A new version of coronavirus has swept the United Kingdom and has been detected in the United States, Canada, and elsewhere. Scientists worry that these new strains can spread more easily.
As an evolutionary biologist, I study how mutations and selection combine to shape changes in populations over time. Never before have we had so much real-time data about evolution as we do with SARS-CoV-2: last year more than 380,000 genomes were sequenced.
SARS-CoV-2 continues to spread, making minor differences in its genome. These mutations allow scientists to find out whom the virus belongs to the family tree.
Evolutionary biologists, including myself, have cautioned against over-explaining the danger posed by mutations. Most mutations will not help the virus, just as it is unlikely to be better than randomly kicking a working machine.
But every once in a while a suit of mutation or mutation gives the virus an advantage. Data are speculating that mutations performed by variants that first appeared in the UK, known as B.1.1.7, make the virus more “fit”.
High fitness or chance?
When a new version becomes common, scientists determine the reason behind its spread. A virus carrying a particular mutation can increase the frequency by chance:
- Performed by a superspreader;
- Moved to a new uninfected location;
- Introduced into a new segment of the population.
The latter two examples are called “founding events”: a rapid increase in frequency can occur if a particular variant is introduced into a new group and a local epidemic begins. Chance events may increase the frequency of several different SARS-CoV-2 variants.
But B.1.1.7 is an exception. This shows a very strong indication of selection.
For the past two months, B.1.1.7 has increased in frequency almost every week and in the health sector in England faster than non-B.1.1.7. This data, reported on December 21, 2020, helped UK Prime Minister Boris Johnson reach most places in the country under lockdown and banned extensive travel from the UK.
The rise of B.1.1.7 cannot be explained by a founding event in new territories, as COVID-19 was already roaming all over Britain.
Founding events (eg, following a conference) in a new segment of the population are also unlikely to be given broad restrictions against larger ceremonies at that time.
Our ability to track the development of SARS-CoV-2 is due to a large-scale effort by scientists to share and analyze data in real-time.
But the incredibly detailed knowledge we have about B.1.1.7 is just plain dumb luck.
One of its mutations altered a portion of the genome used to test for COVID-19 in the UK, drawing the evolutionary picture from over 275,000 cases.
Development in action
Epidemiologists have concluded that B.1.1.7 is more contagious, but there is no indication that it is more fatal.
Some researchers estimate that the number of new cases increases between 40 and 80 percent due to an infected person (called reproduction number or Rt) B.1.1.7; Another preliminary study found that RT increased by 50–74 percent.
A 40–80 percent gain means that B.1.1.7 is not only slightly over-fit, it is over-fit.
Even if the selection is strong, development is not instantaneous. Our mathematical modeling, as well as others in Canada and the US, has shown that it takes B.1.1.7 months to reach its meteorite, as only a small fraction of cases start the new version Does.
For many countries such as the US and Canada, where the number of COVID-19 cases is increasing indefinitely, a variant that increases transmission by 40–80 percent threatens to push us over the top.
It can cause exponential growth in cases and improve medical care already. Evolutionary change takes a little time, it takes us a few weeks to get ready.
More variants
One surprise for the researchers was that B.1.1.7 is a notable number of new mutations.
There are 30-35 changes in B.1.1.7 as compared to the previous year. B.1.1.7 does not mutate at high rates, but it undergoes a range of rapid changes in recent times.
The virus can be carried by an immunologist. People with a weakened immune system constantly fight the virus, with prolonged infections, recurrent rounds of viral replication and only a partial immune response from which the virus continues to develop.
(NextStrain / CC by 4.0)
Above: Each point represents a SARS-CoV-2 genome, with branches connecting viruses belonging to its ancestor. The center represents the virus introduced into humans. Viruses from the center carry the most mutations. There are three new variants highlighted in gold.
Initial research reports that are yet to be verified have described two other forms of concern: one originally from South Africa (B.1.351) and one from Brazil (P1).
Both variants show a history of recent changes and a rapid increase in frequency in local populations. Scientists are currently collecting the data necessary to confirm selection for high transmission and not chance.
What changed to allow the spread?
Selection plays two roles in the development of these variants.
First, consider the role within individuals in which a large number of mutants originated. 23 mutations of B.1.1.7 and 21 mutations of P1 are not randomly in the genome, but are clustered in genes encoding spike proteins.
A change in spike, termed N501Y, occurred independently in all three variants, as well as in immunological patients studied in the US and UK. Other changes in the spike (eg E484K, del69-70) are seen in two of three variants.
Beyond the spike, the three variants of anxiety share an additional mutation that removes a small portion of the name “non-structural protein 6” (NSP6).
We do not yet know what the deletion does, but the associated coronovirus NSP6 operates a cellular defense system and may promote coronavirus infection.
NSP6 also hijacks this system to help mimic the viral genome. Either way, deletion can alter the ability to capture and replicate viruses within our cells.
Easy transmission
The parallel development of similar mutations in different countries and in different immunological patients suggests that they provide a selective advantage to avoid the immune system of individuals in whom mutations occurred. For N501Y, this has been supported by experiments in mice.
But what accounts for the high transmission rate from individual to individual? This is challenging to answer because many mutations that originated at once are now bundled together in these variants, and it may be any one or a combination of them that leads to transmission gain.
That said, many of these variants have arisen earlier on their own and have not caused rapid spread.
One study showed that N501Y in itself had only a weak transmission advantage, increasing rapidly when coupled with the suite of mutations observed only in B.1.1.7.
While the evolutionary story of COVID is still being written, an important message is now emerging. The 40–80 percent transmission gain of B.1.1.7, and possibly other variants B.1.351 and P1, will overwhelm many countries over the next few months.
We are in the race against viral development. We should roll out the vaccines as soon as possible, stop the flow of variants by restricting interactions and travel and expose the spread by eliminating monitoring and contact tracing. 
Sarah Otto, Killam University in Evolutionary Biology, University of British Columbia
This article is republished from Conversation under a Creative Commons license. Read the original article.
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