ArticleJournal of virology2010
Herpes simplex virus glycoprotein D interferes with binding of herpesvirus entry mediator to its ligands through downregulation and direct competition.
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 47 papers.
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.
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Who cites it
47 citing papers in PubMed, 62 citations in OpenAlex.
- Complete disruption of gD binding to HVEM alters virus replication and host receptor homeostasis.PLoS pathogens · 2026Article
- HVEM-LIGHT signaling promotes antibody-dependent neutrophil FcγR-mediated trogocytosis against herpes simplex virus infection.The Journal of clinical investigation · 2026Article
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Rapid glycoprotein evolution enables variant interactions in herpes simplex virus type 1.Virus evolution · 2025Article
- Allosteric mechanism of membrane fusion activation in a herpesvirus.bioRxiv : the preprint server for biology · 2024Article
- HSV-1 Infection of Epithelial Dendritic Cells Is a Critical Strategy for Interfering with Antiviral Immunity.Viruses · 2022Article
- The Implementation of TNFRSF Co-Stimulatory Domains in CAR-T Cells for Optimal Functional Activity.Cancers · 2022Review
- Interleukin-6 and indoleamine-2,3-dioxygenase as potential adjuvant targets for Papillomavirus-related tumors immunotherapy.Frontiers in immunology · 2022Article
- Modulation of Endosome Function, Vesicle Trafficking and Autophagy by Human Herpesviruses.Cells · 2021Review
- Alphaherpesvirus Vaccines.Current issues in molecular biology · 2021Review
- Fragments of gD Protein as Inhibitors of BTLA/HVEM Complex Formation-Design, Synthesis, and Cellular Studies.International journal of molecular sciences · 2020Article
- HVEM signaling promotes protective antibody-dependent cellular cytotoxicity (ADCC) vaccine responses to herpes simplex viruses.Science immunology · 2020Article
- Restoring Herpesvirus Entry Mediator (HVEM) Immune Function in HVEMJournal of virology · 2020Article
- Disulfide-Linked Peptides for Blocking BTLA/HVEM Binding.International journal of molecular sciences · 2020Article
- Structural Basis of CD160:HVEM Recognition.Structure (London, England : 1993) · 2019Article
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- Safety and immunogenicity of a potential checkpoint blockade vaccine for canine melanoma.Cancer immunology, immunotherapy : CII · 2018Article
- A comparative review of viral entry and attachment during large and giant dsDNA virus infections.Archives of virology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
To initiate membrane fusion and virus entry, herpes simplex virus (HSV) gD binds to a cellular receptor such as herpesvirus entry mediator (HVEM). HVEM is a tumor necrosis factor (TNF) receptor family member with four natural ligands that either stimulate (LIGHT and LTα) or inhibit (BTLA and CD160) T cell function. We hypothesized that the interaction of gD with HVEM affects the binding of natural ligands, thereby modulating the immune response during infection. Here, we investigated the effect that gD has on the interaction of HVEM with its natural ligands. First, HSV gD on virions or cells downregulates HVEM from the cell surface. Similarly, trans-interaction with BTLA or LIGHT also downregulates HVEM from the cell surface, suggesting that HSV may subvert a natural mechanism for regulating HVEM activity. Second, we showed that wild-type gD had the lowest affinity for HVEM compared with the four natural ligands. Moreover, gD directly competed for binding to HVEM with BTLA but not LTα or LIGHT, indicating the possibility that gD selectively controls HVEM signals. On the other hand, natural ligands influence the use of HVEM by HSV. For instance, soluble BTLA, LTα, and LIGHT inhibited the binding of wild-type gD to HVEM, and soluble BTLA and LTα blocked HSV infection of HVEM-expressing cells. Thus, gD is at the center of the interplay between HVEM and its ligands. It can interfere with HVEM function in two ways, by competing with the natural ligands and by downregulating HVEM from the cell surface.
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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.