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10.1016/j.virol.2019.11.003 http://scihub22266oqcxt.onion/10.1016/j.virol.2019.11.003 31731106!ä!31731106 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Virology 2020 ; 540 (ä): 17-22 Nephropedia Template TP {{tp|p=31731106|t=2020. IFITM3 and type I interferons are important for the control of influenza A virus replication in murine macrophages |pdf=|usr=}}{{31731106}} gab.com Text IFITM3 and type I interferons are important for the control of influenza A virus replication in murine macrophages JO: Virology http://www.kidney.de/pget.php?&tw=1&pmid=31731106 #FOAvip Abortive infection of macrophages serves as a "dead end" for most seasonal influenza A virus (IAV) strains, and it is likely to contribute to effective host defence. Interferon (IFN)-induced transmembrane protein 3 (IFITM3) restricts the early stages of IAV replication in epithelial cells, but IFITM3 restriction of IAV replication in macrophages has not been previously investigated. Herein, macrophages isolated from IFITM3-deficient mice were more susceptible to initial IAV infection, but late-stage viral replication was still controlled through abortive infection. Strikingly, IFNalpha/beta receptor (IFNAR)-deficient macrophages infected with IAV were not only more susceptible to initial infection, but these cells also supported productive viral replication. Significantly, we have established that abortive IAV infection in macrophages is controlled through a type I IFN-dependent mechanism, where late-stage IAV replication can proceed in the absence of type I IFN responses. These findings provide novel mechanistic insight into macrophage-specific processes that potently shut down IAV replication. Twit Text FOAVip IFITM3 and type I interferons are important for the control of influenza A virus replication in murine macrophages ????Virology http://www.kidney.de/pget.php?&tw=1&pmid=31731106 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31731106 #FOAvip English Wikipedia <ref>{{Cite pmid|31731106}}</ref> IFITM3 and type I interferons are important for the control of influenza A virus replication in murine macrophages #MMPMID31731106 Londrigan SL; Wakim LM; Smith J; Haverkate AJ; Brooks AG; Reading PC Virology 2020[Jan]; 540 (ä): 17-22 PMID31731106show ga Abortive infection of macrophages serves as a "dead end" for most seasonal influenza A virus (IAV) strains, and it is likely to contribute to effective host defence. Interferon (IFN)-induced transmembrane protein 3 (IFITM3) restricts the early stages of IAV replication in epithelial cells, but IFITM3 restriction of IAV replication in macrophages has not been previously investigated. Herein, macrophages isolated from IFITM3-deficient mice were more susceptible to initial IAV infection, but late-stage viral replication was still controlled through abortive infection. Strikingly, IFNalpha/beta receptor (IFNAR)-deficient macrophages infected with IAV were not only more susceptible to initial infection, but these cells also supported productive viral replication. Significantly, we have established that abortive IAV infection in macrophages is controlled through a type I IFN-dependent mechanism, where late-stage IAV replication can proceed in the absence of type I IFN responses. These findings provide novel mechanistic insight into macrophage-specific processes that potently shut down IAV replication. |*Virus Replication/drug effects[MESH] |Animals[MESH] |Cell Line[MESH] |Cells, Cultured[MESH] |Disease Susceptibility[MESH] |Gene Expression[MESH] |Host-Pathogen Interactions[MESH] |Influenza A virus/drug effects/*physiology[MESH] |Interferon Type I/*metabolism/pharmacology[MESH] |Macrophages/immunology/*metabolism/*virology[MESH] |Membrane Proteins/genetics/*metabolism[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Orthomyxoviridae Infections/immunology/*metabolism/*virology[MESH] |Receptor, Interferon alpha-beta/metabolism[MESH]IFITM3 and type I interferons are important for the control of influen(epmc).pdf DeepDyve Pubget Overpricing