ArticleiScience2025
Yip1 interacting factor homolog B mediates the unconventional secretion of ORF8 during SARS-CoV-2 infection.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
- SARS-CoV-2 ORF8: an accessory protein at the interface of immune evasion and inflammation.Frontiers in immunology · 2026Review
- Hidden players of COVID-19: the evolving roles of SARS-CoV-2 accessory proteins.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe cases of COVID-19 are associated with immune responses that lead to a surge in inflammatory molecules, resulting in multi-organ failure and death. This significant increase in inflammatory factors is triggered by viral proteins. Open reading frame 8 (ORF8) has received particular attention as a unique accessory protein of SARS-CoV-2. In a previous study, we have examined the role of unconventionally released ORF8 during cytokine storm associated with SARS-CoV-2 infection. Here, after mass spectrometry analysis and gene knockout/knockdown in cell/hamster models, we further discovered that Yip1 interacting factor homolog B (YIF1B) directly translocates unglycosylated ORF8 into vesicles that mediate cargo transport; specifically, the α4 helix of YIF1B interacts with the β8 sheet. Blocking ORF8 unconventional secretion via YIF1B knockdown attenuates inflammation and yields reduced mortality. Our study suggests that YIF1B directs ORF8 translocation into an unconventional secretion pathway, which has significant implications for the pathogenesis and treatment of COVID-19.
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Registered trials
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