A new type of coronavirus has spread throughout the United Kingdom, detected in the United States, Canada and elsewhere, and scientists are concerned that these strains may easily spread faster.
Sarah Otto, University of Killam Professor of Evolutionary Biology, University of British Columbia studies how mutations and selection combine to shape changes in populations over time. And we never before had as much real-time data on evolution as with SARS-CoV-2: more than 380,000 genomes were sequenced last year.
SARS-CoV-2 mutated as it spread, resulting in slight variations in its genome. These mutations allow scientists to track who relates to who crosses the virus’s family tree.
Evolutionary biologists, including Otto, cautioned against overinterpreting the threat posed by mutations.
But every now and then, a mutation or a combination of mutations gives an advantage to the virus.
The data says that the mutations carried by the variable that first appeared in the United Kingdom, known as B.1.1.7, make the virus more “fit”.
And when a new variable becomes popular, scientists determine the reason behind its spread. And a rapid rise in frequency could occur if a particular variable was introduced into a new population and a local epidemic started. Serendipitous events may explain the high frequency of many different SARS-CoV-2 variants.
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But B.1.1.7 is an exception, as it shows a very strong selection signal.
And over the past two months, the B.1.1.7 recurrence rate has risen faster than non-B.1.1.7 nearly every week, and in the Health Zone in England.
The increased prevalence of B.1.1.7 cannot be explained by an established event in new regions, because “Covid-19” is already spreading through specific events in the United Kingdom in a new segment of the population (for example, after a conference).
Our ability to track the evolution of SARS-CoV-2 is due to the tremendous effort scientists make to share and analyze data in real time. One of the B.1.1.7 mutations changed part of the genome used to test for “Covid-19” in the United Kingdom, allowing the picture of the evolutionary spread to be extracted from more than 275,000 cases.
Epidemiologists 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 individual (called the reproductive number, or Rt), by between 40 and 80%; Another preliminary study found that Rt increased by 50-74%.
And the 40-80% advantage means B.1.1.7 is more convenient. Even when selection is this powerful, evolution is not immediate.
One of the surprises for the researchers was that B.1.1.7 carries a remarkable number of new mutations, accumulating 30-35 changes over the past year. It is also not mutating at a higher rate, but appears to have undergone a bout of rapid change in the recent past.
The virus may have been transmitted by an immunocompromised person. People with weakened immune systems are constantly fighting the virus, with long-term infections, repeated rounds of virus replication, and only a partial immune response with which the virus constantly evolves.
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Unverified, initial research reports described two other variables of concern: one originally from South Africa (B.1.351) and the other from Brazil (P1). Both variables show a recent history of extra mutations and rapid increases in frequency among the local population. Scientists are currently gathering the data needed to confirm that the choice for higher prevalence, rather than chance, is responsible.
What has changed to allow the spread?
Choice plays two roles in the evolution of these variables. Think first about the role within these individuals in which a large number of mutations have arisen: 23 for B.1.1.7 and the 21 P1 mutations, they are not randomly arranged across the genome but clustered into the gene that encodes the spiky protein.
A single alteration in the prickly protein, called N501Y, arose independently in all three variants, as well as in the immunocompromised patients studied in the US and UK.
Apart from the sudden spike, the three worrisome variants share one additional mutation that deletes a small fraction of the non-structural protein called “protein 6” (NSP6). We don’t know yet what deletion does, but in the related NSP6 Coronavirus, it fools the cellular defense system and may enhance MERS infection.
NSP6 also hijacks this system to aid in the transcription of the viral genome. Either way, the deletion may alter the virus’s ability to stick and reproduce within our cells.
And the parallel development of the same mutations in different countries and in different immunocompromised patients indicates that they impart a selective advantage to evade the immune system of individuals. For N501Y, this was supported by experiments in mice.
But what explains the high rate of transmission from one person to another?
It is difficult to answer this question because the many mutations that arose simultaneously are now grouped together in these variants, and it could be any one or a combination of them that gives rise to the transmission advantage.
However, many of these variants had previously arisen on their own, and did not lead to rapid spread. One study showed that N501Y only has a weak transmission advantage on its own, and only rises rapidly when combined with the set of mutations observed in B.1.1.7.
While the evolutionary story of “Covid” is still being written, one important message appears now. The spread advantage of 40-80% for B.1.1.7, and possibly the other variants B.1.351 and P1, will overwhelm many countries in the next few months.
We are in a race against viral evolution. We must roll out vaccines as quickly as possible, stop the flow of variants by restricting interactions and travel, and counter spread by intensifying surveillance and contact tracing.
Source: ScienceAlert
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