ArticleJournal of virology2022
The Role of Long Noncoding RNA BST2-2 in the Innate Immune Response to Viral Infection.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Identification of host lncRNAs that impact Venezuelan equine encephalitis virus TC-83 replication.Journal of virology · 2026Article
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
- Expression Profiles of lncRNAs and mRNAs in the Mouse Brain Infected with Pseudorabies Virus: A Bioinformatic Analysis.Viruses · 2025Article
- The emerging role of exosomal LncRNAs in chronic fatigue syndrome: from intercellular communication to disease biomarkers.Frontiers in molecular biosciences · 2025Review
- Review
- The dual functions of KDM7A in HBV replication and immune microenvironment.Microbiology spectrum · 2023Article
- LncRNA ZNF593-AS alleviates diabetic cardiomyopathy via suppressing IRF3 signaling pathway.Molecular therapy. Nucleic acids · 2023Article
- Transcriptome analysis of PK-15 cells expressing CSFV NS4A.BMC veterinary research · 2022Article
- A novel IFNbeta-induced long non-coding RNA ZAP-IT1 interrupts Zika virus replication in A549 cells.Virologica Sinica · 2022Article
- Schlafen family is a prognostic biomarker and corresponds with immune infiltration in gastric cancer.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) widely exist in the cells and play important roles in various biological processes. The role of lncRNAs in immunity remains largely unknown. lncRNA BST2-2 (lncBST2-2) was upregulated upon viral infection and dependent on the interferon (IFN)/JAK/STAT signaling pathway. There was no coding potential found in the lncBST2-2 transcript. Overexpression of lncBST2-2 inhibited the replication of hepatitis C virus (HCV), Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and herpes simplex virus (HSV), while knockdown of lncBST2-2 facilitated viral replication. Further studies showed that lncBST2-2 promoted the phosphorylation, dimerization, and nuclear transport of IRF3, promoting the production of IFNs. Importantly, lncBST2-2 interacted with the DNA-binding domain of IRF3, which augmented TBK1 and IRF3 interaction, thereby inducing robust production of IFNs. Moreover, lncBST2-2 impaired the interaction between IRF3 and PP2A-RACK1 complex, an essential step for the dephosphorylation of IRF3. These data shown that lncBST2-2 promotes the innate immune response to viral infection through targeting IRF3. Our study reveals the lncRNA involved in the activation of IRF3 and provides a new insight into the role of lncRNA in antiviral innate immunity.
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