Why do some people get severely ill from COVID-19 and others don’t? Scientists find a possible explanation Science and the planet

SARS-CoV-2, the virus that swept the world until recently, belongs to the coronavirus family. Some members of this family cause the common cold. Other conditions, such as SARS, MERS, and SARS-CoV-2, can have more serious and potentially life-threatening consequences, although there are many personality differences as well.

A person who is infected with SARS-CoV-2 for the first time will have no or only mild symptoms in 81 percent of cases. Sometimes it’s serious: Up to five percent of all infections lead to a serious course of the disease, with severe breathing problems or even organ failure.

This is a question that has preoccupied scientists since the outbreak of the epidemic. This includes Professor Gerard Wong and his team at the University of California, UCLA. In cooperation with colleagues from various American universities Recently posted In the Proceedings of the National Academy of Sciences we explore how the SARS-CoV-2 coronavirus can turn our immune system against our own bodies.

They investigated what happens after our immune system eliminates the virus. Using an artificial intelligence system they developed themselves, they scanned all the parts of the protein that could be released when our body breaks down the virus. This examination showed that certain remaining parts of these viral proteins can trigger or strengthen immune signals.

According to scientists, we should consider the virus not only as an infectious particle, but also as a storehouse of protein fragments that may be harmless in themselves, but can bind to other molecules and thus stimulate the immune system. “We have shown that protein fragments of the SARS-CoV-2 virus can ‘recombine’ with other molecules into a new pro-inflammatory entity that can elicit enhanced immune responses.”

In addition to the AI ​​analysis, the researchers also conducted experiments on cells and laboratory animals. This consistently showed that SARS-CoV-2 coronavirus fragments induced an enhanced immune response compared to harmless coronavirus fragments. In mice, protein fragments from SARS-CoV-2 were able to trigger a massive immune response, especially in the lungs.

The findings suggest that some of the most severe cases of Covid-19 could be the result of overstimulation of the immune system, causing uncontrolled inflammation such as the often described “cytokine storms”.

“Therefore, breakdown of the SARS-CoV-2 virus by the immune system is not necessarily the end point,” the researchers wrote. They stress that truly understanding the different forms of Covid-19 will require many large-scale studies in humans. Although this is clearly outside the scope of a machine learning approach, the results confirm that the released viral protein fragments can cause diverse effects on the immune system, and that this was much lower for ‘normal’ common coronaviruses.

“Our results differ from the standard view we have of viral infection,” Wong said in the UCLA press release. “According to this view, the diseased host that destroys the virus has ‘won’, and different parts of the virus then train the immune system to recognize a future invader. COVID-19 reminds us once again that it is not always that simple.”

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