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10.1073/pnas.2111600119 http://scihub22266oqcxt.onion/10.1073/pnas.2111600119 35131898!8872780!35131898     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2022 ; 119 (8): ä Nephropedia Template TP {{tp|p=35131898|t=2022. Differential interferon-alpha subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection |pdf=|usr=}}{{35131898}} gab.com Text Differential interferon-alpha subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=35131898 #FOAvip Type I interferons (IFN-I) exert pleiotropic biological effects during viral infections, balancing virus control versus immune-mediated pathologies, and have been successfully employed for the treatment of viral diseases. Humans express 12 IFN-alpha (alpha) subtypes, which activate downstream signaling cascades and result in distinct patterns of immune responses and differential antiviral responses. Inborn errors in IFN-I immunity and the presence of anti-IFN autoantibodies account for very severe courses of COVID-19; therefore, early administration of IFN-I may be protective against life-threatening disease. Here we comprehensively analyzed the antiviral activity of all IFNalpha subtypes against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to identify the underlying immune signatures and explore their therapeutic potential. Prophylaxis of primary human airway epithelial cells (hAEC) with different IFNalpha subtypes during SARS-CoV-2 infection uncovered distinct functional classes with high, intermediate, and low antiviral IFNs. In particular, IFNalpha5 showed superior antiviral activity against SARS-CoV-2 infection in vitro and in SARS-CoV-2-infected mice in vivo. Dose dependency studies further displayed additive effects upon coadministration with the broad antiviral drug remdesivir in cell culture. Transcriptomic analysis of IFN-treated hAEC revealed different transcriptional signatures, uncovering distinct, intersecting, and prototypical genes of individual IFNalpha subtypes. Global proteomic analyses systematically assessed the abundance of specific antiviral key effector molecules which are involved in IFN-I signaling pathways, negative regulation of viral processes, and immune effector processes for the potent antiviral IFNalpha5. Taken together, our data provide a systemic, multimodular definition of antiviral host responses mediated by defined IFN-I. This knowledge will support the development of novel therapeutic approaches against SARS-CoV-2. Twit Text FOAVip Differential interferon-alpha subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=35131898 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35131898 #FOAvip English Wikipedia <ref>{{Cite pmid|35131898}}</ref> Differential interferon-alpha subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection #MMPMID35131898 Schuhenn J; Meister TL; Todt D; Bracht T; Schork K; Billaud JN; Elsner C; Heinen N; Karakoese Z; Haid S; Kumar S; Brunotte L; Eisenacher M; Di Y; Lew J; Falzarano D; Chen J; Yuan Z; Pietschmann T; Wiegmann B; Uebner H; Taube C; Le-Trilling VTK; Trilling M; Krawczyk A; Ludwig S; Sitek B; Steinmann E; Dittmer U; Lavender KJ; Sutter K; Pfaender S Proc Natl Acad Sci U S A 2022[Feb]; 119 (8): ä PMID35131898show ga Type I interferons (IFN-I) exert pleiotropic biological effects during viral infections, balancing virus control versus immune-mediated pathologies, and have been successfully employed for the treatment of viral diseases. Humans express 12 IFN-alpha (alpha) subtypes, which activate downstream signaling cascades and result in distinct patterns of immune responses and differential antiviral responses. Inborn errors in IFN-I immunity and the presence of anti-IFN autoantibodies account for very severe courses of COVID-19; therefore, early administration of IFN-I may be protective against life-threatening disease. Here we comprehensively analyzed the antiviral activity of all IFNalpha subtypes against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to identify the underlying immune signatures and explore their therapeutic potential. Prophylaxis of primary human airway epithelial cells (hAEC) with different IFNalpha subtypes during SARS-CoV-2 infection uncovered distinct functional classes with high, intermediate, and low antiviral IFNs. In particular, IFNalpha5 showed superior antiviral activity against SARS-CoV-2 infection in vitro and in SARS-CoV-2-infected mice in vivo. Dose dependency studies further displayed additive effects upon coadministration with the broad antiviral drug remdesivir in cell culture. Transcriptomic analysis of IFN-treated hAEC revealed different transcriptional signatures, uncovering distinct, intersecting, and prototypical genes of individual IFNalpha subtypes. Global proteomic analyses systematically assessed the abundance of specific antiviral key effector molecules which are involved in IFN-I signaling pathways, negative regulation of viral processes, and immune effector processes for the potent antiviral IFNalpha5. Taken together, our data provide a systemic, multimodular definition of antiviral host responses mediated by defined IFN-I. This knowledge will support the development of novel therapeutic approaches against SARS-CoV-2. |*COVID-19 Drug Treatment[MESH] |*Transcriptome[MESH] |Animals[MESH] |COVID-19/immunology/virology[MESH] |Chlorocebus aethiops[MESH] |Cloning, Molecular[MESH] |Disease Models, Animal[MESH] |Escherichia coli/genetics/metabolism[MESH] |Gene Expression Profiling[MESH] |Gene Expression Regulation[MESH] |Genetic Vectors/chemistry/metabolism[MESH] |Humans[MESH] |Interferon-alpha/genetics/immunology/*pharmacology[MESH] |Mice[MESH] |Protein Isoforms/classification/genetics/immunology/pharmacology[MESH] |Recombinant Proteins/classification/genetics/immunology/pharmacology[MESH] |SARS-CoV-2/*drug effects/genetics/immunology[MESH] |Signal Transduction[MESH] |Vero Cells[MESH]Differential interferon-alpha subtype induced immune signatures are as(epmc).pdf DeepDyve Pubget Overpricing