Boston University COVID researchers combine omicron spike protein with original virus, test strain on mice

Boston University COVID researchers have combined the omicron variant spike protein with the original virus, testing the created strain on mice “to help fight against future pandemics,” according to BU.

The scientists in BU’s National Emerging Infectious Diseases Laboratories found that all mice infected with only the BA.1 omicron variant had mild cases and survived, while the combined omicron spike protein with original COVID-19 virus strain inflicted severe disease with an 80% mortality rate.

When mice were infected with just the original, ancestral virus strain, 100% of the mice died.

“First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-COV-2 virus strain (original virus from 2020) or make it more dangerous,” BU said in a statement following online reports that the university called “false and inaccurate.”

“In fact, this research made the virus replicate less dangerous,” the university added.

This study provides important insights into omicron’s ability to cause disease, according to the researchers.

“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,” said lead study author Mohsan Saeed.

“Determination of those proteins will lead to better diagnostics and disease management strategies,” Saeed said.

The research was reviewed and approved by the Institutional Biosafety Committee, which consists of scientists as well as local community members. The Boston Public Health Commission also approved the research.

“Furthermore, this research mirrors and reinforces the findings of other, similar research performed by other organizations, including the FDA,” BU said. “Ultimately, this research will provide a public benefit by leading to better, targeted therapeutic interventions to help fight against future pandemics.”

The study did not include humanized mice.

“One potential limitation of our study is the use of K18-hACE2 mice for pathogenesis studies instead of the primate models that have more similarities with humans,” the study reads. “It should however be noted that the K18-hACE2 mouse model is a well-established model for investigating the lethal phenotype of SARS-CoV-2.”