ArticleJournal of virology2010
Herpes simplex virus glycoproteins H/L bind to cells independently of {alpha}V{beta}3 integrin and inhibit virus entry, and their constitutive expression restricts infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed.
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Article
- Hantavirus entry: Perspectives and recent advances.Advances in virus research · 2019Article
- Co-localization of and interaction between duck enteritis virus glycoprotein H and L.BMC veterinary research · 2018Article
- Virus-Receptor Interactions: The Key to Cellular Invasion.Journal of molecular biology · 2018Review
- Novel "Add-On" Molecule Based on Evans Blue Confers Superior Pharmacokinetics and Transforms Drugs to Theranostic Agents.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2017Article
- Herpesvirus Entry into Host Cells Mediated by Endosomal Low pH.Traffic (Copenhagen, Denmark) · 2016Review
- Genital Herpes: Insights into Sexually Transmitted Infectious Disease.Microbial cell (Graz, Austria) · 2016Review
- αvβ3 Integrin Boosts the Innate Immune Response Elicited in Epithelial Cells through Plasma Membrane and Endosomal Toll-Like Receptors.Journal of virology · 2016Article
- Functional Characterization of Glycoprotein H Chimeras Composed of Conserved Domains of the Pseudorabies Virus and Herpes Simplex Virus 1 Homologs.Journal of virology · 2016Article
- Polyethylene glycol-mediated fusion of herpes simplex type 1 virions with the plasma membrane of cells that support endocytic entry.Virology journal · 2015Article
- Article
- Dissociation of HSV gL from gH by αvβ6- or αvβ8-integrin promotes gH activation and virus entry.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Engineering of a Novel Ligand in gH Confers to HSV an Expanded Tropism Independent of gD Activation by Its Receptors.PLoS pathogens · 2015Article
- The epithelial αvβ3-integrin boosts the MYD88-dependent TLR2 signaling in response to viral and bacterial components.PLoS pathogens · 2014Article
- Herpes simplex virus type 2 glycoprotein H interacts with integrin αvβ3 to facilitate viral entry and calcium signaling in human genital tract epithelial cells.Journal of virology · 2014Article
- Type I interferon and NF-κB activation elicited by herpes simplex virus gH/gL via αvβ3 integrin in epithelial and neuronal cell lines.Journal of virology · 2013Article
- Integrins modulate the infection efficiency of West Nile virus into cells.The Journal of general virology · 2013Article
- Possible role of a cell surface carbohydrate in evolution of resistance to viral infections in old world primates.Journal of virology · 2013Article
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Herpes simplex virus (HSV) fusion with cells requires the gD, gB, and gH/gL glycoprotein quartet. gD serves as a receptor binding glycoprotein. gB and gH/gL execute fusion in an as-yet-unclear manner. To better understand the role of gH/gL in HSV entry, we produced a soluble version of gH/gL carrying a One-STrEP tag (gH(t.st)/gL). Previous findings implicated integrins as possible ligands to gH/gL (C. Parry et al., J. Gen. Virol. 86:7-10, 2005). We report that (i) gH(t.st)/gL bound a number of cells in a dose-dependent manner at concentrations similar to those required for the binding of soluble gB or gD. (ii) gH(t.st)/gL inhibited HSV entry at the same concentrations required for binding. It also inhibited cell-cell fusion in transfected cells. (iii) The absence of beta3 integrin did not prevent the binding of gH(t.st)/gL to CHO cells and infection inhibition. Conversely, integrin-negative K562 cells did not acquire the ability to bind gH(t.st)/gL when hyperexpressing alphaVbeta3 integrin. (iv) Constitutive expression of wild-type gH/gL (wt-gH/gL) restricted infection in all of the cell lines tested, a behavior typical of glycoproteins which bind cellular receptors. The extent of restriction broadly paralleled the efficiency of gH/gL transfection. RGD motif mutant gH/gL could not be differentiated from wt-gH with respect to restriction of infection. Cumulatively, the present results provide several lines of evidence that HSV gH/gL interacts with a cell surface cognate protein(s), that this protein is not necessarily an alphaVbeta3 integrin, and that this interaction is required for the process of virus entry/fusion.
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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.