Abstract
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 language | English (US) |
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Pages (from-to) | 57-63 |
Number of pages | 7 |
Journal | Journal of neurovirology |
Volume | 10 |
Issue number | 1 |
DOIs | |
State | Published - Feb 2004 |
Keywords
- IRF-1
- Interferon-gamma
- MAPK
- Neuroimmunology
- STAT-1
- VSV
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Cellular and Molecular Neuroscience
- Virology