ArticleNature communications2024
Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.Science advances · 2026Article
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
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- 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
- The BAHD acyltransferase STBR1 confers both saline-alkali tolerance and blast resistance by stabilizing the non-canonical catalase CATA to promote HPlant communications · 2026Article
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- miR-221 Exerts Antiviral and Anti-Inflammatory Effects against HSV-1 Through Direct Repression of CAMK2A and Immune Pathway Activation.Inflammation · 2026Article
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria.Science advances · 2025Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- BMSC-derived exosomal lncRNA-ZFAS1 regulates the proliferation and differentiation of osteoblasts via the miR-9/IGF-1 signaling axis.Journal of orthopaedic surgery and research · 2025Article
- HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025Review
- Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- Article
- Article
- 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
- Global MicroRNA Profiling of HSV-1 Infected Cornea Identifies miR-329 as a Novel Regulator of Virus Infection.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus 1 (HSV-1) latent infection entails repression of viral lytic genes in neurons. By functional screening using luciferase-expressing HSV-1, we identify ten neuron-specific microRNAs potentially repressing HSV-1 neuronal replication. Transfection of miR-9, the most active candidate from the screen, decreases HSV-1 replication and gene expression in Neuro-2a cells. Ectopic expression of miR-9 from lentivirus or recombinant HSV-1 suppresses HSV-1 replication in male primary mouse neurons in culture and mouse trigeminal ganglia in vivo, and reactivation from latency in the primary neurons. Target prediction and validation identify transcription factors Oct-1, a known co-activator of HSV transcription, and all three Onecut family members as miR-9 targets. Knockdown of ONECUT2 decreases HSV-1 yields in Neuro-2a cells. Overexpression of each ONECUT protein increases HSV-1 replication in Neuro-2a cells, human induced pluripotent stem cell-derived neurons, and primary mouse neurons, and accelerates reactivation from latency in the mouse neurons. Mutagenesis, ChIP-seq, RNA-seq, ChIP-qPCR and ATAC-seq results suggest that ONECUT2 can nonspecifically bind to viral genes via its CUT domain, globally stimulate viral gene transcription, reduce viral heterochromatin and enhance the accessibility of viral chromatin. Thus, neuronal miR-9 promotes viral epigenetic silencing and latency by targeting multiple host transcription factors important for lytic gene activation.
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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.