ArticleJournal of virology2013
Novel mutations in gB and gH circumvent the requirement for known gD Receptors in herpes simplex virus 1 entry and cell-to-cell spread.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed.
- Anatid herpesvirus 1 UL51 protein is palmitoylated by DHHC9 and DHHC18 for viral replication and virulence.PLoS pathogens · 2026Article
- Durable tissue-specific transgene expression in newborn mice following intraperitoneal delivery of non-cytotoxic HSV vectors.Molecular therapy. Methods & clinical development · 2025Article
- Induction of necroptosis in multinucleated giant cells induced by conditionally replicating syncytial oHSV in co-cultures of cancer cells and non-cancerous cells.Molecular therapy. Oncology · 2024Article
- Functions of the UL51 protein during the herpesvirus life cycle.Frontiers in microbiology · 2024Review
- Novel mutations in UMolecular therapy. Methods & clinical development · 2023Article
- Potent anti-tumor effects of receptor-retargeted syncytial oncolytic herpes simplex virus.Molecular therapy oncolytics · 2021Article
- Antibody Screening System Using a Herpes Simplex Virus (HSV)-Based Probe To Identify a Novel Target for Receptor-Retargeted Oncolytic HSVs.Journal of virology · 2021Article
- Research Note: Duck plague virus glycoprotein I influences cell-cell spread and final envelope acquisition.Poultry science · 2020Article
- Generation of an Oncolytic Herpes Simplex Viral Vector Completely Retargeted to the GDNF Receptor GFRα1 for Specific Infection of Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Design of an Interferon-Resistant Oncolytic HSV-1 Incorporating Redundant Safety Modalities for Improved Tolerability.Molecular therapy oncolytics · 2020Article
- Point Mutations in Retargeted gD Eliminate the Sensitivity of EGFR/EGFRvIII-Targeted HSV to Key Neutralizing Antibodies.Molecular therapy. Methods & clinical development · 2020Article
- Identification of 22 Novel Motifs of the Cell Entry Fusion Glycoprotein B of Oncolytic Herpes Simplex Viruses: Sequence Analysis and Literature Review.Frontiers in oncology · 2020Article
- Oncolytic herpes simplex virus tumor targeting and neutralization escape by engineering viral envelope glycoproteins.Drug delivery · 2018Review
- Dual Ligand Insertion in gB and gD of Oncolytic Herpes Simplex Viruses for Retargeting to a Producer Vero Cell Line and to Cancer Cells.Journal of virology · 2018Article
- Insertion of a ligand to HER2 in gB retargets HSV tropism and obviates the need for activation of the other entry glycoproteins.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
- Retargeting of herpes simplex virus (HSV) vectors.Current opinion in virology · 2016Review
- Development of an oncolytic HSV vector fully retargeted specifically to cellular EpCAM for virus entry and cell-to-cell spread.Gene therapy · 2016Article
- The Engineering of a Novel Ligand in gH Confers to HSV an Expanded Tropism Independent of gD Activation by Its Receptors.PLoS pathogens · 2015Article
- Structure-based functional analyses of domains II and III of pseudorabies virus glycoprotein H.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Both entry and cell-to-cell spread of herpes simplex virus (HSV) involve a cascade of cooperative interactions among the essential glycoproteins D, B, and H/L (gD, gB, and gH/gL, respectively) initiated by the binding of gD to a cognate HSV entry receptor. We previously reported that a variant (D285N/A549T) of glycoprotein B (gB:NT) enabled primary virus entry into cells that were devoid of typical HSV entry receptors. Here, we compared the activities of the gB:NT variant with those of a newly selected variant of glycoprotein H (gH:KV) and a frequently coselected gB variant (gB:S668N). In combination, gH:KV and gB:S668N enabled primary virus entry into cells that lacked established HSV entry receptors as efficiently as did gB:NT, but separately, each variant enabled only limited entry. Remarkably, gH:KV uniquely facilitated secondary virus spread between cells that lacked canonical entry receptors. Transient expression of the four essential entry glycoproteins revealed that gH:KV, but not gB:NT, induced fusion between cells lacking the standard receptors. Because the involvement of gD remained essential for virus spread and cell fusion, we propose that gH:KV mimics a transition state of gH that responds efficiently to weak signals from gD to reach the active state. Computational modeling of the structures of wild-type gH and gH:KV revealed relatively subtle differences that may have accounted for our experimental findings. Our study shows that (i) the dependence of HSV-1 entry and spread on specific gD receptors can be reduced by sequence changes in the downstream effectors gB and gH, and (ii) the relative roles of gB and gH are different in entry and spread.
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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.