Cell Reports· 2026Q1
Influenza virus antagonizes self-sensing by RIG-I to enhance viral replication
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- 2026year
Short summary
Influenza virus nucleoprotein (NP) antagonizes RIG-I sensing of host RNAs, which normally signal to suppress viral replication, thereby enhancing viral replication.
AI-generated from the title and abstract; the full text is not read.
Key points
- Host RNAs, particularly non-coding RNAs from RNA polymerase III, activate RIG-I to suppress influenza virus replication.
- Influenza virus nucleoprotein (NP) binds to RIG-I through an RNA bridge.
- NP antagonizes RIG-I's sensing of host RNAs, thereby blocking the antiviral response.
- This mechanism allows influenza virus to enhance its own replication by evading innate immunity.
AI-generated from the title and abstract; the full text is not read.
Abstract
Innate immune sensors must finely distinguish pathogens from the host to mount a response only during infection. RIG-I is a cytoplasmic sensor that triggers a broad antiviral response in response to sensing foreign RNAs. Here, we show that RIG-I not only binds viral RNAs but is activated by host RNAs. These are primarily non-coding RNAs transcribed by RNA polymerase III. They are benign under normal conditions but become immunogenic during influenza virus infection, where they signal via RIG-I to suppress viral replication. These RNAs are also bound by influenza virus nucleoprotein (NP), which normally functions to encapsidate the viral genome. NP interacts with RIG-I via an RNA bridge and antagonizes sensing of self-RNAs to counter innate immune responses. Overall, we demonstrate that self-sensing is strategically deployed by the cell to amplify the antiviral response and reveal a newly identified viral countermeasure that disrupts RIG-I activation by host RNAs.
The authors' abstract, as published at the source. Cell Reports, 2026 · DOI ↗
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ImmunologyImmunology and Microbiology