Why you shouldn’t panic about the UK’s mutant coronavirus strainDecember 21, 2020
A new coronavirus strain detected in the United Kingdom and spreading through southern England is being touted as “highly contagious,” sending the country into a strict lockdown over the Christmas break. The variant, first identified in September, is being closely monitored by scientists and researchers, in an effort to understand if it’s more infectious or transmissible than previous variants.
Cases of the variant, dubbed VUI 202012/01 (for “variant under investigation”), have grown rapidly in the last month, leading to increased scrutiny by UK authorities. It has also been reported in the Netherlands, Denmark, Belgium and Australia. A preliminary study of the new strain shows it has an unusually high 17 mutations in its genetic code, some of which may change key characteristics.
However, it’s unclear if this mutant variant of the coronavirus is more transmissible based on these genetic variations alone. “We can’t tell from the sequence that [the] set of mutations will convey some better transmissibility upon it,” says Ian Mackay, a virologist at the University of Queensland, Australia.
On Saturday, Boris Johnson, UK Prime Minister said “when the virus changes its method of attack, we must change our method of defense” but this, perhaps, oversells the capabilities of the new strain, which we still know very little about. One of the core models of epidemiology is the “triad” which posits diseases spread because of the infectious agent, the host and the environment. “When you get rapid escalation [of cases], all three things are contributing to it,” says Catherine Bennett, chair in epidemiology at Deakin University, Australia.
It may well be that the variant’s genetic mutations have improved its ability to move from person to person or it could be a combination of increased movement and bad luck. Scientists will spend the next few weeks trying to unravel that mystery. The investigations start with the spike protein.
Viruses are always changing. They mutate. These small changes to their genes sometimes provide a survival advantage, or increase the virus’s “fitness.” The coronavirus, SARS-CoV-2, is no different. This is no cause for concern and is not unexpected — thousands of mutations have occurred since SARS-CoV-2’s genome was sequenced in January.
“It mutates constantly as it passes through people,” says Mackay.
Think about the virus’ genetic code as a copy of Harry Potter and the Sorcerer’s Stone and your cells as photocopiers. The virus wants to make millions of copies of Harry Potter. Every time it hijacks a cell, it makes copy-after-copy of Harry Potter. But this process is error-prone. Sometimes entire pages are missing. Other times pages are duplicated or whole new pages are added. Most of the time this doesn’t really change the story. On occasion, it changes it completely.
Since the beginning of the pandemic, scientists have focused on one particular aspect of the SARS-CoV-2 story: the club-shaped spikes affixed to the virus’s shell. It’s the spike that allows the virus to hijack human cells. If we stick with the Harry Potter analogy here, then the genetic code for the spike is like a whole chapter.
In VUI 202012/01, that chapter reads differently.
The new variant has eight mutations in the spike gene, including one known as N501Y, which alters how effectively SARS-CoV-2 sticks to human cells. In mice, this particular mutation was shown to make the virus more infectious and, in South Africa, this mutation in combination with a variety of others, is associated with increasing case numbers. Another mutation, 69-70del, has previously been seen in other coronavirus variants and was associated with an outbreak related to mink in Denmark.
X amount of luck
In his speech Saturday, Boris Johnson suggested the variant “may be up to 70% more transmissible than the old variant” based on early analysis by the UK’s New and Emerging Respiratory Virus Threats (NERVTAG) advisory group. The data behind this figure has not yet been published and relies on computer modeling.
But other scientists suggest the increasing incidence in the UK may just be down to a confluence of circumstances — luck or chance — rather than changes in the viral genome.
“Any apparent increase in transmission now could equally be due to human behaviour during the Christmas period and the increase in movement and social contact associated with it,” says Raina MacIntyre, professor of global biosecurity at the University of New South Wales’ Kirby Institute.
In November, talk of a “particularly sneaky strain” in Adelaide, South Australia, sent the state into lockdown. A cluster of cases appeared to show the virus was spreading more quickly, but later evidence suggested it was not any more infectious or transmissible.
“This could be just another Adelaide event,” says Stuart Turville, an immunovirologist at the Kirby Institute. But, he says, answers will only come when scientists have had a chance to test the new variant in the lab, comparing it to previous variants and seeing how it fares. “Until you get to that point, you can’t really say that the virus is fitter.”
The origin of this variant is still unknown, though NERVTAG propose it may have arisen in a single patient with a compromised immune system over a period of months. Inside the patient, the virus and the immune system are in a constant arms race, trying to outgun each other and get the upper hand. In this environment, there’s more pressure to mutate. The persistent battle means “there’s a higher probability” mutations accumulate in the patient, Turville says.
The number of changes in VUI 202012/01 will challenge researchers to explain if any single mutation or a combination of them contributes to how this variant spreads or how severe it is. “Because there’s so many different changes, it’s gonna be a hard one to really work out,” Turville says.
Researchers will assess these changes with a series of experiments Turville notes could take up to a few weeks. To test if the variant is more transmissible, they compare it to older strains in human cells in the lab or in animal models and see which dominates.
Transmissibility is just the tip of the viral iceberg, however.
“The kinds of mutations that scientists are a bit more worried about are the types that get around vaccines, antibodies, therapeutics — rather than increasing transmissibility,” says Alina Chan, a scientist at the Broad Institute of MIT and Harvard.
That evaluation requires a different type of test. Scientists hit the variant with antibodies created by those infected with older versions of the coronavirus. If the antibodies inhibit the variant from growing, great — but if the variant’s mutations help it evade the antibodies, we may be dealing with an offshoot that could skirt some of our defences.
While scientists and researchers pull apart VUI 202012/01 and determine how its genetic mutations may have altered it, the messaging remains the same. “There’s really nothing to do about it differently, in terms of public health,” says Chan. Social distancing and mask-wearing remain critical for slowing the spread of COVID-19. These measures are the gold standard and will continue to work against the new variant.
It’s too early to tell how the new variant might change our public health messaging or whether it will cause concern for the vaccines now being rolled out across the world. Experts say increased monitoring will be important, but our vaccines won’t be rendered useless overnight.
“We’re a long way from a mutation here or a variant there, really causing us a lot of fear that our vaccine is going to fall over,” says Mackay.