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10.1038/s41586-020-2708-8 http://scihub22266oqcxt.onion/10.1038/s41586-020-2708-8 32854108!8034761!32854108     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2020 ; 586 (7830): 560-566 Nephropedia Template TP {{tp|p=32854108|t=2020. A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures |pdf=|usr=}}{{32854108}} gab.com Text A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=32854108 #FOAvip Coronaviruses are prone to transmission to new host species, as recently demonstrated by the spread to humans of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic(1). Small animal models that recapitulate SARS-CoV-2 disease are needed urgently for rapid evaluation of medical countermeasures(2,3). SARS-CoV-2 cannot infect wild-type laboratory mice owing to inefficient interactions between the viral spike protein and the mouse orthologue of the human receptor, angiotensin-converting enzyme 2 (ACE2)(4). Here we used reverse genetics(5) to remodel the interaction between SARS-CoV-2 spike protein and mouse ACE2 and designed mouse-adapted SARS-CoV-2 (SARS-CoV-2 MA), a recombinant virus that can use mouse ACE2 for entry into cells. SARS-CoV-2 MA was able to replicate in the upper and lower airways of both young adult and aged BALB/c mice. SARS-CoV-2 MA caused more severe disease in aged mice, and exhibited more clinically relevant phenotypes than those seen in Hfh4-ACE2 transgenic mice, which express human ACE2 under the control of the Hfh4 (also known as Foxj1) promoter. We demonstrate the utility of this model using vaccine-challenge studies in immune-competent mice with native expression of mouse ACE2. Finally, we show that the clinical candidate interferon-lambda1a (IFN-lambda1a) potently inhibits SARS-CoV-2 replication in primary human airway epithelial cells in vitro-both prophylactic and therapeutic administration of IFN-lambda1a diminished SARS-CoV-2 replication in mice. In summary, the mouse-adapted SARS-CoV-2 MA model demonstrates age-related disease pathogenesis and supports the clinical use of pegylated IFN-lambda1a as a treatment for human COVID-19(6). Twit Text FOAVip A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=32854108 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32854108 #FOAvip English Wikipedia <ref>{{Cite pmid|32854108}}</ref> A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures #MMPMID32854108 Dinnon KH 3rd; Leist SR; Schafer A; Edwards CE; Martinez DR; Montgomery SA; West A; Yount BL Jr; Hou YJ; Adams LE; Gully KL; Brown AJ; Huang E; Bryant MD; Choong IC; Glenn JS; Gralinski LE; Sheahan TP; Baric RS Nature 2020[Oct]; 586 (7830): 560-566 PMID32854108show ga Coronaviruses are prone to transmission to new host species, as recently demonstrated by the spread to humans of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic(1). Small animal models that recapitulate SARS-CoV-2 disease are needed urgently for rapid evaluation of medical countermeasures(2,3). SARS-CoV-2 cannot infect wild-type laboratory mice owing to inefficient interactions between the viral spike protein and the mouse orthologue of the human receptor, angiotensin-converting enzyme 2 (ACE2)(4). Here we used reverse genetics(5) to remodel the interaction between SARS-CoV-2 spike protein and mouse ACE2 and designed mouse-adapted SARS-CoV-2 (SARS-CoV-2 MA), a recombinant virus that can use mouse ACE2 for entry into cells. SARS-CoV-2 MA was able to replicate in the upper and lower airways of both young adult and aged BALB/c mice. SARS-CoV-2 MA caused more severe disease in aged mice, and exhibited more clinically relevant phenotypes than those seen in Hfh4-ACE2 transgenic mice, which express human ACE2 under the control of the Hfh4 (also known as Foxj1) promoter. We demonstrate the utility of this model using vaccine-challenge studies in immune-competent mice with native expression of mouse ACE2. Finally, we show that the clinical candidate interferon-lambda1a (IFN-lambda1a) potently inhibits SARS-CoV-2 replication in primary human airway epithelial cells in vitro-both prophylactic and therapeutic administration of IFN-lambda1a diminished SARS-CoV-2 replication in mice. In summary, the mouse-adapted SARS-CoV-2 MA model demonstrates age-related disease pathogenesis and supports the clinical use of pegylated IFN-lambda1a as a treatment for human COVID-19(6). |*Betacoronavirus/drug effects/immunology/pathogenicity[MESH] |*Disease Models, Animal[MESH] |Aging/immunology[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Animals[MESH] |COVID-19[MESH] |COVID-19 Vaccines[MESH] |Coronavirus Infections/*drug therapy/genetics/immunology/*prevention & control[MESH] |Female[MESH] |Forkhead Transcription Factors/genetics[MESH] |Humans[MESH] |Interferon-alpha/administration & dosage/pharmacology/therapeutic use[MESH] |Interferons/administration & dosage/*pharmacology/*therapeutic use[MESH] |Interleukins/administration & dosage/*pharmacology/*therapeutic use[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Transgenic[MESH] |Models, Molecular[MESH] |Pandemics/*prevention & control[MESH] |Peptidyl-Dipeptidase A/genetics/metabolism[MESH] |Pneumonia, Viral/*drug therapy/genetics/immunology/*prevention & control[MESH] |Receptors, Virus/genetics/metabolism[MESH] |SARS-CoV-2[MESH]A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures (epmc).pdf DeepDyve Pubget Overpricing