title: Inhibition of phosphorylated-STAT1 nuclear translocation and antiviral protein expression in human brain vascular adventitial fibroblasts infected with varicella-zoster virus.
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.
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA Maria.nagel@ucdenver.edu.
authors: Maria A
authors: MA
authors: Nagel
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Stephanie F
authors: SF
authors: James
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Igor
authors: I
authors: Traktinskiy
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Ann
authors: A
authors: Wyborny
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Alexander
authors: A
authors: Choe
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: April
authors: A
authors: Rempel
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Nicholas L
authors: NL
authors: Baird
authors: Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors: Don
authors: D
authors: Gilden
mesh_terms: D063194:Adventitia / Q000098:blood supply / Q000378:metabolism / Q000473:pathology / Q000821:virology; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology / Q000821:virology; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000473:pathology / Q000821:virology; D005347:Fibroblasts / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D005786:Gene Expression Regulation; D014645:Herpesvirus 3, Human / Q000235:genetics* / Q000378:metabolism; D054884:Host-Pathogen Interactions; D006801:Humans; D016898:Interferon-alpha / Q000235:genetics / Q000378:metabolism; D016899:Interferon-beta / Q000235:genetics / Q000378:metabolism; D064547:Myxovirus Resistance Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D061251:Primary Cell Culture; D021381:Protein Transport; D050794:STAT1 Transcription Factor / Q000235:genetics* / Q000378:metabolism; D050795:STAT2 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D016898:Interferon-alpha; C579071:MX1 protein, human; D064547:Myxovirus Resistance Proteins; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; D050795:STAT2 Transcription Factor; C494084:STAT2 protein, human; D016899:Interferon-beta