- Researchers in the UK have studied the genetic differences between 2,700 coronavirus patients who require intensive care and healthy individuals, which determines five major genetic complications that are favorable for acute COVID-19.
- This improvement will lead to the discovery of new therapies that specifically target the types of genetic imbalances that can lead to life-threatening complications.
- The genetic problems they discovered include antiviral immunity and genes involved in pneumonia.
Doctors save more corona virus patients than they can in March and April because they have come up with new treatment protocols that include new drug discoveries. They are also used for symptoms and have experience managing severe events. But even so, the death toll continues to rise as more and more people become infected every day. Most of them will get over COVID-19 at home within two weeks. But some will create problems that need to be hospitalized. Survival after hospitalization is not guaranteed because we do not yet have drugs that can ensure that complications do not lead to death. Vaccines can prevent severe COVID-19, but should not be used in patients who are already infected. However, that is likely to change soon, and researchers at The Roslin Institute at the University of Edinburgh have released a breakthrough coronavirus study that could explain why some people develop severe COVID-19.
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The researchers recently explained that genetic imbalances related to interferon increase the risk of complications in young patients, which are not expected to produce severe COVID-19. Those genetic issues have always been; They are not the result of a COVID-19 infection. But no other disease brought them to the surface.
It turns out that these are not the only interferon-regulating genes that can affect the COVID-19 prognosis. Interferon is part of the immediate immune system after infection with a pathogen. Roslin’s researchers examined the DNA of 2,700 patients who developed severe COVID-19 in the UK and identified five genetic problems that could lead to a more dangerous version of the disease. This finding will lead to new treatment protocols as physicians are reusing drugs that are currently available to deal with these specific genetic problems.
Researchers at the Genomic Association compared the genetic data of 2,700 ICU patients with samples of healthy volunteers from other studies. They discovered key differences in these five genes: IFNAR2, TYK2, OAS1, DPP9 and CCR. They asked “why some people get seriously ill with Govt-19, others are not affected.”
“Our findings reveal that the major disease in Govit-19 is related to at least two biological mechanisms: endogenous antiviral protection known to be important at the onset of the disease (IFNAR2 and OAS genes), and host-induced pneumonia, which is a late, life-threatening COVID-19. (DPP9, TYK2, and CCR2). ”
“This is a shocking realization of the promise of human genetics to help understand the critical disease,” said Dr. Kenneth Bailey, the project’s lead researcher, in a statement. “Our results immediately show which drugs should be at the top of the list for clinical trials. We can only test a few drugs at a time, so making the right choices can save thousands of lives.
Researchers can predict what types of medications may work in patients with severe COVID-19. They found that a reduction in the activity of the TYK2 gene protects against disease. Anti-inflammatory drugs from the class called JAK inhibitors may help. An example of such a drug is paracetamol.
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Another finding is about the INFAR2 gene. Increasing the activity of the gene may create protection because it reflects the effect of interferon therapy. But this treatment should be used to be effective at the beginning of the infection.
Researchers say anti-inflammatory and antiviral drugs that target these genetic disorders should be the focus of further research.
“We have discovered new and more reliable genetic links to complex disease in COVID-19,” the researchers wrote. “Some of these associations directly lead to potential therapeutic approaches to enhance interferon signals, resist monocyte activation and infiltration into the lungs in particular, or significantly add to the clinical significance of each therapeutic approach to biologic rationale prior to experimentation, although it adds significantly to the clinical rationale based on specific treatment approaches. To be tested. ”
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Chris Smith started writing about gadgets as a hobby and before he knew it he shared his thoughts on technical matters with readers around the world. Whenever he does not write about gadgets he fails to stay away from them, however he tries hard. But that’s not a bad thing at all.