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SARS-CoV-2 Omicron virus causes attenuated disease in mice and hamsters
Peter J Halfmann1, Shun Iida2, Kiyoko Iwatsuki-Horimoto3
1Influenza Research Institute, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Abstract:
The recent emergence of B.1.1.529, the Omicron variant1,2, has raised concerns of escape from protection by vaccines and therapeutic antibodies. A key test for potential countermeasures against B.1.1.529 is their activity in preclinical rodent models of respiratory tract disease. Here, using the collaborative network of the SARS-CoV-2 Assessment of Viral Evolution (SAVE) programme of the National Institute of Allergy and Infectious Diseases (NIAID), we evaluated the ability of several B.1.1.529 isolates to cause infection and disease in immunocompetent and human ACE2 (hACE2)-expressing mice and hamsters. Despite modelling data indicating that B.1.1.529 spike can bind more avidly to mouse ACE2 (refs. 3,4), we observed less infection by B.1.1.529 in 129, C57BL/6, BALB/c and K18-hACE2 transgenic mice than by previous SARS-CoV-2 variants, with limited weight loss and lower viral burden in the upper and lower respiratory tracts. In wild-type and hACE2 transgenic hamsters, lung infection, clinical disease and pathology with B.1.1.529 were also milder than with historical isolates or other SARS-CoV-2 variants of concern. Overall, experiments from the SAVE/NIAID network with several B.1.1.529 isolates demonstrate attenuated lung disease in rodents, which parallels preliminary human clinical data.
Insights
The Omicron variant (B.1.1.529) showed reduced infection and lung disease in rodent models. This suggests milder illness compared to previous SARS-CoV-2 variants, aligning with early human data.
Area of Science:
- Virology
- Infectious Diseases
- Immunology
Background:
- The Omicron variant (B.1.1.529) emerged with concerns about immune escape from vaccines and therapeutics.
- Preclinical rodent models are crucial for evaluating countermeasures against SARS-CoV-2 variants.
Purpose of the Study:
- To assess the pathogenicity of B.1.1.529 isolates in immunocompetent and human ACE2 (hACE2)-expressing mice and hamsters.
- To compare B.1.1.529 disease severity with previous SARS-CoV-2 variants in preclinical models.
Main Methods:
- Utilized the SARS-CoV-2 Assessment of Viral Evolution (SAVE) programme network.
- Inoculated B.1.1.529 isolates into various mouse strains (129, C57BL/6, BALB/c, K18-hACE2) and hamsters (wild-type and hACE2-transgenic).
- Monitored infection levels, weight loss, viral burden, clinical signs, and pathology.
Main Results:
- B.1.1.529 caused less infection and limited weight loss in mice compared to prior SARS-CoV-2 variants.
- Viral burden in the upper and lower respiratory tracts was lower for B.1.1.529 in mice.
- Hamster models showed milder lung infection, disease, and pathology with B.1.1.529 than with historical isolates or other variants of concern.
Conclusions:
- B.1.1.529 isolates demonstrate attenuated lung disease in rodent models.
- Findings in rodents parallel preliminary human clinical observations regarding Omicron's severity.
