Did a Boston lab create a strain of Covid with an 80% mortality rate?

Did a Boston lab create a strain of Covid with an 80% mortality rate?

Question asked by Le Mutin on October 18, 2022.

On October 17, an article in the English tabloid daily mail featured a particularly sensational headline: ‘EXCLUSIVE: ‘You’re playing with fire, it could trigger a lab-generated pandemic’: Experts criticize Boston lab where scientists created deadly new strain of Covid with 80% fatality rate The article, widely shared on social networks, aims to report on a study presented in pre-print on October 14 by a team of researchers from Boston University.

What did the study really consist of? Its authors sought to determine which mutations of the omicron BA.1 variant give a different virulence to the Sars-CoV-2 strain that was circulating at the beginning of the epidemic. More specifically, they wanted to test the hypothesis that omicron’s infectious properties would depend on mutations occurring in its “spike” protein (the protein that allows the virus to attach to human cells).

To test this hypothesis, they introduced the omicron spike protein into the strain discovered in 2019, creating a hybrid virus. Several series of experiments, in vitro or in animals, were carried out to compare the capabilities of this new virus with those of omicron BA.1 and with those of the ancestral virus.

The authors thus observe that this hybrid coronavirus, exposed in vitro to the serum of vaccinated patients, has an immune escape capacity similar to that of omicron (which is not surprising, since most of the available mRNA vaccines are based on exposure of the organism to a spike protein sequenced in 2020, significantly different from that of omicron BA.1).

A second experience especially caught the attention of the daily mail. The hybrid virus, the omicron BA.1 and the ancestral virus were inoculated, respectively, in large quantities, into ten, ten and six mice. “humanized”. In fact, these animals have been genetically modified to express, on the surface of their cells, the same “ACE2” receptor that Spike binds to in the human body (“K18-hACE2” mice).

Lethal… to genetically modified mice

While for the ten mice exposed to omicron BA.1, the infection was “light and non-lethal”, eight of ten humanized mice exposed to the hybrid virus died. For their part, the six mice exposed to the ancestral virus died. In other words, the omicron BA.1 virus does not seem dangerous for these mice that present this human ACE2 receptor on the surface of their cells, while the two viruses that show ancestral characteristics (regardless of the spike protein they express) are fatal. for them. The authors conclude that the virulence characteristics of omicron BA.1 are not based, at least not solely, on mutations present in its spike protein.

At the inoculated dose, 10,000 PFU, the ancestral virus is identified as lethal to K18-hACE2 mice. The researchers note that at the same doses, the hybrid virus saved two of the ten inoculated mice.

When the daily mail mentions a virus in its title “with a mortality rate of 80%”, the tabloid fails to specify that this lethality refers to an experiment with only ten mice, genetically modified to have a very strong sensitivity to Sars-CoV-2. A sensitivity such that the virus that circulated at the beginning of 2020, at the doses in which it is inoculated in these experiments, has a lethality of 100% in these animals. Fortunately, this is not the case with humans.

Boston University reacted to the article in the daily mail calling it a “false and inaccurate”, and judging that it distorted the results obtained by the researchers. “They sensationalized the message, they distorted the entire study and its objectives,” This was stated by Ronald Corley, director of the laboratories on which the authors of the study depend. The university also noted that the research had been reviewed and approved by a biosafety committee and by the Boston Public Health Commission.

Function gain

In its press release, the university also attacks a second claim by the daily mail : these works would be a “gain-of-function search”, defined in the article by these words: “When viruses are deliberately manipulated to make them more infectious or deadly.”

In practice, a search for “gain of function” refers to all work that aims to make an organism acquire new functions, usually by inducing mutations and selection for emergent traits, but also by hybridization or targeted genetic manipulation. All that research, especially that of low-risk organisms, is nothing to worry about. On the contrary, when the organism studied is especially sensitive, and the manipulations carried out tend to increase its danger, it is easy to speak of GoFROC, an acronym for “On gain of function research”. However, there is no consensus and universally accepted definition of GoFROC, which would define its contours without any ambiguity.

