ArticleVeterinary research2024
LINC01197 inhibits influenza A virus replication by serving as a PABPC1 decoy.
Article in Veterinary research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Systematic Identification of the Functional lncRNAs During H7N9 Avian Influenza Virus Infection in Mice.Viruses · 2026Article
- Animal virus-host interactions mediated by non-coding RNAs.Frontiers in cellular and infection microbiology · 2026Review
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
- LINC1467 Activates the IPO8-p65 Axis to Restrict Hand, Foot, and Mouth Disease Virus Replication.Pathogens (Basel, Switzerland) · 2025Article
- Long non-coding RNA C1RL-AS1 aggravates influenza A virus pneumonia through miR-16-5p/LAMP3.Virus genes · 2025Article
- The role of long non-coding RNAs and circular RNAs in immune evasion of influenza A virus: recent advances.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Influenza A viruses (IAVs) significantly impact animal and human health due to their zoonotic potential. A growing body of evidence indicates that the host's long noncoding RNAs (lncRNAs) play crucial roles in regulating host-virus interactions during IAV infection. However, numerous lncRNAs associated with IAV infection have not been well characterised. Here, in this study, we identify the LINC01197 as an antiviral host factor. LINC01197 was significantly upregulated after IAV infection, which is controlled by the NF-κB pathway. Functional analysis revealed that overexpression of LINC01197 inhibited IAV replication and virus production, while knockdown of LINC01197 facilitated IAV replication. Mechanistically, LINC01197 directly interacts with poly(A) binding protein cytoplasmic 1 (PABPC1), which in turn sequesters and restricts its functions. This work shows that LINC01197 acts as a protein decoy, suppressing IAV replication and playing a key role in controlling IAV replication.
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Registered trials
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