ArticleJournal of virology1997
Characterization of a BHK(TK-) cell clone resistant to postattachment entry by herpes simplex virus types 1 and 2.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Exploiting non-permissive CHO cells as a rapid and efficient method for recombinant HSV-1 isolation.AMB Express · 2024Article
- An investigative peptide-acyclovir combination to control herpes simplex virus type 1 ocular infection.Investigative ophthalmology & visual science · 2013Article
- Prophylactic, therapeutic and neutralizing effects of zinc oxide tetrapod structures against herpes simplex virus type-2 infection.Antiviral research · 2012Article
- Tin oxide nanowires suppress herpes simplex virus-1 entry and cell-to-cell membrane fusion.PloS one · 2012Article
- Role of adherens junction proteins in differential herpes simplex virus type 2 infectivity in communication-competent and -deficient cell lines.Intervirology · 2012Article
- An important role for syndecan-1 in herpes simplex virus type-1 induced cell-to-cell fusion and virus spread.PloS one · 2011Article
- Identification of cellular genes affecting the infectivity of foot-and-mouth disease virus.Journal of virology · 2009Article
- Molecular umbrellas: a novel class of candidate topical microbicides to prevent human immunodeficiency virus and herpes simplex virus infections.Journal of virology · 2007Article
- Mutations in herpes simplex virus glycoprotein D that prevent cell entry via nectins and alter cell tropism.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Candidate topical microbicides bind herpes simplex virus glycoprotein B and prevent viral entry and cell-to-cell spread.Antimicrobial agents and chemotherapy · 2004Article
- NP-1, a rabbit alpha-defensin, prevents the entry and intercellular spread of herpes simplex virus type 2.Antimicrobial agents and chemotherapy · 2003Article
- Herpes simplex virus type 1 entry is inhibited by the cobalt chelate complex CTC-96.Journal of virology · 2001Article
- Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread.Journal of virology · 2000Article
- The human cytomegalovirus major immediate-early distal enhancer region is required for efficient viral replication and immediate-early gene expression.Journal of virology · 2000Article
- Herpesvirus entry mediator HVEM mediates cell-cell spread in BHK(TK-) cell clones.Journal of virology · 1998Article
- Sulfated carbohydrate compounds prevent microbial adherence by sexually transmitted disease pathogens.Antimicrobial agents and chemotherapy · 1997Article
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Authors and funding
2 authors.
Funding
Abstract
BHK(TK-) cells selected for resistance to polyethylene glycol-mediated fusion give rise to clones that are resistant to herpes simplex virus (HSV) infection. We have characterized one such clone, designated 95-19, and found that it is resistant to entry of HSV type 1 (HSV-1), HSV-2, and the related alphaherpesvirus pseudorabies virus (PRV). Single-step growth experiments show no detectable replication of multiple strains of HSV-1 and HSV-2 on 95-19 cells. Three lines of evidence suggest that these cells are resistant to postattachment entry. (i) Measurements of binding of radiolabeled virus show that heparin-sensitive binding of HSV-1 and HSV-2 to 95-19 cells is identical to binding to BHK(TK-) cells, suggesting that the block to replication occurs after attachment to heparan sulfate proteoglycan. (ii) 95-19 cells exposed to HSV-1 or HSV-2 at high multiplicity show no detectable immediate-early (IE) mRNA expression. (iii) Exposure of attached virus and cells to polyethylene glycol results in partial recovery of both IE gene expression and virus yield in single-step growth. The degrees of recovery of single-step yield and IE gene expression are similar, suggesting that the only block to single-step replication is at the point of virus entry and that these cells are deficient in some cellular factor required for efficient postattachment entry of free virus. 95-19 cells are also highly resistant to entry by cell-to-cell spread, suggesting that the same cellular factor participates in both types of entry.
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