ArticleJournal of virology1998
Herpesvirus entry mediator HVEM mediates cell-cell spread in BHK(TK-) cell clones.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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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
13 citing papers in PubMed, 27 citations in OpenAlex.
- Structural basis of nectin-1 recognition by pseudorabies virus glycoprotein D.PLoS pathogens · 2017Article
- Syncytial Mutations Do Not Impair the Specificity of Entry and Spread of a Glycoprotein D Receptor-Retargeted Herpes Simplex Virus.Journal of virology · 2016Article
- Role of Nectin-1 and Herpesvirus Entry Mediator as Cellular Receptors for Herpes Simplex Virus 1 on Primary Murine Dermal Fibroblasts.Journal of virology · 2015Article
- 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
- Bispecific adapter-mediated retargeting of a receptor-restricted HSV-1 vector to CEA-bearing tumor cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- 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
- The herpes simplex virus JMP mutant enters receptor-negative J cells through a novel pathway independent of the known receptors nectin1, HveA, and nectin2.Journal of virology · 2004Article
- NP-1, a rabbit alpha-defensin, prevents the entry and intercellular spread of herpes simplex virus type 2.Antimicrobial agents and chemotherapy · 2003Article
- Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread.Journal of virology · 2000Article
- Cell-to-cell spread of wild-type herpes simplex virus type 1, but not of syncytial strains, is mediated by the immunoglobulin-like receptors that mediate virion entry, nectin1 (PRR1/HveC/HIgR) and nectin2 (PRR2/HveB).Journal of virology · 2000Article
- HSV-1-based vectors for gene therapy of neurological diseases and brain tumors: part I. HSV-1 structure, replication and pathogenesis.Neoplasia (New York, N.Y.) · 1999Review
- Inhibition of herpes simplex virus gD and lymphotoxin-alpha binding to HveA by peptide antagonists.Journal of virology · 1999Article
- HveA (herpesvirus entry mediator A), a coreceptor for herpes simplex virus entry, also participates in virus-induced cell fusion.Journal of virology · 1998Article
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
No grant is acknowledged in the PubMed record.
Abstract
95-19 and U(S)11c119.3 are BHK(TK-)-derived cell lines that are highly resistant to postattachment entry of herpes simplex virus type 1 (HSV-1) and HSV-2 but not to later steps in single-step replication. The resistance properties of these two cell types are not identical. U(S)11c119.3 cells are fully susceptible to pseudorabies virus (PRV), as shown by single-step growth experiments, whereas 95-19 cells are resistant to entry of free PRV but not to entry by cell-cell spread. We have tested the ability of HVEM to overcome the block to infection in both cell lines following transient and stable transfection. HVEM was able to mediate entry of free HSV-1 into both cell lines, as shown by an increase in the number of beta-galactosidase-expressing cells in cultures transiently transfected with an HVEM expression plasmid and infected with lacZ-expressing HSV-1. In stably transfected 95-19 cells, HVEM enhanced infection by free HSV-1, as shown by an increase in the number of infectious centers obtained following infection. In both cell types, HVEM strongly enhanced entry of HSV-1 and HSV-2 by cell-cell spread, suggesting that HVEM can function as an entry mediator both in entry of free virus and in entry by cell-cell spread.
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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.