In a secure lab in BU’s National Emerging Infectious Diseases Laboratories (NEIDL), researchers started by looking at the virus’ spike protein, a molecule that helps SARS-CoV-2 invade a cell and begin its infection-and that has also been co-opted into most vaccines. “What is so special about Omicron that it inflicts milder disease? That’s how this project started-we wanted to investigate that question.” “It caused relatively less severe disease,” says Saeed. However, Omicron was also weaker, or attenuated-less deadly. When the Omicron variant crashed onto the scene in late 2021, it soon became clear that it was spreading faster than previous variants. Saeed’s lab has been studying SARS-CoV-2 since the beginning of the outbreak, examining the first coronavirus strain to be recovered from a patient in the United States, known as the Washington or wild-type isolate. This type of research has the potential to not only predict which variants might lead to new waves of infection, but also identify targets for new therapeutics against COVID-19.” Omicron’s Weaknesses Saeed’s research is showing us the relative impact of different SARS-CoV-2 gene segments on disease severity. Studies like this are helping us understand which parts of the viral genome impact pathogenesis, something we still don’t know,” says Li, who points out that it’s not, for example, clear why the Omicron BA.5 subvariant easily outcompeted the BA.4 version-despite the two variants sharing the same spike sequences. “The non-spike portions of the viral genome have been grossly understudied.
One of the coauthors, Jonathan Li, a BWH and HMS associate professor of medicine, says that while lots of research has been concentrated on SARS-CoV-2’s spike protein, little is known about the rest of its genome. The paper, which will also appear in print, was coauthored by researchers from BU and Cleveland Clinic Florida Research and Innovation Center, Loyola University, Brigham and Women’s Hospital (BWH), Harvard Medical School (HMS), University of Wisconsin–Madison, and Friedrich-Alexander-Universität Erlangen-Nürnberg and Johannes Gutenberg-Universität Mainz, both in Germany.
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“This provides us with an exciting new concept for future vaccines and therapeutics-if we know how to weaken the virus, we can better fight it.”
“This is an important piece of work showing that the spike protein has only minimal contribution to Omicron’s lower pathogenicity-and that mutations in another protein, NSP6, play an essential role,” says Saeed, a BU Chobanian & Avedisian School of Medicine assistant professor of biochemistry. But the study’s senior author, BU virologist Mohsan Saeed, says their research could have a major positive impact, potentially helping provide a new target for vaccines and therapeutics.
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A draft containing some of the paper’s early results had previously made international headlines in October when a series of false reports sensationally misconstrued its findings. In a paper published online in Nature, they identify the mutations that help Omicron dodge prior immunity and show that a previously unheralded virus protein-known as NSP6-might be an essential factor in the variant’s lower disease-causing potential, or its pathogenicity. Like, why are some variants weaker than others? Why does the Omicron variant spread fast, yet make people less sick? Do new virus mutations put us at fresh risk or bring us closer to the pandemic’s end? Are there more effective vaccines waiting to be developed?Ī new Boston University–led study by an international team of researchers may provide some answers.
After three years of infections, lockdowns, and vaccinations, we know a lot about SARS-CoV-2, the virus that causes COVID-19-but we don’t know everything.
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