ArticleCell host & microbe2014
A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.
Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 2 of them syntheses that pooled it.
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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
108 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Topical and Systemic Therapeutic Approaches in the Treatment of Oral Herpes Simplex Virus Infection: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- No Significant Effect of ASAP1 Gene Variants on the Susceptibility to Tuberculosis in Chinese Population.Medicine · 2016Pooled it
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
- MicroRNA-138 regulation promotes the efficacy of oncolytic herpes virus G47Δ for malignant brain tumor therapy.Molecular therapy. Oncology · 2026Article
- Optimization of lytic herpes simplex virus infection in human induced pluripotent stem cell-derived cortical neurones.The Journal of general virology · 2026Article
- EGR Proteins Mediate Interferon-Independent Anti-HSV-1 Responses Through Viral and Host Targets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Antiviral responses in peripheral and brain neurons.Current opinion in immunology · 2025Review
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Article
- Article
- Herpesvirus initiation of dementias and autoimmune diseases.Journal of neurovirology · 2025Review
- Cellular miRNAs and viruses: trends in miRNA sequestering and target de-repression.Journal of virology · 2025Review
- Herpesviruses: overview of systematics, genomic complexity and life cycle.Virology journal · 2025Review
- Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Shedding dynamics of a DNA virus population during acute and long-term persistent infection.PLoS pathogens · 2025Article
- Regulation of the innate immune response in human neurons by ICP34.5 maintains herpes simplex virus 1 latency.bioRxiv : the preprint server for biology · 2025Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
48 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
Abstract
After infecting peripheral sites, herpes simplex virus (HSV) invades the nervous system and initiates latent infection in sensory neurons. Establishment and maintenance of HSV latency require host survival, and entail repression of productive cycle ("lytic") viral gene expression. We find that a neuron-specific microRNA, miR-138, represses expression of ICP0, a viral transactivator of lytic gene expression. A mutant HSV-1 (M138) with disrupted miR-138 target sites in ICP0 mRNA exhibits enhanced expression of ICP0 and other lytic proteins in infected neuronal cells in culture. Following corneal inoculation, M138-infected mice have higher levels of ICP0 and lytic transcripts in trigeminal ganglia during establishment of latency, and exhibit increased mortality and encephalitis symptoms. After full establishment of latency, the fraction of trigeminal ganglia harboring detectable lytic transcripts is greater in M138-infected mice. Thus, miR-138 is a neuronal factor that represses HSV-1 lytic gene expression, promoting host survival and viral latency.
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