Matt Hancock was today accused of scaring the public with his dramatic announcement that a mutated strain of coronavirus was spreading through London and the South East.
The Health Secretary yesterday wheeled out the bombshell claim as he laid plans to put 11million more people across the capital, Essex and Hertfordshire into Tier Three from midnight tonight, warning that the mutated strain could be spreading faster than older versions of the virus.
But experts hit back at his claim, saying he used ‘overblown rhetoric’ to frighten people and revealing that the development was ordinary, with this strain unlikely to affect how vaccines work or make people any more ill – and it might even be less deadly.
The coronavirus has already mutated thousands of times in what is a completely natural process, experts say, and many bugs become less dangerous as they evolve.
Scientists said it is definitely important to investigate new strains to see if they change the virus’s behaviour and to keep track of global outbreaks, but called Mr Hancock’s timing into question.
There is some concern that the mutated strain could be a shape that is not well recognised by the immune system and that vaccines might not be as effective. The UK’s Covid-19 Genomics UK Consortium said it was investigating this and also looking into ‘whether or not any of these mutations are contributing to increased transmission’.
Logs of where the mutation has been found show the first record of the strain VUI – 202012/01 is from the Milton Keynes Lighthouse Lab on September 20.
Since then, the mutated version of the virus has been recorded more than 1,000 times, mostly in England but also in Wales, Scotland, Denmark and Australia, Public Health England confirmed.
The reason the mutation is interesting, scientists say, is because it’s on the virus’s spike protein. The spike is used to attach to the body to cause illness, and is the part most often attacked by the immune system, so it could potentially affect either of those processes.
British Health Secretary Matt Hancock yesterday announced the new strain of the virus to the public and said it could be causing Covid-19 to spread faster
The mutation of the coronavirus has caused a change to the spike protein on its outside (shown in red), which is what the bug uses to attach to the human body (Original illustration of the virus by the US Centers for Disease Control and Prevention)
England’s chief medical officer, Professor Chris Whitty said last 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.’
WHAT DO WE KNOW ABOUT THE NEW STRAIN OF CORONAVIRUS?
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 mutations 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 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 Nextstrain.org project, which logs lab reports of the strain, has found samples from records in Wales, Scotland and Denmark.
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.
Scientists reacting to the Department of Health’s announcement about the mysterious new version of the virus – which Mr Hancock didn’t even name – 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.
Professor Hugh Pennington, a bacteriologist from Aberdeen University, wrote in today’s Daily Mail: ‘Some viruses mutate more than others. The Covid virus is one which has fewer mutations but they still happen.
‘If I were to be unkind to our Health Secretary, I would accuse him of having launched a new “Project Fear” yesterday to justify a further tightening of restrictions – and to buttress the new “lockdown” of London as it is placed under Tier Three restrictions.’
Professor Jonathan Ball, a virologist at the University of Nottingham, said on Times Radio: ‘I think many of us were surprised that yesterday was the day of all days to pick on flagging this particular variant of virus, and potentially linking it to the fact that it might have this advantageous spread – because at the moment the biological evidence, the data isn’t there.
‘We suspect some of the changes might impact on behaviour but we’ve not done the necessary laboratory tests so we shouldn’t really be saying that.’
Asked whether he thought the announcement was politically motivated, Professor Ball added: ‘It’s not for me to draw any great conclusions but I think people can see that it was made on the same day that it was announced London and parts of the South East were going to be put into Tier Three.’
Dr Simon Clarke, a professor of cellular microbiology at the University of Reading
The first official case of the strain is recorded in Public Health England’s biggest processing lab in Milton Keynes and the person who provided the swab is thought to be from Kent, PHE said yesterday.
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.
In a report on the new strain, published last night by the UK’s Covid-19 Genomics UK Consortium (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.
Professor Adam Finn, a paediatrician at the University of Bristol and a member of the Government’s Joint Committee on Vaccination and Immunisation, said on BBC Radio 4 this morning: ‘What we tend to see is that viruses do mutate towards being more infectious because that creates an advantage for them, but I think it’s very important that people recognise that pathogens tend to evolve away from being virulent [disease-causing].
‘So there’s not really an expectation that this virus will become more likely to kill you or make you seriously sick over time.
‘In fact, it tends to be an advantage for pathogens to be more benign because their hosts survive for longer and are infectious for longer, and that helps them spread about.’
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
A timeline of the samples, published on Nextstrain.org, shows that the mutation first appeared in late September but did not become widespread until November when England’s second wave really took off (Pictured: The furthest left green dot marks the first recorded instance of the strain, which came from the UK’s Milton Keynes Lighthouse Lab)
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.
But Professor Finn added: ‘All the vaccines that we have coming through at the moment are based on the spike protein.
‘They induce immunity that is directed at many different parts of that protein and any one mutation would tend to change the shape and conformation of just one part, so it would be extremely bad luck if a mutation led to a complete collapse in the protective value of any particular vaccine.’
HOW DID THE MUTATED STRAIN OF CORONAVIRUS EMERGE?
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.