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With 74 million infections on its shoulders, the coronavirus has changed its face. Little, fortunately. But anyone who has looked at the smallest details knows how much a mutation, however small, can turn the tables with the pandemic. While Britain is alarmed by the emergence of a new variant of Sars-Cov-2, Ralph Baric’s team at the University of North Carolina, one of the leading experts on coronavirus, has explained why the D614G mutation it has conquered the world during this second wave has managed to get into such high gear.
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It was enough that one of the 30,000 nucleotides, the building blocks that compose it, changed in the Sars-Cov-2 genome for the D614G variant to be born. And why, writes Baric almost simultaneously in Science and in the New England Journal of Medicine, the virus “identified in February in southern Europe spread rapidly and became prevalent in the world.” To confirm what might appear to be coincidences, the most serious epidemic in Italy in the spring, precisely at the place and time that D614G appeared, and the much higher numbers from the second wave than the first, Baric has contracted a coronavirus , acquired the mutation and measured its replication capacity with a three-step experiment.
In test tubes, in various cell types of human respiratory tissue, the mutated virus has replicated and reached amounts up to 8 times higher than the original virus, the one that appeared in Wuhan. Even when the original virus came into contact with cells in quantities ten times greater than the mutated virus, the latter took over in a few days, conquering the entire culture. Finally, in hamsters and mice used as guinea pigs, the D614G version was able to spread earlier and earlier on the mucous membranes of the nose, the coronavirus’ favorite “launching bridge” for infecting others. Compared to the parent virus, D614G is capable of infecting early (only two days after infection, in guinea pigs) and at lower doses.
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“Our experiments show – writes Baric – that the D614G variant is transmitted significantly faster in hamsters through droplets and aerosols.” The mutation causes “an increase in infectivity and transmission capacity also in the human population.” The severity of symptoms is the same or “marginally greater” for the mutated virus, at least as far as scientists have observed in guinea pigs. Even in men, however, D614G causes “higher viral loads.” And with a greater amount of microorganisms in the nose it is easier to infect those around us. Although more efficient at infecting, the mutated virus is no longer agile at escaping our antibodies. “Study vaccines directed against spikes should also be effective against the D614G variant,” the one from last spring, Baric writes.
However, it is not certain that it can always turn out well, in the Russian roulette of new mutations. And this is where the alarm that was raised in Britain is justified. “Despite a proofreading system that makes the virus genome very faithful,” mutations will always emerge, writes Baric. As more and more people become immunized, a new variant capable of escaping the antibodies generated by the vaccine may emerge and take over. “It is important – the US researchers recommend – to immediately identify the emergence of new variants, especially when herd immunity or other active human interventions will alter the selective pressures on the virus genome.”
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It is still too early to understand what characteristics the English variant will have. But the researchers are concerned. In a preliminary study carried out by several British universities, it is observed that the new strain, called B.1.1.7, was observed for the first time on September 20 in Kent and since then it has multiplied its appearances, reaching 1,623 samples today. of which 519 in London, 555 in Kent, 545 in other regions of the UK and 4 abroad, “with a growing proportion of cases”. The researchers observed in the new strain “a surprisingly large number of genetic changes, especially in the spike protein.” That’s what vaccines are aimed at. “Three of these mutations have potential biological effects.” Which could affect the ability to infect and cause serious symptoms. The N501Y variant could “increase the affinity for the Ace receptor.” So we facilitate the entry of the virus into our cells. “The 69-70del deletion has been described in the context of the ability to evade the human immune response.” It could hamper the work of our defenses. Finally, the P681H mutation could have biological effects that are not yet specified.
Finally, South Africa’s concern adds to British concern. “Our scientists have announced that a new variant called 501.V2 has been identified in our country,” Health Minister Zweli Mkhize said on Friday. “The evidence gathered strongly suggests that the current second wave is driven by this new variant.”
