Abstract
In varicella-zoster virus (VZV)-infected primary human brain vascular adventitial fibroblasts (BRAFs), levels of beta interferon (IFN-β,) STAT1, and STAT2 transcripts as well as STAT1 and STAT2 protein were decreased. IFN-α transcript levels were increased but not secreted IFN-α protein levels. Compared to IFN-α-treated control results, in VZV-infected BRAFs, phosphorylated STAT1 did not translocate to the nucleus, resulting in impaired downstream expression of interferon-inducible antiviral Mx1. Overall, VZV interference with the type I interferon pathway may promote virus persistence in cerebral arteries.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Adventitia / blood supply
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Adventitia / metabolism
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Adventitia / pathology
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Adventitia / virology
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Blood Vessels / metabolism
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Blood Vessels / pathology
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Blood Vessels / virology
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Brain / blood supply
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Brain / metabolism
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Brain / pathology
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Brain / virology
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Fibroblasts / metabolism*
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Fibroblasts / pathology
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Fibroblasts / virology
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Gene Expression Regulation*
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Herpesvirus 3, Human / genetics*
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Herpesvirus 3, Human / metabolism
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Host-Pathogen Interactions
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Humans
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Interferon-alpha / genetics
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Interferon-alpha / metabolism
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Interferon-beta / genetics
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Interferon-beta / metabolism
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Myxovirus Resistance Proteins / antagonists & inhibitors*
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Myxovirus Resistance Proteins / genetics
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Myxovirus Resistance Proteins / metabolism
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Phosphorylation
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Primary Cell Culture
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Protein Transport
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STAT1 Transcription Factor / genetics*
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STAT1 Transcription Factor / metabolism
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STAT2 Transcription Factor / genetics
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STAT2 Transcription Factor / metabolism
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Signal Transduction
Substances
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Interferon-alpha
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MX1 protein, human
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Myxovirus Resistance Proteins
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STAT1 Transcription Factor
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STAT1 protein, human
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STAT2 Transcription Factor
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STAT2 protein, human
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Interferon-beta