A paper published yesterday supports a hypothesis that Richard Nichols and I made in March 2020. We published an article in The Conversation arguing that we need to know if someone’s chances of severe COVID symptoms are affected by their genes.
We suggested:
“It may be that just one or two genes are involved. Perhaps broken genes involved in the immune system or lung cell surfaces…It may be that there are thousands of genes involved. Perhaps a complex mix of genes involved in lung physiology, upper respiratory tract shape, and many other things we have never even thought of.”
Yesterday, the journal Science published a paper that begins to confirm this. It reports the discovery of broken immune system genes in some patients that have severe COVID symptoms.
The paper, titled “Inborn errors of type I IFN immunity in patients with life-threatening COVID-19” gives evidence that thirteen genes involved in the immune system have loss-of-function variants in a subset of patients with severe COVID symptoms.
An accompanying paper, titled “Auto-antibodies against type I IFNs in patients with life-threatening COVID-19” gives additional evidence that type I IFNs are critical to the body’s immune response to COVID. Impairment of their functioning leads to more severe symptoms in the patients they studied.
These studies are based on relatively small numbers of patients, and only studied a handful of genes that seemed likely from the outset to be involve in COVID immunity. If genome-wide association studies were conducted on large numbers of patients, as Richard Nichols and I suggested in March, we may discover that the 13 genes reported yesterday are just the tip of the iceberg.