Injection of ‘decoy proteins’ could stop the coronavirus infecting cells within the body, scientists say

Whey! Somone’s figured it out… Now if only there was some accurate and precise method of molecular modelling!

This may work…


Injection of ‘decoy proteins’ could stop the coronavirus infecting cells within the body, scientists say

By Vanessa Chalmers Health Reporter For Mailonline00:00 17 Apr 2020, updated 00:11 17 Apr 2020

  • The killer virus is understood to invade cells through receptor ‘doorways’ 
  • These ACE-2 receptors coat cells that are found in the lungs and other tissues
  • University of Leicester is working on developing proteins which mimic ACE-2
  • The idea is to trick the virus into binding to those proteins instead of cells 
  • Learn more about how to help people impacted by COVID

Injecting ‘decoy proteins’ into the body could stop the coronavirus infecting someone, according to scientists.

The virus that causes COVID-19 is believed by scientists to enter the body through receptors on the surface of cells in the airways, known as ACE-2 receptors.ADVERTISEMENThttps://tpc.googlesyndication.com/safeframe/1-0-37/html/container.html?n=0

These provide the gateway to the bloodstream and ‘facilitate’ infection with the bug, scientists say. And now they want to inject people with fake ones to lure the coronavirus away and trick it into sticking to a drug instead of lung tissue.

A team of researchers at the University of Leicester is working on creating proteins which mimic these ACE-2 receptors but are even more attractive to the virus.

This could, in theory, distract and soak up the viruses if they get into the body and prevent someone from developing symptoms of COVID-19. 

The approach has been described as ‘hope against the horrible pandemic’.

Other scientists are trying to all but get rid of ACE-2 receptors from people’s bodies to effectively shut the door to the coronavirus, but this may have dangerous side effects. 

The killer virus is understood to invade cells by sticking to proteins on the surface, called ACE-2 receptors (pictured in blue).  A team at University of Leicester are working on developing proteins which mimic ACE-2 receptors, tricking the virus into latching on to them


ACE-2 receptors are structures found on the surface of cells in the lungs and airways which work with an enyzme called ACE (angiotensin-converting enzyme) to regulate blood pressure.

Its exact function in the lungs is not well understood but studies suggest it is protective against lung damage and low levels of it can worsen the impact of viral infections.

Scientists say that the coronavirus which causes COVID-19 enters the body through the ACE-2 receptor, which the shape of it allows it to latch on to.

This means that someone with more ACE-2 receptors may be more susceptible to a large viral load – first infectious dose of a virus – entering their bloodstream.

ACE-2 receptors have a shape which matches the outside of the coronavirus, effectively providing it with a doorway into the bloodstream, scientists say

People who have higher than usual numbers of ACE-2 receptors may include those with diabetes or high blood pressure because they have genetic defects which make them produce more. Emerging evidence shows that smokers may also produce more.

High levels of ACE-2 receptors may also be protective, however.

They are thought to be able to protect the lungs during infection and a study on mice in 2008 found that mice which had ACE-2 blocked in their bodies suffered more damage when they were infected with SARS, which is almost identical to COVID-19.

Smoking has in the past been repeatedly linked to lower than normal levels of ACE-2 receptors, potentially increasing the risk of lung damage from COVID-19.

‘By creating an attractive decoy protein for the virus to bind to, we are aiming to block the ability of this virus to infect cells and protect the function of the cell surface receptors,’ said Professor Nick Brindle, from the University of Leicester.     

‘By “hijacking” the receptors on cells in our lungs and other tissues the virus can grow and spread throughout the body and lead to disease. 

‘If this approach is successful, it could have the potential to prevent new cases of this deadly disease across the globe.’   

ACE-2 receptors are found on the surface of cells throughout the body, but the ones inside the lungs and airways appear to be the ones targeted by the coronavirus.

Elsewhere in the body the receptors are used to regulate blood pressure by controlling enzymes – angiotensin converting enzymes (ACE) – linked to the heart and blood flow. Their function inside the lungs is not well understood. 

The coronavirus ‘depends’ on the receptors for a way into the human body, according to German researchers writing in the scientific journal, Cell, in March.

The receptors were also critical for SARS, the closest relative of the coronavirus, to invade the human body, scientists found during an outbreak of that in 2002.

Since the discovery that ACE-2 receptors are the entry point for the virus, scientists have been desperate to find a way to weaponise them to stop the virrus.

There are different routes, however. Scientists such as those at Leicester are working on decoy ACE-2 receptors to confuse the killer virus.

Researchers from the Karolinska Institutet in Sweden and the University of British Columbia (UBC) in Canada, have had promising early results using this approach.

That team added a genetically modified ‘soluble’ form of ACE-2 – called hrsACE-2 – to human cells in the lab. 

It essentially stopped the virus from multiplying at an early stage by ‘catching’ the viruses and blocking their routes to ACE-2 on the cells it was targeting.

The research, published in the journal Cell, showed that hrsACE-2 stopped the viral growth of SARS-CoV-2, and reduced it by a factor of 1,000 to 5,000 in cell cultures. 

‘We believe adding this enzyme copy, hrsACE-2, lures the virus to attach itself to the copy instead of the actual cells,’ study author Professor Ali Mirazimi said.

‘It distracts the virus from infecting the cells to the same degree and should lead to a reduction in the growth of the virus in the lungs and other organs.’

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