Abstract
The varicella-zoster virus (VZV) ORF61 protein is necessary for normal replication in vitro and virulence in human skin xenografts in the severe combined immunodeficiency mouse model in vivo. These experiments identify a hydrophobic domain that mediates ORF61 self-interaction. While not needed to inhibit host cell defenses, disruption of this domain (residues 250 to 320) severely impairs VZV growth, transactivation of the immediate early 63 and glycoprotein E genes, and the pathogenesis of VZV skin infection in vivo.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Amino Acid Sequence
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Animals
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Base Sequence
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Chickenpox / physiopathology*
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Herpesvirus 3, Human / genetics
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Herpesvirus 3, Human / metabolism*
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Herpesvirus 3, Human / pathogenicity
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Humans
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Hydrophobic and Hydrophilic Interactions
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Immediate-Early Proteins / metabolism
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Immunoblotting
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Immunoprecipitation
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Mice
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Microscopy, Confocal
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Molecular Sequence Data
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Protein Structure, Tertiary
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Sequence Analysis, DNA
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Skin / pathology
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Skin / virology*
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Viral Envelope Proteins / metabolism
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Viral Proteins / chemistry*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
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Virus Replication / genetics
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Virus Replication / physiology*
Substances
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Immediate-Early Proteins
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Viral Envelope Proteins
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Viral Proteins
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glycoprotein E, varicella-zoster virus
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immediate early protein 63, Human herpesvirus 3
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protein 61, Varicella-zoster virus