ArticlePloS one2008
The murid herpesvirus-4 gH/gL binds to glycosaminoglycans.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 29 citations in OpenAlex.
- Gammaherpesvirus BoHV-4 infects bovine respiratory epithelial cells mainly at the basolateral side.Veterinary research · 2019Article
- Multivalent binding of herpesvirus to living cells is tightly regulated during infection.Science advances · 2018Article
- The Major Envelope Glycoprotein of Murid Herpesvirus 4 Promotes Sexual Transmission.Journal of virology · 2017Article
- Structural Proteomics of Herpesviruses.Viruses · 2016Review
- Rhadinovirus host entry by co-operative infection.PLoS pathogens · 2015Article
- Herpes simplex virus 1 targets the murine olfactory neuroepithelium for host entry.Journal of virology · 2013Article
- Article
- Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.PLoS pathogens · 2012Article
- Murine gammaherpesvirus 68 glycoprotein 150 does not contribute to latency amplification in vivo.Virology journal · 2012Article
- Virion endocytosis is a major target for murid herpesvirus-4 neutralization.The Journal of general virology · 2012Article
- Bovine herpesvirus type 4 glycoprotein L is nonessential for infectivity but triggers virion endocytosis during entry.Journal of virology · 2012Article
- A heparan-dependent herpesvirus targets the olfactory neuroepithelium for host entry.PLoS pathogens · 2012Article
- Article
- The bovine herpesvirus 4 Bo10 gene encodes a nonessential viral envelope protein that regulates viral tropism through both positive and negative effects.Journal of virology · 2011Article
- Vaccination with murid herpesvirus-4 glycoprotein B reduces viral lytic replication but does not induce detectable virion neutralization.The Journal of general virology · 2010Article
- A gammaherpesvirus complement regulatory protein promotes initiation of infection by activation of protein kinase Akt/PKB.PloS one · 2010Article
- An unusual dependence of human herpesvirus-8 glycoproteins-induced cell-to-cell fusion on heparan sulfate.Biochemical and biophysical research communications · 2009Article
- Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions.The Journal of general virology · 2009Article
- From carbohydrate leads to glycomimetic drugs.Nature reviews. Drug discovery · 2009Review
- Glycoprotein L sets the neutralization profile of murid herpesvirus 4.The Journal of general virology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The first contact a virus makes with cells is an important determinant of its tropism. Murid Herpesvirus-4 (MuHV-4) is highly dependent on glycosaminoglycans (GAGs) for cell binding. Its first contact is therefore likely to involve a GAG-binding virion glycoprotein. We have previously identified two such proteins, gp70 and gp150. Gp70 binds strongly to GAGs. However, deleting it makes little difference to MuHV-4 cell binding or GAG-dependence. Deleting gp150, by contrast, frees MuHV-4 from GAG dependence. This implies that GAGs normally displace gp150 to allow GAG-independent cell binding. But the gp150 GAG interaction is weak, and so would seem unlikely to make an effective first contact. Since neither gp70 nor gp150 matches the expected profile of a first contact glycoprotein, our understanding of MuHV-4 GAG interactions must be incomplete. Here we relate the seemingly disconnected gp70 and gp150 GAG interactions by showing that the MuHV-4 gH/gL also binds to GAGs. gH/gL-blocking and gp70-blocking antibodies individually had little effect on cell binding, but together were strongly inhibitory. Thus, there was redundancy in GAG binding between gp70 and gH/gL. Gp150-deficient MuHV-4 largely resisted blocks to gp70 and gH/gL binding, consistent with its GAG independence. The failure of wild-type MuHV-4 to do the same argues that gp150 is normally engaged only down-stream of gp70 or gH/gL. MuHV-4 GAG dependence is consequently two-fold: gp70 or gH/gL binding provides virions with a vital first foothold, and gp150 is then engaged to reveal GAG-independent binding.
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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.