Potential COVID-19 vaccines should NOT be affected by mutations to the coronavirus because different strains respond to treatment in the same way, study claims

  • Scientist infected ferret blood with two forms of the SARS-CoV-2 coronavirus 
  • These were the initially dominant ‘D’ strain and the now prevalent ‘G’ variant  
  • A vaccine currently in development was found to be effective against both
  • Reassuring research indicates a vaccine should be effective against all strains 
  • Means vaccines for the coronavirus pandemic will not have to be regularly changed and adapted, as is the case for seasonal flu  

Mutations to the SARS-CoV-2 coronavirus that causes Covid-19 will not affect the effectiveness of vaccines, a study shows. 

The virus has mutated at a critical location since it first emerged in Wuhan late last year, and there were concerns future changes could render vaccines useless.  

In the early days of the Covid-19 pandemic the dominant guise of the virus was a variant now called the ‘D strain’. 

However, a mutation at one specific location, called position 614, turned one amino acid from a D (aspartate) to a G (glycine), and this ‘G strain’ is now dominant. 

Viral mutations are common and can make creating vaccines difficult as it causes the virus to change shape, rendering previous vaccines useless, as is the case with seasonal flu. 

Researchers were concerned that if this was the case for SARS-CoV-2 a new vaccine would be needed for every time the coronavirus mutated. 

However, a study from the Commonwealth Scientific and Industrial Research Organisation (CSIRO) has found the change from the D to G strain will not impact on vaccine effectiveness. 

They are hopeful that any future mutations will also not impact vaccine efficacy.   

Mutations to the SARS-CoV-2 coronavirus that causes Covid-19 will not affect the effectiveness of vaccines, a study shows. The virus has mutated at a critical location since it first emerged in Wuhan late last year

SARS-CoV-2, the virus which leads to Covid-19, has a protein on its surface which binds to a receptor on cells called ACE2 and this is how it invades the body 

The G strain of the virus initially accounted for barely any SARS-CoV-2 positive cases, and now makes up around 85 per cent of all cases worldwide.

It emerged due to a mutation called D614G, which occurred at position 614 and is located on the S-protein viral spike which sticks out from the coronavirus and latches onto the human receptor ACE2.

This human receptor protrudes from surface of some cells and acts as a gateway for the coronavirus, triggering an infection. 

One recent study from the US found 99 per cent of cases in one hospital were of the G strain.   

As the mutation is on this critical part of the virus, scientists feared it would mean the virus may rapidly change shape.

If this was to occur, it could mean a new vaccine would be needed every time a new mutation emerged, similar to seasonal flu. 

Professor Seshadri Vasan leads the Dangerous Pathogens Team at CSIRO and is senior author of the latest paper. 

His team used blood samples from ferrets to see how the mutation would impact vaccines. 

The animals were infected with either the D or the G strain and given a vaccine currently in development.

How one amino acid led to a major mutation  

A study by the Royal Society’s SET-C (Science in Emergencies Tasking – COVID-19) task force studied the one major mutation SARS-CoV-2 underwent. 

It is located on the S-protein which sticks out from the surface of the virus. 

This spike latches on to the ACE2 receptor of human cells, tricks it into opening the cell, and allows the pathogen to infect a person. 

At one specific location — residue 614 on the S1 terminus — the original form of the coronavirus had the amino acid aspartate, labelled with a D.

However, a random mutation saw this amino acid replaced with a glycine, labelled with a G. 

The so-called D614G mutation was seen in barely any samples taken in February. 

However, by March, more than a quarter (26 per cent) of isolated SARS-CoV-2 strains contained the mutation. 

By May this figure had reached 70 per cent. 

An estimate for October claims 85 per cent of global cases are now due to the D614G mutation, making it by far the most dominant one seen globally. 

This mutation appears to help more virus infect a person and for more efficient infection of cells. 

The D614G virus is also almost always accompanied with three other minor mutations. The role of these changes remains unknown. 

Data from the peer-reviewed study, published in the journal npj Vaccines shows the vaccine worked just as well on either strain. 

