The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
SARS-Coronavirus Open Reading Frame-9b Suppresses Innate Immunity by Targeting Mitochondria and the MAVS/TRAF3/TRAF6 Signalosome
Open accessAbstract
Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002–2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b–mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells.
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Cites
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Cited by
Coronavirus biology and replication: implications for SARS-CoV-2
V’kovski, P., Kratzel, A., Steiner, S., Stalder, H., & Thiel, V. (2021) · Nature Reviews Microbiology · doi:10.1038/s41579-020-00468-6 · Cited by 3,197
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Immune response, inflammation, and the clinical spectrum of COVID-19
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COVID-19: Drug Targets and Potential Treatments
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Interplay between SARS-CoV-2 and the type I interferon response
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Metadata
- Authors
- Shi, C.-S., Qi, H.-Y., Boularan, C., Huang, N.-N., Abu-Asab, M., Shelhamer, J. H., & Kehrl, J. H.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-09
- Volume
- 193
- Issue
- 6
- Pages
- 3080-3089
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2111058723
- Cited by
- 473
- References
- 47
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: SARS-Coronavirus Open Reading Frame-9b Suppresses Innate Immunity by Targeting Mitochondria and the MAVS/TRAF3/TRAF6 Signalosome. https://app.cochat.ai/papers/10.4049/jimmunol.1303196
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- Shi, C.-S., Qi, H.-Y., Boularan, C., Huang, N.-N., Abu-Asab, M., Shelhamer, J. H., & Kehrl, J. H. (2014). SARS-Coronavirus Open Reading Frame-9b Suppresses Innate Immunity by Targeting Mitochondria and the MAVS/TRAF3/TRAF6 Signalosome. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1303196
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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