A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response

72Citations
Citations of this article
76Readers
Mendeley users who have this article in their library.

This article is free to access.

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.

Cite

CITATION STYLE

APA

Zhao, Y., Sui, L., Wu, P., Wang, W., Wang, Z., Yu, Y., … Wang, G. (2021). A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response. Signal Transduction and Targeted Therapy, 6(1). https://doi.org/10.1038/s41392-021-00742-w

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free