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SARS-CoV-2 infection activates a subset of intrinsic pathways to inhibit type I interferons in vitro and in vivo.
Luo, Weisheng; Huang, Lianzhou; Wang, Xiaohui; Ma, Yuying; Xiao, Ji; Song, Xiaowei; Liu, Ping; Wang, Yifei; Wang, Yiliang; Ren, Zhe.
  • Luo W; Guangzhou Jinan Biomedicine Research and Development Center, Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, PR China.
  • Huang L; Key Laboratory of Virology of Guangzhou, Jinan University, Guangzhou 510632, PR China.
  • Wang X; Guangzhou Jinan Biomedicine Research and Development Center, Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, PR China.
  • Ma Y; Key Laboratory of Virology of Guangzhou, Jinan University, Guangzhou 510632, PR China.
  • Xiao J; Guangzhou Jinan Biomedicine Research and Development Center, Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, PR China.
  • Song X; Key Laboratory of Virology of Guangzhou, Jinan University, Guangzhou 510632, PR China.
  • Liu P; Guangzhou Jinan Biomedicine Research and Development Center, Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, PR China.
  • Wang Y; Key Laboratory of Virology of Guangzhou, Jinan University, Guangzhou 510632, PR China.
  • Wang Y; Guangzhou Jinan Biomedicine Research and Development Center, Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, PR China.
  • Ren Z; Key Laboratory of Virology of Guangzhou, Jinan University, Guangzhou 510632, PR China.
Int J Med Sci ; 18(12): 2561-2569, 2021.
Article in English | MEDLINE | ID: covidwho-1389722
ABSTRACT
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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Interferon-gamma / Host-Pathogen Interactions / SARS-CoV-2 / COVID-19 Type of study: Prognostic study / Reviews Limits: Animals / Humans Language: English Journal: Int J Med Sci Journal subject: Medicine Year: 2021 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Interferon-gamma / Host-Pathogen Interactions / SARS-CoV-2 / COVID-19 Type of study: Prognostic study / Reviews Limits: Animals / Humans Language: English Journal: Int J Med Sci Journal subject: Medicine Year: 2021 Document Type: Article