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Experts say that this discovery will eventually lead to the development of effective treatments against the SARS-CoV-2 disease. “Vaccines should dramatically reduce the number of COVID-19 cases, but physicians around the world will likely continue to treat the disease in intensive care for several years, so we urgently need to find new treatments,” said Dr. Kenneth Baillie. , who coordinated the investigation.
Cells get “angry”
Over several months, specialists analyzed the DNA of patients in more than 200 intensive care units operating in UK hospitals. Each person’s genes were scanned, including those responsible for fighting infections. These genomes were then compared to the DNA of healthy people to identify differences, shows nature.com. Therefore, it was discovered that a gene called TYK2 may be “faulty”. “Because of this, the immune cells become more ‘angry’ and very inflammatory,” said Kenneth Baillie. Fortunately, there is a class of anti-inflammatory drugs, already used for conditions like rheumatoid arthritis, that target this biological mechanism. “One of them is baricitinib, which is emerging as a viable candidate for a new treatment, but of course we need to do large-scale clinical trials,” said Dr. Baillie.
Very little interferon
Genetic differences have also been found in a gene called DPP9, which plays a role in controlling inflammation, but also in a gene called OAS, which helps stop the virus from multiplying. Then, differences were also found in the IFNAR2 gene, which has a direct link to interferon, a powerful antiviral molecule, in intensive care patients. This helps activate the immune system as soon as an infection is detected. Due to the abnormalities found in IFNAR2, the infected body produces less interferon, giving the new coronavirus an advantage, allowing it to multiply rapidly, leading to more serious illness. Thus, interferon can be administered as a treatment, although initially a clinical study by the World Health Organization concluded that it did not help very sick patients. “Given in the first two, three, or four days of infection, interferon would work because it would essentially provide the molecule that the patient does not make,” said Professor Jean-Laurent Casanova of Rockefeller University. from New York.
Vanessa Sancho-Shimizu, a geneticist at Imperial College London, said the genetic findings offer unprecedented insight into the principle behind which COVID-19 works. “The findings of these genetic studies will help us to identify certain molecular pathways that could help us in therapeutic intervention,” said the expert.
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