Professor Vasan said: ‘This is good news for the hundreds of vaccines in development around the world, with the majority targeting the spike protein as this binds to the ACE2 receptors in our lungs and airways, which are the entry point to infect cells.

‘Despite this D614G mutation to the spike protein, we confirmed through experiments and modelling that vaccine candidates are still effective.

‘We’ve also found the G-strain is unlikely to require frequent “vaccine matching” where new vaccines need to be developed seasonally to combat the virus strains in circulation, as is the case with influenza.’

CSIRO Chief Executive Dr Larry Marshall said the research was critically important in the race to develop a vaccine.

Dr Marshall said: ‘This brings the world one step closer to a safe and effective vaccine to protect people and save lives.

‘Research like this, at speed, is only possible through collaboration with partners in Australia and globally. 

‘We are tackling these challenges head on and delivering solutions through world-leading science.’

It has been claimed the G strain is more infectious, but less lethal than the original D strain, but this is hotly contested. 

Previous research by scientists at The Scripps Research Institute in Florida offers a potential explanation for the virus’s altering traits. 

It found the mutated version, D614G, has four to five times more ‘spikes’ that protrude from the viral surface, allowing it to latch onto human cells. 

The original coronavirus that first jumped into humans, known as the D strain, had a spike which often snapped off when trying to fuse with the receptor. 

The mutated G strain, they say, is more robust and less likely to snap, making it better at infecting cells. 

In the early days of the Covid-19 pandemic the dominant guise of the virus was a variant now called the ‘D strain’. However, a mutation at one specific location, called position 614, turned one amino acid from a D (aspartate) to a G (glycine), and this ‘G strain’ is now dominant. Pictured, a biomolecular model of the viral spike and the 614 residue 

But although the mutation makes the virus better at infecting cells, it does not appear to make it any more potent or deadly. 

This, researchers suggest, could be because the spike had nothing to do with the virus’s ability to reproduce – to replicate – once it was inside the body. 

The process of reproduction, and using the body’s resources to achieve this, is how the coronavirus causes illness and happens when the pathogen is already inside a cell and is an independent process to initial infection.  

Researchers in the UK and US noted in May that the mutated version of the virus had become ‘the dominant pandemic form in many countries’, including the then- hotspots of Italy, the US and the UK. 

They said it was first found in Germany in February and had since become the most common form of the virus in patients worldwide – it appears to force out the older version whenever they clash.

Viruses mutate naturally all the time and it is not usually cause for alarm, but should be studied in case they change so much they become unrecognisable to the body and immunity from a first infection cannot protect against them, as is the case with flu.

A study by scientists at the University of Sheffield and Los Alamos National Laboratory, New Mexico, found that the original virus made up the vast majority of all Covid-19 infections in China, and Asia as a whole, and also seemed to be the first version of the virus to appear in the countries they studied.

However, the mutated version started to appear soon after in Europe and North America in particular, before going on to take over as the dominant virus.

Scientists have been focusing much of their research on understanding the interaction between the glycoprotein viral spike and the ACE2 receptor. 

It is hoped that a deep understanding of this will allow either therapeutics or a vaccine to be created, which can help cure or prevent COVID-19. 

For example, specific points on the spike are the landing sites for the ACE2 receptor, and spotting these allows researchers to try and inhibit them, so the virus can not latch on to human cells. 

Investigations into other coronaviruses found that these sites, known as receptor binding domains, are completely different to the virus’s closest cousins. 

In dozens of other coronavirus circulating in bats, none had the same sites and would therefore be very unlikely to bind to ACE2, rendering them harmless to humans.

In fact, high-resolution images reveal the spike on the surface of SARS-CoV-2 is 97 per cent identical to the spike on the coronavirus it most closely resembles, called RaTG13, which is found in bats.

However, the slight differences make SARS-CoV-2 far more stable and 1,000 times more infectious in humans.  

Genetic analysis found the SARS-CoV-2 virus is unique, and evolved around 70 years ago, but never before made the jump from bats to humans.  


ACE-2 receptors are structures found on the surface of cells in the lungs and airways which work with an enzyme 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.

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.

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.

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