ArticleJournal of virology2004
The herpes simplex virus ICP0 RING finger domain inhibits IRF3- and IRF7-mediated activation of interferon-stimulated genes.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 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
163 citing papers in PubMed, 269 citations in OpenAlex.
- IFN-κ directs antiviral immunity in human skin.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic Impact of Caffeic Acid Phenethyl Ester and Acyclovir Combination on Human Gingival Fibroblasts (HGF-1) Infected With Herpes Simplex Type 1 ICP0.MicrobiologyOpen · 2026Article
- Article
- Article
- Article
- Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- 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
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Herpes simplex virus infected cell protein 8 is required for viral inhibition of the cGAS pathway.Virology · 2023Article
- Article
- Inborn Errors of Immunity Predisposing to Herpes Simplex Virus Infections of the Central Nervous System.Pathogens (Basel, Switzerland) · 2023Review
- Recent advances in ZBP1-derived PANoptosis against viral infections.Frontiers in immunology · 2023Review
- Article
- A 77 Amino Acid Region in the N-Terminal Half of the HSV-1 E3 Ubiquitin Ligase ICP0 Contributes to Counteracting an Established Type 1 Interferon Response.Microbiology spectrum · 2022Article
- Noncognate Signals Drive Enhanced Effector CD8Journal of virology · 2022Article
- Modulation of Ubiquitin Signaling in Innate Immune Response by Herpesviruses.International journal of molecular sciences · 2022Review
- 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
103 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virus infection induces a rapid cellular response in cells characterized by the induction of interferon. While interferon itself does not induce an antiviral response, it activates a number of interferon-stimulated genes that collectively function to inhibit virus replication and spread. Previously, we and others reported that herpes simplex virus type 1 (HSV-1) induces an interferon -independent antiviral response in the absence of virus replication. Here, we report that the HSV-1 proteins ICP0 and vhs function in concert to disable the host antiviral response. In particular, we show that ICP0 blocks interferon regulatory factor IRF3- and IRF7-mediated activation of interferon-stimulated genes and that the RING finger domain of ICP0 is essential for this activity. Furthermore, we demonstrate that HSV-1 modifies the IRF3 pathway in a manner different from that of the small RNA viruses most commonly studied.
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.