New Covid strain has 17 mutations, scientist say

The new strain of coronavirus spreading through Britain has a ‘striking’ amount of mutations, scientists have claimed.

Members of the UK’s Covid-19 Genomics UK Consortium (COG-UK), who have been investigating the evolved strain, say they have uncovered 17 alterations, which they described as ‘a lot’.

Many of the changes have occurred on the virus’s spike protein, which it uses to latch onto human cells and cause illness.

Alterations to the spike are significant because most Covid vaccines in the works, including Pfizer/BioNTech’s approved jab, work by targeting this protein.

It is feared these changes could also stop people from becoming immune if they have been infected with a different strain previously.  

But scientists, including England’s chief medical officer Chris Whitty, have said there is ‘currently no evidence’ the mutation — which has been spotted in Wales, Scotland, Denmark and Australia — will have any impact on vaccines.  

Professor Nick Loman, from the Institute of Microbiology and Infection at the University of Birmingham and COG-UK member, said: ‘There is actually 17 changes that would affect the protein structure in some way that distinguish this variant from its kind of common ancestor of other variants that are circulating, which is a lot.

‘It’s striking. There’s a really long branch going back to the common ancestor, and it’s a matter of great interest as to why that is the case.”

The mutations of the coronavirus has caused changes to the spike protein on its outside (shown in red), which is what the virus uses to attach to the human body (Original illustration of the virus by the US Centers for Disease Control and Prevention)

Mapping of coronavirus samples confirmed to have the mutations of the VUI ¿ 202012/01 shows that almost all of them have been in England (large green circle denotes the proportional number of samples in England, not the geographic area covered), but it has also been found in Scotland, Wales and Denmark

Mapping of coronavirus samples confirmed to have the mutations of the VUI – 202012/01 shows that almost all of them have been in England (large green circle denotes the proportional number of samples in England, not the geographic area covered), but it has also been found in Scotland, Wales and Denmark

Surveillance of the strain shows it is increasing faster than all other strains except the dominant one, and has been making up an increasing share of the total infections (The new strain is shown in pink, and the timeline runs from May to December)

Surveillance of the strain shows it is increasing faster than all other strains except the dominant one, and has been making up an increasing share of the total infections (The new strain is shown in pink, and the timeline runs from May to December)

Most Covid vaccines work by training the immune system to recognise the virus’s spike proteins and attack them when the virus tries to infect in future.

But if the shape of the spike proteins are altered through mutations, the virus may be able to slip by the body’s natural defences.

The new strain, called ‘VUI – 202012/01’, was first picked up in September in Kent and appears to be linked to an explosion of infections in London and the South East.

There have been more than 1,000 confirmed cases of the new strain, mostly in southern England. But exact locations have not been revealed.

COG-UK said it was spreading spreading faster than the dominant strain, which was imported by holidaymakers from Spain in the summer and now accounts for the majority of infections. 


What is the strain?

The strain, named VUI – 202012/01 by Public Health England, is a version of the SARS-CoV-2 coronavirus that is slightly different to older versions of the virus.

It has a series of 17 mutations, some of them on its spike protein, that change its shape slightly.

The spike protein is a part on the outside that the virus uses to attach to the body to cause infection. It is also the main target of the immune system. 

Specifically, the three main mutations are the changing of one amino acid to another and the deletion of two other amino acids. The amino acids are the building blocks of the virus.

The change is called N501Y, and the deleted parts are named His69 and Val70.

When was the strain discovered? 

Matt Hancock said yesterday that Public Health England identified the mutations as a separate, significant strain of the virus last week.

Lab sequences show that the earliest trace of the strain dates back to September 20, to a lab in Milton Keynes that is used to analyse people’s swab tests.

Not all mutations are logged as new strains as soon as they are found, because some don’t appear many times more, and others turn out to be totally insignificant. 

The UK’s Covid-19 Genomics UK Consortium (COG-UK) said: ‘It is difficult to predict whether any given mutation is important when it first emerges, against a backdrop of the continuous emergence of new mutations.’  

