Cited by 351interferon and immune responsesSARS-CoV-2 and COVID-19 ResearchCOVID-19 Clinical Research Studies

SARS-CoV-2 Orf9b suppresses type I interferon responses by targeting TOM70

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Jiang, He-wei, Zhang, Hai-nan, Meng, Qing-feng, Xie, Jia, Li, Yang, Chen, Hong, Zheng, Yun-xiao, Wang, Xue-ning +5 more·2020·Cellular & Molecular Immunology

Abstract

COVID-19 is caused by SARS-CoV-2. 1 As of July 16th, 2020, there were 13,579,581 diagnosed cases and 584,782 deaths attributed to COVID-19 reported globally ( https://coronavirus.jhu.edu/map.html ). 2 Unfortunately, there is still no effective drug or vaccine for treating this disease. To accelerate drug development, there is an urgent need to identify critical molecular targets and the role they play in infection. Herein, we reported that Orf9b localizes on the membrane of mitochondria and suppresses type I interferon (IFN-I) responses through association with TOM70, and TOM70 overexpression could largely rescue this inhibition. Our results suggest the potential of targeting Orf9b-TOM70 interaction as a novel therapeutic strategy of COVID-19.

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  • The Alpha variant contains non-spike mutations including nsp6:Δ106-108 and nucleocapsid mutations D3L, R203K and G204R, which may increase transmission by antagonizing innate immunity.

    “The Alpha variant also contains several non-spike mutations including nsp6:Δ106-108 and the nucleocapsid mutations D3L, R203K and G204R, which may increase transmission by antagonizing innate immunity 25,[185][186][187] .”

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  1. Stukalov, A.et al. Multi-level proteomics reveals host-perturbation strategies of SARS-CoV-2 and SARS-CoV. https://www.biorxiv.org/content/10.1101/ 2020.06.17.156455v1 (2020). · DOI

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Authors
Jiang, H.-W., Zhang, H.-N., Meng, Q.-F., Xie, J., Li, Y., Chen, H., Zheng, Y.-X., Wang, X.-N., Qi, H., Zhang, J., Wang, P.-H., Han, Z.-G., & Tao, S.-C.
Affiliations
  • Shanghai Jiao Tong University (CN)
  • Shandong University (CN)
Corresponding author
Tao, Sheng-ce
Venue
Cellular & Molecular Immunology
Published
2020-07-29
Volume
17
Issue
9
Pages
998-1000
ISSN
  • 1672-7681 (ISSN-L)
  • 2042-0226
OpenAlex
W3045756756
Cited by
351
References
16
Citations by year
2026: 18 · 2025: 34 · 2024: 40 · 2023: 57 · 2022: 81 · 2021: 106 · 2020: 15
FWCI
22.73
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (31670831, 31970130, 31900112, 21907065)
  • National Key Research and Development Program of China Grant
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 › Infectious Diseases › COVID-19 Clinical Research Studies
Keywords
SARS-CoV-2, ORF9b, Tom70, type I interferon, interferon inhibition, mitochondrial membrane, COVID-19 pandemic, antiviral drug targets, host-virus interaction
MeSH terms
Betacoronavirus, SARS-CoV-2, Mitochondrial Precursor Protein Import Complex Proteins, Amino Acid Sequence, Gene Expression Regulation, Humans, Mitochondria, Promoter Regions, Genetic, Protein Binding, Viral Proteins, Signal Transduction, Open Reading Frames, Sequence Alignment, Interferon-beta, Sequence Homology, Amino Acid, Mitochondrial Membrane Transport Proteins, Severe acute respiratory syndrome-related coronavirus, Host-Pathogen Interactions, HEK293 Cells

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