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Boston University has pushed back on media reports that their researchers created a new and deadly strain of the SARS-CoV-2 virus.

The institution emphatically denied stories by various outlets that implied the spawning of a dangerous new COVID strain in the lab -- some of which cited an 80% kill rate -- calling them "false and inaccurate" in a statement issued in response to the articles circulating online.

"First, this research is not gain-of-function research, meaning it did not amplify the [ancestral] SARS-CoV-2 virus strain or make it more dangerous," Boston University (BU) said in the statement. "In fact, this research made the virus replicate less dangerous."

The university went on to add that the work was approved by the Institutional Biosafety Committee as well as the Boston Public Health Commission, and that it "mirrors and reinforces the findings of other, similar research performed by other organizations, including the FDA."

The research aimed to study whether the Omicron spike protein, with its many mutations, is responsible for the COVID variant's high transmissibility and association with attenuated disease, published on Friday.

In order to study those areas, researchers combined the Omicron spike protein with the ancestral strain of the virus, and compared it with the naturally circulating Omicron variant.

They found in the animal model that while the naturally circulating Omicron variant caused mild, non-fatal infection, the combined virus inflicted severe disease with a mortality rate of 80% in 10 mice (the wild type virus led to a 100% mortality rate in six mice). The finding indicates that while vaccine escape is defined by mutations in the Omicron spike protein, major determinants of viral pathogenicity reside outside of the spike protein, the researchers stated.

Ronald Corley, PhD, director of the BU National Emerging Infectious Diseases Laboratories and chair of microbiology at the Chobanian & Avedisian School of Medicine, explained in a on Monday that the work began in a tissue culture, and then moved to an animal model.

"The animal model that was used was a particular type of mouse that is highly susceptible, and 80 to 100 percent of the infected mice succumb to disease from the original strain, the so-called Washington strain," Corley stated in the article. "Whereas Omicron causes a very mild disease in these animals."

He said that the 80% figure used in media headlines "totally misrepresents not only the findings, but [also] the purpose of the study."

But BU is said to have drawn government scrutiny as a result of the research, , which reported that "the research team did not clear the work with the National Institute of Allergy and Infectious Diseases [NIAID], which was one of the funders of the project."

"The agency indicated it is going to be looking for some answers as to why it first learned of the work through media reports," STAT said. As of press time, NIAID did not provide further comment to 番茄社区app.

BU maintained in its statement that all required regulatory obligations and protocols were fulfilled: "Following NIAID's guidelines and protocols, we did not have an obligation to disclose this research for two reasons. The experiments reported in this manuscript were carried out with funds from Boston University. NIAID funding was acknowledged because it was used to help develop the tools and platforms that were used in this research; they did not fund this research directly. NIH funding was also acknowledged for a shared instrumentation grant that helped support the pathology studies. We believe that funding streams for tools do not require an obligation to report."

If at any point there was evidence that the research was gaining function "under both NIAID and our own protocols we would immediately stop and report," BU stated.

The university also said that is in continued conversation with NIAID.

Lead researcher Mohsan Saeed, PhD, DVM, said in the statement that "Consistent with studies published by others, this work shows that it is not the spike protein that drives Omicron pathogenicity, but instead other viral proteins. Determination of those proteins will lead to better diagnostics and disease management strategies."

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