Interferon-γ-induced inhibition of neuronal vesicular stomatitis virus infection is STAT1 dependent

David A. Chesler, Cindy Dodard, Grace Y. Lee, David E. Levy, Carol Shoshkes Reiss

Research output: Contribution to journalArticlepeer-review


In this report, the signaling pathways utilized by interferon (IFN)-γ in neurons and their respective roles in the inhibition of vesicular stomatitis virus (VSV) replication were studied. The authors have previously shown that IFN-γ treatment of NB41A3 neuroblastoma cells results in a 2-log inhibition of VSV production. This inhibition of VSV replication is dependent both in vitro and in vivo on nitric oxide (NO) production by NO synthase (NOS)-1. In NB41A3 neuroblastoma cells, IFN-γ was found to induce the signal transducer and activator of transcription (STAT) STAT1 phosphorylation, interferon regulatory factor (IRF)-1 expression, and p42/p44 mitogen-activated protein kinase (MAPK) phosphorylation; MAPK, however, was not required for inhibition of viral replication. Using olfactory bulb-enriched primary neuronal cultures, the inhibition of VSV replication was found to be STAT1 dependent, but did not require IRF-1.

Original languageEnglish (US)
Pages (from-to)57-63
Number of pages7
JournalJournal of neurovirology
Issue number1
StatePublished - Feb 2004


  • IRF-1
  • Interferon-gamma
  • MAPK
  • Neuroimmunology
  • STAT-1
  • VSV

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Virology


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