The body’s immune response drives the production of a faulty coronavirus...

The body’s immune response drives the production of a faulty coronavirus...
The body’s immune response drives the production of a faulty coronavirus...
London, 25 October
Some molecules in the immune system trigger the production of a non-functional variant of the human protein, which the novel coronavirus uses to penetrate host cells and infect them. This comes from a study that shed light on the body’s natural defenses against COVID-19.

The study, 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 at the Francis Crick Institute in London, analyzed existing genetic databases and human cells to identify a new variant or isoform of ACE2 called MIRb-ACE2 that the SARS-CoV-2 virus cannot bind to .

“This variant of genetic information is the result of retro elements in our DNA that can jump around the genome and affect gene expression,” said Kevin Ng, co-author of the study at the Francis Crick Institute.

“If you look at what other species have this variant, it seems to be widespread in mammals, so it must have entered the human genome a long time ago,” he added.

To understand what role this variant plays in the body’s own immune response to SARS-CoV-2, the scientists examined the effects of exposure of cells to interferons – signaling proteins that are produced and released by virus-infected cells.

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

According to the researchers, the results allay concerns that interferon-based treatments for SARS-CoV-2 could inadvertently help the virus by causing an increase in coronavirus cell receptors in the body.

They said that the coronavirus cannot bind to MIRb-ACE2, which is also very unstable.

“The non-functional MIRb-ACE2 isoform was likely responsible for results from previous studies that indicated that interferons could upregulate ACE2 because there was no difference between these two isoforms,” ​​said George Kassiotis, another co-author of the study.

“This shows how the 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’re making rapid progress, ”said Kassiotis.

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

They believe more research is needed to understand why this difference occurs and what impact it could have on the spread of the virus throughout the body. PTI

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