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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Nat+Immunol 2020 ; 21 (11): 1327-1335 Nephropedia Template TP
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SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function #MMPMID32839612
Winkler ES; Bailey AL; Kafai NM; Nair S; McCune BT; Yu J; Fox JM; Chen RE; Earnest JT; Keeler SP; Ritter JH; Kang LI; Dort S; Robichaud A; Head R; Holtzman MJ; Diamond MS
Nat Immunol 2020[Nov]; 21 (11): 1327-1335 PMID32839612show ga
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-kappaB-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.