ArticleProceedings of the National Academy of Sciences of the United States of America2012
Herpesvirus entry mediator is a serotype specific determinant of pathogenesis in ocular herpes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- A case report of long-delayed diagnosis of pseudorabies virus encephalitis with endophthalmitis: lessons from metagenomic next generation sequencing.BMC neurology · 2023Article
- Targeting NECTIN-1 Based on CRISPR/Cas9 System Attenuated the Herpes Simplex Virus Infection in Human Corneal Epithelial Cells In Vitro.Translational vision science & technology · 2022Article
- Nectin-1 and Non-muscle Myosin Heavy Chain-IIB: Major Mediators of Herpes Simplex Virus-1 Entry Into Corneal Nerves.Frontiers in microbiology · 2022Article
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
- Pathogenesis of Herpes Stromal Keratitis: Immune Inflammatory Response Mediated by Inflammatory Regulators.Frontiers in immunology · 2020Review
- Article
- Transcriptional changes after herpes simplex virus type 1 infection in human trabecular meshwork cells.PloS one · 2019Article
- Article
- First Impressions-the Potential of Altering Initial Host-Virus Interactions for Rational Design of Herpesvirus Vaccine Vectors.Current clinical microbiology reports · 2018Article
- The pUL37 tegument protein guides alpha-herpesvirus retrograde axonal transport to promote neuroinvasion.PLoS pathogens · 2017Article
- Article
- Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye.Journal of virology · 2017Review
- Innate Immune Mechanisms and Herpes Simplex Virus Infection and Disease.Advances in anatomy, embryology, and cell biology · 2017Review
- Murine Corneal Inflammation and Nerve Damage After Infection With HSV-1 Are Promoted by HVEM and Ameliorated by Immune-Modifying Nanoparticle Therapy.Investigative ophthalmology & visual science · 2017Article
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- Review
- Article
- Heparanase is a host enzyme required for herpes simplex virus-1 release from cells.Nature communications · 2015Article
- Herpes simplex virus 2 infection: molecular association with HIV and novel microbicides to prevent disease.Medical microbiology and immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Infection with herpes simplex virus type 1 (HSV-1) and HSV-2 is initiated by viral glycoprotein D (gD) binding to a receptor on the host cell. Two receptors, herpesvirus entry mediator (HVEM) and nectin-1, mediate entry in murine models of HSV-1 and HSV-2. HVEM is dispensable for HSV-2 infection of the vagina and brain, but is required for WT pathogenesis of HSV-1 infection of the cornea. By challenging WT and HVEM KO mice with multiple strains of HSV-1 and HSV-2, we demonstrate that without HVEM, all HSV-1 strains tested do not replicate well in the cornea and infection does not result in severe symptoms, as observed in WT mice. In contrast, all HSV-2 strains tested had no requirement for HVEM to replicate to WT levels in the cornea and still cause severe disease. These findings imply that HSV-2 does not require HVEM to cause disease regardless of route of entry, but HVEM must be present for HSV-1 to cause full pathogenesis in the eye. These findings uncover a unique role for HVEM in mediating HSV-1 infection in an area innervated by the trigeminal ganglion and may explain why the presence of HVEM can lead to severe inflammation in the cornea. Thus, the dependence on HVEM is a dividing point between HSV-1 and HSV-2 that evolved to infect areas innervated by different sensory ganglia.
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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.