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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
SARS-CoV-2 Omicron (B.1.1.529) infection in rhesus macaques, hamsters, and BALB/c mice with severe lung
Wenhai Yu1, Junbin Wang1, Yun Yang1
1National Kunming High-level Biosafety Primate Research Center, Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming, Yunnan, China.
Abstract:
Since the first SARS-CoV-2 outbreak in late 2019, the SARS-CoV-2 genome has harbored multiple mutations, especially spike protein mutations. The currently fast-spreading Omicron variant that manifests without symptoms or with upper respiratory diseases has been recognized as a serious global public health problem. However, its pathological mechanism is largely unknown. In this work, rhesus macaques, hamsters, and BALB/C mice were employed as animal models to explore the pathogenesis of Omicron (B.1.1.529). Notably, Omicron (B.1.1.529) infected the nasal turbinates, tracheae, bronchi, and lungs of hamsters and BALB/C mice with higher viral loads than in those of rhesus macaques. Severe histopathological damage and inflammatory responses were observed in the lungs of Omicron (B.1.1.529)-infected animals. In addition, viral replication was found in multiple extrapulmonary organs. Results indicated that hamsters and BALB/c mice are potential animal models for studies on the development of drugs/vaccines and therapies for Omicron (B.1.1.529).
Insights
The Omicron variant (B.1.1.529) causes significant lung damage and inflammation in hamsters and mice, with higher viral loads than in macaques. These findings highlight hamsters and mice as valuable models for Omicron research.
Area of Science:
- Virology
- Pathology
- Infectious Diseases
Background:
- The SARS-CoV-2 Omicron variant (B.1.1.529) is a rapidly spreading global health concern.
- Its pathological mechanisms and disease progression remain largely uncharacterized.
- Mutations, particularly in the spike protein, contribute to variant transmissibility and immune evasion.
Purpose of the Study:
- To investigate the pathogenesis of the SARS-CoV-2 Omicron variant (B.1.1.529) in distinct animal models.
- To compare viral loads and tissue tropism of Omicron infection across species.
- To identify suitable animal models for evaluating Omicron-specific therapeutics and vaccines.
Main Methods:
- Utilized rhesus macaques, hamsters, and BALB/C mice as experimental models.
- Inoculated animals with the Omicron (B.1.1.529) variant.
- Assessed viral loads in respiratory and extrapulmonary organs.
- Evaluated histopathological damage and inflammatory responses in infected tissues.
Main Results:
- Omicron (B.1.1.529) exhibited higher viral loads in the nasal turbinates, tracheae, bronchi, and lungs of hamsters and BALB/C mice compared to rhesus macaques.
- Severe histopathological damage and significant inflammatory responses were observed in the lungs of infected hamsters and mice.
- Viral replication was detected in multiple extrapulmonary organs in the studied animal models.
Conclusions:
- Hamsters and BALB/C mice demonstrate susceptibility to Omicron (B.1.1.529) infection with pronounced pulmonary pathology.
- These species serve as appropriate animal models for studying Omicron pathogenesis.
- The findings support the use of hamsters and BALB/C mice in preclinical research for developing drugs, vaccines, and therapies against the Omicron variant.
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