Researchers have found that some immune system molecules trigger the production of a non-functional variant of the human protein used by the novel coronavirus to enter and infect host cells, reported PTI, quoting a study that sheds light on the body’s natural defence against the deadly virus.

The research, which was published in the journal Nature Genetics, examined the genetic information that codes for the ACE2 receptor, to which the SARS-CoV-2 virus must bind in order to enter and infect human cells.

In the study, scientists, including those from the Francis Crick Institute in London, analysed existing genetic databases and human cells to identify a new variant, or isoform, of ACE2 called MIRb-ACE2, which the SARS-CoV-2 virus cannot bind to.

Kevin Ng, a co-author of the study from the Francis Crick Institute said, “This variant of genetic information is the result of retroelements in our DNA, which can ‘jump’ around the genome impacting gene expression.”

He added, “From looking at which other species also have this variant, it appears to be widely present in mammals, so it must have entered the human genome a long time ago.”

The scientists, in order to understand the role this variant plays in the body’s immune response to SARS-CoV-2, assessed the effects of exposing cells to interferons, signalling proteins that are made and released by virus-infected cells. 

The scientists found that interferons increase the response and production specifically of MIRb-ACE2, while ACE2 is not affected.

The researchers said the findings allay concerns that interferon-based treatments for SARS-CoV-2 could inadvertently be helping the virus by bringing about an increase in coronavirus cell receptors in the body. They said that the coronavirus is not able to bind to MIRb-ACE2, which is also highly unstable.

George Kassiotis, another co-author of the study, said, “The non-functional MIRb-ACE2 isoform was likely responsible for results from previous studies that suggested interferons could be upregulating ACE2, as there was no distinction between these two isoforms.”

He added, “This highlights how scientific knowledge about SARS-CoV-2 is constantly being revised and updated as new research is carried out. We still have a lot to learn, but we are making rapid progress.”

The researchers also found that cells in the upper aero-digestive tract, including the mouth and the nose, express more MIRb-ACE2 than the functional ACE2, and this balance changes lower in this tract and in the intestines.

Researchers believe further research is required to understand why this difference occurs and the impact it might have on how the virus spreads in the body.