Nature: Severe new crown patients may be closely related to five genes

BEIJING, Dec. 14 (Reporter Hu Dingkun Zhang Mengran) Recently, an international team of researchers from the University of Edinburgh, Oxford University, Cambridge University, Dublin University in Ireland, Zhongshan University in China, West Lake University and other institutions in the journal Nature said that patients with severe new coronary pneumonia or closely related to five key genes, this discovery provides important clues for the screening of new coronary drugs.
team analyzed the genetic sequences of more than 2,700 patients with neo-coronary pneumonia in 208 intensive care units in the UK and found that IFNAR2 gene expression was lower in patients with severe neo-coronary pneumonia, which is associated with the synthesis of interferon, which has antiviral effects, compared to the control group. At the same time, the OSA gene cluster mutation is also one of the characteristics of severe patients, the gene helps to stop virus replication. Abnormalities in IFNAR2 and OSA make patients less immune innariable.
In addition, the study found higher levels of expression of the TYK2 and CCR2 genes in patients with severe neo-coronary pneumonia, which showed more mutations in the DEP9 gene, which may have led to a stronger inflammatory response in patients with more severe lung damage and fibrosis.
Usually, when the body's immune system senses an alien invader, white blood cells are produced to eliminate the threat, and when the innate immune response is not sufficient to defeat the coronavirus immediately, it can cause severe inflammation, damage to healthy tissue or lead to organ failure. It can be said that these five key genes lead to severe disease potential mechanism is to inhibit the body's defenses, promote inflammatory response.
in addition to trying to solve the genetic mystery behind the severe new coronary pneumonia, the team also gave clues to the search for a cure. Dr Kenneth Bailey, co-author of the paper and at the Roslin Institute at the University of Edinburgh, said that, like sepsis and influenza, the damage to the lungs from neo-coronary pneumonia is caused by our own immune system, not the virus itself. The findings show the route to key drug targets, highlighting which drugs should be the drug of choice for clinical trials.
paper points out that increasing interferon gene expression such as IFNAR2 and curbing harmful inflammatory channels are potential new treatments for coronary pneumonia. For example, the high expression gene TYK2 in severe patients is one of the four targets of JAK inhibitors such as barrettinib, so the drug may be used in the treatment of neo-coronary pneumonia.