ArticlemBio2025
The miR-302 cluster-IRFs-IRF1AS axis regulates influenza A virus replication in a species-specific manner.
Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Investigating the Role of microRNA in Host-Influenza A and Other Respiratory RNA Virus Interactions.Pathogens (Basel, Switzerland) · 2026Review
- Long Non-Coding RNAs Can Govern the Antiviral Immune Response Through Interferon-Mediated Mechanisms in Respiratory Tract.Viruses · 2026Review
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Non-coding RNAs are crucial orchestrators in the intricate dance between viruses and host cells, among which the expression and function of enhancer RNAs (eRNAs) during influenza virus infection remain largely unexplored. This study utilized whole transcriptome high-throughput sequencing to investigate the molecular mechanisms underpinning the species-specific regulation of influenza virus replication by the miR-302 cluster-IRFs-IRF1AS axis both IMPORTANCE: Non-coding RNAs play a crucial role in regulating the three-dimensional structure of chromatin. They influence gene expression through various mechanisms and thereby contribute to the onset and progression of influenza A virus pathogenicity. Our comprehensive whole transcriptome sequencing analysis reveals a novel finding: the species-specific regulation of influenza virus replication by the miR-302 cluster-IRFs-IRF1AS axis. Our findings indicate that the miR-302 cluster-IRFs axis facilitates the transcription of key hub genes and hub lncRNAs, most of which significantly inhibit influenza virus replication. Notably, the downstream IRF1AS assembles into an enhancer cluster, orchestrating and
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