ORF68

Summary

Gene Symbol: ORF68
Description: type 1 membrane protein; contains a signal peptide; complexed with envelope glycoprotein I to form an Fc-receptor
Alias: envelope glycoprotein E
Species: Human herpesvirus 3

Top Publications

  1. ncbi Functions of the C-terminal domain of varicella-zoster virus glycoprotein E in viral replication in vitro and skin and T-cell tropism in vivo
    Jennifer Moffat
    Department of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA
    J Virol 78:12406-15. 2004
  2. ncbi Incorporation of three endocytosed varicella-zoster virus glycoproteins, gE, gH, and gB, into the virion envelope
    Lucie Maresova
    University of Iowa Hospital 2501 JCP, 200 Hawkins Dr, Iowa City, IA 52242, USA
    J Virol 79:997-1007. 2005
  3. ncbi 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 entry
    Barbara Berarducci
    Institut Pasteur, Départment de Virologie, 25 rue du Dr Roux, 75015 Paris, France
    J Virol 83:228-40. 2009
  4. ncbi 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 infection
    Mir A Ali
    Medical Virology Section, Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Virology 386:270-9. 2009
  5. ncbi Insulin-degrading enzyme binds to the nonglycosylated precursor of varicella-zoster virus gE protein found in the endoplasmic reticulum
    J E Carpenter
    Children s Hospital, University of Iowa, Iowa City, Iowa 52242, USA
    J Virol 84:847-55. 2010
  6. ncbi Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infection
    Barbara Berarducci
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 107:282-7. 2010
  7. ncbi Varicella-zoster virus glycoprotein E is a critical determinant of virulence in the SCID mouse-human model of neuropathogenesis
    Leigh Zerboni
    Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305, USA
    J Virol 85:98-111. 2011
  8. ncbi 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
    Stefan L Oliver
    Stanford University School of Medicine, Stanford, CA 94305, USA
    J Virol 85:4095-110. 2011

Research Grants

  1. Cdk inhibitors: novel antivirals for VZV
    Jennifer Moffat; Fiscal Year: 2007

Scientific Experts

Detail Information

Publications8

  1. ncbi Functions of the C-terminal domain of varicella-zoster virus glycoprotein E in viral replication in vitro and skin and T-cell tropism in vivo
    Jennifer Moffat
    Department of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA
    J Virol 78:12406-15. 2004
    ....
  2. ncbi Incorporation of three endocytosed varicella-zoster virus glycoproteins, gE, gH, and gB, into the virion envelope
    Lucie 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...
  3. ncbi 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 entry
    Barbara 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...
  4. ncbi 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 infection
    Mir 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...
  5. ncbi Insulin-degrading enzyme binds to the nonglycosylated precursor of varicella-zoster virus gE protein found in the endoplasmic reticulum
    J 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...
  6. ncbi Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infection
    Barbara 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...
  7. ncbi Varicella-zoster virus glycoprotein E is a critical determinant of virulence in the SCID mouse-human model of neuropathogenesis
    Leigh Zerboni
    Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305, USA
    J Virol 85:98-111. 2011
    ....
  8. ncbi 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
    Stefan 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...

Research Grants5

  1. Cdk inhibitors: novel antivirals for VZV
    Jennifer Moffat; Fiscal Year: 2007
    ..Understanding precisely how cdk inhibitors block VZV growth is the starting point for development of effective antiviral agents. ..