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10.1371/journal.ppat.1007125 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1007125 C6042795!6042795!30001425     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2018 ; 14 (7): ä Nephropedia Template TP {{tp|p=30001425|t=2018. DDX3 suppresses type I interferons and favors viral replication during Arenavirus infection |pdf=|usr=}}{{30001425}} gab.com Text DDX3 suppresses type I interferons and favors viral replication during Arenavirus infection JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=30001425 #FOAvip Several arenaviruses cause hemorrhagic fever (HF) diseases that are associated with high morbidity and mortality in humans. Accordingly, HF arenaviruses have been listed as top-priority emerging diseases for which countermeasures are urgently needed. Because arenavirus nucleoprotein (NP) plays critical roles in both virus multiplication and immune-evasion, we used an unbiased proteomic approach to identify NP-interacting proteins in human cells. DDX3, a DEAD-box ATP-dependent-RNA-helicase, interacted with NP in both NP-transfected and virus-infected cells. Importantly, DDX3 deficiency compromised the propagation of both Old and New World arenaviruses, including the HF arenaviruses Lassa and Junin viruses. The DDX3 role in promoting arenavirus multiplication associated with both a previously un-recognized DDX3 inhibitory role in type I interferon production in arenavirus infected cells and a positive DDX3 effect on arenavirus RNA synthesis that was dependent on its ATPase and Helicase activities. Our results uncover novel mechanisms used by arenaviruses to exploit the host machinery and subvert immunity, singling out DDX3 as a potential host target for developing new therapies against highly pathogenic arenaviruses. Twit Text FOAVip DDX3 suppresses type I interferons and favors viral replication during Arenavirus infection ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=30001425 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30001425 #FOAvip English Wikipedia <ref>{{Cite pmid|30001425}}</ref> DDX3 suppresses type I interferons and favors viral replication during Arenavirus infection #MMPMID30001425 Loureiro ME; Zorzetto-Fernandes AL; Radoshitzky S; Chi X; Dallari S; Marooki N; Lèger P; Foscaldi S; Harjono V; Sharma S; Zid BM; López N; de la Torre JC; Bavari S; Zúñiga E PLoS Pathog 2018[Jul]; 14 (7): ä PMID30001425show ga Several arenaviruses cause hemorrhagic fever (HF) diseases that are associated with high morbidity and mortality in humans. Accordingly, HF arenaviruses have been listed as top-priority emerging diseases for which countermeasures are urgently needed. Because arenavirus nucleoprotein (NP) plays critical roles in both virus multiplication and immune-evasion, we used an unbiased proteomic approach to identify NP-interacting proteins in human cells. DDX3, a DEAD-box ATP-dependent-RNA-helicase, interacted with NP in both NP-transfected and virus-infected cells. Importantly, DDX3 deficiency compromised the propagation of both Old and New World arenaviruses, including the HF arenaviruses Lassa and Junin viruses. The DDX3 role in promoting arenavirus multiplication associated with both a previously un-recognized DDX3 inhibitory role in type I interferon production in arenavirus infected cells and a positive DDX3 effect on arenavirus RNA synthesis that was dependent on its ATPase and Helicase activities. Our results uncover novel mechanisms used by arenaviruses to exploit the host machinery and subvert immunity, singling out DDX3 as a potential host target for developing new therapies against highly pathogenic arenaviruses. äDDX3 suppresses type I interferons and favors viral replication during(epmc).pdf DeepDyve Pubget Overpricing