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10.1038/s41590-020-0778-2 http://scihub22266oqcxt.onion/10.1038/s41590-020-0778-2 32839612!7578095!32839612     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32839612&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function |pdf=|usr=}}{{32839612}} gab.com Text SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32839612 #FOAvip 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. Twit Text FOAVip SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32839612 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32839612 #FOAvip English Wikipedia <ref>{{Cite pmid|32839612}}</ref> 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. |Angiotensin-Converting Enzyme 2[MESH] |Animals[MESH] |Betacoronavirus/*immunology[MESH] |COVID-19[MESH] |Chlorocebus aethiops[MESH] |Coronavirus Infections/immunology/*pathology[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Humans[MESH] |Immunity, Innate/*immunology[MESH] |Interferon Type I/immunology[MESH] |Interferon-gamma/immunology[MESH] |Keratin-18/genetics[MESH] |Leukocytes/immunology[MESH] |Lymphocyte Activation/immunology[MESH] |Male[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Monocytes/immunology[MESH] |NF-kappa B/immunology[MESH] |Neutrophil Infiltration/immunology[MESH] |Neutrophils/immunology[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/*genetics[MESH] |Pneumonia, Viral/immunology/*pathology[MESH] |Pneumonia/genetics/*pathology/virology[MESH] |Promoter Regions, Genetic/genetics[MESH] |SARS-CoV-2[MESH] |T-Lymphocytes/immunology[MESH] |Vero Cells[MESH]SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung (epmc).pdf DeepDyve Pubget Overpricing