ArticlemSphere2020
Herpes Simplex Virus Glycoprotein C Regulates Low-pH Entry.
Article in mSphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed, 27 citations in OpenAlex.
- Comprehensive genomic characterization of herpes B virus isolated from a wild long-tailed macaque reveals conserved entry mechanisms and zoonotic potential.Emerging microbes & infections · 2026Article
- Host Cell Receptor and Herpes Simplex Virus 1 Glycoprotein B Are Determinants of Low Temperature Entry.Viruses · 2026Article
- Optimized isolation and purification of native glycoprotein B from herpes simplex virus 1: a streamlined approach.Iranian journal of microbiology · 2025Article
- Herpes simplex virus 1 envelope glycoprotein C shields glycoprotein D to protect virions from entry-blocking antibodies.Journal of virology · 2025Article
- Herpes simplex virus 1 glycoprotein C promotes virus penetration from endosomes during entry, independent of interaction with heparan sulfate.Frontiers in microbiology · 2025Article
- Herpes Simplex Virus 1 Envelope Glycoprotein C Shields Glycoprotein D to Protect Virions from Entry-Blocking Antibodies.bioRxiv : the preprint server for biology · 2024Article
- Article
- Article
- Herpes Simplex Virus 1 Glycoprotein B from a Hyperfusogenic Virus Mediates Enhanced Cell-Cell Fusion.Viruses · 2024Article
- Prunella vulgaris polysaccharide inhibits herpes simplex virus infection by blocking TLR-mediated NF-κB activation.Chinese medicine · 2024Article
- Bis-Benzylisoquinoline Alkaloids Inhibit Porcine Epidemic Diarrhea Virus by Disrupting Virus Entry.Pathogens (Basel, Switzerland) · 2023Article
- Impact of actin polymerization and filopodia formation on herpes simplex virus entry in epithelial, neuronal, and T lymphocyte cells.Frontiers in cellular and infection microbiology · 2023Review
- Deletion of Double Copies of the US1 Gene Reduces the Infectivity of Recombinant Duck Plague VirusMicrobiology spectrum · 2022Article
- Host Cell Neddylation Facilitates Alphaherpesvirus Entry in a Virus-Specific and Cell-Dependent Manner.Microbiology spectrum · 2022Article
- A Human Stem Cell-Derived Neurosensory-Epithelial Circuitry on a Chip to Model Herpes Simplex Virus Reactivation.Biomedicines · 2022Article
- Conformational Changes in Herpes Simplex Virus Glycoprotein C.Journal of virology · 2022Article
- Review
- Modulation of Endosome Function, Vesicle Trafficking and Autophagy by Human Herpesviruses.Cells · 2021Review
- Article
- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex viruses (HSVs) cause significant morbidity and mortality in humans worldwide. Herpesviruses mediate entry by a multicomponent virus-encoded machinery. Herpesviruses enter cells by endosomal low-pH and pH-neutral mechanisms in a cell-specific manner. HSV mediates cell entry via the envelope glycoproteins gB and gD and the heterodimer gH/gL regardless of pH or endocytosis requirements. Specifics concerning HSV envelope proteins that function selectively in a given entry pathway have been elusive. Here, we demonstrate that gC regulates cell entry and infection by a low-pH pathway. Conformational changes in the core herpesviral fusogen gB are critical for membrane fusion. The presence of gC conferred a higher pH threshold for acid-induced antigenic changes in gB. Thus, gC may selectively facilitate low-pH entry by regulating conformational changes in the fusion protein gB. We propose that gC modulates the HSV fusion machinery during entry into pathophysiologically relevant cells, such as human epidermal keratinocytes.
Indexed as
Identifiers
What OpenQuestion holds
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.