ArticleJournal of virology2009
Herpes simplex virus type 1 glycoprotein E mediates retrograde spread from epithelial cells to neurites.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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
36 citing papers in PubMed, 49 citations in OpenAlex.
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- HSV1 glycoprotein D utilizes an LY6-like binding domain to inhibit alpha7 nicotinic receptors.Npj viruses · 2025Article
- Article
- Recent Advances in the Study of Alphaherpesvirus Latency and Reactivation: Novel Guidance for the Design of Herpesvirus Live Vector Vaccines.Pathogens (Basel, Switzerland) · 2024Review
- Review
- Evaluation of safety and immunogenicity of duck-plague virus gC/gE double gene deletion.Frontiers in immunology · 2022Article
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Article
- A putative WAVE regulatory complex (WRC) interacting receptor sequence (WIRS) in the cytoplasmic tail of HSV-1 gE does not function in WRC recruitment or neuronal transport.Access microbiology · 2021Article
- Viral cell-to-cell spread: Conventional and non-conventional ways.Advances in virus research · 2020Review
- Antibody responses to crucial functional epitopes as a novel approach to assess immunogenicity of vaccine adjuvants.Vaccine · 2019Article
- Article
- Roles of the Phosphorylation of Herpes Simplex Virus 1 UL51 at a Specific Site in Viral Replication and Pathogenicity.Journal of virology · 2018Article
- Vaccine-induced antibodies to herpes simplex virus glycoprotein D epitopes involved in virus entry and cell-to-cell spread correlate with protection against genital disease in guinea pigs.PLoS pathogens · 2018Article
- The pUL37 tegument protein guides alpha-herpesvirus retrograde axonal transport to promote neuroinvasion.PLoS pathogens · 2017Article
- What Goes Around, Comes Around - HSV-1 Replication in Monocyte-Derived Dendritic Cells.Frontiers in microbiology · 2017Review
- Axonal transport of AAV9 in nonhuman primate brain.Gene therapy · 2016Article
- Blocking herpes simplex virus 2 glycoprotein E immune evasion as an approach to enhance efficacy of a trivalent subunit antigen vaccine for genital herpes.Journal of virology · 2014Article
- Different modes of herpes simplex virus type 1 spread in brain and skin tissues.Journal of neurovirology · 2014Article
- Rapid host immune response and viral dynamics in herpes simplex virus-2 infection.Nature medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In animal models of infection, glycoprotein E (gE) is required for efficient herpes simplex virus type 1 (HSV-1) spread from the inoculation site to the cell bodies of innervating neurons (retrograde direction). Retrograde spread in vivo is a multistep process, in that HSV-1 first spreads between epithelial cells at the inoculation site, then infects neurites, and finally travels by retrograde axonal transport to the neuron cell body. To better understand the role of gE in retrograde spread, we used a compartmentalized neuron culture system, in which neurons were infected in the presence or absence of epithelial cells. We found that gE-deleted HSV-1 (NS-gEnull) retained retrograde axonal transport activity when added directly to neurites, in contrast to the retrograde spread defect of this virus in animals. To better mimic the in vivo milieu, we overlaid neurites with epithelial cells prior to infection. In this modified system, virus infects epithelial cells and then spreads to neurites, revealing a 100-fold retrograde spread defect for NS-gEnull. We measured the retrograde spread defect of NS-gEnull from a variety of epithelial cell lines and found that the magnitude of the spread defect from epithelial cells to neurons correlated with epithelial cell plaque size defect, indicating that gE plays a similar role in both types of spread. Therefore, gE-mediated spread between epithelial cells and neurites likely explains the retrograde spread defect of gE-deleted HSV-1 in vivo.
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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.