The wave of Covid-19 infections engulfing the UK seems to be due largely to a new variant of the coronavirus, which transmits more readily between people. Called B117, it is a mutant form that seems to have been present in the British population at least since early September, although it only came to light towards the end of that month. Already it has been the subject of studies by epidemiologists and virologists, so we can now say some things for sure—and other things with less certainty—about this deeply alarming new adversary.
Two studies, conducted by researchers at Imperial College in London (led by Neil Ferguson) and by a collaboration between the Wellcome Sanger Institute and the European Bioinformatics Institute (EBI), both in Hinxton, Cambridgeshire, have provided some insight—reassuring in its consistency, alarming in its implications—into how B117 spreads.
B117 (also sometimes called Variant of Concern [VOC] 202012/01) may have originated as far back as the late summer. It has no fewer than 17 mutations in its genome—a surprisingly large number to occur all at once in a virus. A different, fast-spreading variant has also been identified in South Africa, and already cases of B117 have been reported in other countries beyond the UK, including the Netherlands, Italy and the US. It is not even clear that it originated in the UK; it might simply have been spotted here first, because Britain’s viral gene sequencing efforts are relatively advanced.
The Imperial team looked at the data gathered from Covid-19 tests and coronavirus sequencing in the UK since October. B117 shows up in the standard test in a distinctive way. Most testing uses a method called the polymerase chain reaction to multiply (“amplify”) any viral DNA in swabs, and then looks for three of the key viral genes. One of these encodes the “spike” protein that enables the virus to attach to human cells that it then infects. But in B117 this spike protein has mutated—its chemical makeup is slightly different—in a way that makes the tests unable to pick up the gene’s presence: they show a “spike dropout,” although the presence of the virus is still clear from the signal provided by the other two genes that the tests identify.
So an infection by the B117 variant is indicated by tests that have this dropout. (It’s possible that other mutants could induce spike dropouts too, but the researchers have also analysed data on the entire viral genome, and shown that since at least mid-November more than 97 per cent of all spike dropouts are caused by B117.) The test results show that London and southeast England have been at the centre of B117 infections, which accounted for more than 80 per cent of all infections by mid-December. In contrast, only around 15 per cent of infections in Yorkshire were due to this variant at that time. But it’s spreading fast to other regions, rising quickly, for example, in Oxford and Birmingham.
Mutations to an infectious virus are normal and inevitable. They arise from rare, random errors when a proliferating virus copies its genome in infected human cells, and may spread by chance or because they confer some slight advantage. They are nothing to be concerned about unless they increase the virus’ spreading rate, its virulence in causing disease—or a decrease in its susceptibility to vaccines.
Which of these apply with the B117 variant? There is no evidence that you’re more likely to get sick or to die if you catch it, and many experts believe that the vaccine should work just as well as it does against other forms of coronavirus. That’s a big relief.
But the new mutant’s faster spreading rate is a massive problem. Current estimates from both the Imperial and EBI-Sanger teams show that the transmissibility of B117 might be around 50 per cent greater than the previous forms of the virus, which means a big rise in the R value—the reproduction number which describes the average number of people an infected person will themselves infect. For Covid-19 to stop spreading, R must be below 1. But B117 has the potential to raise an R of 0.9 (roughly the value last August) to around 1.6.
The consequences are huge. Epidemiologist Adam Kucharski of the London School of Hygiene and Tropical Medicine (LSHTM) says that a 50 per cent increase in infectiousness is worse than a 50 per cent increase in virulence, in terms of the number of fatalities it can cause: simply, in a given time interval, more people will get ill and more will die.
