An antiviral drug that could be taken as a nasal spray can block the coronavirus from latching onto lung cells, according to laboratory trials.
The medicine, marketed as Neumifil, was developed as a treatment for flu but may be able to prevent COVID-19, scientists say.
A study by the University of St Andrews in Scotland found it could bind to the ‘spike’-shaped proteins on the outside of the virus and stop it latching to cells found in human airways.
Only lab tests have been done so far but the results, watched over by Public Health England, give hope that the drug could be used on COVID-19 patients.
Scientists around the world are scrambling to find a cure for COVID-19 so countries can come out of lockdown without fear of a second outbreak.
So far two of the most promising drugs, remdesivir and hydroxychloroquine, have not been found to be beneficial in clinical trials. The latter might even make the disease more deadly, some results have suggested.
Neumifil works by blocking the coronavirus’s interaction with structures called ACE-2 receptors in the airways, which are the virus’s doorway into the body. These receptors are a big point of focus for scientists trying to stop the disease.
Some suggest they could be a reason that smokers appear to have lower rates of serious illness when infected with COVID-19 – there is speculation that nicotine may reduce numbers of the receptors, blocking access.
But scientists also say they may have a protective effect in the lungs and low levels are linked to worse damage from viral infection. Other studies have shown smoking raises levels of ACE-2 receptors.
A new Scottish antiviral drug is being rushed into clinical trials after it successfully treated coronavirus in lab studies overseen by Public Health England. University of St Andrews researchers, behind the drug , say they envisage it being given to patients via a nasal spray
The drug (shows as mCBMs) works by binding to the virus and blocking it from hooking onto cells in the airways and invading the body
Neumifil was created by Pneumagen Ltd, a spin-off company from the University of St Andrews which focuses on new treatments for infectious diseases and cancer.
Unlike most antiviral drugs, which attack viruses, it works by binding to sugar molecules both on the surface of respiratory cells – those in the airways and the lungs – and on the virus.
This hinders the ability of the virus to attack the respiratory cells by latching its unique ‘spike’ proteins onto the ACE-2 receptors.
Lead researcher Gary Taylor, professor of biology at St Andrews, told MailOnline: ‘Classic antivirals actually attack some part of the virus’s machinery, whereas our drug actually inhibits the virus from even getting into cells.
‘We envision it being given as a nasal spray, and imagine it being given weekly or every other day.
HOW IS NEUMIFIL SAID TO PREVENT AND TREAT COVID-19?
Most antiviral drugs work by attacking viruses or blocking their ability to multiply and spread in the body.
But Neumifil is said to inhibit the virus from even getting into cells.
It binds to sugar molecules which are on the surface of all cells in the respiratory tract.
These same types of carbs are on the surfaces of virus’ spike proteins, which it uses to enter cells.
This hinders the ability of the virus to unleash its spikes and attach itself to ACE-2 receptors.
ACE-2 receptors, which are found on cells in the airways and lungs, have been said to work as the virus’ doorway into the body and to ‘facilitate’ infection.
‘Our drug binds to sugar molecules which are on the surface of all cells in the respiratory tract.
‘These same types of carbs are on the surfaces of virus’ spike proteins, which it uses to enter cells.
‘The spike protein has complex carbohydrates attached to it, and we supposed that our drug binds to these and blocks access of the spike protein to its ACE-2 receptor.
‘Likewise, ACE-2 is sitting on a cell surface which is covered in complex carbohydrates. Our drug also binds to those, and being a relatively large molecule, blocks the ability of ACE-2 to bind to the spike.’
Some scientists have suggested that smoking cigarettes may actually protect people against the coronavirus by altering levels of ACE-2.
ACE-2 is the virus’ route into the body, therefore having more of them would seem to be a bad thing.
But scientists say they may have a protective effect in the lungs and low levels are linked to worse damage from viral infection.
A study published earlier this month by researchers in New York and Athens suggested that while the virus causes lung damage by depleting the numbers of ACE-2, smoking actually increases the number of them, reversing the effect.
In the University of St Andrews lab trials, Neumifil was able to both prevent and treat coronavirus infection in three separate studies in test tubes.
The studies were conducted at Public Health England’s Porton Down lab in Wiltshire, and at the University of Glasgow’s MRC Centre for Virus Research.
Following the promising results, scientists are now pushing to have the drug trialled on animals and eventually humans.
However, it could be the first quarter of next year before the drug is ready to be rolled out.
Pneumagen had already been developing Neumifil to treat respiratory tract infections (RTIs) including the flu and respiratory syncytial birus (RSV).
But the Fife-based firm switched its research focus to treating COVID-19 amid the pandemic.
Douglas Thomson, CEO of Pneumagen, said the goal was now to ‘rapidly’ push the drug through clinical trials, first on animals then on humans.
He said: ‘Today’s positive results from in vitro studies… against coronaviruses show that glycan binding has the potential to prevent and treat infection.
‘This further supports the value of our universal therapeutic modality to block access to lung cells of SARS-CoV-2, as well as other viruses, that cause respiratory tract infections, providing the potential for a pan-viral respiratory product.
‘Our goal is now to rapidly begin clinical testing for the prevention and treatment of COVID-19.’
WHAT IS AN ACE-2 RECEPTOR AND WHAT DOES IT HAVE TO DO WITH COVID-19?
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.