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10.1261/rna.078923.121 http://scihub22266oqcxt.onion/10.1261/rna.078923.121 34315815!8522697!34315815     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34315815&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 infection triggers widespread host mRNA decay leading to an mRNA export block |pdf=|usr=}}{{34315815}} gab.com Text SARS-CoV-2 infection triggers widespread host mRNA decay leading to an mRNA export block JO: RNA http://www.kidney.de/pget.php?&tw=1&pmid=34315815 #FOAvip The transcriptional induction of interferon (IFN) genes is a key feature of the mammalian antiviral response that limits viral replication and dissemination. A hallmark of severe COVID-19 disease caused by SARS-CoV-2 is the low presence of IFN proteins in patient serum despite elevated levels of IFN-encoding mRNAs, indicative of post-transcriptional inhibition of IFN protein production. Here, we performed single-molecule RNA visualization to examine the expression and localization of host mRNAs during SARS-CoV-2 infection. Our data show that the biogenesis of type I and type III IFN mRNAs is inhibited at multiple steps during SARS-CoV-2 infection. First, translocation of the interferon regulatory factor 3 (IRF3) transcription factor to the nucleus is limited in response to SARS-CoV-2, indicating that SARS-CoV-2 inhibits RLR-MAVS signaling and thus weakens transcriptional induction of IFN genes. Second, we observed that IFN mRNAs primarily localize to the site of transcription in most SARS-CoV-2 infected cells, suggesting that SARS-CoV-2 either inhibits the release of IFN mRNAs from their sites of transcription and/or triggers decay of IFN mRNAs in the nucleus upon exiting the site of transcription. Lastly, nuclear-cytoplasmic transport of IFN mRNAs is inhibited during SARS-CoV-2 infection, which we propose is a consequence of widespread degradation of host cytoplasmic basal mRNAs in the early stages of SARS-CoV-2 replication by the SARS-CoV-2 Nsp1 protein, as well as the host antiviral endoribonuclease, RNase L. Importantly, IFN mRNAs can escape SARS-CoV-2-mediated degradation if they reach the cytoplasm, making rescue of mRNA export a viable means for promoting the immune response to SARS-CoV-2. Twit Text FOAVip SARS-CoV-2 infection triggers widespread host mRNA decay leading to an mRNA export block ????RNA http://www.kidney.de/pget.php?&tw=1&pmid=34315815 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34315815 #FOAvip English Wikipedia <ref>{{Cite pmid|34315815}}</ref> SARS-CoV-2 infection triggers widespread host mRNA decay leading to an mRNA export block #MMPMID34315815 Burke JM; St Clair LA; Perera R; Parker R RNA 2021[Nov]; 27 (11): 1318-1329 PMID34315815show ga The transcriptional induction of interferon (IFN) genes is a key feature of the mammalian antiviral response that limits viral replication and dissemination. A hallmark of severe COVID-19 disease caused by SARS-CoV-2 is the low presence of IFN proteins in patient serum despite elevated levels of IFN-encoding mRNAs, indicative of post-transcriptional inhibition of IFN protein production. Here, we performed single-molecule RNA visualization to examine the expression and localization of host mRNAs during SARS-CoV-2 infection. Our data show that the biogenesis of type I and type III IFN mRNAs is inhibited at multiple steps during SARS-CoV-2 infection. First, translocation of the interferon regulatory factor 3 (IRF3) transcription factor to the nucleus is limited in response to SARS-CoV-2, indicating that SARS-CoV-2 inhibits RLR-MAVS signaling and thus weakens transcriptional induction of IFN genes. Second, we observed that IFN mRNAs primarily localize to the site of transcription in most SARS-CoV-2 infected cells, suggesting that SARS-CoV-2 either inhibits the release of IFN mRNAs from their sites of transcription and/or triggers decay of IFN mRNAs in the nucleus upon exiting the site of transcription. Lastly, nuclear-cytoplasmic transport of IFN mRNAs is inhibited during SARS-CoV-2 infection, which we propose is a consequence of widespread degradation of host cytoplasmic basal mRNAs in the early stages of SARS-CoV-2 replication by the SARS-CoV-2 Nsp1 protein, as well as the host antiviral endoribonuclease, RNase L. Importantly, IFN mRNAs can escape SARS-CoV-2-mediated degradation if they reach the cytoplasm, making rescue of mRNA export a viable means for promoting the immune response to SARS-CoV-2. |*RNA Stability[MESH] |A549 Cells[MESH] |Angiotensin-Converting Enzyme 2/genetics/metabolism[MESH] |COVID-19/*genetics/virology[MESH] |Cell Line[MESH] |Endoribonucleases/genetics/metabolism[MESH] |Host-Pathogen Interactions/*genetics[MESH] |Humans[MESH] |In Situ Hybridization, Fluorescence/methods[MESH] |Interferon Regulatory Factor-3/genetics/metabolism[MESH] |Interferons/*genetics/metabolism[MESH] |RNA, Messenger/metabolism[MESH] |SARS-CoV-2/*pathogenicity[MESH] |Single Molecule Imaging[MESH]SARS-CoV-2 infection triggers widespread host mRNA decay leading to an(epmc).pdf DeepDyve Pubget Overpricing