SARS-CoV-2 S protein disrupts the formation of ISGF3 complex through conserved S2 subunit to antagonize type I interferon response

This study unveils a new mechanism by which the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) protein attenuates the host's antiviral immune response. The interferon-inhibitory mechanism of the S protein was universal among SARS-CoV-2 variants and other human coronaviruses, including SARS-CoV, MERS-CoV, HCoV-229E, HCoV-NL63, and HCoV-HKU1, through conserved S2 domains. Our study expands the understanding of SARS-CoV-2 and other human coronaviruses in evading antiviral immune strategies, which is very important for the design and optimization of vaccine antigens, thus providing a theoretical basis for human anti-coronavirus immunity and understanding the interaction between the host and coronavirus.

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Publication Details

Journal
Journal of Virology
Published
2024-12-19
DOI
https://doi.org/10.1128/jvi.01516-24
Citations
11
Primary Topic
interferon and immune responses
Type
article
Field-Weighted Citation Impact
2.65

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article

SARS-CoV-2 S protein disrupts the formation of ISGF3 complex through conserved S2 subunit to antagonize type I interferon response

Wenkang Li, Yu Chen, Xiaoqian Yao, Weifeng Yuan et al.
11 citations
Journal of Virology
interferon and immune responses
2.65
article

SARS-CoV-2 S protein disrupts the formation of ISGF3 complex through conserved S2 subunit to antagonize type I interferon response

Wenkang Li, Yu Chen, Xiaoqian Yao, Weifeng Yuan, Wenjia Ni, Simeng Liang, Mingliang Tang, Ke Lan, Yongliang Zhao, Zhixuan Wu, Li Zhou, Ke Xu, Zeng Cai, Yucheng Zheng, Qi Wang
article en
11 citations

Abstract

This study unveils a new mechanism by which the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) protein attenuates the host's antiviral immune response. The interferon-inhibitory mechanism of the S protein was universal among SARS-CoV-2 variants and other human coronaviruses, including SARS-CoV, MERS-CoV, HCoV-229E, HCoV-NL63, and HCoV-HKU1, through conserved S2 domains. Our study expands the understanding of SARS-CoV-2 and other human coronaviruses in evading antiviral immune strategies, which is very important for the design and optimization of vaccine antigens, thus providing a theoretical basis for human anti-coronavirus immunity and understanding the interaction between the host and coronavirus.

Journal of VirologyVol. 99(1)
Chengdu Medical College (CN), Wuhan University (CN), State Key Laboratory of Virology
National Natural Science Foundation of China, China Postdoctoral Science Foundation, Wuhan University, Fundamental Research Funds for the Central Universities
Good health and well-being
Openalex Percentile: Top 9%
interferon and immune responses
2.65
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