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  • 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]
  • |SARS-CoV-2/genetics/*immunology[MESH]

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  • suck abstract from ncbi

    382 1.6 2021