It is this faster spreading that explains why B117 is coming to dominate new infections: it out-competes other forms of the virus in a Darwinian manner. This advantage was disturbingly evident during the four-week UK “lockdown” from 5th November (which was more of a quasi-lockdown, since schools, colleges and other establishments stayed open). Older variants of the virus declined during the lockdown—but B117 went right on spreading, increasing its “market share” of infections. The Imperial team estimates that while the lockdown reduced R for other forms of the virus to 0.92 on average, for B117 it stayed at around 1.45. “If we look across all English regions, in the overwhelming majority B117 expands during lockdown while other lineages contract,” says Jeffrey Barrett of the Sanger Institute.
Importantly, this does not mean that lockdowns somehow encourage or even create faster-spreading variants, as some lockdown sceptics have suggested. Without any lockdown at all, the virus variants would all have spread faster, albeit with B117 gaining the advantage anyway. “If there had been no lockdown there would have been much stronger growth of both [old and new] variants,” says Moritz Gerstung, who led the EBI team. Tight social restrictions are not comparable to the way antibiotics allow “superbug” pathogenic bacteria to emerge, he stresses.
B117 seems to be more prevalent than the older variants in children and young people aged 0-19 years. The reasons aren't yet clear. It’s possible that the variant is better at infecting young people than previous strains, but also possible that this increase reflects the fact that schools remained open during the lockdown, so more spreading went on there than elsewhere. At any rate, despite higher infection levels, reports that B117 might be causing more hospitalised casualties among children do not seem to be borne out. Russell Viner, of the Royal College of Paediatrics and Child Health in London, has said that “The overwhelming majority of children and young people have no symptoms or very mild illness only... as yet, we are not seeing any greater severity amongst children and young people.”
But children can act as conduits for B117 to be passed on to adults, who are at far greater risk of illness and death. Given this, it was unconscionable that the UK government was even thinking, before its U-turn on 1st January, of opening any schools in London. And given the rate at which B117 is spreading elsewhere, it was deeply irresponsible to open schools anywhere else in the country today (other than for children of key workers or those who are at serious social or educational risk if kept at home). Scotland has announced full closures, and it now appearsEngland and Wales are likely to follow suit within hours.
The government’s delay in implementing a new, tougher national lockdown, which many scientists have called for, is also hard to comprehend. Certainly, “lockdowns” of the kind practised in November won’t be enough to deal with B117. “Our interventions (masks, social distancing, etc) work less well, and gaps (non-compliance, open schools, etc) are riskier,” says Barrett, while the Imperial team writes that “Social distancing measures will need to be more stringent than they would have otherwise.”
A study of B117 spreading by Nicholas Davies and colleagues at the LSHTM, released on 23rd December—which also finds the new virus variant to be around 50 per cent more transmissible—said: “Our estimates suggest that control measures of a similar stringency to the national lockdown implemented in England in November 2020 are unlikely to reduce the effective reproduction number to less than 1, unless primary schools, secondary schools, and universities are also closed.”
Among the urgent questions now to be addressed are what allows the virus to spread faster. Is it better at getting into human cells? (This seems likely—the mutations of the spike protein allow it to bind more avidly to its docking protein on the human cell.) Does it replicate better and create a higher viral load? Or might it, as some studies have suggested, create more virus specifically in the throat and nose, so that it is more easily passed on?
The new variant also raises the urgency of vaccination programmes. While the new studies don’t say anything about whether specific vaccines will be more or less efficient, Gerstung says that the estimated 50 per cent or so higher spreading rate means that more people need to be protected, and more quickly. He says the higher R value raises the threshold proportion of people that need to be immunised to achieve herd immunity, from about 60-70 per cent to around 80 per cent. So combating anti-vaccination sentiment just got more urgent too.
That touches on a more general, vital aspect of managing this dreadful situation: it needs to be done by frank and open communication with the public. No one could have foreseen the appearance of this fast-spreading variant of the virus (even if such things come as no surprise to virologists). The public would surely have forgiven a government that recognised the need, before schools returned, to take tougher measures, however exhausted and straitened we all are by them. Whether it will forgive a government that takes them so belatedly and chaotically remains to be seen.