ArticleJournal of virology2012
Bovine herpesvirus type 4 glycoprotein L is nonessential for infectivity but triggers virion endocytosis during entry.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- A novel replication-deficient feline herpesvirus type 1 vector-based vaccine provides strong immune protection in cats.Journal of virology · 2026Article
- Ovine Herpesvirus 2 Glycoprotein B Complementation Restores Infectivity to a Bovine Herpesvirus 4 gB-Null Mutant.Pathogens (Basel, Switzerland) · 2024Article
- Functional Role of N-Linked Glycosylation in Pseudorabies Virus Glycoprotein gH.Journal of virology · 2018Article
- Epstein-Barr Virus Fusion with Epithelial Cells Triggered by gB Is Restricted by a gL Glycosylation Site.Journal of virology · 2017Article
- Primary replication and invasion of the bovine gammaherpesvirus BoHV-4 in the genital mucosae.Veterinary research · 2017Article
- Functional Relevance of the N-Terminal Domain of Pseudorabies Virus Envelope Glycoprotein H and Its Interaction with Glycoprotein L.Journal of virology · 2017Article
- Bovine Herpesvirus 4 Modulates Its β-1,6-N-Acetylglucosaminyltransferase Activity through Alternative Splicing.Journal of virology · 2016Article
- Structural Proteomics of Herpesviruses.Viruses · 2016Review
- Deletion of Murid Herpesvirus 4 ORF63 Affects the Trafficking of Incoming Capsids toward the Nucleus.Journal of virology · 2015Article
- Mutations in Pseudorabies Virus Glycoproteins gB, gD, and gH Functionally Compensate for the Absence of gL.Journal of virology · 2015Article
- A Functional Interaction between Herpes Simplex Virus 1 Glycoprotein gH/gL Domains I and II and gD Is Defined by Using Alphaherpesvirus gH and gL Chimeras.Journal of virology · 2015Article
- Structure-based functional analyses of domains II and III of pseudorabies virus glycoprotein H.Journal of virology · 2015Article
- The highly conserved proline at position 438 in pseudorabies virus gH is important for regulation of membrane fusion.Journal of virology · 2014Article
- A gammaherpesvirus uses alternative splicing to regulate its tropism and its sensitivity to neutralization.PLoS pathogens · 2013Article
- Article
- Proteomic characterization of bovine herpesvirus 4 extracellular virions.Journal of virology · 2012Article
- Structure-based mutational analysis of the highly conserved domain IV of glycoprotein H of pseudorabies virus.Journal of virology · 2012Article
- Virion endocytosis is a major target for murid herpesvirus-4 neutralization.The Journal of general virology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The core entry machinery of mammalian herpesviruses comprises glycoprotein B (gB), gH, and gL. gH and gL form a heterodimer with a central role in viral membrane fusion. When archetypal alpha- or betaherpesviruses lack gL, gH misfolds and progeny virions are noninfectious. However, the gL of the rhadinovirus murid herpesvirus 4 (MuHV-4) is nonessential for infection. In order to define more generally what role gL plays in rhadinovirus infections, we disrupted its coding sequence in bovine herpesvirus 4 (BoHV-4). BoHV-4 lacking gL showed altered gH glycosylation and incorporated somewhat less gH into virions but remained infectious. However, gL(-) virions showed poor growth associated with an entry deficit. Moreover, a major part of their entry defect appeared to reflect impaired endocytosis, which occurs upstream of membrane fusion itself. Thus, the rhadinovirus gL may be more important for driving virion endocytosis than for incorporating gH into virions, and it is nonessential for membrane fusion.
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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.