tetano
Editor, Senior Moderator
Signal Transduct Target Ther
. 2021 Sep 1;6(1):331.
doi: 10.1038/s41392-021-00742-w.
A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response
Yinghua Zhao[SUP] 1 [/SUP], Liyan Sui[SUP] 1 [/SUP], Ping Wu[SUP] 2 [/SUP], Wenfang Wang[SUP] 3 [/SUP], Zedong Wang[SUP] 1 [/SUP], Yang Yu[SUP] 4 [/SUP], Zhijun Hou[SUP] 2 [/SUP], Guangyun Tan[SUP] 5 [/SUP], Quan Liu[SUP] 6 7 8 9 [/SUP], Guoqing Wang[SUP] 10 [/SUP]
Affiliations
Abstract
The recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative agent of ongoing global pandemic of COVID-19, may trigger immunosuppression in the early stage and overactive immune response in the late stage of infection; However, the underlying mechanisms are not well understood. Here we demonstrated that the SARS-CoV-2 nucleocapsid (N) protein dually regulated innate immune responses, i.e., the low-dose N protein suppressed type I interferon (IFN-I) signaling and inflammatory cytokines, whereas high-dose N protein promoted IFN-I signaling and inflammatory cytokines. Mechanistically, the SARS-CoV-2 N protein dually regulated the phosphorylation and nuclear translocation of IRF3, STAT1, and STAT2. Additionally, low-dose N protein combined with TRIM25 could suppress the ubiquitination and activation of retinoic acid-inducible gene I (RIG-I). Our findings revealed a regulatory mechanism of innate immune responses by the SARS-CoV-2 N protein, which would contribute to understanding the pathogenesis of SARS-CoV-2 and other SARS-like coronaviruses, and development of more effective strategies for controlling COVID-19.
. 2021 Sep 1;6(1):331.
doi: 10.1038/s41392-021-00742-w.
A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response
Yinghua Zhao[SUP] 1 [/SUP], Liyan Sui[SUP] 1 [/SUP], Ping Wu[SUP] 2 [/SUP], Wenfang Wang[SUP] 3 [/SUP], Zedong Wang[SUP] 1 [/SUP], Yang Yu[SUP] 4 [/SUP], Zhijun Hou[SUP] 2 [/SUP], Guangyun Tan[SUP] 5 [/SUP], Quan Liu[SUP] 6 7 8 9 [/SUP], Guoqing Wang[SUP] 10 [/SUP]
Affiliations
- PMID: 34471099
- DOI: 10.1038/s41392-021-00742-w
Abstract
The recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative agent of ongoing global pandemic of COVID-19, may trigger immunosuppression in the early stage and overactive immune response in the late stage of infection; However, the underlying mechanisms are not well understood. Here we demonstrated that the SARS-CoV-2 nucleocapsid (N) protein dually regulated innate immune responses, i.e., the low-dose N protein suppressed type I interferon (IFN-I) signaling and inflammatory cytokines, whereas high-dose N protein promoted IFN-I signaling and inflammatory cytokines. Mechanistically, the SARS-CoV-2 N protein dually regulated the phosphorylation and nuclear translocation of IRF3, STAT1, and STAT2. Additionally, low-dose N protein combined with TRIM25 could suppress the ubiquitination and activation of retinoic acid-inducible gene I (RIG-I). Our findings revealed a regulatory mechanism of innate immune responses by the SARS-CoV-2 N protein, which would contribute to understanding the pathogenesis of SARS-CoV-2 and other SARS-like coronaviruses, and development of more effective strategies for controlling COVID-19.