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SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function
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SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function
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Journal Article
SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function
2020
Overview
Although animal models have been evaluated for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, none have fully recapitulated the lung disease phenotypes seen in humans who have been hospitalized. Here, we evaluate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs. A decline in pulmonary function occurs 4 days after peak viral titer and correlates with infiltration of monocytes, neutrophils and activated T cells. SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with signatures of nuclear factor-κB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.
Diamond and colleagues generate a K18-hACE2 model of SARS-CoV-2 infection that shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ ACE2
/ Angiotensin converting enzyme
/ Angiotensin-Converting Enzyme 2
/ Animals
/ Betacoronavirus - immunology
/ Biomedical and Life Sciences
/ Coronavirus Infections - immunology
/ Coronavirus Infections - pathology
/ COVID-19
/ Female
/ Humans
/ Immunity, Innate - immunology
/ Interferon Type I - immunology
/ Interferon-gamma - immunology
/ Lymphocyte Activation - immunology
/ Male
/ Mice
/ Neutrophil Infiltration - immunology
/ Peptidyl-Dipeptidase A - genetics
/ Pneumonia, Viral - immunology
/ Pneumonia, Viral - pathology
/ Promoter Regions, Genetic - genetics
/ Respiratory tract infections
