But scientists still don't know why some people develop severe disease while others suffer only mild symptoms – or no symptoms at all.
The research, which has yet to be peer-reviewed and published in a journal, suggests that in patients with severe COVID, the body produces "autoantibodies".
instead of attacking the invading virus – attack the patient's own immune system and organs. https://www.sciencealert.com/virus 
The researchers found that people with severe COVID had autoantibodies that latched onto crucial proteins involved in recognising, alerting and clearing cells infected with the coronavirus.
These proteins include cytokines and chemokines – important messengers in the immune system. This interfered with the normal immune system function, blocking antiviral defences, potentially making the disease more severe.
They searched for autoantibodies in 170 hospitalised patients and compared them with autoantibodies found in people who suffered mild illness or asymptomatic infection, as well as people who had not been infected with the virus.
In the blood of the hospitalised patients, they found autoantibodies that could attack interferons, as well as autoantibodies that could interfere with other critical cells of the immune system such as natural killer cells and T cells.
The findings showed that autoantibodies were a very common feature of severely ill COVID patients.
The Yale researchers conducted further tests in mice, which showed that the presence of these autoantibodies could make the disease worse, suggesting that these autoantibodies could contribute to the severity of COVID in humans.
Not the whole story

Though COVID patients had many autoantibodies that targeted immune system proteins, the researchers didn't find any COVID-specific autoantibodies that could be used to distinguish severely ill COVID patients.
What determines if a person is going to suffer from severe COVID depends on many things, and autoantibodies are not the whole story.
But the research suggests that people with existing autoantibodies may be at higher risk of getting severe COVID.
These people may have deficiencies in their immune response during early coronavirus infection or be predisposed to making new autoantibodies that could hinder their immune response to the virus.
The presence of autoantibodies suggests that, for some patients, COVID could be an autoimmune disease triggered by the coronavirus.
Understanding what drives the production of autoantibodies will help scientists to develop new treatments for this disease.
Scientists don't know how long these autoantibodies last for after the infection has cleared. An important unanswered question is whether long-term damage caused by autoantibodies could explain some symptoms of long COVID.

https://www.medrxiv.org/content/10.1101/2020.10.19.20214494v1.full.pdf
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