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10.1038/s41392-021-00800-3 http://scihub22266oqcxt.onion/10.1038/s41392-021-00800-3 34732709!8564796!34732709     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34732709&cmd=llinks): Failed to open stream: HTTP request failed! 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Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infection |pdf=|usr=}}{{34732709}} gab.com Text Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infection JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34732709 #FOAvip The global coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense RNA virus. How the host immune system senses and responds to SARS-CoV-2 infection remain largely unresolved. Here, we report that SARS-CoV-2 infection activates the innate immune response through the cytosolic DNA sensing cGAS-STING pathway. SARS-CoV-2 infection induces the cellular level of 2'3'-cGAMP associated with STING activation. cGAS recognizes chromatin DNA shuttled from the nucleus as a result of cell-to-cell fusion upon SARS-CoV-2 infection. We further demonstrate that the expression of spike protein from SARS-CoV-2 and ACE2 from host cells is sufficient to trigger cytoplasmic chromatin upon cell fusion. Furthermore, cytoplasmic chromatin-cGAS-STING pathway, but not MAVS-mediated viral RNA sensing pathway, contributes to interferon and pro-inflammatory gene expression upon cell fusion. Finally, we show that cGAS is required for host antiviral responses against SARS-CoV-2, and a STING-activating compound potently inhibits viral replication. Together, our study reported a previously unappreciated mechanism by which the host innate immune system responds to SARS-CoV-2 infection, mediated by cytoplasmic chromatin from the infected cells. Targeting the cytoplasmic chromatin-cGAS-STING pathway may offer novel therapeutic opportunities in treating COVID-19. In addition, these findings extend our knowledge in host defense against viral infection by showing that host cells' self-nucleic acids can be employed as a "danger signal" to alarm the immune system. Twit Text FOAVip Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infection ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34732709 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34732709 #FOAvip English Wikipedia <ref>{{Cite pmid|34732709}}</ref> Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infection #MMPMID34732709 Zhou Z; Zhang X; Lei X; Xiao X; Jiao T; Ma R; Dong X; Jiang Q; Wang W; Shi Y; Zheng T; Rao J; Xiang Z; Ren L; Deng T; Jiang Z; Dou Z; Wei W; Wang J Signal Transduct Target Ther 2021[Nov]; 6 (1): 382 PMID34732709show ga The global coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense RNA virus. How the host immune system senses and responds to SARS-CoV-2 infection remain largely unresolved. Here, we report that SARS-CoV-2 infection activates the innate immune response through the cytosolic DNA sensing cGAS-STING pathway. SARS-CoV-2 infection induces the cellular level of 2'3'-cGAMP associated with STING activation. cGAS recognizes chromatin DNA shuttled from the nucleus as a result of cell-to-cell fusion upon SARS-CoV-2 infection. We further demonstrate that the expression of spike protein from SARS-CoV-2 and ACE2 from host cells is sufficient to trigger cytoplasmic chromatin upon cell fusion. Furthermore, cytoplasmic chromatin-cGAS-STING pathway, but not MAVS-mediated viral RNA sensing pathway, contributes to interferon and pro-inflammatory gene expression upon cell fusion. Finally, we show that cGAS is required for host antiviral responses against SARS-CoV-2, and a STING-activating compound potently inhibits viral replication. Together, our study reported a previously unappreciated mechanism by which the host innate immune system responds to SARS-CoV-2 infection, mediated by cytoplasmic chromatin from the infected cells. Targeting the cytoplasmic chromatin-cGAS-STING pathway may offer novel therapeutic opportunities in treating COVID-19. In addition, these findings extend our knowledge in host defense against viral infection by showing that host cells' self-nucleic acids can be employed as a "danger signal" to alarm the immune system. |*Immunity, Innate[MESH] |Animals[MESH] |COVID-19/genetics/*immunology[MESH] |Chromatin/genetics/*immunology[MESH] |Cytoplasm/genetics/*immunology[MESH] |Disease Models, Animal[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Humans[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Nucleotidyltransferases/genetics/*immunology[MESH]Sensing of cytoplasmic chromatin by cGAS activates innate immune respo(epmc).pdf DeepDyve Pubget Overpricing