“Everyone has a hard time defining this research,” comment to Release Bruno Canard, CNRS research director at the Laboratory of Architecture and Functions of Biological Macromolecules at the University of Aix-Marseille. “There hasn’t been much of a debate on this topic, and no one really agrees on what to include behind these terms. One of the issues is also that the research activity, in this field, is in itself uncertain: one can very well predict a loss of function and obtain a gain of function, and vice versa…”

For Boston University, however, things would be simple, as she writes: “This research is not gain-of-function research, in the sense that it did not involve amplification of the Sars-CoV-2 virus strain. [ancestrale]And that didn’t make it more dangerous. In fact, this research has made virus replication less dangerous. (referring to the fact that only eight out of ten mice died with the hybrid virus, compared to six out of six with the ancestral virus).

However, this argument raises several problems. First of all, it is based on an arbitrary and narrow definition of gain-of-function research (reduced here to two criteria, recourse to a technique “amplification” produce the viruses used in the experiment and, above all, to the production of a more dangerous virus). In addition, the university hides that the hybrid virus does present a greater immune escape than the ancestral strain (as shown by the experiment carried out in vitro). This corresponds to a new function conferred on the virus, which makes it more dangerous.

Finally, the argument that the lethality of the hybrid virus is lower (for humanized mice) than that of the ancestral virus… is an observation resulting from the experiment. In the event that the researchers had described a virus as lethal as the ancestral strain, and presenting more significant pathogenic characteristics than the initial virus, would the university then have judged that it was a “gain-of-function research” ? In other words, does this qualifier depend on the outcome of the experiment or on the simple implementation of an experimental protocol? Intent or result?

An answer is given in the university press release, in a passage explaining why this work was not the subject of a prior disclosure to the National Institute of Infectious Diseases (Niaid): “In the first place because the experiments were carried out with funds from the university […] and second, because this research did not lead to a gain of function. If at any point there was evidence of an improvement in functionality, per Niaid’s protocols and our own, we would stop and report the investigation immediately.”

Similar research recently published in “Nature Communications”

Boston University also wants to reassure by specifying that this research was carried out in laboratories of “biosafety level 3” : “All studies take place in a biosafety cabinet, with researchers entering their workspace through a series of locked doors. All floors and walls are sealed and the laboratory is equipped with sophisticated filtration and decontamination technology. And if the researchers had seen anything abnormal during the study, they would have immediately stopped it and reported it.”

While gain-of-function research involving infectious pathogens raises legitimate questions, one may be surprised at the attention paid to the Boston study, when similar but larger work is published without generating the slightest media reaction. In fact, at the end of September, a Chinese team presented in the review NatureCommunications the results of experiments carried out with several hybrid viruses, integrating into an ancestral Sars-CoV-2 the spike proteins of the alpha, beta, gamma, kappa, delta, lambda, omicron and N.1.618 variants.

With the usual reservations related to the fact that these results have not yet been peer-reviewed, Bruno Canard judges the experiment carried out in the Boston laboratory, “which was carried out in correct security conditions”, “allows obtaining interesting scientific information”. “It shows that there are additional mutations in the virus backbone that play a role in increasing innate immunity, or the ability of viruses to replicate, etc.”

why this study “It was carried out on viruses that are already circulating, of which we already know the spike and the skeleton, and to which populations have already been exposed,” Bruno Canard judges this investigation “Clearly much less worrisome than others.” “It is remarkably much less dangerous than going looking for new viruses, often under poorly defined safety conditions, to bring them back to the lab and have them cross the species barrier to determine if they will ever get through. for the man.”A type of research that, he insists, “never made it possible to predict an epidemic”,and returns, according to him, “looking for a gas leak with a lighter”.

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