Injection of 'decoy proteins' could stop the coronavirus infecting cells within the body, scientists say
The killer virus is known to invade cells through receptor 'doorways'
These ACE-2 receptors coat cells that are found within the lungs and other tissues
University of Leicester is functioning on developing proteins which mimic ACE-2
The idea is to trick the virus into binding to those proteins rather than cells
Learn more about a way to help people impacted by COVID
Injecting 'decoy proteins' into the body could stop the coronavirus infecting someone, in step with scientists.
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
The virus that causes COVID-19 is believed by scientists to enter the body through receptors on the surface of cells within the airways, called ACE-2 receptors.
These provide the gateway to the bloodstream and 'facilitate' infection with the bug, scientists say. And now they require to inject people with fake ones to lure the coronavirus away and trick it into sticking to a drug rather than lung tissue.
A team of researchers at the University of Leicester is functioning on creating proteins which mimic these ACE-2 receptors but are even more attractive to the virus.
This could, in theory, distract and absorb the viruses if they get into the body and stop someone from developing symptoms of COVID-19.
The approach has been described as 'hope against the horrible pandemic'.
Other scientists try to all or any but get obviate ACE-2 receptors from people's bodies to effectively shut the door to the coronavirus, but this might have dangerous side effects.
The killer virus is known to invade cells by sticking to proteins on the surface, called ACE-2 receptors (pictured in blue). A team at University of Leicester are acting on developing proteins which mimic ACE-2 receptors, tricking the virus into latching on to them
'By creating a lovely decoy protein for the virus to bind to, we are planning to block the flexibility 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 cause disease.
'If this approach is successful, it could have the potential to stop new cases of this deadly disease across the world.'
ACE-2 receptors are found on the surface of cells throughout the body, but those inside the lungs and airways appear to be those targeted by the coronavirus.
Elsewhere within the body the receptors are accustomed regulate vital sign by controlling enzymes - angiotensin converting enzymes (ACE) - linked to the center and blood flow. Their function inside the lungs isn't well understood.
The coronavirus 'depends' on the receptors for the way into the figure, in step with German researchers writing within the scientific journal, Cell, in March.
The receptors were also critical for SARS, the closest relative of the coronavirus, to invade the figure, scientists found during a scourge of that in 2002.
Since the invention that ACE-2 receptors are the entry point for the virus, scientists are desirous to find the way to weaponise them to prevent the virrus.
There are different routes, however. Scientists like those at Leicester are acting on decoy ACE-2 receptors to confuse the killer virus.
Researchers from the Karolinska Institutet in Sweden and therefore the University of Canadian province (UBC) in Canada, have had promising early results using this approach.
That team added a genetically modified 'soluble' type of ACE-2 - called hrsACE-2 - to human cells within 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 absolutely was targeting.
The research, published within the journal Cell, showed that hrsACE-2 stopped the viral growth of SARS-CoV-2, and reduced it by an element of 1,000 to 5,000 in cell cultures.
'We believe adding this enzyme copy, hrsACE-2, lures the virus to connect itself to the copy rather than the particular cells,' study author Professor Ali Mirazimi said.
'It distracts the virus from infecting the cells to the identical degree and may cause a discount within the growth of the virus within the lungs and other organs.'
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