Let’s talk of this strain of COVID-19 “more contagious” (and “pre-prints”)…
BLOG / When the dust will have begun to fall on this crisis of the COVID-19, and even before if you can, it will be necessary to ask serious questions about the articles in the “pre-publication”, both in the media and in the research world. Because I’m not sure that they have done more good than harm in the current crisis.
The latest example is this story, repeated in many media of the planet, around a new strain of “now dominant” of the COVID-19 which would be “more contagious” than the original . As you might expect, this “new” has caused a lot of excitement and anxiety on social networks. And all this for frankly not much else.
The L. A. Times was the first to report this “news”, which goes back to an article placed recently on the server prepublication bioRxiv. The document deals with a mutation observed in the virus of the COVID-19 and that seems to be widespread thereafter. The authors of the study, who are serious people also interpret this as the sign that this mutation gives an advantage to the virus mutants by making them more contagious. And the tone of the prépapier actually has something of an alarmist, because he speaks of an “emergency” (urgent concern, in the summary) about the mutation in question, the poetically named “D614G”.
However, here, as in all the other studies that find themselves on bioRxiv, it is a “pre-publication”, that is to say, a sort of “rough draft” that has not yet gone through the process of peer review which leads (eventually) to a publication in scientific journals. We can’t rely on it as much as on a study review published in good and due form. Already that when a study is published, it remains “just a study” whose results need to be corroborated by other work, so imagine the caution with which we must deal with the preprints.
But neither the Timesnor the JdeM, nor most of the others do not have this nuance. Many have taken these results to cash, have taken headlines of apocalyptic and often did not even bother to seek the input of other experts.
It would have been necessary. Personally, I’ve stopped counting the number of virologists and epidemiologists that I’ve seen fart checkmarks on my network at sujetde this “new” in the last few days. Essentially, they say, it is possible that this mutation D614G to have an influence on the infectiousness of the COVID-19. It could be… maybe… But the article to bioRxiv makes no demonstration.
First, note the epidemiologist from Harvard, Bill Hanage in an illuminating series of tweets, one of the main arguments of this preprint to defend the thesis of natural selection is that the mutant variant has eventually become more widespread than the original that broke at the start in China (and a few other places in the world). But in and of itself, says Hanage, it doesn’t mean anything. It can be a sign of a greater transmissibility of the mutant, but this can also be explained simply by what geneticists call the “founder effect” : the first virus to have infected Europe belonged to the mutant strain, and it is shown that a time that China and Asia are managed to control their outbreaks, it is Europe that has become the main source of contagion. It would therefore be dealing with a strain of virus which are not more contagious than the other, but who have just been “lucky” to find himself in the right place, at the right time.
It is not yet certain of anything, but a sign that to believe Mr. Hanage that there was no doubt the case that a strain “lucky” is a chart of the prépapier (figure 3 on page 19 (33), which shows the way in which the epidemic took place in the State of Washington. This place was one of the first (and most severely) affected in North America because of its links with Asia. In the State of Washington, the epidemic started with the original strain (in orange on the graph), then the mutant strain (in blue) is gradually arriving from the east coast of the u.s., where the coronavirus was mainly happened in Europe.