ArticleJournal of virology2003
Herpes simplex virus gE/gI expressed in epithelial cells interferes with cell-to-cell spread.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 53 citations in OpenAlex.
- Viral Factors in Modulation of Host Immune Response: A Route to Novel Antiviral Agents and New Therapeutic Approaches.International journal of molecular sciences · 2024Review
- A Recombinant Duck Plague Virus Containing the ICP27 Deletion Marker Provides Robust Protection in Ducks.Microbiology spectrum · 2023Article
- Cell-to-cell spread inhibiting antibodies constitute a correlate of protection against herpes simplex virus type 1 reactivations: A retrospective study.Frontiers in immunology · 2023Article
- Discovery and Characterization of an Aberrant Small Form of Glycoprotein I of Herpes Simplex Virus Type I in Cell Culture.Microbiology spectrum · 2022Article
- Review
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- 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
- The LORF5 Gene Is Non-essential for Replication but Important for Duck Plague Virus Cell-to-Cell Spread Efficiently in Host Cells.Frontiers in microbiology · 2021Article
- Article
- Differential Requirements for gE, gI, and UL16 among Herpes Simplex Virus 1 Syncytial Variants Suggest Unique Modes of Dysregulating the Mechanism of Cell-to-Cell Spread.Journal of virology · 2019Article
- The Fc Domain of Immunoglobulin Is Sufficient to Bridge NK Cells with Virally Infected Cells.Immunity · 2017Article
- Genital Herpes: Insights into Sexually Transmitted Infectious Disease.Microbial cell (Graz, Austria) · 2016Review
- HSV-1 Glycoproteins Are Delivered to Virus Assembly Sites Through Dynamin-Dependent Endocytosis.Traffic (Copenhagen, Denmark) · 2016Article
- The herpes simplex virus 1 UL51 protein interacts with the UL7 protein and plays a role in its recruitment into the virion.Journal of virology · 2015Article
- Prospects and perspectives for development of a vaccine against herpes simplex virus infections.Expert review of vaccines · 2014Review
- The herpes simplex virus 1 UL51 gene product has cell type-specific functions in cell-to-cell spread.Journal of virology · 2014Article
- Article
- Rapid host immune response and viral dynamics in herpes simplex virus-2 infection.Nature medicine · 2013Article
- Mucosal HSV-2 Specific CD8+ T-Cells Represent Containment of Prior Viral Shedding Rather than a Correlate of Future Protection.Frontiers in immunology · 2013Article
- A network of protein interactions around the herpes simplex virus tegument protein VP22.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The herpes simplex virus (HSV) glycoprotein heterodimer gE/gI plays an important role in virus cell-to-cell spread in epithelial and neuronal tissues. In an analogous fashion, gE/gI promotes virus spread between certain cell types in culture, e.g., keratinocytes and epithelial cells, cells that are polarized or that form extensive cell junctions. One mechanism by which gE/gI facilitates cell-to-cell spread involves selective sorting of nascent virions to cell junctions, a process that requires the cytoplasmic domain of gE. However, the large extracellular domains of gE/gI also appear to be involved in cell-to-cell spread. Here, we show that coexpression of a truncated form of gE and gI in a human keratinocyte line, HaCaT cells, decreased the spread of HSV between cells. This truncated gE/gI was found extensively at cell junctions. Expression of wild-type gE/gI that accumulates at intracellular sites, in the trans-Golgi network, did not reduce cell-to-cell spread. There was no obvious reduction in production of infectious HSV in cells expressing gE/gI, and virus particles accumulated at cell junctions, not at intracellular sites. Expression of HSV gD, which is known to bind virus receptors, also blocked cell-to-cell spread. Therefore, like gD, gE/gI appears to be able to interact with cellular components of cell junctions, gE/gI receptors which can promote HSV cell-to-cell spread.
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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.