Journal
CELL
Volume 182, Issue 3, Pages 744-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.06.011
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Categories
Funding
- NIH [75N93019C00062, R01 AI127828, P01 AI60699, R21 AI139813, U01 AI141990, R01 AI130591, R35 HL145242, HHSN272201400008C]
- Defense Advanced Research Projects Agency [HR001117S0019]
- Helen Hay Whitney Foundation postdoctoral fellowship
- [F32 AI138392]
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a pandemic with millions of human infections. One limitation to the evaluation of potential therapies and vaccines to inhibit SARS-CoV-2 infection and ameliorate disease is the lack of susceptible small animals in large numbers. Commercially available laboratory strains of mice are not readily infected by SARS-CoV-2 because of species-specific differences in their angiotensin-converting enzyme 2 (ACE2) receptors. Here, we transduced replication-defective adenoviruses encoding human ACE2 via intranasal administration into BALB/c mice and established receptor expression in lung tissues. hACE2-transduced mice were productively infected with SARS-CoV-2, and this resulted in high viral titers in the lung, lung pathology, and weight loss. Passive transfer of a neutralizing monoclonal antibody reduced viral burden in the lung and mitigated inflammation and weight loss. The development of an accessible mouse model of SARS-CoV-2 infection and pathogenesis will expedite the testing and deployment of therapeutics and vaccines.
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