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10.1038/s41590-021-00942-0 http://scihub22266oqcxt.onion/10.1038/s41590-021-00942-0 33976430!ä!33976430 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33976430.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Immunol 2021 ; 22 (7): 820-828 Nephropedia Template TP {{tp|p=33976430|t=2021. RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells |pdf=|usr=}}{{33976430}} gab.com Text RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33976430 #FOAvip Efficient immune responses against viral infection are determined by sufficient activation of nucleic acid sensor-mediated innate immunity(1,2). Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains an ongoing global pandemic. It is an urgent challenge to clarify the innate recognition mechanism to control this virus. Here we show that retinoic acid-inducible gene-I (RIG-I) sufficiently restrains SARS-CoV-2 replication in human lung cells in a type I/III interferon (IFN)-independent manner. RIG-I recognizes the 3' untranslated region of the SARS-CoV-2 RNA genome via the helicase domains, but not the C-terminal domain. This new mode of RIG-I recognition does not stimulate its ATPase, thereby aborting the activation of the conventional mitochondrial antiviral-signaling protein-dependent pathways, which is in accordance with lack of cytokine induction. Nevertheless, the interaction of RIG-I with the viral genome directly abrogates viral RNA-dependent RNA polymerase mediation of the first step of replication. Consistently, genetic ablation of RIG-I allows lung cells to produce viral particles that expressed the viral spike protein. By contrast, the anti-SARS-CoV-2 activity was restored by all-trans retinoic acid treatment through upregulation of RIG-I protein expression in primary lung cells derived from patients with chronic obstructive pulmonary disease. Thus, our findings demonstrate the distinctive role of RIG-I as a restraining factor in the early phase of SARS-CoV-2 infection in human lung cells. Twit Text FOAVip RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33976430 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33976430 #FOAvip English Wikipedia <ref>{{Cite pmid|33976430}}</ref> RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells #MMPMID33976430 Yamada T; Sato S; Sotoyama Y; Orba Y; Sawa H; Yamauchi H; Sasaki M; Takaoka A Nat Immunol 2021[Jul]; 22 (7): 820-828 PMID33976430show ga Efficient immune responses against viral infection are determined by sufficient activation of nucleic acid sensor-mediated innate immunity(1,2). Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains an ongoing global pandemic. It is an urgent challenge to clarify the innate recognition mechanism to control this virus. Here we show that retinoic acid-inducible gene-I (RIG-I) sufficiently restrains SARS-CoV-2 replication in human lung cells in a type I/III interferon (IFN)-independent manner. RIG-I recognizes the 3' untranslated region of the SARS-CoV-2 RNA genome via the helicase domains, but not the C-terminal domain. This new mode of RIG-I recognition does not stimulate its ATPase, thereby aborting the activation of the conventional mitochondrial antiviral-signaling protein-dependent pathways, which is in accordance with lack of cytokine induction. Nevertheless, the interaction of RIG-I with the viral genome directly abrogates viral RNA-dependent RNA polymerase mediation of the first step of replication. Consistently, genetic ablation of RIG-I allows lung cells to produce viral particles that expressed the viral spike protein. By contrast, the anti-SARS-CoV-2 activity was restored by all-trans retinoic acid treatment through upregulation of RIG-I protein expression in primary lung cells derived from patients with chronic obstructive pulmonary disease. Thus, our findings demonstrate the distinctive role of RIG-I as a restraining factor in the early phase of SARS-CoV-2 infection in human lung cells. |A549 Cells[MESH] |Animals[MESH] |COVID-19/*immunology[MESH] |Cell Line[MESH] |Cell Line, Tumor[MESH] |Chlorocebus aethiops[MESH] |DEAD Box Protein 58/*immunology[MESH] |Dogs[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Interferon Lambda[MESH] |Interferon Type I/immunology[MESH] |Interferons/immunology[MESH] |Lung/*immunology/virology[MESH] |Madin Darby Canine Kidney Cells[MESH] |Pulmonary Disease, Chronic Obstructive/immunology[MESH] |RNA-Dependent RNA Polymerase/immunology[MESH] |Receptors, Immunologic/*immunology[MESH] |SARS-CoV-2/*immunology[MESH] |Sf9 Cells[MESH] |Signal Transduction/immunology[MESH] |Vero Cells[MESH]RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human l(epmc).pdf DeepDyve Pubget Overpricing