What we know about the new coronavirus strain
Scientists are racing to discover how infectious the variant is and if vaccines can beat it
Scientists are scrambling to understand the new coronavirus variant that has devastated the Christmas plans of millions of people in Britain and left the UK largely isolated from the rest of the world as a result of travel bans imposed by other countries. Labelled B.1.1.7, we look at what we know and do not know about the new strain.
Where did the new variant come from?
It was first detected in mid-October when the Covid-19 Genomics UK Consortium (Cog-UK) read the full genetic code of coronavirus in two samples that had been collected in Kent and London on September 20 and 21. But scientists did not became alarmed about B.1.1.7 until mid December when they associated it with rapidly rising case numbers in south-east England.
B.1.1.7 has far more mutations than in any previous variant of the Sars-Cov-2 virus analysed since the pandemic started. Twenty-three letters of the viral genetic code have changed, of which 17 could alter the behaviour of the virus. They include several mutations on the key “spike protein” that it uses to enter human cells.
Virologists suspect that the multiple mutations occurred in a patient with a severely suppressed immune system who incubated Sars-Cov-2 for many weeks and then infected someone else. These conditions are likely to supercharge the mutation process.
Efforts to trace the original “index patient” have failed. “We don’t know whether the new variant originated in the UK or was introduced from elsewhere,” said Sharon Peacock, Cog-UK director.
How infectious is it and how far has it spread?
B.1.1.7 has multiplied rapidly in London and south-east England, supplanting older variants. It was responsible for 28 per cent of infections in London by early November and 63 per cent since November 29. It is also present at much lower levels in Scotland, Wales and the rest of England.
Computer modelling of the viral spread suggests the new variant could be 50 to 70 per cent more transmissible than other Sars-Cov-2 strains circulating in the UK. The modelling shows it may raise the R value of the virus — the average number of people to whom someone with Covid-19 passes the infection — by at least 0.4, making the pandemic far harder to control without stringent lockdown measures. Some specific mutations on B.1.1.7 also look as though they might make it easier to infect people.
However, no laboratory studies of the transmissibility of the new virus have been completed and some independent experts were cautious about the meaning of the UK government’s modelling. The variant’s rapid spread could be a coincidence, they said, because people who happened to be carrying the variant had behaved in ways that were more likely to transmit the virus, such as ignoring social-distancing measures.
Outside the UK, the new Covid-19 variant has been identified in Denmark, Australia, Italy, the Netherlands and Iceland. Scientists suspect that it has spread much farther afield than this smattering of cases would indicate. The UK is one of the few countries doing the intensive genomic sequencing required to identify variants; Cog-UK has produced half of all the world’s publicly released Sars-Cov-2 sequences.
“There are very few countries that look — and if you don’t look for it, you won’t find it,” said Mads Albertsen, an expert in microbial genetics at Aalborg University in Denmark. “I cannot imagine that it hasn’t spread worldwide by now . . . It’s been in the UK for so long it must be in all countries around the world.”
Will the variant affect the immune system enough to stop Covid-19 vaccines working?
The vaccines completing trials and beginning mass inoculation programmes — from Pfizer/BioNTech, Moderna and Oxford/AstraZeneca — achieve protection by training the recipient’s immune system to recognise many different sites on the viral spike protein. Experts do not expect the mutations on B.1.1.7 to interfere with that.
“The prediction is that the new variant is unlikely to have more than a minor impact on vaccine effectiveness,” said Professor Adam Finn, a vaccine specialist at the University of Bristol. Scientists at the UK government’s Porton Down microbiology labs and colleagues at the vaccine companies are racing to confirm the veracity of that reassuring prediction.
Ugur Sahin, BioNTech chief executive, said it was “highly likely” that the company’s vaccine would work effectively against B.1.1.7, though it would take two weeks to complete the laboratory work needed to reach a definitive assessment.
One lab test involves infecting human cell cultures with coronavirus and then exposing them to antibodies from people who have been vaccinated. The scientists then look for any differences between the ability of the antibodies to neutralise different variants of the virus.
In the longer term, researchers will examine the health records of people who have been vaccinated to find out whether they are more susceptible to some variants than others.
Does the variant affect how ill people become if they are infected?
Scientists are analysing the viral genetics of Covid-19 patients to discover whether B.1.1.7 might affect their symptoms. “We have had no signal,” said Judith Breuer, professor of virology at University College London. “If it was much more virulent we would see signals emerging.”
There is provisional clinical evidence that B.1.1.7 is increasing the “viral load” — the amount of virus present in patients’ upper respiratory tract — which is also a feature of another variant called 501.V2 that has evolved independently in South Africa. This may make the new variants transmit more readily between people but it is not clear how the greater viral load would affect symptoms in those who are infected.
Might the new variant spread more easily in children?
Adults are more susceptible than children to Covid-19 partly because the so-called ACE receptor — the gateway into human cells for the virus — changes shape as people grow up. Some scientists have suggested that mutations in B.1.1.7 enable the virus to enter the juvenile form of these receptors more easily.
As Wendy Barclay, professor of virology at Imperial College London, put it, the genetic changes might give the virus a “more level playing field” for infecting children.
But experts emphasised that this theory was unproven and urged caution. “We are not aware of any increased incidence of the new variant in children,” said Prof Peacock.
