A mutation of the gene could suppress the reproduction of the virus, the researchers found, but people carrying this mutation tended to have problems with their neurons that were linked to schizophrenia and other mental disorders, according to some previous studies.

The new discovery added to mounting evidence that “common genetic variation can impact viral infection”, the research team led by Dr Kristen Brennand, of the Icahn School of Medicine at Mount Sinai in New York, said in a non-peer-reviewed paper posted on bioRxiv.org on Monday.

In China, nearly 20 per cent of Covid-19 cases developed severe or critical conditions, according to a study published by the China Medical Treatment Expert Group for Covid-19 in the New England Journal of Medicine in April.

In June, French researchers reported in the same journal that a third of patients studied had neurological symptoms, such as inattention, disorientation or poorly organised movements.

Brennand’s team infected human neurons carrying the rs4702 gene with a small dose of Sars-CoV-2, the official name for the coronavirus. In 24 hours, the viral copies increased nearly 150,000 times. They then induced the mutation of the rs4702 gene in the neurons with gene editing technology. The number of viral copies dropped to about a third.

Variation in human genes is known to affect the deadliness of an infectious disease. Chinese people are more vulnerable to the H1N1 flu virus than Europeans, for instance.

Part of the reason, according to an Oxford University study published in the journal Nature in 2013, is because of a mutation that was much more prevalent among Chinese than white people. The mutation could increase the risk of severe or critical symptoms six-fold.

The rs4702 gene controlled the production of furin, an enzyme critical for the proper functioning of many proteins. The gene not only occurred in the brain but also in lung and gut cells, according to Brennand and her colleagues.

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They believe the Sars-CoV-2 virus had “hijacked” furin to initiate a series of binding mechanisms that would eventually lead to the fusion of the viral envelope, or outermost layer, and the host cell membrane.

Such an ability – enabled by a unique four-letter insertion in the virus’s genetic codes – was not seen in other coronaviruses such as Sars, according to the researchers.

Previous studies by Brennand’s team and others found the mutation of the rs4702 gene can lead to reduced neuron growth and altered activity. These changes were considered common risk factors for schizophrenia, a serious mental disorder that can result in hallucinations, delusions and extreme thinking or behaviour.

Even though the mutation might reduce viral replication in individual patients, it might not be good news for the control of the pandemic by “permitting low levels of virus to spread successfully while remaining undetected by the immune system”, Brennand said.

Doctors in the central Chinese city of Wuhan, where the first Covid-19 outbreak was first reported, were the first to observe different outcomes among patients with different blood types that were closely related to genes.

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European researchers reported genetic variants that affected the generation of angiotensin-converting enzyme 2, a protein used by the virus to enter the host cell in the Italian population. Scientists from many countries have also launched a worldwide collaboration to track the most relevant genes in this global health crisis.

“[These efforts] will help to better identify high-risk individuals,” Brennand said.