A new variant of the coronavirus has crossed the United Kingdom and has been detected in the United States, Canada and elsewhere. Scientists are concerned that these new species may spread more easily.
As an evolutionary biologist, I study how mutation and selection combine to shape changes in populations over time. Never before have we had so much real-time data on evolution as with SARS-CoV-2: more than 380,000 genomes were sequenced last year.
SARS-CoV-2 is mutating as it spreads, creating small differences in the genome. These mutations allow scientists to trace who is related to whom in the virus family tree.
Evolutionary biologists, myself included, have warned against over-interpretations of the threat of mutations. Most mutations won’t help the virus, just as randomly kicking a working machine probably won’t improve it.
But occasionally a mutation or series of mutations gives the virus an advantage. The data is conclusive that the mutations carried by the variant that first appeared in the UK, known as B.1.1.7, make the virus more “fit”.
Higher fitness or chance?
When a new variant becomes common, scientists determine the reason behind its spread. A virus carrying a particular mutation can accidentally increase in frequency if it:
- worn by a superspreader;
- moved to a new uninfected location;
- introduced to a new segment of the population.
The last two examples are called “founder events”: a rapid increase in frequency can occur if a particular variant is introduced in a new group and a local epidemic starts. Coincidental events may explain the increase in frequency of different SARS-CoV-2 variants.
But B.1.1.7 is an exception. It shows a very strong selection signal.
In the past two months, B.1.1.7 has increased in frequency in almost every week and health region in England at a faster rate than non-B.1.1.7. These data, reported on December 21, 2020, helped convince British Prime Minister Boris Johnson to lock up much of the country and led to widespread travel bans from the UK.
The emergence of B.1.1.7 cannot be explained by a founder event in new regions as COVID-19 was already circulating in the UK.
Founder events in a new segment of the population (eg After a conference) are also unlikely given the widespread restrictions on large gatherings at the time.
Our ability to track the evolution of SARS-CoV-2 is due to the enormous effort of scientists to share and analyze data in real time.
But the incredibly detailed knowledge we have about B.1.1.7 is also due to stupid luck.
One of the mutations altered part of the genome used to test for COVID-19 in the UK, allowing the picture of the evolutionary distribution to be drawn from more than 275,000 cases.
Evolution in action
Epidemiologists have concluded that B.1.1.7 is more transmissible, but there is no evidence that it is more deadly.
Some researchers estimate that B.1.1.7 increases the number of new cases caused by an infected person (called the reproductive number or Rt) by 40 to 80 percent; another preliminary study found that the Rt increased by 50-74 percent.
An advantage of 40-80 percent means that B.1.1.7 is not only a little fitter, but also a lot fitter.
Even if the selection is so strong, the evolution is not immediate. Our mathematical models, as well as those of others in Canada and the US, show that it takes a few months for B.1.1.7 to reach its rapid emergence, as only a small fraction of cases initially carry the new variant.
For many countries, like the US and Canada, where the number of COVID-19 cases has risen dangerously, a variant that increases transmission by 40-80 percent threatens to push us over the top.
It can lead to an exponential growth in the number of cases and overwhelm already worn-out medical care. Evolutionary change takes time, so we may need a few weeks to prepare.
More variants
A surprise to researchers was that B.1.1.7 contains a striking number of new mutations.
B.1.1.7 has added 30-35 changes in the past year. B.1.1.7 is not mutating at a faster rate, but appears to have undergone rapid change in the recent past.
The virus could have been passed on from an immunocompromised person. People with weaker immune systems are constantly fighting the virus, with long-lasting infections, recurring rounds of viral replication and only a partial immune response to which the virus is constantly evolving.
(NextStrain / CC BY 4.0)
Above: each dot represents a SARS-CoV-2 genome, with branches connecting related viruses to their ancestors. The center represents the virus that has been introduced to humans. The viruses furthest from the center carry more mutations. The three new variants are marked with gold.
Preliminary research reports that have yet to be verified have described two other worrying variants: one originally from South Africa (B.1.351) and one from Brazil (P1).
Both variants show a recent history of excessive mutations and rapid increases in frequency within local populations. Scientists are currently collecting the data needed to confirm that selection is responsible for higher transmission, not chance.
What has changed to enable dissemination?
Selection plays two roles in the evolution of these variants.
First consider the role within those individuals in which the great number of mutants arose. The 23 mutations of B.1.1.7 and the 21 mutations of P1 are not randomly arranged across the genome, but clustered in the gene encoding the spike protein.
One change in the peak, called N501Y, occurred independently in all three variants, as well as in immunocompromised patients studied in the US and UK. Other changes in the peak (eg, E484K, del69-70) are seen in two of the three variants.
In addition to the peak, the three variants of concern share another mutation that removes a small portion of the boringly named “nonstructural protein 6” (NSP6).
We don’t know yet what the removal does, but in a related coronavirus, NSP6 cheats a cellular defense system and can promote coronavirus infection.
NSP6 also hijacks this system to help copy the viral genome. Either way, the deletion could alter the virus’s ability to hold onto and replicate in our cells.
Easier shipping
The parallel evolution of the same mutations in different countries and in different immunocompromised patients suggests that they provide a selective advantage in bypassing the immune systems of the individuals in which the mutations occurred. For N501Y this is supported by experiments in mice.
But what explains the higher transmission speed from individual to individual? This is a challenge to answer because the many mutations that have arisen simultaneously are now bundled into these variants, and it may be one of the variants or a combination thereof that leads to the transmission advantage.
That said, several of these variants on their own have emerged before and have not led to rapid spread.
One study showed that N501Y on its own had only a weak transmission advantage and increased rapidly only in conjunction with the set of mutations seen in B.1.1.7.
While the evolutionary story of COVID is still being written, an important message is now emerging. The transmission advantage of 40-80 percent of B.1.1.7, and possibly the other variants B.1.351 and P1, will overwhelm many countries in the coming months.
We are in a race against viral evolution. We need to roll out vaccines as quickly as possible, stop the flow of variants by limiting interactions and travel, and prevent their spread by increasing surveillance and contact tracking. 
Sarah Otto, Killam University Professor of Evolutionary Biology, University of British Columbia
This article has been republished from The Conversation under a Creative Commons license. Read the original article.