ArticleScience advances2026
Molecular mechanism by which SARS-CoV-2 Orf9b suppresses the Tom70-Hsp90 interaction to evade innate immunity.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Dynamic disorder is crucial for mitochondrial protein import.Protein science : a publication of the Protein Society · 2026Review
- Inhibiting the interaction between the mitochondrial receptor Tom70 and SARS CoV 2 Orf9b with small molecules.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
The Tom70-Hsp90 interaction is critical for MAVS-mediated interferon (IFN) production. Upon RNA virus infection, cytosolic Hsp90 recruits key innate immune signaling proteins to MAVS on mitochondria through its interaction with Tom70. To evade this innate immune response, SARS-CoV-2 Orf9b binds to Tom70, thereby disrupting the Tom70-Hsp90 interaction and suppressing IFN production. Despite its importance, the molecular mechanism underlying the Orf9b-mediated IFN antagonism has remained unclear. Here, using an integrative approach including cryo-electron microscopy and
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