ArticleNature communications2015
Heparanase is a host enzyme required for herpes simplex virus-1 release from cells.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 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
111 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Effect of Anticoagulant Administration on the Mortality of Hospitalized Patients With COVID-19: An Updated Systematic Review and Meta-Analysis.Frontiers in medicine · 2021Pooled it
- Glycoprotein G enables HSV-2 neuroinvasion and provides protection as a glycosylated vaccine antigen.PLoS pathogens · 2026Article
- Challenges in developing broad-spectrum viral attachment inhibitors targeting heparan sulfates and sialic acids.Journal of virology · 2026Review
- Glycocalyx degradation: exploring related mechanisms, pathophysiological significance, and therapeutic prospects.Journal of physiology and biochemistry · 2026Review
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- Oral SARS-CoV-2 Infection and Risk for Long Covid.Reviews in medical virology · 2025Review
- Recruitment of apolipoprotein E facilitates Herpes simplex virus 1 attachment and release.Npj viruses · 2025Article
- Global MicroRNA Profiling of HSV-1 Infected Cornea Identifies miR-329 as a Novel Regulator of Virus Infection.Investigative ophthalmology & visual science · 2025Article
- Herpes simplex virus 1 glycoprotein C promotes virus penetration from endosomes during entry, independent of interaction with heparan sulfate.Frontiers in microbiology · 2025Article
- Article
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Article
- Aspergillus Fumigatus Spore Proteases Alter the Respiratory Mucosa Architecture and Facilitate Equine Herpesvirus 1 Infection.Viruses · 2024Article
- Hypoxia-induced activation of HIF-1alpha/IL-1beta axis in microglia promotes glioma progression via NF-κB-mediated upregulation of heparanase expression.Biology direct · 2024Article
- Exploring Heparanase Levels in Tears: Insights From Herpes Simplex Virus-1 Keratitis Patients and Animal Studies.Investigative ophthalmology & visual science · 2024Article
- Validation of Candidate Host Cell Entry Factors for Bovine Herpes Virus Type-1 Based on a Genome-Wide CRISPR Knockout Screen.Viruses · 2024Article
- The underlying mechanisms of arenaviral entry through matriglycan.Frontiers in molecular biosciences · 2024Review
- Glycoengineered keratinocyte library reveals essential functions of specific glycans for all stages of HSV-1 infection.Nature communications · 2023Article
51 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
9 authors at 2 institutions in 1 country.
Funding
Abstract
Herpesviruses exemplified by herpes simplex virus-1 (HSV-1) attach to cell surface heparan sulfate (HS) for entry into host cells. However, during a productive infection, the HS moieties on parent cells can trap newly exiting viral progenies and inhibit their release. Here we demonstrate that a HS-degrading enzyme of the host, heparanase (HPSE), is upregulated through NF-kB and translocated to the cell surface upon HSV-1 infection for the removal of HS to facilitate viral release. We also find a significant increase in HPSE release in vivo during infection of murine corneas and that knockdown of HPSE in vivo inhibits virus shedding. Overall, we propose that HPSE acts as a molecular switch for turning a virus-permissive 'attachment mode' of host cells to a virus-deterring 'detachment mode'. Since many human viruses use HS as an attachment receptor, the HPSE-HS interplay may delineate a common mechanism for virus release.
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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.