ArticleCell reports2017
Viral Activation of Heparanase Drives Pathogenesis of Herpes Simplex Virus-1.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 88 citations in OpenAlex.
- Molecular Pathways Driving Corneal Neovascularization in Herpes Simplex Keratitis.Pathogens (Basel, Switzerland) · 2026Review
- The PI3K/Akt Pathway in Herpesvirus Biology: A Double-Edged Sword in Host-Virus Interactions.Microorganisms · 2026Review
- Heparan Sulfate Proteoglycans (HSPGs) and Their Degradation in Health and Disease.Biomolecules · 2025Review
- Collagen Analogs Promote Tissue Regeneration in HSV-1-Infected Corneas in Animal Models.Journal of functional biomaterials · 2025Article
- Article
- Article
- Review
- Global MicroRNA Profiling of HSV-1 Infected Cornea Identifies miR-329 as a Novel Regulator of Virus Infection.Investigative ophthalmology & visual science · 2025Article
- 3D Tissue Culture Model for Virology Studies.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer.Breast cancer research : BCR · 2024Article
- Chronic inflammation as a proposed risk factor for ocular surface squamous neoplasia.The ocular surface · 2024Article
- Emerging drugs for the treatment of herpetic keratitis.Expert opinion on emerging drugs · 2024Review
- Exploring Heparanase Levels in Tears: Insights From Herpes Simplex Virus-1 Keratitis Patients and Animal Studies.Investigative ophthalmology & visual science · 2024Article
- Viral MicroRNAs in Herpes Simplex Virus 1 Pathobiology.Current pharmaceutical design · 2024Review
- The underlying mechanisms of arenaviral entry through matriglycan.Frontiers in molecular biosciences · 2024Review
- Unique Attributes of Guinea Pigs as New Models to Study Ocular Herpes Pathophysiology and Recurrence.Investigative ophthalmology & visual science · 2023Article
- Synthetic Heparanase Inhibitors Can Prevent Herpes Simplex Viral Spread.Angewandte Chemie (International ed. in English) · 2023Article
- Pathophysiology of reinfection by exogenous HSV-1 is driven by heparanase dysfunction.Science advances · 2023Article
- Heparanase Modulates Chromatin Accessibility.Cells · 2023Article
6 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus-1 (HSV-1) causes lifelong recurrent pathologies without a cure. How infection by HSV-1 triggers disease processes, especially in the immune-privileged avascular human cornea, remains a major unresolved puzzle. It has been speculated that a cornea-resident molecule must tip the balance in favor of pro-inflammatory and pro-angiogenic conditions observed with herpetic, as well as non-herpetic, ailments of the cornea. Here, we demonstrate that heparanase (HPSE), a host enzyme, is the molecular trigger for multiple pathologies associated with HSV-1 infection. In human corneal epithelial cells, HSV-1 infection upregulates HPSE in a manner dependent on HSV-1 infected cell protein 34.5. HPSE then relocates to the nucleus to regulate cytokine production, inhibits wound closure, enhances viral spread, and thus generates a toxic local environment. Overall, our findings implicate activated HPSE as a driver of viral pathogenesis and call for further attention to this host protein in infection and other inflammatory disorders.
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.