ArticleMolecular cell2025
Exposure of negative-sense viral RNA in the cytoplasm initiates innate immunity to West Nile virus.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Characterization of Orsay virus replication intermediates inMolecular biology of the cell · 2026Article
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Detection of Orsay viral replication intermediates reveals spatial and regulatory links tobioRxiv : the preprint server for biology · 2025Article
- Innate immune sensing and vaccine strategies against West Nile virus: role of Toll-like receptors and viral evasion mechanisms.Frontiers in microbiology · 2025Review
- Differential TLR-ERK1/2 Activity Promotes Viral ssRNA and dsRNA Mimic-Induced Dysregulated Immunity in Macrophages.Pathogens (Basel, Switzerland) · 2024Article
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Abstract
For many RNA viruses, immunity is triggered when RIG-I-like receptors (RLRs) detect viral RNA. However, only a minority of infected cells undergo innate immune activation. By examining these "first-responder" cells during West Nile virus infection, we found that specific accumulation of antigenomic negative-sense viral RNA (-vRNA) underlies innate immune activation and that RIG-I preferentially interacts with -vRNA. However, flaviviruses sequester -vRNA into membrane-bound replication compartments away from cytosolic sensors. We found that single-stranded -vRNA accumulates outside of replication compartments in first-responder cells, rendering it accessible to RLRs. Exposure of this -vRNA occurs at late time points of infection, is linked to viral assembly, and depends on the expression of viral structural proteins. These findings reveal that, although most infected cells replicate high levels of vRNA, release of -vRNA from replication compartments during assembly occurs at low frequency and is critical for initiation of innate immunity during flavivirus infection.
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