ArticleVirology2016
Neuronal IFN signaling is dispensable for the establishment of HSV-1 latency.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- HSV-1 LAT promotes ocular diseases in the absence of type I IFN responses in sensory neurons.Journal of virology · 2026Article
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025Review
- Article
- MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8Journal of neuroinflammation · 2025Article
- Temporally resolved single-cell RNA sequencing reveals protective and pathological responses during herpes simplex virus CNS infection.Journal of neuroinflammation · 2025Article
- Unveiling the Involvement of Herpes Simplex Virus-1 in Alzheimer's Disease: Possible Mechanisms and Therapeutic Implications.Molecular neurobiology · 2025Review
- 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
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- Article
- Mice with type I interferon signaling deficiency are prone to epilepsy upon HSV-1 infection.Virologica Sinica · 2024Article
- Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes.Nature communications · 2024Article
- Human cytomegalovirus UL138 interaction with USP1 activates STAT1 in infection.PLoS pathogens · 2023Article
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
- Human Cytomegalovirus UL138 Interaction with USP1 Activates STAT1 in infection.bioRxiv : the preprint server for biology · 2023Article
- Disrupting Neurons and Glial Cells Oneness in the Brain-The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Interferon Regulatory Factor 3 Supports the Establishment of Chronic Gammaherpesvirus Infection in a Route- and Dose-Dependent Manner.Journal of virology · 2021Article
- Stunning symmetries involved in the self-assembly of the HSV-1 capsid.The journal of the Korean Physical Society · 2021Review
- Disturbed Yin-Yang balance: stress increases the susceptibility to primary and recurrent infections of herpes simplex virus type 1.Acta pharmaceutica Sinica. B · 2020Review
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
IFN responses control acute HSV infection, but their role in regulating HSV latency is poorly understood. To address this we used mice lacking IFN signaling specifically in neural tissues. These mice supported a higher acute viral load in nervous tissue and delayed establishment of latency. While latent HSV-1 genome copies were equivalent, ganglia from neuronal IFN signaling-deficient mice unexpectedly supported reduced reactivation. IFNβ promoted survival of primary sensory neurons after infection with HSV-1, indicating a role for IFN signaling in sustaining neurons. We observed higher levels of latency associated transcripts (LATs) per HSV genome in mice lacking neuronal IFN signaling, consistent with a role for IFN in regulating LAT expression. These data show that neuronal IFN signaling modulates the expression of LAT and may conserve the pool of neurons available to harbor latent HSV-1 genome. The data also show that neuronal IFN signaling is dispensable for the establishment of latency.
Indexed as
Identifiers
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.