About: SARS-CoV-2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation, immune cell infiltration, and compromised respiratory function

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About: SARS-CoV-2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation, immune cell infiltration, and compromised respiratory function Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	SARS-CoV-2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation, immune cell infiltration, and compromised respiratory function
Creator	Yu, Jinsheng Diamond, Michael Nair, Sharmila Fox, Julie Earnest, James Holtzman, Michael Mccune, Broc Winkler, Emma Kafai, Natasha Bailey, Adam Chen, Rita Dort, Sarah Head, Richard Kang, Liang-I Keeler, Shamus Ritter, Robichaud, Annette
Source	BioRxiv; Medline
abstract	Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) emerged in late 2019 and has spread worldwide resulting in the Coronavirus Disease 2019 (COVID-19) pandemic. Although animal models have been evaluated for SARS-CoV-2 infection, none have recapitulated the severe lung disease phenotypes seen in hospitalized human cases. Here, we evaluate heterozygous transgenic mice expressing the human ACE2 receptor driven by the epithelial cell cytokeratin-18 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 lung tissues with additional spread to other organs. Remarkably, a decline in pulmonary function, as measured by static and dynamic tests of respiratory capacity, occurs 4 days after peak viral titer and correlates with an inflammatory response marked by infiltration into the lung of monocytes, neutrophils, and activated T cells resulting in pneumonia. Cytokine profiling and RNA sequencing analysis of SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with prominent signatures of NF-kB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection recapitulates many features of severe COVID-19 infection in humans and can be used to define the mechanistic basis of lung disease and test immune and antiviral-based countermeasures.
has issue date	2020-07-10(xsd:dateTime)
bibo:doi	10.1101/2020.07.09.196188
bibo:pmid	32676600
has license	biorxiv
sha1sum (hex)	22b9c5f51b428433eb3220fa06073b99d32b42e6
schema:url	https://doi.org/10.1101/2020.07.09.196188
resource representing a document's title	SARS-CoV-2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation, immune cell infiltration, and compromised respiratory function
has PubMed identifier	32676600
schema:publication	bioRxiv
resource representing a document's body	covid:22b9c5f51b428433eb3220fa06073b99d32b42e6#body_text
is schema:about of	named entity 'tissues' named entity 'signaling' named entity 'Intranasal' named entity 'promoter' named entity 'humans' named entity 'biology' named entity 'epithelial cell' named entity 'transgenic mice' named entity 'NEUTROPHILS' named entity 'HOSPITALIZED' named entity 'CYTOKERATIN-18' named entity 'PATHWAYS' named entity 'COVID-19' named entity 'SEVERE' named entity 'TYPE I' named entity 'RNA SEQUENCING' named entity 'neutrophils' named entity 'decline' named entity 'basis' named entity 'severe' named entity 'emerged' named entity 'evaluated' named entity 'pneumonia' named entity 'Cytokine' named entity 'promoter' named entity 'evaluate' named entity 'profiling' named entity 'T cells' named entity '2019' named entity 'leukocyte' named entity 'test' named entity 'hypertension' named entity 'viral vectors' named entity 'Tyk2' named entity 'coagulopathy' named entity 'lung' named entity 'lung' named entity 'severe' named entity 'While' named entity 'human' named entity 'massively' named entity 'driven' named entity 'function' named entity 'infection' named entity 'Severe Acute Respiratory Syndrome Coronavirus' named entity 'infection' named entity 'infection' named entity 'SARS-CoV-2' named entity 'SARS-CoV-2' named entity 'ACE2 receptor' named entity 'monocytes' named entity 'infection' named entity 'pneumonia' named entity 'upregulated' named entity 'COVID-19' named entity 'COVID' named entity 'SARS-CoV-2' named entity 'infection' named entity 'ACE2' named entity 'infection' named entity 'disease' named entity 'SARS-CoV-2' named entity 'natural killer cells' named entity 'tropism' named entity 'IFN' named entity 'SARS-CoV-2'

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