Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling
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Abstract
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has quickly spread worldwide and has affected more than 10 million individuals. A typical feature of COVID-19 is the suppression of type I and III interferon (IFN)-mediated antiviral immunity. However, the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive. Here, we reported that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5-MAVS signaling. In addition, the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly (I:C) transfection. Mechanistically, the SARS-CoV-2 M protein interacts with RIG-I, MAVS, and TBK1, thus preventing the formation of the multiprotein complex containing RIG-I, MAVS, TRAF3, and TBK1 and subsequently impeding the phosphorylation, nuclear translocation, and activation of IRF3. Consequently, ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis virus. Taken together, these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling, which subsequently attenuates antiviral immunity and enhances viral replication. This study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19.
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IFNs inhibit viral replication and are elevated during COVID-19, which helps drive Th1 and Th17 responses.
“As is typical for many viruses, IFNs inhibit viral replication and are elevated during COVID-19, which helps drive Th1 and Th17 responses. 149,150”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [149]
The Introduction (page unavailable) says IFNs can inhibit SARS-CoV-2 replication and remain elevated in severe COVID-19, but describes their induction as suppressed in moderate cases. It does not say that IFNs drive Th1 or Th17 responses. (LLM, conf=0.88)
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- Authors
- Zheng, Y., Zhuang, M.-W., Han, L., Zhang, J., Nan, M.-L., Zhan, P., Kang, D., Liu, X., Gao, C., & Wang, P.-H.
- Affiliations
- Shandong University (CN)
- Corresponding author
- Gao, Chengjiang
- Wang, Pei-Hui
- ORCID
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2020-12-28
- Volume
- 5
- Issue
- 1
- Pages
- 299-299
- ISSN
- 2059-3635 (ISSN-L)
- PMC
- PMC7768267
- OpenAlex
- W3115832826
- Cited by
- 302
- References
- 47
- Citations by year
- 2026: 13 · 2025: 23 · 2024: 36 · 2023: 56 · 2022: 93 · 2021: 80 · 2020: 1
- FWCI
- 20.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Shandong University (2020XGB03)
- National Natural Science Foundation of China (81525012, 81930039, 31730026, 81901604, COVID-19)
- China Postdoctoral Science Foundation (2018M642662)
- Government of Jiangsu Province
- Natural Science Foundation of Jiangsu Province (SBK2020042706)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- SARS-CoV-2, membrane proteins, interferon evasion, type I interferon, interferon lambda, RIG-I, MDA5, MAVS, TBK1, IRF3, vesicular stomatitis virus, poly(I:C), viral replication
- MeSH terms
- DEAD Box Protein 58, Interferon-Induced Helicase, IFIH1, COVID-19, SARS-CoV-2, Coronavirus M Proteins, Interferon Lambda, Animals, Chlorocebus aethiops, HeLa Cells, Humans, Interferon Type I, Interferons, Receptors, Immunologic, Vero Cells, Viral Matrix Proteins, Signal Transduction, HEK293 Cells
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