A study found that life-threatening cases of COVID-19 may be linked to five major genes. It is a guide on how to treat disease.

A new study found that five genes appear to be linked to life-threatening COVID-19 cases. The results provide a possible explanation for why some patients become very ill while others do not. Two of these genes are linked to the innate immune response, while three are associated with inflammation and lung damage. The study provides direction for further research into some potential COVID-19 treatments.

A growing body of research is shining light on a selection of genes that may explain why some people develop more severe cases of COVID-19 than others. Some genes, for example, instruct the body to make more ACE2 receptors, which the Corona virus uses to invade our cells. Studies show that people whose bodies naturally encode more of these receptors may be more likely to develop a severe infection.

Researchers at the University of Edinburgh announced Friday that they have identified five genes that may be linked to the life-threatening conditions of COVID-19. Perhaps not surprisingly, genes are associated with a weaker innate immune response and more aggressive inflammation.

The new study compared more than 2,200 coronavirus patients in intensive care units in the United Kingdom with patients of the same strain who had not tested positive for COVID-19. Critically ill COVID-19 patients were found to have lower expression of IFNAR2, which is a gene that helps encode proteins called interferons. This works as an emergency flame to warn the immune system of an intruder. The patients also showed variation in a set of genes called OAS, which normally help prevent the virus from replicating.

Moreover, critically ill patients had higher expressions of the TYK2 and CCR2 genes, which can cause inflammation and possibly lead to lung injury. They showed a variation in the DPP9 gene, which scientists have linked to pulmonary fibrosis (damaged or scarred lung tissue).

A weak immune system is usually at risk of collapse, when our immune system senses a foreign gas, it sends white blood cells to destroy the threat. But in some patients, this innate immune response is not strong enough to defeat the Coronavirus immediately. This can lead to an aggressive inflammation that damages healthy tissue or lead to organ failure

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Dr. Panagis Galiatos, a pulmonologist at Johns Hopkins Bayview Medical Center, compared this process to an earthquake – in general, falling buildings are what kill a person, not the earthquake itself.

He previously told Business Insider: “Your infection rattles off your immune system.” “If your immune system isn’t well-regulated, it will collapse.” This means that genetic signals that suppress the body’s normal defenses or encourage inflammation may trigger a chain reaction that ultimately leads to serious respiratory failure.

Other factors, including age and underlying health conditions, play a role in severe cases of COVID-19 as well.

Implications for COVID-19 treatments A vial of remdesivir is being examined at the Gilead manufacturing site in the United States.

In solving some of the mysteries surrounding severe COVID-19, Edinburgh researchers have also found clues about how to treat patients.

“Our results immediately highlight which drugs should be at the top of the clinical test list,” Kenneth Bailey, an academic advisor in critical care medicine who co-led the research, told Reuters.

Medicines that enhance INFAR2 expression, for example, may help patients fight the virus before it wreaks havoc in the body.

One potential treatment, a multiple sclerosis drug called Rebif, attempts a similar approach by giving patients a boost of interferon. Merck, the company behind the drug, hopes the treatment will prevent the coronavirus from replicating.

The Edinburgh study also suggests that drugs that target inflammation can play a key role in stopping the disease’s progression. In particular, the researchers point to a class of anti-inflammatory drugs called Janus kinase (JAK) inhibitors, which are already used to treat rheumatoid arthritis. One of these arthritis medications, Eli Lilly’s baricitinib, was recently approved by the Food and Drug Administration for use with remdesivir.

Among other genes, paritinib targets TYK2: a highly expressed gene found in critically ill patients. In September, Eli Lilly announced that together, paritinib and remdesivir reduced the average recovery time for patients by one day compared to patients who only received remdesivir.

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