The most concerning versions of the virus are not simply mutating—they’re mutating in similar ways.
For most of 2020, the coronavirus, which causes COVID-19, jumped from person to person and accumulated mutations at a steady rate of two per month – not particularly impressive for a virus. These mutations had much of little effect.
But recently, three different versions of the virus appear to have independently adopted some of the same mutations, even though they live thousands of miles apart in the UK, South Africa and Brazil. (A mutation is a genetic modification; a variant is a virus with a certain set of mutations). The fact that these mutations have appeared not only once, not twice, but now three times – as far as we know – in variants with unusual behavior suggests that they give the virus an evolutionary advantage. All three variants seem to be appearing more and more frequently. And all three are potentially more transferable.
“Every time you have mutations that occur independently in multiple places, that’s really a sign,” said Vineet Menachery, a coronavirus researcher at the University of Texas Medical Branch. Now scientists are trying to figure out if and how these mutations could give viruses an advantage.
It is still early, and the data on the variant in Brazil are particularly sparse. However, these variants have not only certain mutations in common, but also a large number of mutations, some of which are unique to each variant. The rapid occurrence of a whole range of mutations should be a very rare event. But because the virus is so widespread at the moment, very unusual events will happen – and more than once. The usual mutation rate of two per month may underestimate how the coronavirus can mutate in unusual situations. “It’s a little wake-up call,” Kristian Andersen, a microbiologist at Scripps Research, told me.
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The role of each mutation is still unclear, but a specific mutation in the spike protein called N501Y is remarkable because all three variants have it. The spike protein causes the coronavirus to enter the cells, and N501Y is located in a particularly important region, the so-called receptor binding domain, which is stuck in the cell. An N501Y mutation could make the spike protein stickier, making it easier to bind to and penetrate cells. Such a virus could be more easily transmitted. On the positive side, however, the mutation does not appear to affect the immunity of vaccines.
Here, by the way, is how to read the names of the mutations: proteins are made up of building blocks called amino acids. N501Y means that the 501st amino acid was originally an N that stands for the amino acid asparagine, but has been changed to a Y that stands for tyrosine.
However, N501Y is not unique to these three variants; it has been found in a number of sequences around the world. The unusual thing about these three variants is that they also have a constellation of other mutations in other parts of the virus. A change in the behavior of a variant, such as .B increased transferability, is probably “not only due to one mutation, but to multiple mutations,” says Emma Hodcroft, a molecular epidemiologist at the University of Bern. The British variant has more than a dozen other mutations that have not been studied as strongly as N501Y. But the increased portability of the variant looks increasingly secure: it is becoming more common not only in the UK, but also in Ireland and Denmark, two other countries that regularly sequence large amounts of samples. The CDC recently warned that it is likely to become the dominant variant in the United States by March.
(Scientists have given all three variants more accurate names, but unfortunately they have not yet standardized them. The British variant is also under the names B.1.1.7, 20I/501Y. V1 and VOC 202012/01. The South African variant is sometimes called B.1.351 or 20C/501Y. V2. The Brazil variant is available as P.1 and 20J/501Y. V3).
The South African and Brazilian variants also have a second and third mutation in the receptor-binding domain of the spike in common: E484K and K417. Scientists know a little more about the E484K mutation. It exchanges a negatively charged amino acid for a positively charged amino acid; it’s like turning a magnet around. This probably changes the shape of the spike protein when it binds to a cell, but this change appears to work in synergy with the N501Y mutation, Andersen said. These mutations, possibly along with others, can make the virus better bind to cells.
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But the variants from South Africa and Brazil could have an added advantage. A recent study suggests that viruses with the E484K mutation may be better able to dodge antibodies from the blood plasma of recovered COVID-19 patients. Some viruses with this mutation might become better at infecting people again or even infecting vaccinated people.
However, it is unlikely that this mutation alone renders immunity from previous infections or vaccines completely ineffective. With current vaccines, “you have more than enough antibodies, and even if you halve that amount, you still have more than enough antibodies to control the virus,” Menachery said. “If the new variant is effective … reduced by 50 percent, you still have a lot of protection.” Studies are underway to find out exactly how much this mutation affects vaccines, but it suggests that vaccine manufacturers need to update their vaccines as more mutations like E484K accumulate over a period of years. Influenza vaccination is already done every year, and the current mRNA-COVID-19 vaccines can be updated particularly quickly, in just six weeks, according to the manufacturer.
Scientists are now wondering whether the variants are spreading in South Africa and Brazil precisely because they have this slight advantage in overcoming the existing immunity. Both variants were originally found in parts of countries where there were high COVID-19 infection rates – especially in Manaus, Brazil, where a particularly high proportion of people already had the virus. (A December study said 76 percent, which is probably an overestimation, but the high COVID-19 death rate in the region suggests that there was actually a major outbreak in 2020). The South African variant becomes dominant in the country; the situation in Brazil is less clear because there is less data, but Manaus is currently experiencing another big increase in COVID-19. Menachery said he doesn’t believe that previous immunity is necessarily a reason these variants become more common, especially because South Africa is not so close to herd immunity. Better portability is already an advantage.
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But others outlined this plausible, if still hypothetical, scenario: The variants may have evolved in immunocompromised patients infected with the virus for months. Normally, Hodcroft says, “your immune system goes to the bottom of it. It’s really trying to beat it up.’ But immunocompromised patients have a weaker immune response. “It’s almost like a training course on how to live with the human immune system,” she says. This could be the reason why these variants have so many new mutations at once, as if one or two years of evolution had been compressed into months. This is probably quite rare, but with tens of millions of infections around the globe, rare things also appear.
So a variant could emerge from the training ground of a chronic infection, with mutations that make the virus better bind to cells and thus make it more portable. This could be the case with the British variant. It could also turn out to be a little more capable of re-infection. This could be the case in Brazil, where there are already two documented cases of pure infections with the new variant. In a place where many people are already infected with COVID-19, a variant that can escape the existing immunity a little better has an advantage. These pure infections may not be serious, nor may they be the norm, but over time this variant will prevail. The coronavirus is in a constant arms race against our immune system. It will continue to evolve.
This means that our vaccines must also evolve with him. But the United States sequences only a tiny percentage of its COVID-19 cases. (Standard COVID-19 diagnostic tests examine some regions of the viral genome, but they do not sequence the entire genome). “San Diego is one of the places in the country where we perform well, and we only sequence 2 percent of cases. This is ridiculous compared to the UK and Denmark,” Andersen said. “And we need to change that.” The sequencing data, when collected, is scattered across individual laboratories across the country. What the US needs, Andersen said, is a federal mandate for genomic surveillance. This is the only way for the US to keep up with an ever-changing virus.