Severe COVID-19 patients may be closely related to five genes
December 14 Recently, an international research team composed of researchers from the University of Edinburgh, Oxford University, Cambridge University, the University of Dublin in Ireland, Sun Yat-sen University of China, West Lake University and other institutions published an article in the journal Nature that the severe coronavirus Patients with pneumonia may be closely related to five key genes, and this discovery provides important clues for screening of drugs for the treatment of COVID-19.
Analyzing the gene sequences of more than 2,700 patients with COVID-19 in 208 intensive care units in the United Kingdom, the research team found that compared with the control group, the expression level of IFNAR2 gene in severe COVID-19 patients was lower, which was related to the synthesis of interferon, which had antiviral effects.
At the same time, OSA cluster mutation is also one of the characteristics of severe patients, which helps to curb viral replication. Abnormalities in IFNAR2 and OSA make patients’ innate immunity poor.
In addition, the study found that patients with severe COVID-19 have higher levels of expression of TYK2 and CCR2 genes and more mutations in the DPP9 gene, which may make patients have a stronger inflammatory response and lung damage and fibrosis worse.
Usually, when the body’s immune system senses an alien invader, it produces white blood cells to eliminate the threat. When the innate immune response is not enough to defeat the coronavirus immediately, it will cause serious inflammation, damage healthy tissues or lead to organ failure.
It can be said that the potential mechanism of action of these five key genes to cause severe illness is to inhibit the body’s defense ability and promote the inflammatory response.
In addition to trying to solve the genetic mystery behind severe COVID-19, the research team also gave clues to find a therapeutic drug. “Like sepsis and flu, the damage to the lungs caused by COVID-19 is caused by our own immune system, not the virus itself,” said Dr. Kenneth Bailey, the correspondent author of the paper and the Roslyn Institute of the University of Edinburgh in the United Kingdom.
The results of the study show the route to key drug targets, highlighting which drugs should be the preferred drugs in clinical trials.
The paper points out that increasing the expression of interferon genes such as IFNAR2 and curbing harmful inflammatory channels are potential treatments for COVID-19.
For example, the high-expression gene TYK2 in severe patients is one of the four target targets of JAK inhibitors such as baretinib, so the drug may be used for the treatment of COVID-19.
