ArticleJournal of virology2012
Herpes B virus utilizes human nectin-1 but not HVEM or PILRα for cell-cell fusion and virus 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 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- HSV-1 inhibits melanogenesis of PIG1 cells through downregulation of VN1R5/ERK pathway.Archives of dermatological research · 2025Article
- Nectin1 is a pivotal host factor involved in attachment and entry of red-spotted grouper nervous necrosis virus in the early stages of the viral life cycle.Journal of virology · 2024Article
- Article
- Archaic connectivity between the sulfated heparan sulfate and the herpesviruses - An evolutionary potential for cross-species interactions.Computational and structural biotechnology journal · 2023Review
- Towards a comprehensive view of the herpes B virus.Frontiers in immunology · 2023Review
- Primate Simplexviruses Differ in Tropism for Macaque Cells.Microorganisms · 2022Article
- Nectin-1 Is an Entry Mediator for Varicella-Zoster Virus Infection of Human Neurons.Journal of virology · 2021Article
- Article
- Questioning the Extreme Neurovirulence of Monkey B VirusAdvances in virology · 2018Review
- Structural basis of nectin-1 recognition by pseudorabies virus glycoprotein D.PLoS pathogens · 2017Article
- Mapping sites of herpes simplex virus type 1 glycoprotein D that permit insertions and impact gD and gB receptors usage.Scientific reports · 2017Article
- Understanding Primate Herpesviruses.Journal of emerging diseases and virology · 2017Article
- Identification of unique B virus (Macacine Herpesvirus 1) epitopes of zoonotic and macaque isolates using monoclonal antibodies.PloS one · 2017Article
- Regulation of Herpes Simplex Virus Glycoprotein-Induced Cascade of Events Governing Cell-Cell Fusion.Journal of virology · 2016Article
- B Virus (Macacine Herpesvirus 1) Divergence: Variations in Glycoprotein D from Clinical and Laboratory Isolates Diversify Virus Entry Strategies.Journal of virology · 2016Article
- Optimized Expression, Purification of Herpes B Virus gD Protein in Escherichia coli, and Production of Its Monoclonal Antibodies.Jundishapur journal of microbiology · 2016Article
- Article
- B Virus (Macacine herpesvirus 1) Glycoprotein D Is Functional but Dispensable for Virus Entry into Macaque and Human Skin Cells.Journal of virology · 2015Article
- Isolation and characterization of a novel alphaherpesvirus in fruit bats.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
To investigate the requirements of herpesvirus entry and fusion, the four homologous glycoproteins necessary for herpes simplex virus (HSV) fusion were cloned from herpes B virus (BV) (or macacine herpesvirus 1, previously known as cercopithecine herpesvirus 1) and cercopithecine herpesvirus 2 (CeHV-2), both related simian simplexviruses belonging to the alphaherpesvirus subfamily. Western blots and cell-based enzyme-linked immunosorbent assay (ELISA) showed that glycoproteins gB, gD, and gH/gL were expressed in whole-cell lysates and on the cell surface. Cell-cell fusion assays indicated that nectin-1, an HSV-1 gD receptor, mediated fusion of cells expressing glycoproteins from both BV and CeHV-2. However, herpesvirus entry mediator (HVEM), another HSV-1 gD receptor, did not facilitate BV- and CeHV-2-induced cell-cell fusion. Paired immunoglobulin-like type 2 receptor alpha (PILRα), an HSV-1 gB fusion receptor, did not mediate fusion of cells expressing glycoproteins from either simian virus. Productive infection with BV was possible only with nectin-1-expressing cells, indicating that nectin-1 mediated entry while HVEM and PILRα did not function as entry receptors. These results indicate that these alphaherpesviruses have differing preferences for entry receptors. The usage of the HSV-1 gD receptor nectin-1 may explain interspecies transfer of the viruses, and altered receptor usage may result in altered virulence, tropism, or pathogenesis in the new host. A heterotypic cell fusion assay resulting in productive fusion may provide insight into interactions that occur to trigger fusion. These findings may be of therapeutic significance for control of deadly BV infections.
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