Journal
JOURNAL OF VIROLOGY
Volume 88, Issue 19, Pages 11634-11637Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01945-14
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Funding
- Public Health Service grants from the National Institutes of Health [AG006127, AG032958, NS 067070]
- National Institutes of Health [NS007321]
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In varicella-zoster virus (VZV)-infected primary human brain vascular adventitial fibroblasts (BRAFs), levels of beta interferon (IFN-beta,) STAT1, and STAT2 transcripts as well as STAT1 and STAT2 protein were decreased. IFN-alpha transcript levels were increased but not secreted IFN-beta protein levels. Compared to IFN-alpha-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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