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- Five genes appear to be associated with life-threatening cases of COVID-19, a new study found.
- The finding offers a possible explanation for why some patients get seriously ill and others don’t.
- Two of these genes are related to the innate immune response, while three are related to inflammation and lung damage.
- The study offers a direction for more research on certain potential COVID-19 treatments.
- Visit the Business Insider home page for more stories.
A growing body of research is highlighting a select set of genes that may explain why some people develop more severe COVID-19 cases than others. Certain genes, for example, instruct the body to make more ACE2 receptors, which the coronavirus uses to invade our cells. Studies show that people whose bodies naturally code for more of these receptors may be at higher risk of serious infection.
On Friday, researchers from the University of Edinburgh announced that they had identified five genes that may be associated with life-threatening COVID-19 cases. The genes are, perhaps unsurprisingly, associated with a weaker innate immune response and more aggressive inflammation.
The new study compared more than 2,200 coronavirus patients in UK intensive care units with patients of similar descent who had not tested positive for COVID-19.
Critically ill COVID-19 patients were found to have lower expression of IFNAR2, a gene that helps encode proteins called interferons. These act as an emergency flash to warn the immune system of an intruder. The patients also showed variation in a group of genes called OAS, which normally helps prevent a virus from replicating.
Additionally, critically ill patients had higher expressions of the TYK2 and CCR2 genes, which can cause inflammation and potentially lead to lung injury. And they showed a variation in the DPP9 gene, which scientists have linked to pulmonary fibrosis (damaged or scarred lung tissue).
A weak immune system runs the risk of collapse
Normally, when our immune system detects a foreign invader, it sends out white blood cells to destroy the threat. But in some patients, that innate immune response is not strong enough to defeat the coronavirus immediately. This can trigger aggressive inflammation that damages healthy tissue or leads to organ failure.
Dr. Panagis Galiatsatos, a pulmonary physician at Johns Hopkins Bayview Medical Center, likened that process to an earthquake; in general, it is the buildings that fall that kill someone, not the earthquake itself.
“His infection is a rattle of his immune system,” he previously told Business Insider. “If your immune system is just not well structured, it will just crash.”
That means genetic signals that inhibit the body’s natural defenses or stimulate inflammation can set off a chain reaction that ultimately leads to critical respiratory failure.
Other factors, including age and underlying health conditions, also play a role in severe cases of COVID-19.
Implications for COVID-19 treatments
A vial of remdesivir is inspected at a Gilead manufacturing site in the USA.
Gilead Sciences via AP
By unraveling some of the mysteries surrounding severe COVID-19, the Edinburgh researchers also found clues on how to treat patients.
“Our results immediately highlight which drugs should be at the top of the list for clinical trials,” Kenneth Baillie, academic consultant in critical care medicine who co-led the research, told Reuters.
Medications that increase the expression of INFAR2, for example, can help patients fight the virus before it wreaks havoc in the body.
One potential treatment, a multiple sclerosis drug called Rebif, is trying a similar approach by giving patients an interferon booster. Merck, the company behind the drug, hopes the therapy will prevent the replication of the coronavirus.
The Edinburgh study also suggests that drugs targeting inflammation could play a key role in stopping the progression of the disease. In particular, the researchers point to a class of anti-inflammatory drugs called Janus kinase inhibitors (JAKs), which are already used to treat rheumatoid arthritis.
One of these arthritis medications, Eli Lilly’s baricitinib, was recently cleared by the FDA for use in combination with remdesivir.
Among other genes, baricitinib targets TYK2: one of the highly expressed genes found in critically ill patients. In September, Eli Lilly announced that together, baricitinib and remdesivir reduced the mean recovery time of patients by one day compared to patients who received only remdesivir.
