sensing and extinguishing harmful viruses and pathogens – responds to a COVID-19 infection. “These findings show how the immune system malfunctions during coronavirus infections, leading to serious illness, and pointing to potential therapeutic targets,” said senior study author Bali Pulendran, PhD, professor of pathology and microbiology and immunology. 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 in severely ill COVID-19 cases, many of the patients “had improved levels of molecules that promote inflammation.” Three of these molecules have been shown to be associated with inflammatory lung disease alongside others, “but were not previously detected in COVID-19 infections.” “These three molecules and their receptors could represent attractive therapeutic targets in the fight against COVID-19,” Pulendran said. “The scientists also found elevated levels of bacterial debris, such as bacterial DNA and cell wall material, in the blood of that COVID-19. “Patients with severe cases. The more pounds, the safer 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 commonly present in places such as the intestine, lungs and throat may make their way into the bloodstream, kick-starting improved inflammation that is transmitted to all points via the circular system, “added the university. Although always present in numbers within severe cases of COVID-19, the reaction time of these cells is delayed and their effectiveness in combating COVID-19 is under-par. These cells would normally respond quickly and effectively to other viral compounds, such as the “first-responder” of the immune system. This led the researchers to ask: If the numerical presence of these molecules makes mild COVID-19 infections separate from bad ones and the bloodstream does not produce them in its own place, where do they come from? Pulendran is thought to originate from tissues in other parts of the body, purely from the site of infection – in this case, the patient’s lungs. “One of the big mysteries of COVID-19 infections was that some people develop serious illness, while others seem to recover,” Pulendran said. “Now we have some insight into why that happens.”
