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10.1128/JVI.01257-21 http://scihub22266oqcxt.onion/10.1128/JVI.01257-21 34523966!8577386!34523966     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2021 ; 95 (23): e0125721 Nephropedia Template TP {{tp|p=34523966|t=2021. The NF-kappaB Transcriptional Footprint Is Essential for SARS-CoV-2 Replication |pdf=|usr=}}{{34523966}} gab.com Text The NF-kappaB Transcriptional Footprint Is Essential for SARS-CoV-2 Replication JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=34523966 #FOAvip SARS-CoV-2, the etiological agent of COVID-19, is characterized by a delay in type I interferon (IFN-I)-mediated antiviral defenses alongside robust cytokine production. Here, we investigate the underlying molecular basis for this imbalance and implicate virus-mediated activation of NF-kappaB in the absence of other canonical IFN-I-related transcription factors. Epigenetic and single-cell transcriptomic analyses show a selective NF-kappaB signature that was most prominent in infected cells. Disruption of NF-kappaB signaling through the silencing of the NF-kappaB transcription factor p65 or p50 resulted in loss of virus replication that was rescued upon reconstitution. These findings could be further corroborated with the use of NF-kappaB inhibitors, which reduced SARS-CoV-2 replication in vitro. These data suggest that the robust cytokine production in response to SARS-CoV-2, despite a diminished IFN-I response, is the product of a dependency on NF-kappaB for viral replication. IMPORTANCE The COVID-19 pandemic has caused significant mortality and morbidity around the world. Although effective vaccines have been developed, large parts of the world remain unvaccinated while new SARS-CoV-2 variants keep emerging. Furthermore, despite extensive efforts and large-scale drug screenings, no fully effective antiviral treatment options have been discovered yet. Therefore, it is of the utmost importance to gain a better understanding of essential factors driving SARS-CoV-2 replication to be able to develop novel approaches to target SARS-CoV-2 biology. Twit Text FOAVip The NF-kappaB Transcriptional Footprint Is Essential for SARS-CoV-2 Replication ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=34523966 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34523966 #FOAvip English Wikipedia <ref>{{Cite pmid|34523966}}</ref> The NF-kappaB Transcriptional Footprint Is Essential for SARS-CoV-2 Replication #MMPMID34523966 Nilsson-Payant BE; Uhl S; Grimont A; Doane AS; Cohen P; Patel RS; Higgins CA; Acklin JA; Bram Y; Chandar V; Blanco-Melo D; Panis M; Lim JK; Elemento O; Schwartz RE; Rosenberg BR; Chandwani R; tenOever BR J Virol 2021[Nov]; 95 (23): e0125721 PMID34523966show ga SARS-CoV-2, the etiological agent of COVID-19, is characterized by a delay in type I interferon (IFN-I)-mediated antiviral defenses alongside robust cytokine production. Here, we investigate the underlying molecular basis for this imbalance and implicate virus-mediated activation of NF-kappaB in the absence of other canonical IFN-I-related transcription factors. Epigenetic and single-cell transcriptomic analyses show a selective NF-kappaB signature that was most prominent in infected cells. Disruption of NF-kappaB signaling through the silencing of the NF-kappaB transcription factor p65 or p50 resulted in loss of virus replication that was rescued upon reconstitution. These findings could be further corroborated with the use of NF-kappaB inhibitors, which reduced SARS-CoV-2 replication in vitro. These data suggest that the robust cytokine production in response to SARS-CoV-2, despite a diminished IFN-I response, is the product of a dependency on NF-kappaB for viral replication. IMPORTANCE The COVID-19 pandemic has caused significant mortality and morbidity around the world. Although effective vaccines have been developed, large parts of the world remain unvaccinated while new SARS-CoV-2 variants keep emerging. Furthermore, despite extensive efforts and large-scale drug screenings, no fully effective antiviral treatment options have been discovered yet. Therefore, it is of the utmost importance to gain a better understanding of essential factors driving SARS-CoV-2 replication to be able to develop novel approaches to target SARS-CoV-2 biology. |*SARS-CoV-2[MESH] |*Transcriptome[MESH] |*Virus Replication[MESH] |A549 Cells[MESH] |Animals[MESH] |COVID-19/*metabolism/virology[MESH] |Chlorocebus aethiops[MESH] |Cytokines/*metabolism[MESH] |Epigenomics[MESH] |Gene Expression Regulation[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Host Microbial Interactions[MESH] |Humans[MESH] |Interferon Type I/*metabolism[MESH] |Signal Transduction[MESH] |Single-Cell Analysis[MESH] |Transcription Factor RelA/antagonists & inhibitors/genetics/*metabolism[MESH] |Transcription Factors/metabolism[MESH]The NF-kappaB Transcriptional Footprint Is Essential for SARS-CoV-2 Re(epmc).pdf DeepDyve Pubget Overpricing