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Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2
Published on: November 5, 2021
Revisiting endothelial tropism of SARS-CoV-2 using a cell-specific hACE2 mouse model
Sahine Lameire1,2, Nincy Debeuf1,2, Julie Deckers1,2
1Laboratory of Immunoregulation and Mucosal Immunology, VIB Center for Inflammation Research, Ghent, Belgium.
Microbiology Spectrum
|August 11, 2026
Summary
Direct infection of endothelial cells by SARS-CoV-2 (the virus that causes COVID-19) is not sufficient to cause disease. This research shows that endothelial-restricted viral tropism alone does not lead to severe COVID-19 symptoms in vivo.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- Severe COVID-19 often involves vascular complications, prompting investigation into direct SARS-CoV-2 endothelial cell infection.
- The role of endothelial-restricted viral tropism in COVID-19 pathogenesis remains unclear, despite endothelial cells expressing ACE2.
Purpose of the Study:
- To directly assess the in vivo consequences of endothelial-restricted SARS-CoV-2 tropism.
- To determine if direct endothelial infection by SARS-CoV-2 can cause disease.
Main Methods:
- Generated a transgenic mouse model (Cdh5-hACE2) expressing human ACE2 specifically in endothelial cells.
- Infected Cdh5-hACE2 mice with SARS-CoV-2 to evaluate viral tropism and disease development.
Main Results:
- Confirmed pulmonary endothelial expression and presence of human ACE2 in Cdh5-hACE2 mice.
- SARS-CoV-2 infection did not result in clinical illness, detectable viral replication, or immune cell influx in the lungs.
- No significant histopathological abnormalities were observed in the lungs or brains of infected mice.
Conclusions:
- Endothelial-restricted SARS-CoV-2 tropism alone is insufficient to drive productive infection and clinical disease in vivo.
- Endothelial involvement in COVID-19 likely stems from broader cellular infection or systemic host responses, not primary endothelial infection.
