ArticleJournal of virology2000
Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed.
- Syncytium-forming HSV-1 in cancer gene therapy: From molecular mechanisms to clinical translation.Virulence · 2026Review
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Enterocin DD14 can inhibit the infection of eukaryotic cells with enveloped viruses.Archives of microbiology · 2024Article
- Virus-Induced Cell Fusion and Syncytia Formation.Results and problems in cell differentiation · 2024Article
- Entry receptor bias in evolutionarily distant HSV-1 clinical strains drives divergent ocular and nervous system pathologies.The ocular surface · 2021Article
- 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
- Development of an oncolytic HSV vector fully retargeted specifically to cellular EpCAM for virus entry and cell-to-cell spread.Gene therapy · 2016Article
- Rapid genome assembly and comparison decode intrastrain variation in human alphaherpesviruses.mBio · 2015Article
- 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
- The epithelial αvβ3-integrin boosts the MYD88-dependent TLR2 signaling in response to viral and bacterial components.PLoS pathogens · 2014Article
- Varicella-zoster virus and herpes simplex virus 1 can infect and replicate in the same neurons whether co- or superinfected.Journal of virology · 2014Article
- Displacement of the C terminus of herpes simplex virus gD is sufficient to expose the fusion-activating interfaces on gD.Journal of virology · 2013Article
- Griffithsin protects mice from genital herpes by preventing cell-to-cell spread.Journal of virology · 2013Article
- Novel mutations in gB and gH circumvent the requirement for known gD Receptors in herpes simplex virus 1 entry and cell-to-cell spread.Journal of virology · 2013Article
- Herpes simplex virus glycoproteins gB and gD function in a redundant fashion to promote secondary envelopment.Journal of virology · 2011Article
- The virological synapse facilitates herpes simplex virus entry into T cells.Journal of virology · 2009Article
- Generation of herpesvirus entry mediator (HVEM)-restricted herpes simplex virus type 1 mutant viruses: resistance of HVEM-expressing cells and identification of mutations that rescue nectin-1 recognition.Journal of virology · 2009Article
- Glycoprotein D-independent spread of pseudorabies virus infection in cultured peripheral nervous system neurons in a compartmented system.Journal of virology · 2007Article
- Cytoplasmic residues of herpes simplex virus glycoprotein gE required for secondary envelopment and binding of tegument proteins VP22 and UL11 to gE and gD.Journal of virology · 2007Article
- Human cytomegalovirus entry into epithelial and endothelial cells depends on genes UL128 to UL150 and occurs by endocytosis and low-pH fusion.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) glycoprotein D (gD) is an essential component of the entry apparatus that is responsible for viral penetration and subsequent cell-cell spread. To test the hypothesis that gD may serve distinguishable functions in entry of free virus and cell-cell spread, mutants were selected for growth on U(S)11cl19.3 cells, which are resistant to both processes due to the lack of a functional gD receptor, and then tested for their ability to enter as free virus and to spread from cell to cell. Unlike their wild-type parent, HSV-1(F), the variants that emerged from this selection, which were named SP mutants, are all capable of forming macroscopic plaques on the resistant cells. This ability is caused by a marked increase in cell-cell spread without a concomitant increase in efficiency of entry of free virus. gD substitutions that arose within these mutants are sufficient to mediate cell-cell spread in U(S)11cl19.3 cells but are insufficient to overcome the restriction to entry of free virions. These results suggest that mutations in gD (i) are sufficient but not necessary to overcome the block to cell-cell spread exhibited by U(S)11cl19.3 cells and (ii) are insufficient to mediate entry of free virus in the same cells.
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