ArticleJournal of virology2013
Polarized cell migration during cell-to-cell transmission of herpes simplex virus in human skin keratinocytes.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Herpes simplex virus spreads rapidly in human foreskin, partly driven by chemokine-induced redistribution of Nectin-1 on keratinocytes.PLoS pathogens · 2024Article
- Genome-wide CRISPR screen for HSV-1 host factors reveals PAPSS1 contributes to heparan sulfate synthesis.Communications biology · 2022Article
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Herpes simplex virus 2 (HSV-2) evolves faster in cell culture than HSV-1 by generating greater genetic diversity.PLoS pathogens · 2021Article
- Volume measurement and biophysical characterization of mounds in epithelial monolayers after intracellular bacterial infection.STAR protocols · 2021Article
- Life as a Vector of Dengue Virus: The Antioxidant Strategy of Mosquito Cells to Survive Viral Infection.Antioxidants (Basel, Switzerland) · 2021Review
- Mechanical competition triggered by innate immune signaling drives the collective extrusion of bacterially infected epithelial cells.Developmental cell · 2021Article
- Microbial Biofilms: Human T-cell Leukemia Virus Type 1 First in Line for Viral Biofilm but Far Behind Bacterial Biofilms.Frontiers in microbiology · 2020Review
- Host Src controls gallid alpha herpesvirus 1 intercellular spread in a cellular fatty acid metabolism-dependent manner.Virology · 2019Article
- Vaccinia virus hijacks EGFR signalling to enhance virus spread through rapid and directed infected cell motility.Nature microbiology · 2019Article
- Upsetting the Balance: When Viruses Manipulate Cell Polarity Control.Journal of molecular biology · 2018Review
- The HSV-1 mechanisms of cell-to-cell spread and fusion are critically dependent on host PTP1B.PLoS pathogens · 2018Article
- Extracellular Matrix in Plants and Animals: Hooks and Locks for Viruses.Frontiers in microbiology · 2017Review
- Article
- Viruses exploit the tissue physiology of the host to spread in vivo.Current opinion in cell biology · 2016Review
- Global Mapping of O-Glycosylation of Varicella Zoster Virus, Human Cytomegalovirus, and Epstein-Barr Virus.The Journal of biological chemistry · 2016Article
- Herpes simplex virus downregulation of secretory leukocyte protease inhibitor enhances human papillomavirus type 16 infection.The Journal of general virology · 2016Article
- Secreted herpes simplex virus-2 glycoprotein G modifies NGF-TrkA signaling to attract free nerve endings to the site of infection.PLoS pathogens · 2015Article
- Update on herpes virus infections of the nervous system.Current neurology and neuroscience reports · 2013Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to transmission involving extracellular free particles, a generally accepted model of virus propagation is one wherein virus replicates in one cell, producing infectious particles that transmit to the next cell via cell junctions or induced polarized contacts. This mechanism of spread is especially important in the presence of neutralizing antibody, and the concept underpins analysis of virus spread, plaque size, viral and host functions, and general mechanisms of virus propagation. Here, we demonstrate a novel process involved in cell-to-cell transmission of herpes simplex virus (HSV) in human skin cells that has not previously been appreciated. Using time-lapse microscopy of fluorescent viruses, we show that HSV infection induces the polarized migration of skin cells into the site of infection. In the presence of neutralizing antibody, uninfected skin cells migrate to the initial site of infection and spread over infected cells to become infected in a spatially confined cluster containing hundreds of cells. The cells in this cluster do not undergo cytocidal cell lysis but harbor abundant enveloped particles within cells and cell-free virus within interstitial regions below the cluster surface. Cells at the base and outside the cluster were generally negative for virus immediate-early expression. We further show, using spatially separated monolayer assays, that at least one component of this induced migration is the paracrine stimulation of a cytotactic response from infected cells to uninfected cells. The existence of this process changes our concept of virus transmission and the potential functions, virus, and host factors involved.
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