Why has the British variant gained the upper hand over the South African and Brazilian strains in France?
We can explain it by its contagiousness: in an estimate made by our team in collaboration with the Cerba laboratories, it was calculated that the V2 and V3 variants detected in South Africa and Brazil are less contagious than the V1, identified in England. This one has 40% more transmission advantages compared to the lines which circulated before, while, for the other two, it is rather around 25%. In addition, the control measures put in place from January were more or less sufficient to prevent the spread of these V2 and V3 variants.
Why is the British variant more contagious than the other two? Is it due to specific mutations?
It does seem that the explanations are biological. But linking them to particular mutations is tricky: a number of them stand out because they have been shown to have a big effect. We have, for example, the N501Y mutation which is part of those encoding the spike protein (which allows the virus to enter the cell to reproduce, Editor’s note). In the V2 and V3 variants, E484 is found, which appears to be associated with immune escape. But there is also a whole other series of mutations which, taken in isolation, are not going to have an effect, but which, together, can.
Has the fact that the British variant seems to have arrived a little earlier than the other two on our territory work in his favor?
I don’t think it is. Natural or vaccine immunity was extremely low when they arrived. Suddenly, as my colleague epidemiologist Mircea Sofonea says, it’s a bit like a race where everyone is in their own lane but not directly in the same area. The question of the order of arrival would play more in Brazil where a large part of the population was infected because the leaders did anything. When a large part of the population has been infected, a variant that comes second, meets immunized, and suddenly, it has difficulty in transmission. In France, we don’t think this is the case. And anyway, the V2 and V3 variants detected in South Africa and Brazil seem capable of re-infecting previously infected people. So arriving after other variants seems to be less of a concern for them.
The South African variant almost became the majority in Moselle at the beginning of March, but its share is now only 30%. What analysis do you draw from it?
This confirms this idea that, compared to the speed of propagation of V1, V2 diffuses less quickly. We also see that measures such as the 6 p.m. curfew seemed to be about sufficient to control the V2 and V3 variants but not the V1.
Are the South African and Brazilian variants more resistant to the vaccine? Can this help them gain the upper hand over the British variant?
Immune escape seems limited if taking RNA vaccines. For the time being, there is good efficacy regardless of the type of virus and infection. In the short term, there is not much doubt that vaccination will control the epidemic. In the medium and long term, questions arise about the duration of protection against severe forms, which however appears to be quite long, and that of the blocking of transmissions.
Could a new variant resist vaccination and relaunch the epidemic?
Viral evolution is also a big unknown. We have seen variants appear which have changed the situation a little. Before, our knowledge of the virus’s evolutionary capacities dated from the first sequence obtained from a virus in Wuhan, China, in December 2019. We knew roughly the direction in which it could evolve: rather neutral, which was positive. The variant has put everything back: the new starting point for evolution is the genome of this variant, in particular the one detected in England, and there, we do not really know in which direction it can go. This is quite worrying, because at the moment vaccination is working well on most viruses, although there are differences between vaccines. However, we are not immune to variants for which this would be less the case. The more we let the epidemic circulate, the more we expose ourselves to these unknowns.
Has the virus reached its evolutionary limits or, on the contrary, does it still have room to change again and again?
The answer is, we don’t know. Many people will use what we have learned from other coronaviruses to say that there are indeed very strong genomic constraints to its evolution. From a personal point of view, my conclusion is that all those who made predictions about this epidemic based on known viruses, even on other coronaviruses, were wrong in large widths: they neglected the transmission asymptomatic, said it was going to become a seasonal virus, and that there would be no epidemic, the summer. You have to be humble in the face of novelty. The evolution of variants that has been observed since the end of 2020 should encourage us to be cautious.
Little information is known about the “Breton variant”, but what do you think of this new virus which seems difficult to detect?
This is an opportunity to recall that we must avoid speaking of a “Breton variant” but rather of a “variant detected in Brittany”, for aspects of discrimination. The inhabitants have nothing to do with it if the variant has been detected in them… There is no scientific publication on the subject yet. The Institut Pasteur and other labs are working on it. We talk about variant when a virus causes an infection with different symptoms, and there, for this line detected at Lannion, it would be very possible that this is the case. It could also be that the virus has a really pronounced tropism for the lower respiratory tract potentially linked to certain mutations in its genome. In the same way that the variant detected in England has been shown to cause more contagious and more virulent infections, it would be possible that this line identified with Lannion is also at the origin of a higher virulence because it generally comes from ‘tropism for the lower respiratory tract. We can make the connection between the two. This line detected at Lannion would, however, potentially be less transmissible because the contagiousness is, a priori, higher when the virus infects the upper respiratory tract. These are possible hypotheses which remain to be confirmed.
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