ABSTRACT
Since the end of 2019, new coronavirus pneumonia caused by infection with a new type of coronavirus has become widespread in the world, posing a serious threat to life and health. However, after individuals are infected with SARS-CoV-2, significantly different outcomes occur, which can manifest as simple, mild, common, severe, and dangerous pneumonia. Previous research published in the New England Journal of Medicine suggested that severe infections in individuals may be related to genetic variation, but the genetic contribution and associated mechanisms of severe COVID-19 is still not well understood. Recently, JeanLaurent Casanova's team at Rockefeller University performed genomic testing on 1,193 patients with new coronary pneumonia and found that the critically ill patients carried rare harmful mutations. These mutations originate from 13 loci and related genes that are enriched in the TLR3/IRF7-dependent type I interferon pathway. Further studies of the function of all 118 non-synonymous mutations at these 13 loci revealed that cells harboring these mutations were more susceptible to SARS-CoV-2. This study suggests that TLR3/IRF7-dependent interferon immunity associated with dsRNA sensing may play an important role in the control of SARS-CoV-2, and that genetic defects in these genes are implicated in immunity may be responsible for the development of severe COVID-19 in some individuals.