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10.1038/s41467-020-17665-9 http://scihub22266oqcxt.onion/10.1038/s41467-020-17665-9 32733001!7392898!32733001     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       Nat+Commun 2020 ; 11 (1): 3810 Nephropedia Template TP {{tp|p=32733001|t=2020. Activation and evasion of type I interferon responses by SARS-CoV-2 |pdf=|usr=}}{{32733001}} gab.com Text Activation and evasion of type I interferon responses by SARS-CoV-2 JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=32733001 #FOAvip The pandemic of COVID-19 has posed an unprecedented threat to global public health. However, the interplay between the viral pathogen of COVID-19, SARS-CoV-2, and host innate immunity is poorly understood. Here we show that SARS-CoV-2 induces overt but delayed type-I interferon (IFN) responses. By screening 23 viral proteins, we find that SARS-CoV-2 NSP1, NSP3, NSP12, NSP13, NSP14, ORF3, ORF6 and M protein inhibit Sendai virus-induced IFN-beta promoter activation, whereas NSP2 and S protein exert opposite effects. Further analyses suggest that ORF6 inhibits both type I IFN production and downstream signaling, and that the C-terminus region of ORF6 is critical for its antagonistic effect. Finally, we find that IFN-beta treatment effectively blocks SARS-CoV-2 replication. In summary, our study shows that SARS-CoV-2 perturbs host innate immune response via both its structural and nonstructural proteins, and thus provides insights into the pathogenesis of SARS-CoV-2. Twit Text FOAVip Activation and evasion of type I interferon responses by SARS-CoV-2 ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=32733001 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32733001 #FOAvip English Wikipedia <ref>{{Cite pmid|32733001}}</ref> Activation and evasion of type I interferon responses by SARS-CoV-2 #MMPMID32733001 Lei X; Dong X; Ma R; Wang W; Xiao X; Tian Z; Wang C; Wang Y; Li L; Ren L; Guo F; Zhao Z; Zhou Z; Xiang Z; Wang J Nat Commun 2020[Jul]; 11 (1): 3810 PMID32733001show ga The pandemic of COVID-19 has posed an unprecedented threat to global public health. However, the interplay between the viral pathogen of COVID-19, SARS-CoV-2, and host innate immunity is poorly understood. Here we show that SARS-CoV-2 induces overt but delayed type-I interferon (IFN) responses. By screening 23 viral proteins, we find that SARS-CoV-2 NSP1, NSP3, NSP12, NSP13, NSP14, ORF3, ORF6 and M protein inhibit Sendai virus-induced IFN-beta promoter activation, whereas NSP2 and S protein exert opposite effects. Further analyses suggest that ORF6 inhibits both type I IFN production and downstream signaling, and that the C-terminus region of ORF6 is critical for its antagonistic effect. Finally, we find that IFN-beta treatment effectively blocks SARS-CoV-2 replication. In summary, our study shows that SARS-CoV-2 perturbs host innate immune response via both its structural and nonstructural proteins, and thus provides insights into the pathogenesis of SARS-CoV-2. |*Immune Evasion[MESH] |*Signal Transduction/drug effects[MESH] |Betacoronavirus/genetics/immunology/metabolism/*physiology[MESH] |COVID-19[MESH] |Cell Line[MESH] |Coronavirus Infections/immunology/*virology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Interferon Type I/*metabolism[MESH] |Interferon-beta/genetics/metabolism/pharmacology[MESH] |Mutation[MESH] |Open Reading Frames[MESH] |Pandemics[MESH] |Pneumonia, Viral/immunology/*virology[MESH] |Promoter Regions, Genetic[MESH] |SARS-CoV-2[MESH] |Viral Proteins/genetics/metabolism[MESH]Activation and evasion of type I interferon responses by SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing