SARS-CoV-2 Nucleocapsid Protein Targets RIG-I-Like Receptor Pathways to Inhibit the Induction of Interferon Response
- Authors
- Oh, Soo Jin; Shin, Ok Sarah
- Issue Date
- 3월-2021
- Publisher
- MDPI
- Keywords
- coronavirus disease 2019; SARS-CoV-2 N protein; antiviral immune response; interferon; RIG-I like receptors
- Citation
- CELLS, v.10, no.3, pp.1 - 13
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELLS
- Volume
- 10
- Number
- 3
- Start Page
- 1
- End Page
- 13
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/128492
- DOI
- 10.3390/cells10030530
- ISSN
- 2073-4409
- Abstract
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19) that has resulted in the current pandemic. The lack of highly efficacious antiviral drugs that can manage this ongoing global emergency gives urgency to establishing a comprehensive understanding of the molecular pathogenesis of SARS-CoV-2. We characterized the role of the nucleocapsid protein (N) of SARS-CoV-2 in modulating antiviral immunity. Overexpression of SARS-CoV-2 N resulted in the attenuation of retinoic acid inducible gene-I (RIG-I)-like receptor-mediated interferon (IFN) production and IFN-induced gene expression. Similar to the SARS-CoV-1 N protein, SARS-CoV-2 N suppressed the interaction between tripartate motif protein 25 (TRIM25) and RIG-I. Furthermore, SARS-CoV-2 N inhibited polyinosinic: polycytidylic acid [poly(I:C)]-mediated IFN signaling at the level of Tank-binding kinase 1 (TBK1) and interfered with the association between TBK1 and interferon regulatory factor 3 (IRF3), subsequently preventing the nuclear translocation of IRF3. We further found that both type I and III IFN production induced by either the influenza virus lacking the nonstructural protein 1 or the Zika virus were suppressed by the SARS-CoV-2 N protein. Our findings provide insights into the molecular function of the SARS-CoV-2 N protein with respect to counteracting the host antiviral immune response.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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