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northATURAL SELECTION it is a powerful force. In still disputed circumstances, he took a bat coronavirus and adapted it to people. The result has spread throughout the world. Now, in two separate but coincident events, it has further modified that virus, creating new variants that are displacing the original versions. It seems possible that one or the other of these new viruses will soon become a dominant form of SARS–CORV-2.
Knowledge of both became general in mid-December. In Britain, a group of researchers called Covid-19 Genomics uK Consortium (CORGRAM–ORK) published the genetic sequence of the variant SECOND.1.1.7 and northERVTAG, a group that studies emerging viral threats, warned the government that this version of the virus was 67-75% more transmissible than those already circulating in the country. Meanwhile, in South Africa, Salim Abdool Kalim, a prominent epidemiologist, informed the country on all three television channels about a variant called 501.v2, which by then accounted for almost 90% of new COVID-19 infections in the United States. West Cape province.
Britain responded on December 19 by tightening the restrictions already in place. South Africa’s response came on December 28, in the wake of its one millionth recorded case of the disease, with measures that extended the night curfew by two hours and reimposed the ban on the sale of alcohol. Other countries have reacted by discouraging even more vigorously than ever before any travel between them and Britain and South Africa. At least in the case of second.1.1.7, however, this has simply closed the stable door after the horse has run off. That variant has now been detected in a score of countries other than Great Britain, and from these new sites, or from Great Britain, it will spread even further. Isolated cases of 501.v2 have also been reported outside of South Africa in Australia, Great Britain, Japan and Switzerland.
So far, the evidence suggests that despite its additional transmissibility, no new variant is more dangerous, on a case-by-case basis, than existing versions of the virus. In this, they are both treading the path predicted by evolutionary biologists to lead to the long-term success of a new pathogen, which is to become more contagious (increasing the likelihood of transmission) rather than more deadly (reducing it). . And the speed with which they have spread is impressive.
The first sample of SECOND.1.1.7 was collected on September 20, southeast of London. The second was found the next day in London itself. A few weeks later, in early November, second.1.1.7 accounted for 28% of new infections in London. By the first week of December, it had risen to 62%. It’s probably above 90% now.
Variant 501.V2 has a similar story. It started in the Eastern Cape, the first samples date from mid-October and has since spread to other coastal provinces.
The rapid rise of SECOND.1.1.7 and 501.v2 raise several questions. One is why these particular variants have been so successful. A second is in what circumstances they arose. A third is whether they will resist any of the new vaccines in which said warehouse is now placed.
The answers to the first of these questions lie in the variant genomes. CORGRAM–ORKResearch SECOND.1.1.7 shows that it differs significantly from the original version of SARS–COV-2 in 17 places. That’s a lot. Additionally, several of these differences are found in the beak gene, the protein by which coronaviruses attach to their cellular prey. Three of the spike mutations particularly caught the researchers’ attention.
One, north501AND, affects link 501 of the Spike amino acid chain. This linkage is part of a structure called the receptor-binding domain, which extends from linkages 319 to 541. It is one of six key contact points that help lock the spike to its target, a protein called ACE2 that occurs in the surface membranes of certain cells that line the airways of the lungs. The letters in the name of the mutation refer to the replacement of an amino acid called asparagine (“north“, In biological abbreviation) by one called tyrosine (“AND”). That’s important because previous lab work has shown that the change in chemical properties caused by this substitution binds the two proteins more closely than normal. Perhaps tellingly, this particular mutation (though not another) is shared with 501.V2.
Golden peak
SECOND.The other two intriguing peak mutations of 1.1.7 are 69-70del, which removes two amino acids from the chain entirely, and P681H, which replaces another amino acid, histidine, with one called proline in chain link 681. The double deletion attracted the attention of researchers for several reasons, including that it was also found in a viral variant that affected some mink crops in Denmark in November, causing concern about the development of an animal reservoir of the disease. The substitution is considered significant because it is at one end of a part of the protein called S1 /S2 furin cleavage site (linkages 681-688), which helps activate the spike in preparation for its encounter with the target cell. This site is absent from related coronavirus spike proteins, such as the original SARSand it may be one of the reasons why SARS–CORV-2 is so contagious.
The South African variant, 501.v2, has only three significant mutations and all are in the spike receptor-binding domain. further north501AND, are K417north and me484K (K and me are amino acids called lysine and glutamic acid). These other two links are now under intense scrutiny.
Even three significant mutations is enough to have a variant. Only one would be more common. The 17 found in SECOND.1.1.7 are therefore a major anomaly. How this plethora of changes came together into a single virus is therefore the second question that needs an answer.
The authors of the CORGRAM–UK paper has a suggestion. This is that, instead of being a casual accumulation of changes, SECOND.1.1.7 could itself be the consequence of an evolutionary process, but it happened in a single human being rather than in a population. They note that some people develop chronic COVID-19 infections because their immune system is not working properly and therefore cannot clear the infection. These unfortunates, they hypothesize, may act as incubators for new viral variants.
The theory is the following. At first, the lack of natural immunity in such a patient relaxes the pressure on the virus, allowing the multiplication of mutations that would otherwise be eliminated by the immune system. However, the treatment of chronic COVID-19 often involves what is known as convalescent plasma. This is the serum obtained from recovered covid patients, which is therefore rich in antibodies against SARS–CORV-2. As a therapy, that approach often works. But the administration of such a cocktail of antibodies applies strong selection pressure to what is now a diverse viral population in the patient’s body. This the CORGRAM–UK The researchers estimate that it may result in the success of mutational combinations that otherwise would not have seen the light of day. It is possible that SECOND.1.1.7 is one of these.
The answer to the third question, whether any of the new variants will withstand the vaccines that are being released now, is “probably not.” It would be a great coincidence if the mutations that spread in the absence of a vaccine 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 appearance of these two variants shows the power of evolution. If there is a combination of mutations that can circumvent the immune response that a vaccine induces, then there is a great chance that 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.”
