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10.1016/j.antiviral.2016.07.008 http://scihub22266oqcxt.onion/10.1016/j.antiviral.2016.07.008 27451344!ä!27451344 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       Antiviral+Res 2016 ; 133 (ä): 23-31 Nephropedia Template TP {{tp|p=27451344|t=2016. JNJ872 inhibits influenza A virus replication without altering cellular antiviral responses |pdf=|usr=}}{{27451344}} gab.com Text JNJ872 inhibits influenza A virus replication without altering cellular antiviral responses JO: Antiviral Res http://www.kidney.de/pget.php?&tw=1&pmid=27451344 #FOAvip JNJ-63623872 (formally known as VX-787; referred to here as JNJ872) is an orally bioavailable compound, which is in phase II clinical trials for the treatment of influenza A virus (IAV) infections. Here we show that JNJ872 inhibits at nanomolar concentrations the transcription of viral RNA in IAV-infected human macrophages by targeting a highly conserved site on the cap-snatching domain of influenza polymerase basic 2 protein (PB2). Furthermore, even lower concentrations of JNJ872 protected macrophages from IAV-mediated death when given in combination with 100 nM gemcitabine, which also attenuated transcription and replication of viral RNA. Importantly, treating human macrophages with JNJ872 allowed expression of many immune-related and other genes, involved in antiviral responses, such as indoleamine 2,3-dioxygenase 1 (IDO), and cytosolic 5'-nucleotidase 3A (NT5C3A). Moreover, our targeted metabolomics analysis indicate that treatment with JNJ782 did not interfere with metabolic responses to infection, which further supported our transcriptomics results. Thus, VX-737 alone or in combination with other drugs could be beneficial for treating IAV infected patients, because it would allow the development of antiviral responses and, thereby, protect individuals from current and future infections with closely related IAV strains. Twit Text FOAVip JNJ872 inhibits influenza A virus replication without altering cellular antiviral responses ????Antiviral Res http://www.kidney.de/pget.php?&tw=1&pmid=27451344 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27451344 #FOAvip English Wikipedia <ref>{{Cite pmid|27451344}}</ref> JNJ872 inhibits influenza A virus replication without altering cellular antiviral responses #MMPMID27451344 Fu Y; Gaelings L; Soderholm S; Belanov S; Nandania J; Nyman TA; Matikainen S; Anders S; Velagapudi V; Kainov DE Antiviral Res 2016[Sep]; 133 (ä): 23-31 PMID27451344show ga JNJ-63623872 (formally known as VX-787; referred to here as JNJ872) is an orally bioavailable compound, which is in phase II clinical trials for the treatment of influenza A virus (IAV) infections. Here we show that JNJ872 inhibits at nanomolar concentrations the transcription of viral RNA in IAV-infected human macrophages by targeting a highly conserved site on the cap-snatching domain of influenza polymerase basic 2 protein (PB2). Furthermore, even lower concentrations of JNJ872 protected macrophages from IAV-mediated death when given in combination with 100 nM gemcitabine, which also attenuated transcription and replication of viral RNA. Importantly, treating human macrophages with JNJ872 allowed expression of many immune-related and other genes, involved in antiviral responses, such as indoleamine 2,3-dioxygenase 1 (IDO), and cytosolic 5'-nucleotidase 3A (NT5C3A). Moreover, our targeted metabolomics analysis indicate that treatment with JNJ782 did not interfere with metabolic responses to infection, which further supported our transcriptomics results. Thus, VX-737 alone or in combination with other drugs could be beneficial for treating IAV infected patients, because it would allow the development of antiviral responses and, thereby, protect individuals from current and future infections with closely related IAV strains. |Antiviral Agents/chemistry/*pharmacology[MESH] |Binding Sites[MESH] |Cluster Analysis[MESH] |Cytokines/genetics/metabolism[MESH] |Dose-Response Relationship, Drug[MESH] |Gene Expression Profiling[MESH] |Host-Pathogen Interactions/*drug effects/genetics[MESH] |Humans[MESH] |Influenza A virus/*drug effects/*physiology[MESH] |Influenza, Human/genetics/metabolism/virology[MESH] |Macrophages/drug effects/metabolism/virology[MESH] |Metabolome[MESH] |Metabolomics/methods[MESH] |Models, Molecular[MESH] |Molecular Conformation[MESH] |Protein Binding[MESH] |Protein Interaction Domains and Motifs[MESH] |RNA-Dependent RNA Polymerase/chemistry/metabolism[MESH] |Viral Proteins/chemistry/metabolism[MESH]JNJ872 inhibits influenza A virus replication without altering cellula(epmc).pdf DeepDyve Pubget Overpricing