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Interleukin-6 and type 1 interferons inhibit varicella zoster virus replication in human neurons.

Authors
  • Como, Christina N1
  • Pearce, Catherine M1
  • Cohrs, Randall J2
  • Baird, Nicholas L3
  • 1 Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA.
  • 2 Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
  • 3 Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: [email protected]
Type
Published Article
Journal
Virology
Publisher
Elsevier
Publication Date
Sep 01, 2018
Volume
522
Pages
13–18
Identifiers
DOI: 10.1016/j.virol.2018.06.013
PMID: 29979960
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus that, following primary infection (varicella), establishes latency in sensory, autonomic, sympathetic and parasympathetic neurons, where it remains until reactivation (zoster). VZV-specific cell-mediated immune responses maintain VZV latency; thus, immunosuppressed and elderly persons are at risk of reactivation and associated neurological diseases. However, the cytokines produced by the immune system that control VZV in neurons are largely unknown. Therefore, to better understand how the immune system may restrict VZV in neurons, we studied interleukin-6, tumor necrosis factor-alpha and type 1 interferons for their ability to inhibit VZV replication in human neurons in vitro. Our studies revealed that VZV transcription and viral spread were significantly reduced by interleukin-6 and type 1 interferons, and to a lesser extent by tumor necrosis factor-alpha. These findings will help in understanding how the innate immune system limits virus replication in neurons in vivo. Copyright © 2018 Elsevier Inc. All rights reserved.

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