ArticlePloS one2014
MiR-23a facilitates the replication of HSV-1 through the suppression of interferon regulatory factor 1.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 65 citations in OpenAlex.
- IRF1 amplifies HSV-1-triggered antiviral innate immunity in a feed-forward manner.Cell insight · 2025Article
- Viperin: A Multifunctional Protein in Antiviral Immunity and Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Overview of host-directed antiviral targets for future research and drug development.Acta pharmaceutica Sinica. B · 2025Review
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Global MicroRNA Profiling of HSV-1 Infected Cornea Identifies miR-329 as a Novel Regulator of Virus Infection.Investigative ophthalmology & visual science · 2025Article
- Editorial: Viral infection pathogenesis and pathology in nervous system.Frontiers in cellular and infection microbiology · 2025Article
- Small RNA sequencing analysis reveals regulation of microRNA expression in Madin-Darby canine kidney epithelial cells infected with Canid alphaherpesvirus 1.Virus genes · 2024Article
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- miRNAs: Targets to Investigate Herpesvirus Infection Associated with Neurological Disorders.International journal of molecular sciences · 2023Review
- Review
- Alzheimer's disease and microorganisms: the non-coding RNAs crosstalk.Frontiers in cellular neuroscience · 2023Review
- Article
- Enhancing the HSV-1-mediated antitumor immune response by suppressing Bach1.Cellular & molecular immunology · 2022Article
- Article
- Interaction Between Non-Coding RNAs and Interferons: With an Especial Focus on Type I Interferons.Frontiers in immunology · 2022Review
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021Review
- miR-23a/b suppress cGAS-mediated innate and autoimmunity.Cellular & molecular immunology · 2021Article
- Hidden in plain sight: The effects of BCG vaccination in the COVID-19 pandemic.Journal of medical virology · 2021Review
- Circular RNA circDtx1 regulates IRF3-mediated antiviral immune responses through suppression of miR-15a-5p-dependent TRIF downregulation in teleost fish.PLoS pathogens · 2021Article
Corrections and comments
- Expression of concern
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are small, non-coding RNAs that negatively regulate gene expression. It has been reported that miRNAs are involved in host-virus interaction, but evidence that cellular miRNAs promote virus replication has been limited. Here, we found that miR-23a promoted the replication of human herpes simplex virus type 1 (HSV-1) in HeLa cells, as demonstrated by a plaque-formation assay and quantitative real-time PCR. Furthermore, interferon regulatory factor 1 (IRF1), an innate antiviral molecule, is targeted by miR-23a to facilitate viral replication. MiR-23a binds to the 3'UTR of IRF1 and down-regulates its expression. Suppression of IRF1 expression reduced RSAD2 gene expression, augmenting HSV-1 replication. Ectopic expression of IRF1 abrogated the promotion of HSV-1 replication induced by miR-23a. Notably, IRF1 contributes to innate antiviral immunity by binding to IRF-response elements to regulate the expression of interferon-stimulated genes (ISGs) and apoptosis, revealing a complex interaction between miR-23a and HSV-1. MiR-23a thus contributes to HSV-1 replication through the regulation of the IRF1-mediated antiviral signal pathway, which suggests that miR-23a may represent a promising target for antiviral treatments.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.