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Inhibition of phosphorylated-STAT1 nuclear translocation and antiviral protein expression in human brain vascular adventitial fibroblasts infected with varicella-zoster virus.

Authors:
Maria A Nagel Stephanie F James Igor Traktinskiy Ann Wyborny Alexander Choe April Rempel Nicholas L Baird Don Gilden

J Virol 2014 Oct 23;88(19):11634-7. Epub 2014 Jul 23.

Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA.

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.

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http://dx.doi.org/10.1128/JVI.01945-14DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178816PMC
October 2014

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