Gene Symbol: ORF68
Description: type 1 membrane protein; contains a signal peptide; complexed with envelope glycoprotein I to form an Fc-receptor
Alias: type 1 membrane protein, contains a signal peptide, complexed with envelope glycoprotein I to form an Fc-receptor, envelope glycoprotein E
Species: Human herpesvirus 3
- Autophagy and the effects of its inhibition on varicella-zoster virus glycoprotein biosynthesis and infectivityErin M Buckingham
Virology Laboratory, University of Iowa Children s Hospital, Iowa City, Iowa, USA
J Virol 88:890-902. 2014....
- [Sequence analysis of varicella-zoster virus gE gene in varicella-zoster virus strains with different clades]Long feng Jiang
Department of Microbiology, Anhui Medical University, Hefei 230032, China
Bing Du Xue Bao 29:112-8. 2013..The analysis of gE gene sequences,revealed a novel non-synonymous mutations in the e1 and c1 epitopes, corresponding to the amino acid change of serine to tyrosine...
- Functions of the C-terminal domain of varicella-zoster virus glycoprotein E in viral replication in vitro and skin and T-cell tropism in vivoJennifer Moffat
Department of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA
J Virol 78:12406-15. 2004....
- Incorporation of three endocytosed varicella-zoster virus glycoproteins, gE, gH, and gB, into the virion envelopeLucie Maresova
University of Iowa Hospital 2501 JCP, 200 Hawkins Dr, Iowa City, IA 52242, USA
J Virol 79:997-1007. 2005..Furthermore, since a recombinant VZV genome lacking only endocytosis-competent gE cannot replicate, these results supported the conclusion that the endocytosis-envelopment pathway is an essential component of the VZV life cycle...
- Deletion of the first cysteine-rich region of the varicella-zoster virus glycoprotein E ectodomain abolishes the gE and gI interaction and differentially affects cell-cell spread and viral entryBarbara Berarducci
Institut Pasteur, Départment de Virologie, 25 rue du Dr Roux, 75015 Paris, France
J Virol 83:228-40. 2009..Blocking gE binding to gI resulted in severe impairment of VZV infection of human skin xenografts in SCIDhu mice in vivo, documenting the importance of cell fusion mediated by this complex for VZV virulence in skin...
- The insulin degrading enzyme binding domain of varicella-zoster virus (VZV) glycoprotein E is important for cell-to-cell spread and VZV infectivity, while a glycoprotein I binding domain is essential for infectionMir A Ali
Medical Virology Section, Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Virology 386:270-9. 2009..We conclude that the IDE binding domain is important for efficient cell-to-cell spread and infectivity of cell-free virus...
- Insulin-degrading enzyme binds to the nonglycosylated precursor of varicella-zoster virus gE protein found in the endoplasmic reticulumJ E Carpenter
Children s Hospital, University of Iowa, Iowa City, Iowa 52242, USA
J Virol 84:847-55. 2010..We conclude that IDE protease binds to the 73-kDa gE precursor and that this event occurs in the cytosol but not as a receptor/ligand interaction...
- Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infectionBarbara Berarducci
Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 107:282-7. 2010..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...
- Varicella-zoster virus glycoprotein E is a critical determinant of virulence in the SCID mouse-human model of neuropathogenesisLeigh Zerboni
Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305, USA
J Virol 85:98-111. 2011....
- Mutagenesis of varicella-zoster virus glycoprotein I (gI) identifies a cysteine residue critical for gE/gI heterodimer formation, gI structure, and virulence in skin cellsStefan L Oliver
Stanford University School of Medicine, Stanford, CA 94305, USA
J Virol 85:4095-110. 2011..Thus, residues C95 and 105 to 125 are critical for gI structure required for gE/gI heterodimer formation, virion incorporation, and ultimately, effective viral spread in human skin...
- Cdk inhibitors: novel antivirals for VZVJennifer Moffat; Fiscal Year: 2007..Understanding precisely how cdk inhibitors block VZV growth is the starting point for development of effective antiviral agents. [unreadable] [unreadable]..