ArticleJournal of virology2007
The amino terminus of varicella-zoster virus (VZV) glycoprotein E is required for binding to insulin-degrading enzyme, a VZV receptor.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
- Altered Surface Expression of Insulin-Degrading Enzyme on Monocytes and Lymphocytes from COVID-19 Patients Both at Diagnosis and after Hospital Discharge.International journal of molecular sciences · 2022Article
- Role of Epitranscriptomic and Epigenetic Modifications during the Lytic and Latent Phases of Herpesvirus Infections.Microorganisms · 2022Review
- Review
- Nectin-1 Is an Entry Mediator for Varicella-Zoster Virus Infection of Human Neurons.Journal of virology · 2021Article
- A putative WAVE regulatory complex (WRC) interacting receptor sequence (WIRS) in the cytoplasmic tail of HSV-1 gE does not function in WRC recruitment or neuronal transport.Access microbiology · 2021Article
- The Roles of Envelope Glycoprotein M in the Life Cycle of Some Alphaherpesviruses.Frontiers in microbiology · 2021Review
- Recombinant Glycoprotein E of Varicella Zoster Virus Contains Glycan-Peptide Motifs That Modulate B Cell Epitopes into Discrete Immunological Signatures.International journal of molecular sciences · 2019Article
- Functional Relevance of the Transmembrane Domain and Cytoplasmic Tail of the Pseudorabies Virus Glycoprotein H for Membrane Fusion.Journal of virology · 2018Article
- Varicella-Zoster Virus Glycoproteins: Entry, Replication, and Pathogenesis.Current clinical microbiology reports · 2016Article
- Global Mapping of O-Glycosylation of Varicella Zoster Virus, Human Cytomegalovirus, and Epstein-Barr Virus.The Journal of biological chemistry · 2016Article
- Review
- Herpes simplex virus and varicella zoster virus, the house guests who never leave.Herpesviridae · 2012Article
- Anion activation site of insulin-degrading enzyme.The Journal of biological chemistry · 2012Article
- Investigation of varicella-zoster virus neurotropism and neurovirulence using SCID mouse-human DRG xenografts.Journal of neurovirology · 2011Review
- Mutagenesis of varicella-zoster virus glycoprotein I (gI) identifies a cysteine residue critical for gE/gI heterodimer formation, gI structure, and virulence in skin cells.Journal of virology · 2011Article
- Insulin degrading enzyme induces a conformational change in varicella-zoster virus gE, and enhances virus infectivity and stability.PloS one · 2010Article
- Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Insulin-degrading enzyme binds to the nonglycosylated precursor of varicella-zoster virus gE protein found in the endoplasmic reticulum.Journal of virology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Varicella-zoster virus (VZV) glycoprotein E (gE) is required for VZV infection. Although gE is well conserved among alphaherpesviruses, the amino terminus of VZV gE is unique. Previously, we showed that gE interacts with insulin-degrading enzyme (IDE) and facilitates VZV infection and cell-to-cell spread of the virus. Here we define the region of VZV gE required to bind IDE. Deletion of amino acids 32 to 71 of gE, located immediately after the predicted signal peptide, resulted in loss of the ability of gE to bind IDE. A synthetic peptide corresponding to amino acids 24 to 50 of gE blocked its interaction with IDE in a concentration-dependent manner. However, a chimeric gE in which amino acids 1 to 71 of VZV gE were fused to amino acids 30 to 545 of herpes simplex virus type 2 gE did not show an increased level of binding to IDE compared with that of full-length HSV gE. Thus, amino acids 24 to 71 of gE are required for IDE binding, and the secondary structure of gE is critical for the interaction. VZV gE also forms a heterodimer with glycoprotein gI. Deletion of amino acids 163 to 208 of gE severely reduced its ability to form a complex with gI. The amino portion of IDE, as well an IDE mutant in the catalytic domain of the protein, bound to gE. Therefore, distinct motifs of VZV gE are important for binding to IDE or to gI.
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