ArticleProceedings of the National Academy of Sciences of the United States of America2010
Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Trial
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Inhibitory effect of Alantolactone against varicella-zoster virus in vitro.Virology journal · 2025Article
- Structures of the Varicella Zoster Virus Glycoprotein E and Epitope Mapping of Vaccine-Elicited Antibodies.Vaccines · 2024Article
- Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine.NPJ vaccines · 2024Article
- Immunogenicity in Mice Immunized with Recombinant Adenoviruses Expressing Varicella-Zoster Virus Envelope Glycoprotein E.Viruses · 2023Article
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
- Humanized Severe Combined Immunodeficient (SCID) Mouse Models for Varicella-Zoster Virus Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Novel BC02 Compound Adjuvant Enhances Adaptive and Innate Immunity Induced by Recombinant Glycoprotein E of Varicella-Zoster Virus.Vaccines · 2022Article
- Sirt3 deficiency induced down regulation of insulin degrading enzyme in comorbid Alzheimer's disease with metabolic syndrome.Scientific reports · 2022Article
- 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
- Review
- Modulation of Insulin Sensitivity by Insulin-Degrading Enzyme.Biomedicines · 2021Review
- The N-terminus of varicella-zoster virus glycoprotein B has a functional role in fusion.PLoS pathogens · 2021Article
- Varicella-zoster virus: molecular controls of cell fusion-dependent pathogenesis.Biochemical Society transactions · 2020Review
- Insights into the pathogenesis of varicella viruses.Current clinical microbiology reports · 2019Article
- Breadth and Functionality of Varicella-Zoster Virus Glycoprotein-Specific Antibodies Identified after Zostavax Vaccination in Humans.Journal of virology · 2018Article
- Global aspects of viral glycosylation.Glycobiology · 2018Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Varicella-zoster virus (VZV) is an alphaherpesvirus that infects skin, lymphocytes, and sensory ganglia. VZV glycoprotein E (gE) has a unique N-terminal region (aa1-188), which is required for replication and includes domains involved in secondary envelopment, efficient cell-cell spread, and skin infection in vivo. The nonconserved N-terminal region also mediates binding to the insulin-degrading enzyme (IDE), which is proposed to be a VZV receptor. Using viral mutagenesis to make the recombinant rOka-DeltaP27-G90, we showed that amino acids in this region are required for gE/IDE binding in infected cells; this deletion reduced cell-cell spread in vitro and skin infection in vivo. However, a gE point mutation, linker insertions, and partial deletions in the aa27-90 region, and deletion of a large portion of the unique N-terminal region, aa52-187, had similar or more severe effects on VZV replication in vitro and in vivo without disrupting the gE/IDE interaction. VZV replication in T cells in vivo was not impaired by deletion of gE aa27-90, suggesting that these gE residues are not essential for VZV T cell tropism. However, the rOka-DeltaY51-P187 mutant failed to replicate in T cell xenografts as well as skin in vivo. VZV tropism for T cells and skin, which is necessary for its life cycle in the human host, requires this nonconserved region of the N-terminal region of VZV gE.
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