SARS-CoV-2 Nucleocapsid Protein Targets RIG-I-Like Receptor Pathways to Inhibit the Induction of Interferon Response
DC Field | Value | Language |
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dc.contributor.author | Oh, Soo Jin | - |
dc.contributor.author | Shin, Ok Sarah | - |
dc.date.accessioned | 2021-11-23T15:40:58Z | - |
dc.date.available | 2021-11-23T15:40:58Z | - |
dc.date.created | 2021-08-30 | - |
dc.date.issued | 2021-03 | - |
dc.identifier.issn | 2073-4409 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/128492 | - |
dc.description.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. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.title | SARS-CoV-2 Nucleocapsid Protein Targets RIG-I-Like Receptor Pathways to Inhibit the Induction of Interferon Response | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Ok Sarah | - |
dc.identifier.doi | 10.3390/cells10030530 | - |
dc.identifier.scopusid | 2-s2.0-85103919672 | - |
dc.identifier.wosid | 000633483700001 | - |
dc.identifier.bibliographicCitation | CELLS, v.10, no.3, pp.1 - 13 | - |
dc.relation.isPartOf | CELLS | - |
dc.citation.title | CELLS | - |
dc.citation.volume | 10 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 13 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | SARS CORONAVIRUS | - |
dc.subject.keywordPlus | IMMUNE-RESPONSES | - |
dc.subject.keywordPlus | VIRUS | - |
dc.subject.keywordPlus | DIMERIZATION | - |
dc.subject.keywordPlus | COMPLEX | - |
dc.subject.keywordPlus | GENES | - |
dc.subject.keywordAuthor | coronavirus disease 2019 | - |
dc.subject.keywordAuthor | SARS-CoV-2 N protein | - |
dc.subject.keywordAuthor | antiviral immune response | - |
dc.subject.keywordAuthor | interferon | - |
dc.subject.keywordAuthor | RIG-I like receptors | - |
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