A new study confirms that, compared to earlier versions of the SARS-CoV-2 virus, the omicron variant causes less severe disease in mice and hamsters, which are reliable models for understanding COVID-19.
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Yoshihiro Kawaoka |
The findings, previously available as a
preprint and published following peer review today (Jan. 21) in the
journal Nature, align with preliminary data from studies of people infected with the variant and offer insight into the nature of the disease with omicron. The variant emerged in late November 2021 and was first identified by scientists in Botswana and South Africa.
Led by Yoshihiro Kawaoka at the University of Wisconsin–Madison, along with Michael Diamond and Adrianus (Jacco) Boon at the Washington University School of Medicine in St. Louis, the collaborative effort was the work of the SARS-CoV-2 Assessment of Viral Evolution (SAVE) program of the National Institute of Allergy and Infectious Diseases.
“SAVE meets four times per week,” Kawaoka explains, and includes teams analyzing sequences from viruses isolated across the world and screening for new variants; teams studying the biology of new variants in animal models; and teams working to isolate viruses for study, examining viral replication and testing how well previous infection or vaccination provides protection against emerging variants. Researchers who typically compete for publications and funding have come together in light of the COVID-19 crisis.
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Peter Halfmann |
Peter Halfmann, a research associate professor at UW–Madison, was among the first in the world to isolate the omicron variant from human samples for study. The samples came from infected patients in Wisconsin, New York, Georgia and Tokyo, and each contained slight sequence differences.
Once the viruses were isolated from the samples, scientists throughout the SAVE network began to test them in mice and hamsters. Animal studies are an important step in understanding new variants and how well they respond to existing countermeasures, such as vaccines and therapies.
The spike protein of omicron contains more than 30 mutations — a striking number relative to earlier variants. Because current vaccines and antibody treatments are based on these earlier versions, researchers were concerned that vaccines and therapies would be rendered less effective.
Computer models and studies that looked at the binding capacity of the virus to ACE2 receptors, which grant the virus entry into cells, also suggested that omicron would better attach to cells.