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10.7150/ijms.56630

http://scihub22266oqcxt.onion/10.7150/ijms.56630
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34104087!8176179!34104087
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suck abstract from ncbi


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pmid34104087      Int+J+Med+Sci 2021 ; 18 (12): 2561-2569
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  • SARS-CoV-2 infection activates a subset of intrinsic pathways to inhibit type I interferons in vitro and in vivo #MMPMID34104087
  • Luo W; Huang L; Wang X; Ma Y; Xiao J; Song X; Liu P; Wang Y; Wang Y; Ren Z
  • Int J Med Sci 2021[]; 18 (12): 2561-2569 PMID34104087show ga
  • SARS-CoV-2 infection poses a global challenge to human health. Upon viral infection, host cells initiate the innate antiviral response, which primarily involves type I interferons (I-IFNs), to enable rapid elimination of the invading virus. Previous studies revealed that SARS-CoV-2 infection limits the expression of I-IFNs in vitro and in vivo, but the underlying mechanism remains incompletely elucidated. In the present study, we performed data mining and longitudinal data analysis using SARS-CoV-2-infected normal human bronchial epithelial (NHBE) cells and ferrets, and the results confirmed the strong inhibitory effect of SARS-CoV-2 on the induction of I-IFNs. Moreover, we identified genes that are negatively correlated with IFNB1 expression in vitro and in vivo based on Pearson correlation analysis. We found that SARS-CoV-2 activates numerous intrinsic pathways, such as the circadian rhythm, phosphatidylinositol signaling system, peroxisome, and TNF signaling pathways, to inhibit I-IFNs. These intrinsic inhibitory pathways jointly facilitate the successful immune evasion of SARS-CoV-2. Our study elucidates the underlying mechanism by which SARS-CoV-2 evades the host innate antiviral response in vitro and in vivo, providing theoretical evidence for targeting these immune evasion-associated pathways to combat SARS-CoV-2 infection.
  • |Animals[MESH]
  • |Bronchi/cytology[MESH]
  • |COVID-19/*immunology/virology[MESH]
  • |Cell Line[MESH]
  • |Datasets as Topic[MESH]
  • |Disease Models, Animal[MESH]
  • |Epithelial Cells[MESH]
  • |Ferrets[MESH]
  • |Gene Expression Regulation/immunology[MESH]
  • |Host-Pathogen Interactions/genetics/*immunology[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Interferon-gamma/immunology/*metabolism[MESH]
  • |RNA-Seq[MESH]
  • |Respiratory Mucosa/cytology[MESH]
  • |SARS-CoV-2/*immunology[MESH]


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