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NOTATURAL SELECTION is a mighty force. In still disputed circumstances, it took a bat coronavirus and adapted it to people instead. The result has spread around the world. Now, in two independent but coincidental events, he has further modified this virus, creating new variants that replace the original versions. It seems possible that either of these new viruses will soon itself become a dominant form of SARS–VSOV-2.
Knowledge of the two became widespread in mid-December. In Britain, a group of researchers called the Covid-19 Genomics uK Consortium (VSOg–UK) published the genetic sequence of the variant B.1.1.7, and NOTERVTAG, a group that studies emerging viral threats, has informed the government that this version of the virus is 67-75% more transmissible than those already circulating in the country. In South Africa, meanwhile, Salim Abdool Kalim, a leading epidemiologist, informed the country on all three TV channels of a variant called 501.v2 which, at that time, accounted for nearly 90%. of new covid-19 infections in Cape Western Province.
Britain responded on December 19 by tightening restrictions already in place. South Africa’s response came on December 28, following its one millionth recorded case of the disease, with measures that extended a nighttime curfew by two hours and reimposed a ban on the sale of alcohol. Other countries have reacted by discouraging even more forcefully than before any travel between them and Britain and South Africa. At least in the case of B.1.1.7, however, it simply closed the stable door after the horse locked. This variant has now been detected in about 20 countries besides Great Britain – and from these new sites, or Great Britain, it will spread even more. Isolated cases of 501.v2 outside of South Africa have also been reported in Australia, Britain, Japan and Switzerland.
Evidence so far suggests that despite their additional transmissibility, none of the newer variants are more dangerous on a case-by-case basis than existing versions of the virus. In this, both follow the path predicted by evolutionary biologists to lead to the long-term success of a new pathogen – which must become more contagious (which increases the chances of transmission) rather than more deadly (which reduces it). . And the speed at which they have spread is impressive.
The first sample of B.1.1.7 was collected on September 20, South East London. The second was found the next day in London itself. A few weeks later, at the beginning of November, B.1.1.7 accounted for 28% of new infections in London. By the first week of December, this percentage had risen to 62%. It is now probably over 90%.
Variant 501.V2 has a similar story. It started in the Eastern Cape, with the first samples dating from mid-October, and has since spread to other coastal provinces.
The rapid rise of B.1.1.7 and 501.v2 raises several questions. One is the reason why these particular variations have been so successful. A second is the circumstances in which they appeared. A third is whether they will resist any of the new vaccines in which such a reserve is now placed.
The answers to the first of these questions lie in the variant genomes. VSOg–UKin order to B.1.1.7 shows that it differs significantly from the original version of SARS–COV-2 in 17 places. It’s a lot. In addition, many of these differences relate to the peak gene, the protein by which coronaviruses attach themselves to their cellular prey. Three of the peak mutations particularly caught the attention of researchers.
A, NOT501AND, affects the 501st link of the tip amino acid chain. This link is part of a structure called the receptor binding domain, which spans from links 319 to 541. It is one of the six key contact points that help lock the peak onto its target, a protein called AS2 which occurs on the surface membranes of certain cells lining the airways of the lungs. The letters in the name of the mutation refer to the replacement of an amino acid called asparagine (“NOT”, In biological shorthand) by a called tyrosine (“AND”). This is important because previous lab work has shown that the change in chemical properties this substitution causes binds the two proteins together more tightly than normal. Perhaps revealing, this particular mutation (although no other) is shared with 501.V2.
Golden woodpecker
B.The other two intriguing tip mutations in 1.1.7 are 69-70del, which completely removes two amino acids from the chain, and P681H, which replaces yet another amino acid, histidine, with an acid called proline at link 681. Double deletion has caught the attention of researchers for several reasons, not least because it was also found in a variant viral affecting some mink in Denmark in November, causing concerns about the development of an animal reservoir of the disease. The substitution is considered significant because it is located at one end of a part of the protein called S1 /S2 furin cleavage site (links 681-688), which helps activate the peak in preparation for its encounter with the target cell. This site is absent from the spike proteins of related coronaviruses, such as the original SARS, and may be one of the reasons why SARS–VSOV-2 is so infectious.
The South African variant, 501.v2, has only three significant mutations, and all of them are in the Spike receptor binding domain. outraged NOT501AND, they are K417NOT and E484K (K and E are amino acids called lysine and glutamic acid). These other two links are now under close scrutiny.
Even three significant mutations is a lot for one variant. Only one would be more usual. The 17 found in B.1.1.7 is therefore a huge anomaly. How this plethora of changes came together in a single virus is therefore the second question that requires an answer.
The authors of VSOg–United Kingdom paper have a suggestion. It is that, rather than being a fortuitous accumulation of changes, B.1.1.7 could itself be the result of an evolutionary process – but one that occurred in a single human being rather than in a population. They observe that some people develop chronic covid-19 infections because their immune system is not functioning properly and therefore cannot clear the infection. According to them, these unfortunates could serve as incubators for new viral variants.
The theory goes like this. At first, such a patient’s lack of natural immunity eases the pressure on the virus, allowing mutations to multiply that would otherwise be cleared by the immune system. However, the treatment of chronic covid-19 often involves what is called convalescent plasma. This is serum taken from convicted patients recovered, which is therefore rich in antibodies SARS–VSOV-2. As a therapy, this approach frequently works. But administering such a cocktail of antibodies puts strong selective pressure on what is now a diverse viral population in the patient’s body. This, the VSOg–United Kingdom researchers believe, may lead to the success of mutational combinations that would not have emerged otherwise. It’s possible that B.1.1.7 is one of them.
The answer to the third question – whether any of the new variants will withstand the vaccines being deployed – is “probably not”. It would be a long-standing coincidence if mutations that spread in the absence of a vaccine nevertheless protected the virus that carries them from the immune response elicited by that vaccine.
However, this is not a guarantee for the future. The rapid emergence of these two variants shows the power of evolution. If there is a combination of mutations that can bypass a vaccine-induced immune response, there’s a good chance nature will find it.■
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This article appeared in the Science and Technology section of the print edition under the title “Variations on a Theme”
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