ArticlePloS one2010
Binding of herpes simplex virus type-1 virions leads to the induction of intracellular signalling in the absence of virus entry.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 36 citations in OpenAlex.
- Loss of Akt3 enhances antiviral immunity while disrupting corneal homeostasis during ocular HSV-1 infection.Frontiers in immunology · 2026Article
- Inositol metabolism as a broad-spectrum antiviral target.Frontiers in microbiology · 2025Review
- Quindoline-derivatives display potent G-quadruplex-mediated antiviral activity against herpes simplex virus 1.Antiviral research · 2022Article
- Alphaherpesvirus-induced activation of plasmacytoid dendritic cells depends on the viral glycoprotein gD and is inhibited by non-infectious light particles.PLoS pathogens · 2021Article
- Review
- Porcine Hemagglutinating Encephalomyelitis Virus Activation of the Integrin α5β1-FAK-Cofilin Pathway Causes Cytoskeletal Rearrangement To Promote Its Invasion of N2a Cells.Journal of virology · 2019Article
- The Amino Terminus of Herpes Simplex Virus 1 Glycoprotein K (gK) Is Required for gB Binding to Akt, Release of Intracellular Calcium, and Fusion of the Viral Envelope with Plasma Membranes.Journal of virology · 2018Article
- First Impressions-the Potential of Altering Initial Host-Virus Interactions for Rational Design of Herpesvirus Vaccine Vectors.Current clinical microbiology reports · 2018Article
- Herpesviruses in the Activated Phosphatidylinositol-3-Kinase-δ Syndrome.Frontiers in immunology · 2018Review
- Dendritic cell-targeted lentiviral vector immunization uses pseudotransduction and DNA-mediated STING and cGAS activation.Science immunology · 2017Article
- Participation of 3-FEBS open bio · 2017Article
- Article
- HSV-1-induced activation of NF-κB protects U937 monocytic cells against both virus replication and apoptosis.Cell death & disease · 2016Article
- Genome-Wide Gene Expression Analysis Identifies the Proto-oncogene Tyrosine-Protein Kinase Src as a Crucial Virulence Determinant of Infectious Laryngotracheitis Virus in Chicken Cells.Journal of virology · 2016Article
- Oncolytic herpes simplex virus kills stem-like tumor-initiating colon cancer cells.Molecular therapy oncolytics · 2016Article
- Induction of ROS generation and NF-κB activation in MARC-145 cells by a novel porcine reproductive and respiratory syndrome virus in Southwest of China isolate.BMC veterinary research · 2015Article
- Review
- Article
- Host nectin-1 is required for efficient Chlamydia trachomatis serovar E development.Frontiers in cellular and infection microbiology · 2014Article
- An image-based genetic assay identifies genes in T1D susceptibility loci controlling cellular antiviral immunity in mouse.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The envelope of HSV-1 contains a number of glycoproteins, four of which are essential for virus entry. Virus particles lacking gB, gD, gH or gL are entry-defective, although these viruses retain the ability to bind to the plasma membrane via the remaining glycoproteins. Soluble forms of gD have been shown to trigger the nuclear translocation of the NF-kappaB transcriptional complex in addition to stimulating the production of Type I interferon. By taking advantage of the entry-defective phenotype of glycoprotein-deficient HSV-1 virus particles, the results presented here show that binding of virions to cellular receptors on the plasma membrane is sufficient to stimulate a change in cellular gene expression. Preliminary microarray studies, validated by quantitative real-time PCR, identified the differential expression of cellular genes associated with the NF-kappaB, PI3K/Akt, Jak/Stat and related Jak/Src pathways by virions lacking gB or gH but not gD. Gene induction occurred at a few particles per cell, corresponding to physiological conditions during primary infection. Reporter assay studies determined that NF-kappaB transcriptional activity is stimulated within an hour of HSV-1 binding, peaks between two and three hours post-binding and declines to background levels by five hours after induction. The immediate, transient nature of these signalling events suggests that HSV-1 glycoproteins, particularly gD, may alter the cellular environment pre-entry so as to condition the cell for viral replication.
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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.