ArticlePLoS pathogens2011
The herpes simplex virus-1 transactivator infected cell protein-4 drives VEGF-A dependent neovascularization.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- A Systematic Review of Tear Vascular Endothelial Growth Factor and External Eye Diseases.International journal of molecular sciences · 2024Pooled it
- Molecular Pathways Driving Corneal Neovascularization in Herpes Simplex Keratitis.Pathogens (Basel, Switzerland) · 2026Review
- Research progress on the correlation between corneal neovascularization and lymphangiogenesis (Review).Molecular medicine reports · 2025Review
- Review
- Rational strategies for designing next-generation oncolytic viruses based on transcriptome analysis of tumor cells infected with oncolytic herpes simplex virus-1.Frontiers in oncology · 2024Article
- The Host-Pathogen Interplay: A Tale of Two Stories within the Cornea and Posterior Segment.Microorganisms · 2023Review
- HSV-1 0∆NLS vaccine elicits a robust B lymphocyte response and preserves vision without HSV-1 glycoprotein M or thymidine kinase recognition.Scientific reports · 2022Article
- Mucosal immunology of the ocular surface.Mucosal immunology · 2022Review
- Host Molecules That Promote Pathophysiology of Ocular Herpes.Frontiers in microbiology · 2022Review
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- The Durability of Vaccine Efficacy against Ocular HSV-1 Infection Using ICP0 Mutants 0∆NLS and 0∆RING Is Lost over Time.Pathogens (Basel, Switzerland) · 2021Article
- The Herpes Simplex Virus 1 Protein ICP4 Acts as both an Activator and a Repressor of Host Genome Transcription during Infection.Molecular and cellular biology · 2021Article
- An intact complement system dampens cornea inflammation during acute primary HSV-1 infection.Scientific reports · 2021Article
- Parallel G-quadruplexes recruit the HSV-1 transcription factor ICP4 to promote viral transcription in herpes virus-infected human cells.Communications biology · 2021Article
- Corneal angiogenic privilege and its failure.Experimental eye research · 2021Review
- Heparanase, cell signaling, and viral infections.Cellular and molecular life sciences : CMLS · 2020Review
- Distinguishing Features of High- and Low-Dose Vaccine against Ocular HSV-1 Infection Correlates with Recognition of Specific HSV-1-Encoded Proteins.ImmunoHorizons · 2020Article
- Loss of Osteopontin Expression Reduces HSV-1-Induced Corneal Opacity.Investigative ophthalmology & visual science · 2020Article
- HSV-1 Hijacks the Host DNA Damage Response in Corneal Epithelial Cells through ICP4-Mediated Activation of ATM.Investigative ophthalmology & visual science · 2020Article
- Pathological processes activated by herpes simplex virus-1 (HSV-1) infection in the cornea.Cellular and molecular life sciences : CMLS · 2019Review
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 3 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus-1 (HSV-1) causes lifelong infection affecting between 50 and 90% of the global population. In addition to causing dermal lesions, HSV-1 is a leading cause of blindness resulting from recurrent corneal infection. Corneal disease is characterized by loss of corneal immunologic privilege and extensive neovascularization driven by vascular endothelial growth factor-A (VEGF-A). In the current study, we identify HSV-1 infected cells as the dominant source of VEGF-A during acute infection, and VEGF-A transcription did not require TLR signaling or MAP kinase activation. Rather than being an innate response to the pathogen, VEGF-A transcription was directly activated by the HSV-1 encoded immediate early transcription factor, ICP4. ICP4 bound the proximal human VEGF-A promoter and was sufficient to promote transcription. Transcriptional activation also required cis GC-box elements common to the VEGF-A promoter and HSV-1 early genes. Our results suggest that the neovascularization characteristic of ocular HSV-1 disease is a direct result of HSV-1's major transcriptional regulator, ICP4, and similarities between the VEGF-A promoter and those of HSV-1 early genes.
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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.