ArticleJournal of virology2013
The amino terminus of herpes simplex virus 1 glycoprotein K is required for virion entry via the paired immunoglobulin-like type-2 receptor alpha.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Combinatorial genome engineering of pseudorabies virus Bartha by developing a reverse genetic system based on three overlapping genomic segments.Journal of advanced research · 2026Article
- Screening of host proteins interacting with the African swine fever virus outer membrane protein CD2v.Frontiers in microbiology · 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 Glycoprotein B from a Hyperfusogenic Virus Mediates Enhanced Cell-Cell Fusion.Viruses · 2024Article
- Review
- Review
- Article
- Identification and Visualization of Functionally Important Domains and Residues in Herpes Simplex Virus Glycoprotein K(gK) Using a Combination of Phylogenetics and Protein Modeling.Scientific reports · 2019Article
- The Amino Terminus of Herpes Simplex Virus 1 Glycoprotein K (gK) Is Required for gB Binding to Akt, Release of Intracellular Calcium, and Fusion of the Viral Envelope with Plasma Membranes.Journal of virology · 2018Article
- First Impressions-the Potential of Altering Initial Host-Virus Interactions for Rational Design of Herpesvirus Vaccine Vectors.Current clinical microbiology reports · 2018Article
- Role of Herpes Simplex Virus Type 1 (HSV-1) Glycoprotein K (gK) Pathogenic CD8Frontiers in immunology · 2018Review
- Herpes simplex virus Membrane Fusion.Advances in anatomy, embryology, and cell biology · 2017Review
- Herpesvirus Entry into Host Cells Mediated by Endosomal Low pH.Traffic (Copenhagen, Denmark) · 2016Review
- Article
- Deletion of a Predicted β-Sheet Domain within the Amino Terminus of Herpes Simplex Virus Glycoprotein K Conserved among Alphaherpesviruses Prevents Virus Entry into Neuronal Axons.Journal of virology · 2015Article
- Herpes simplex virus internalization into epithelial cells requires Na+/H+ exchangers and p21-activated kinases but neither clathrin- nor caveolin-mediated endocytosis.Journal of virology · 2014Article
- Article
- Single dose of glycoprotein K (gK)-deleted HSV-1 live-attenuated virus protects mice against lethal vaginal challenge with HSV-1 and HSV-2 and induces lasting T cell memory immune responses.Virology journal · 2013Article
- Herpes simplex virus 1 glycoprotein M and the membrane-associated protein UL11 are required for virus-induced cell fusion and efficient virus entry.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The herpes simplex virus 1 (HSV-1) glycoprotein K (gK)/UL20 protein complex is incorporated into virion envelopes and cellular membranes and functions during virus entry and cell-to-cell spread. To investigate the role of gK/UL20 in the context of a highly neurovirulent virus strain, the HSV-1(McKrae) genome was cloned into a bacterial artificial chromosome plasmid (McKbac) and utilized to construct the mutant virus McK(gKΔ31-68), carrying a 37-amino-acid deletion within the gK amino terminus. The McKbac virus entered efficiently into Chinese hamster ovary (CHO) cells constitutively expressing HSV-1 human receptors, nectin-1, herpesvirus entry mediator (HVEM), or paired immunoglobulin-like type-2 receptor alpha (PILRα). In contrast, the McK(gKΔ31-68) virus failed to enter into CHO-PILRα cells, while it entered CHO cells expressing HVEM and nectin-1 more efficiently than the McKbac virus. Both McKbac and McK(gKΔ31-68) viruses entered all CHO cells expressing HSV-1 receptors via a pH-independent pathway. The HSV-1(F) gBΔ28syn mutant virus, encoding a carboxyl-terminal truncated gB, causes extensive cell fusion. Previously, we showed that the gKΔ31-68 amino acid deletion abrogated gBΔ28syn virus-induced cell fusion, indicating that the amino terminus of gK is required for gB-mediated virus-induced cell fusion (V. N. Chouljenko, A. V. Iyer, S. Chowdhury, D. V. Chouljenko, and K. G. J. Kousoulas, Virology 83:12301-12313, 2009). Surprisingly, the gKΔ31-68/gBΔ28syn virus caused extensive fusion of CHO-nectin-1 cells but limited cell fusion of CHO-PILRα cells. Coimmunoprecipitation experiments revealed that both gK and PILRα bound gB in infected cells. Collectively, these results indicate that the amino terminus of gK is functionally and physically associated with the gB-PILRα protein complex and regulates membrane fusion of the viral envelope with cellular membranes during virus entry as well as virus-induced cell-to-cell fusion.
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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.