How common is this strain of the virus?

This is unclear. 

Not every swab test done in the UK has the genes analysed – COG-UK records the genetic sequence of around 10 per cent of swab tests done through the Department of Health.

It has so far identified VUI – 202012/01 in more than 1,000 people, according to Matt Hancock.

The samples have become significantly more common in October and November, but this may simply be a consequence of more people getting infected. 

There have been reports of the strain in at least 60 local authority areas in England, the Health Secretary said, but most evidence has come from London and the South East.

Where else has the strain been found?

The project, which logs lab reports of the strain, has found samples from records in Wales, Scotland and Denmark. 

Public Health England confirmed it was also in Australia. 

The vast majority are in England.

The virus strain is likely to be present in other countries but may not have been picked up by surveillance studies. 

Do the mutations make the virus more infectious or deadly, or make a vaccine less likely to work?

There is currently no reason to think the mutation changes the function of the virus in any way, nor the immune system’s ability to prevent Covid-19. 

Matt Hancock said experts think it may make the virus spread faster, but there is not yet evidence to support this.

COG-UK said: ‘The vast majority of the mutations observed in SARS-CoV-2 have no apparent effect on the virus and only a very small minority are likely to be important and change the virus in any appreciable way.’

The coronavirus has mutated thousands of times since it was first discovered in December but none appear to have changed how it behaves in a fundamental way.

Researchers suspect the mutations may mean the disease is more infectious, but they said even if it is spreading more rapidly, it may not make the virus more deadly. Some viruses evolve to become less deadly, in order to survive for longer.

Health Secretary Matt Hancock announced the strain’s existence on Monday, revealing there was no hard evidence that this version could spread any faster, but that it was increasing at a far greater rate than any other strain in the country.

Neither Public Health England or COG-UK, the organisations which discovered the strain, could confirm where the cases have been found.

Online lab records suggest the first instance of the virus came from the Government’s Lighthouse Lab in Milton Keynes on September 20, and PHE said yesterday that the person who provided the swab was from Kent.

Professor Tom Connor, a genomics and virus expert from Cardiff University and a member of COG-UK said: ‘It’s quite clear that it has spread beyond that [South East England] and it is it is spreading into other parts of the country.’

A history of the virus published online by the Neher Lab, at the University of Basel in Switzerland, shows how it has become more common over time.

After the first official records of the virus in September, progress was slow, and it wasn’t until England’s second wave took hold in late October that cases exploded.

This, scientists say, could be because the virus strain is faster spreading and made cases rise quicker – or it could be that it was simply found more often as cases surged naturally.

At the time of the first sample the UK was averaging just 3,700 positive coronavirus tests per day. By the start of November, when samples were coming in thick and fast, the average number of positive results had skyrocketed to 23,000 per day.

Professor Loman said there was ‘no evidence’ the strain had come from any other countries, adding: ‘It’s sort of come out of nowhere.

‘We have a long gap between the first cases we saw with this variant in late September [and recent surge in cases]… It’s more likely to have evolved in the UK but we don’t know that.

‘There are very few examples of this variant in other countries at the moment – it’s really a kind of UK phenomenon.’

And he said the reason that the strain had been brought to public attention now was that it was spreading so fast.

Although it still makes up a small proportion of cases it is rapidly becoming a bigger factor and this could be because it spreads more quickly than other strains. 

Up to 20 per cent of cases in Norfolk are thought to be down to the new strain — but officials haven’t confirmed the figures.

The scientists admitted it could be a coincidence but said they would expect other strains to see similar surges, which they haven’t.

The variant seems to be spreading faster than the dominant strain (20A.EU1) did when it arrived in the UK from Spain in the summer.

Professor Loman called it ‘unusual’ and added: ‘That one did sweep the country and become the dominant variant quite quickly, and remains the dominant variant in the UK. The initial modelling shows this one is growing faster than that one.’

Professor Connor said: ‘There are a large number of circulating lineages within the UK, but the key thing to think about is the observation of the increase over time.

‘The results that came initially from modelling were that this is something that seems a bit out of ordinary, in our experience.’

