- Researchers from the UK have studied genetic differences between 2,700 coronavirus patients who required intensive care and healthy individuals, determining five key genetic issues that might favor severe COVID-19.
- The breakthrough could lead to the discovery of new therapies that specifically target the types of genetic imbalances that can lead to life-threatening complications.
- The genetic issues they discovered include genes that are involved in antiviral immunity and lung inflammation.
Doctors are saving more coronavirus patients than they could in March and April, as they’ve come up with new treatment protocols that involve new drug discoveries. They’re also used to the symptoms and have experience managing severe cases. But even so, the death toll continues to remain high because so many people get infected every day. Most of them will get over COVID-19 at home within two weeks. But some will develop complications that require hospitalization. Survival isn’t guaranteed after admission to the hospital, as we still lack the drugs that could ensure that complications won’t lead to death. Vaccines will prevent severe COVID-19, but the drugs can’t be used on patients who are already infected. That might change soon enough, however, and researchers from The Roslin Institute at the University of Edinburgh just released a breakthrough coronavirus study that explains why some people develop severe COVID-19.
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Researchers explained recently that interferon-related genetic imbalances might increase the risk of complications in young patients that aren’t expected to develop severe COVID-19. Those genetic problems were always there; they’re not the results of a COVID-19 infection. But no other illness brought them to the surface.
It turns out that it’s not just genes that control interferon that can impact the COVID-19 prognosis. Interferon is a protein that’s part of the immediate immune response after an infection with a pathogen. The Roslin researchers studied the DNA of 2,700 patients who developed severe COVID-19 in the UK and found five genetic issues that can lead to a more dangerous version of the illness. The discovery could lead to new treatment protocols, as doctors repurpose currently-available medicines to deal with these particular genetic issues.
Researchers from the GenOMICC consortium compared the 2,700 ICU patients’ genetic information with samples from healthy volunteers from other studies. They discovered key differences in these five genes: IFNAR2, TYK2, OAS1, DPP9, and CCR. They “partially explain why some people become severely sick with Covid-19, while others are not affected.”
“Our findings reveal that critical illness in Covid-19 is related to at least two biological mechanisms: innate antiviral defenses, which are known to be important early in disease (IFNAR2 and OAS genes), and host-driven inflammatory lung injury, which is a key mechanism of late, life-threatening COVID-19 (DPP9, TYK2, and CCR2),” the researchers wrote.
“This is a stunning realization of the promise of human genetics to help understand critical illness,” the project’s chief investigator Dr. Kenneth Baillie said in a statement. “Our results immediately highlight which drugs should be at the top of the list for clinical testing. We can only test a few drugs at a time, so making the right choices will save thousands of lives.
The researchers can predict what sort of drugs could work in patients with severe COVID-19. They found that a reduction in the activity of the TYK2 gene protects against the illness. Anti-inflammatory drugs from a class called JAK inhibitors might help. One example of such a drug is baricitinib.
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Another discovery concerns the INFAR2 gene. Boosting the gene’s activity could create protection, as it would mimic the effect of interferon treatment. But this therapy should be used early in the infection to be effective.
The researchers say that anti-inflammatory and antiviral drugs that can target these genetic issues should be the focus of additional research.
“We have discovered new and highly plausible genetic associations with critical illness in COVID-19,” the researchers wrote. “Some of these associations lead directly to potential therapeutic approaches to augment interferon signaling, antagonize monocyte activation and infiltration into the lungs, or specifically target harmful inflammatory pathways. While this adds substantially to the biological rationale underpinning specific therapeutic approaches, each treatment must be tested in large-scale clinical trials before entering clinical practice.”
The full study is available in Nature.
Chris Smith started writing about gadgets as a hobby, and before he knew it he was sharing his views on tech stuff with readers around the world. Whenever he's not writing about gadgets he miserably fails to stay away from them, although he desperately tries. But that's not necessarily a bad thing.
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Breakthrough study might explain why people develop severe COVID-19 - BGR
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