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10.1002/jmv.27965

http://scihub22266oqcxt.onion/10.1002/jmv.27965
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35765167!9350412!35765167
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suck abstract from ncbi


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pmid35765167      J+Med+Virol 2022 ; 94 (11): 5174-5188
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  • SARS-CoV-2 ORF10 antagonizes STING-dependent interferon activation and autophagy #MMPMID35765167
  • Han L; Zheng Y; Deng J; Nan ML; Xiao Y; Zhuang MW; Zhang J; Wang W; Gao C; Wang PH
  • J Med Virol 2022[Nov]; 94 (11): 5174-5188 PMID35765167show ga
  • A characteristic feature of COVID-19, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is the dysregulated immune response with impaired type I and III interferon (IFN) expression and an overwhelming inflammatory cytokine storm. RIG-I-like receptors (RLRs) and cGAS-STING signaling pathways are responsible for sensing viral infection and inducing IFN production to combat invading viruses. Multiple proteins of SARS-CoV-2 have been reported to modulate the RLR signaling pathways to achieve immune evasion. Although SARS-CoV-2 infection also activates the cGAS-STING signaling by stimulating micronuclei formation during the process of syncytia, whether SARS-CoV-2 modulates the cGAS-STING pathway requires further investigation. Here, we screened 29 SARS-CoV-2-encoded viral proteins to explore the viral proteins that affect the cGAS-STING signaling pathway and found that SARS-CoV-2 open reading frame 10 (ORF10) targets STING to antagonize IFN activation. Overexpression of ORF10 inhibits cGAS-STING-induced interferon regulatory factor 3 phosphorylation, translocation, and subsequent IFN induction. Mechanistically, ORF10 interacts with STING, attenuates the STING-TBK1 association, and impairs STING oligomerization and aggregation and STING-mediated autophagy; ORF10 also prevents the endoplasmic reticulum (ER)-to-Golgi trafficking of STING by anchoring STING in the ER. Taken together, these findings suggest that SARS-CoV-2 ORF10 impairs the cGAS-STING signaling by blocking the translocation of STING and the interaction between STING and TBK1 to antagonize innate antiviral immunity.
  • |*COVID-19[MESH]
  • |*Interferon Type I/genetics[MESH]
  • |Autophagy[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Interferons[MESH]
  • |Membrane Proteins/genetics/metabolism[MESH]
  • |Nucleotidyltransferases/genetics[MESH]
  • |Open Reading Frames[MESH]
  • |Protein Serine-Threonine Kinases/genetics[MESH]
  • |SARS-CoV-2[MESH]


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