The reason why some people infected with the coronavirus have no symptoms at all, while others are seriously ill is one of the biggest puzzles in the pandemic.
A study published in the scientific journal Nature of more than 2,200 patients admitted to intensive care facilities identified a specific gene that may be the reason.
That gene makes some people more susceptible to severe Covid-19 symptoms.
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These findings explain how the immune system is failing, so hopefully it will help identify new treatments.
This study will continue to be needed even though a vaccine is being developed, said Dr. Kenneth Baillie, a consultant medicine at the Royal Infirmary in Edinburgh, is leading the Genomicc project.
"Vaccines are supposed to reduce the number of Covid-19 cases drastically, but it is likely that doctors will still treat patients infected with the disease over the next few years around the world.
"So there is an urgent need to find new treatments," he said.
The 'angry' cells
Scientists looked at the DNA of patients in more than 200 intensive care units in British hospitals.
Scientists scan their genes, which contain instructions for every biological process - including how to fight viruses.
Their genomes are then compared with the DNA of healthy people to show genetic differences.
Some of the differences found were the first of which was a gene called TYK2.
"It's part of the system that makes your immune cells angrier and more inflamed," says Dr. Baillie.
But if the genes don't work, the immune response can become too rapid, putting patients at risk of developing lung inflammation.
Anti-inflammatory drugs already used for conditions such as rheumatoid arthritis target these biological mechanisms, including a drug called Baricitinib.
"That makes him a very reasonable candidate for a new treatment," said Dr. Baillie. "But of course, we need to do large-scale clinical trials to find out if this is true or not."
Too little interferon
Genetic differences were also found in the DPP9 gene, which plays a role in inflammation, and in a gene called OAS, which helps stop the virus from making copies of itself.
Variations in a gene called IFNAR2 were also identified in patients in intensive care.
IFNAR2 is linked to a powerful anti-viral molecule called interferon, which helps turn on the immune system as soon as an infection is detected.
Too little interferon production can cause the virus to multiply rapidly, leading to more severe symptoms.
Two other recent studies published in the journal Science also implicated the role of interferon in the case of Covid, through genetic mutations and autoimmune disorders that affect its production.
Prof Jean-Laurent Casanova, who conducted the research from The Rockefeller University in New York, said: "[Interferon] accounted for nearly 15% of critical Covid-19 cases reported internationally in the group of people we studied."
Interferon can be given as treatment, but World Health Organization clinical trials have concluded that it does not help very sick patients.
However, Prof. Casanova said when interferon was given important.
He explained: "I hope that if interferon is given in the first two, three, four days of infection, it will work, because basically interferon will provide molecules that [the patient] does not produce themselves."
'When things go wrong'
Dr Vanessa Sancho-Shimizu, a geneticist from Imperial College London, said that the genetic discovery provides unprecedented insights into the biology of the disease.
"This is really an example of precision medicine, allowing us to really identify when things go wrong in the patient's body," he told BBC News.
"The findings from this genetic study will help us identify specific molecular pathways that can be targeted for therapeutic interventions," he said.
But there are still some mysteries regarding this genome study.
The Genomicc study - and several others - have revealed a cluster of genes on chromosome 3 that are strongly associated with severe symptoms.
However, the biology underlying this is still not understood.
This study will involve more patients in the future.
Dr Baillie said: "We need everyone, but we are very interested in recruiting people from ethnic minority groups, which are a population with a large number of critical cases."
He added: "There is still a very urgent need to find new treatments for this disease and we have to make the right choices about which treatments to try next because we don't have time to make mistakes."
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