So, they are looking at autoantibodies reacting against proteins outside cells, in people with Covid-19: People with Covid-19 had a higher level of overall reactivity to their own proteins than uninfected people and people with SLE, (but a lower level of overall reactivity than people with a genetic mutation that causes them to not make a protein that helps distinguish own proteins from pathogen proteins). There was no difference between the overall reactivity of men and women with Covid-19. People with more severe Covid-19 had a higher level of reactivity. They were able to track reactivity levels for each protein over time. They found some reactivities that could be assumed to pre-date the infection, while others developed after. And many of the proteins being reacted to by people with severe Covid-19 were immune-related. They found that autoantibodies could affect immune function. So, perhaps the virus is disrupting things? Causing people's immune systems to be distracted with a civil war, rather than fighting the invader? That seems like a good strategy for a virus. But, by itself, the finding doesn't explain why some people, including some people with mild infections, develop Long Covid, while many people with severe infections don't.
It does not explain serious illness caused by organ damage but a lot of what we see as illness is the immune system's response to the infection. Interferons cause fever, runny nose and coughs, malaise and so on. A mild disease could be because the immune system fights of the invader quickly before it replicates very much but it could also be because of immune failure while the virus multiplies unchecked. It could be that the virus can get deeper into the body with mild disease.