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10.1074/jbc.AC120.013788 http://scihub22266oqcxt.onion/10.1074/jbc.AC120.013788 32587093!7549028!32587093     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       J+Biol+Chem 2020 ; 295 (41): 13958-13964 Nephropedia Template TP {{tp|p=32587093|t=2020. Inhibition of SARS-CoV-2 by type I and type III interferons |pdf=|usr=}}{{32587093}} gab.com Text Inhibition of SARS-CoV-2 by type I and type III interferons JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=32587093 #FOAvip The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-alpha in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19. Twit Text FOAVip Inhibition of SARS-CoV-2 by type I and type III interferons ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=32587093 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32587093 #FOAvip English Wikipedia <ref>{{Cite pmid|32587093}}</ref> Inhibition of SARS-CoV-2 by type I and type III interferons #MMPMID32587093 Felgenhauer U; Schoen A; Gad HH; Hartmann R; Schaubmar AR; Failing K; Drosten C; Weber F J Biol Chem 2020[Oct]; 295 (41): 13958-13964 PMID32587093show ga The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-alpha in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19. |Animals[MESH] |Antiviral Agents/*pharmacology[MESH] |Betacoronavirus/*drug effects/isolation & purification/physiology[MESH] |COVID-19[MESH] |Cell Line[MESH] |Chlorocebus aethiops[MESH] |Coronavirus Infections/pathology/virology[MESH] |Humans[MESH] |Interferon Lambda[MESH] |Interferon Type I/*pharmacology[MESH] |Interferons/*pharmacology[MESH] |Janus Kinases/metabolism[MESH] |Nitriles[MESH] |Pandemics[MESH] |Pneumonia, Viral/pathology/virology[MESH] |Pyrazoles/pharmacology[MESH] |Pyrimidines[MESH] |SARS-CoV-2[MESH] |Severe acute respiratory syndrome-related coronavirus/drug effects/physiology[MESH] |Signal Transduction/drug effects[MESH] |Vero Cells[MESH]Inhibition of SARS-CoV-2 by type I and type III interferons (epmc).pdf DeepDyve Pubget Overpricing