ArticleVirology2008
Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
85 citing papers in PubMed, 130 citations in OpenAlex.
- IFN-κ directs antiviral immunity in human skin.bioRxiv : the preprint server for biology · 2026Article
- Review
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- In the Absence of Type-1 IFN, HSV-1 LAT Increases γ34.5 Expression and Enhances Mortality in Infected Mice.Viruses · 2025Article
- IFNβ absence compensates for LAT functions in latency reactivation and T cell exhaustion.Journal of virology · 2025Article
- A microengineered 3D human neurovascular unit model to probe the neuropathogenesis of herpes simplex encephalitis.Nature communications · 2025Article
- The antiviral activity of myricetin against pseudorabies virus through regulation of the type I interferon signaling pathway.Journal of virology · 2025Article
- The functions of herpesvirus shuttling proteins in the virus lifecycle.Frontiers in microbiology · 2025Review
- The importance of IFNα2A (Roferon-A) in HSV-1 latency and T cell exhaustion in ocularly infected mice.PLoS pathogens · 2024Article
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1).International journal of molecular sciences · 2024Article
- HSV1-induced enhancement of productive HIV-1 replication is associated with interferon pathway downregulation in human macrophages.Memorias do Instituto Oswaldo Cruz · 2024Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Inborn Errors of Immunity Predisposing to Herpes Simplex Virus Infections of the Central Nervous System.Pathogens (Basel, Switzerland) · 2023Review
- Deletion of Double Copies of the US1 Gene Reduces the Infectivity of Recombinant Duck Plague VirusMicrobiology spectrum · 2022Article
- Host MOV10 is induced to restrict herpes simplex virus 1 lytic infection by promoting type I interferon response.PLoS pathogens · 2022Article
- Article
- Pseudorabies Virus Inhibits Type I and Type III Interferon-Induced Signaling via Proteasomal Degradation of Janus Kinases.Journal of virology · 2021Article
- Absence of CD28-CTLA4-PD-L1 Costimulatory Molecules Reduces Herpes Simplex Virus 1 Reactivation.mBio · 2021Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Host cells respond to viral infection by many mechanisms, including the production of type I interferons which act in a paracrine and autocrine manner to induce the expression of antiviral interferon-stimulated genes (ISGs). Viruses have evolved means to inhibit interferon signaling to avoid induction of the innate immune response. Herpes simplex virus 1 (HSV-1) has several mechanisms to inhibit type I interferon production, the activities of ISGs, and the interferon signaling pathway itself. We report that the inhibition of the Jak/STAT pathway by HSV-1 requires viral gene expression and that viral immediate-early protein ICP27 plays a role in downregulating STAT-1 phosphorylation and in preventing the accumulation of STAT-1 in the nucleus. We also show that expression of ICP27 by transfection causes an inhibition of IFN-induced STAT-1 nuclear accumulation. Therefore, ICP27 is necessary and sufficient for at least some of the effects of HSV infection on STAT-1.
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.