The scientists detailed how interferons – proteins that alert other cells to the presence of viruses – have been found to stimulate the ACE2 gene, potentially allowing the virus to infect a greater number of cells.

The team published its findings about Sars-CoV-2, the scientific name for the new coronavirus, in the journal Cell last Tuesday.

Jose Ordovas-Montanes, a research scientist from the Boston Children’s Hospital at Harvard who led the study, described the role of ACE2 and why it might be vulnerable to Covid-19, a pneumonia-like disease.

“ACE2 is also critical in protecting people during various types of lung injury,” he said in a statement released by the hospital.

“When ACE2 comes up, that’s usually a productive response. But since the virus uses ACE2 as a target, we speculate that it might be exploiting that normal protective response.”

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The report said ACE2 had been identified as a receptor for severe acute respiratory syndrome (Sars) coronavirus, which broke out from southern China in 2002-03.

But this team studying Covid-19 found that the enzyme might be stimulated by interferons, creating more targets for Sars-CoV-2.

The study, done in collaboration with the Human Cell Atlas Lung Biological Network group, said there were three types of interferons, two of which were found to stimulate ACE2 in cells in the primary human upper airway.

Their latest findings highlighted how ACE2 might have been missed as an interferon-stimulated gene, adding to “growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN [interferon] pathway”, the report said.

To identify susceptible cells, the researchers looked for cells that expressed both ACE2 and TMPRSS2, which they found made up only a small percentage – often well below 10 per cent – of human respiratory and intestinal cells. These cells fell into three types found in the nose, lung and small intestines.

“Once you understand which cells are infected you can start to ask, ‘How do these cells work?’ ‘Is there anything within these cells that is critical for the virus’s life cycle’,” Ordovas-Montanes said.

“With more refined cellular models, we can perform better screens to find what existing drugs target that biology, providing a stepping stone to go into mice or non-human primates.”

Interferons have been tested as a treatment for Covid-19, and have been used in clinical studies against the Middle Eastern respiratory syndrome (Mers) coronavirus.

French researchers said in a report published on the ScienceDirect platform in early April that there had been mixed efficacy for Type I interferons as treatment against Sars and Mers, but that Sars-CoV-2 would likely be more sensitive to the interferons than Sars.

But Ordovas-Montanes said it was not yet clear if interferons would be harmful or beneficial to patients with Covid-19. More research was needed, he said.

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“It might be that in some patients, because of the timing or the dose, interferon can contain the virus, while in others, interferon promotes more infection,” he said. “We want to better understand where the balance lies and how we can maintain a productive antiviral response without producing more target cells for the virus to infect.”

The Covid-19 virus that first began to spread from central China late last year has led to more than 3 million confirmed cases and over 200,000 deaths in 185 countries.