Scientists trace severe COVID-19 to faulty genes and autoimmune condition
https://www.rockefeller.edu/news/29183-severe-covid-19-faulty-genes-autoimmune-condition/

Here's the SMMRY:
https://smmry.com/https://www.rockefeller.edu/news/29183-severe-covid-19-faulty-genes-autoimmune-condition/#&SM_LENGTH=10
> More than 10 percent of young and healthy people who develop severe COVID-19 
> have misguided antibodies that attack not the virus, but the immune system 
> itself, new research shows.
> 
> Whether the proteins have been neutralized by so-called auto-antibodies, or 
> were not produced in sufficient amounts in the first place due to a faulty 
> gene, their missing-in-action appears to be a common theme among a subgroup 
> of COVID-19 sufferers whose disease has thus far been a mystery.
> 
> Published in two papers in Science, the findings help explain why some people 
> develop a disease much more severe than others in their age group-including, 
> for example, individuals who required admission to the ICU despite being in 
> their 20s and free of underlying conditions.
> 
> "These findings provide compelling evidence that the disruption of type I 
> interferon is often the cause of life-threatening COVID-19," says 
> Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of 
> Infectious Diseases at The Rockefeller University and a Howard Hughes Medical 
> Institute investigator.
> 
> The findings are the first results being published out of the COVID Human 
> Genetic Effort, an ongoing international project spanning over 50 sequencing 
> hubs and hundreds of hospitals around the world, co-led by Casanova and Helen 
> Su at the National Institute of Allergy and Infectious Diseases.
> 
> It soon became obvious that a significant number of people with severe 
> disease carried rare variants in these 13 genes, and more than 3 percent of 
> them were in fact missing a functioning gene.
> 
> Further experiments showed that immune cells from these patients did not 
> produce any detectable type I interferons in response to SARS-CoV-2.
> 
> Examining 987 patients with life-threatening COVID-19 pneumonia, they found 
> that more than 10 percent had auto-antibodies against interferons at the 
> onset of their infection.
> 
> Biochemical experiments confirmed these auto-antibodies can effectively curb 
> the activity of interferon type I. In some cases, they could be detected in 
> blood samples taken before patients became infected; in others, they were 
> found in the early stages of the infection, before the immune system had the 
> time to mount a response.
> 
> The team continues to look for genetic variations that may affect other types 
> of interferons or additional aspects of the immune response in COVID-19 
> outliers.



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