tetano
Editor, Senior Moderator
Viruses
. 2020 Dec 30;13(1):E47.
doi: 10.3390/v13010047.
SARS-CoV-2 Nucleocapsid Protein Interacts with RIG-I and Represses RIG-Mediated IFN-β Production
Keli Chen[SUP] 1 [/SUP], Feng Xiao[SUP] 1 [/SUP], Dingwen Hu[SUP] 1 [/SUP], Weiwei Ge[SUP] 1 [/SUP], Mingfu Tian[SUP] 1 [/SUP], Wenbiao Wang[SUP] 2 [/SUP], Pan Pan[SUP] 2 [/SUP], Kailang Wu[SUP] 1 [/SUP], Jianguo Wu[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
SARS-CoV-2 is highly pathogenic in humans and poses a great threat to public health worldwide. Clinical data shows a disturbed type I interferon (IFN) response during the virus infection. In this study, we discovered that the nucleocapsid (N) protein of SARS-CoV-2 plays an important role in the inhibition of interferon beta (IFN-β) production. N protein repressed IFN-β production induced by poly(I:C) or upon Sendai virus (SeV) infection. We noted that N protein also suppressed IFN-β production, induced by several signaling molecules downstream of the retinoic acid-inducible gene I (RIG-I) pathway, which is the crucial pattern recognition receptor (PRR) responsible for identifying RNA viruses. Moreover, our data demonstrated that N protein interacted with the RIG-I protein through the DExD/H domain, which has ATPase activity and plays an important role in the binding of immunostimulatory RNAs. These results suggested that SARS-CoV-2 N protein suppresses the IFN-β response through targeting the initial step, potentially the cellular PRR-RNA-recognition step in the innate immune pathway. Therefore, we propose that the SARS-CoV-2 N protein represses IFN-β production by interfering with RIG-I.
Keywords: COVID-19; IFN; RIG-I; SARS-CoV-2; coronavirus disease 2019; interferon; nucleocapsid; retinoic acid-inducible gene I; severe acute respiratory syndrome coronavirus 2.
. 2020 Dec 30;13(1):E47.
doi: 10.3390/v13010047.
SARS-CoV-2 Nucleocapsid Protein Interacts with RIG-I and Represses RIG-Mediated IFN-β Production
Keli Chen[SUP] 1 [/SUP], Feng Xiao[SUP] 1 [/SUP], Dingwen Hu[SUP] 1 [/SUP], Weiwei Ge[SUP] 1 [/SUP], Mingfu Tian[SUP] 1 [/SUP], Wenbiao Wang[SUP] 2 [/SUP], Pan Pan[SUP] 2 [/SUP], Kailang Wu[SUP] 1 [/SUP], Jianguo Wu[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 33396605
- DOI: 10.3390/v13010047
Abstract
SARS-CoV-2 is highly pathogenic in humans and poses a great threat to public health worldwide. Clinical data shows a disturbed type I interferon (IFN) response during the virus infection. In this study, we discovered that the nucleocapsid (N) protein of SARS-CoV-2 plays an important role in the inhibition of interferon beta (IFN-β) production. N protein repressed IFN-β production induced by poly(I:C) or upon Sendai virus (SeV) infection. We noted that N protein also suppressed IFN-β production, induced by several signaling molecules downstream of the retinoic acid-inducible gene I (RIG-I) pathway, which is the crucial pattern recognition receptor (PRR) responsible for identifying RNA viruses. Moreover, our data demonstrated that N protein interacted with the RIG-I protein through the DExD/H domain, which has ATPase activity and plays an important role in the binding of immunostimulatory RNAs. These results suggested that SARS-CoV-2 N protein suppresses the IFN-β response through targeting the initial step, potentially the cellular PRR-RNA-recognition step in the innate immune pathway. Therefore, we propose that the SARS-CoV-2 N protein represses IFN-β production by interfering with RIG-I.
Keywords: COVID-19; IFN; RIG-I; SARS-CoV-2; coronavirus disease 2019; interferon; nucleocapsid; retinoic acid-inducible gene I; severe acute respiratory syndrome coronavirus 2.