England’s chief medical officer, Professor Chris Whitty said on Monday night: ‘It does appear to be in an area of the country, particularly Kent and bits of London, [where cases] are increasing rapidly.

‘Now we don’t know what’s cause and effect – is it getting more frequent because it’s in a part of the country where the rate of increase is going faster anyway, and therefore inevitably there’s a higher proportion [of the strain]?

‘Or is it this virus [strain] itself is possible to transmit more easily? That isn’t immediately clear.’

In a report on the new strain, published last night by COG-UK, experts said: ‘It is difficult to predict whether any given mutation is important when it first emerges, against a backdrop of the continuous emergence of new mutations.’

They added: ‘Efforts are under way to confirm whether or not any of these mutations are contributing to increased transmission.’

Making the virus spread faster currently appears to be the only possible danger posed by this mutation.

Scientists say it’s unlikely that it will make the disease any worse or affect how well vaccines work.

One of the concerns about the mutation was that antibodies developed for one strain of the virus might not work on the mutated version.

Antibodies are substances made by the immune system which can attack and destroy the coronavirus when it is inside the body. People who have had the virus once – or a vaccine – produce and keep the antibodies to protect them in case the virus gets into their body again, so they can get rid of it before they get ill.

But they are extremely specific. Antibodies for one virus generally won’t work for another, and may not even work for other strains of the same virus. This is why people don’t get immune to the flu – because influenza viruses mutate so often.

There is a chance that antibodies to the strain without the virus mutation might not work for the new strain, although this does not yet seem to be the case.

The consequence would be that a vaccine might not work as well, or that people would have a greater risk of catching the virus a second time.

Some scientists reacting to the Department of Health’s announcement about the mysterious new version of the virus – which Mr Hancock didn’t name at the time – said it was totally normal for viruses to evolve.

They pointed out that the coronavirus has changed thousands of times this year since it was discovered, and none of the mutations appear to have changed it.


Like all viruses, the coronavirus (SARS-CoV-2) has a piece of genetic code which contains all the information the virus needs to survive and reproduce. 

It is made of RNA, which is a single stranded version of its more famous bigger brother, DNA. RNA is made of four types of molecules, known simply as A, U, C and G.

Three of these bases in a row provide the blueprint for bigger molecules known as amino acids, which are the building blocks of every organic thing on Earth. 

Once the virus has infected a person’s cells, such as a human lung cell, it reproduces by forcing the human cell to read its RNA and make more viruses.

These replicas are designed to be exactly the same, which is made possible because the RNA is the same, but sometimes the the cells can ‘misread’ the genetic code and introduce an error. This is where mutation occurs.

A glitch in the process can cause one of the A, U, C, G to be either deleted or swapped for another one, which changes how the physical form of the virus is produced. 

Other causes of mutations include interactions with other viruses infecting the same cell and changes induced by the host’s or a person’s own immune system. 

Most mutations to SARS-CoV-2 are due to the latter, researchers have said previously.  

These happen completely at random and are common. 

Researchers have found the mutation rate of SARS-CoV-2 to be unusually slow compared to other viruses, such as flu and HIV. 

Nevertheless, the SARS-CoV-2 has mutated, with several different strains emerging. 

One, D614G, emerged in February and is now the dominant strain worldwide. 

This happens on the spike protein which binds to the ACE2 receptor, allowing the virus to infect the cell. The mutation, at the 614th location on the spike, saw a ‘D’ code for aspartate to a ‘G’ for glycine.

The new mutation occured at the 501st location on the spike protein and saw a ‘N’ code for the amino acid Asparagine which changed to a ‘Y’ for Tyrosine.

Of the three bases which code for the amino acid, only one was incorrect. Instead of being AAU, it ended up being UAU. This single change altered the amino acid that was produced, affecting the structure of the spike. 

As well as this swap, two amino acids were deleted, called H69/V70, which are found on the first subunit of the spike protein in the receptor-binding domain, a key location as it is where the spike latches on to the ACE2 receptor.  

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