A gene that doubles the risk of respiratory failure caused by COVID-19 has been identified by scientists at Oxford University.

They found that a “relatively unstudied gene called LZTFL1” appears to stop cells in the airways and lungs from responding to the virus properly, potentially leading to respiratory failure and death.

Sixty percent of people with South Asian ancestry carry the “high-risk genetic signal”, partly explaining the excess deaths seen in some UK communities, researchers said.

It is found in about 15% of those with European ancestry, while for people of Afro-Caribbean ancestry, it is 2%.

Crucially, those carrying it respond normally to vaccines because it does not affect the immune system.

Professor James Davies, who co-led the study, said the increased risk “should be cancelled out” by immunisation.

Researchers are also hopeful that drugs and other therapies could help the lungs fight off COVID-19, raising the prospect of customised treatments.

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Prof Davies, who worked in intensive care during the coronavirus pandemic, said the discovery shows the “way in which the lung responds to the infection is critical”.

This is an important step forward, he added, because “most treatments (until now) have focused on changing the way in which the immune system reacts to the virus”.

An “artificial intelligence algorithm” was used to analyse large quantities of genetic data from “hundreds of types of cells from all parts of the body”.

Then, using a new, “highly accurate” technique, scientists were able to “zoom down on the DNA”.

Dr Damien Downes, who led laboratory work from the Hughes Research Group, said: “Surprisingly, as several other genes were suspected, the data showed that a relatively unstudied gene called LZTFL1 causes the effect.”

Professor Jim Hughes, professor of gene regulation, also co-led the study and said it had been made more difficult because they were examining an “indirect switch effect”.

He added: “We found that the increased risk is not because of a difference in gene coding for a protein, but because of a difference in the DNA that makes a switch to turn a gene on.

“It’s much harder to detect the gene which is affected by this kind of indirect switch effect.”

The study is published in the journal Nature Genetics.

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