ArticleEMBO reports2021
PML-NB-dependent type I interferon memory results in a restricted form of HSV latency.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 citing papers in PubMed, 37 citations in OpenAlex.
- The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.Proteomics. Clinical applications · 2026Article
- DNA damage responses in HCMV infection: emerging mechanisms and outstanding questions.Journal of virology · 2026Review
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- 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
- Interferon dependent immune memory during HSV-1 neuronal latency via increased H3K9me3 and restriction by ATRX.Nature communications · 2025Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Article
- Daxx mediated histone H3.3 deposition on HSV-1 DNA restricts genome decompaction and the progression of immediate-early transcription.PLoS pathogens · 2025Article
- Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.PLoS pathogens · 2025Article
- Co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Co-option of mitochondrial nucleic acid sensing pathways by HSV-1 UL12.5 for reactivation from latent Infection.bioRxiv : the preprint server for biology · 2024Article
- Comparative proteomic analysis of PK-15 cells infected with wild-type strain and its EP0 gene-deleted mutant strain of pseudorabies virus.Journal of veterinary science · 2024Article
- Article
- Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes.Nature communications · 2024Article
- c-Jun signaling during initial HSV-1 infection modulates latency to enhance later reactivation in addition to directly promoting the progression to full reactivation.Journal of virology · 2024Article
- Single-genome analysis reveals heterogeneous association of the Herpes Simplex Virus genome with H3K27me2 and the reader PHF20L1 following infection of human fibroblasts.bioRxiv : the preprint server for biology · 2023Article
- Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.Viruses · 2023Review
- c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation.bioRxiv : the preprint server for biology · 2023Article
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
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9 authors at 2 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus (HSV) establishes latent infection in long-lived neurons. During initial infection, neurons are exposed to multiple inflammatory cytokines but the effects of immune signaling on the nature of HSV latency are unknown. We show that initial infection of primary murine neurons in the presence of type I interferon (IFN) results in a form of latency that is restricted for reactivation. We also find that the subnuclear condensates, promyelocytic leukemia nuclear bodies (PML-NBs), are absent from primary sympathetic and sensory neurons but form with type I IFN treatment and persist even when IFN signaling resolves. HSV-1 genomes colocalize with PML-NBs throughout a latent infection of neurons only when type I IFN is present during initial infection. Depletion of PML prior to or following infection does not impact the establishment latency; however, it does rescue the ability of HSV to reactivate from IFN-treated neurons. This study demonstrates that viral genomes possess a memory of the IFN response during de novo infection, which results in differential subnuclear positioning and ultimately restricts the ability of genomes to reactivate.
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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.