Abstract
The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-beta consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-alpha1, IFN-alpha4, IFN-alpha5, IFN-alpha6, or IFN-alpha9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2'-5' oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-beta was lost.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antiviral Agents / deficiency
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Antiviral Agents / genetics
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Antiviral Agents / physiology*
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Cell Line
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Cells, Cultured
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Chlorocebus aethiops
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Endoribonucleases / deficiency
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Endoribonucleases / genetics
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Endoribonucleases / physiology*
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Female
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Gene Expression Regulation, Viral / immunology
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Herpesvirus 1, Human / genetics
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Herpesvirus 1, Human / immunology*
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Immunity, Innate / genetics
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Immunophenotyping
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Interferon-beta / physiology*
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Mice
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Mice, Inbred C57BL
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Mice, Inbred ICR
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Signal Transduction / genetics
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Signal Transduction / immunology*
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Transfection
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Trigeminal Ganglion / cytology
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Trigeminal Ganglion / enzymology
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Trigeminal Ganglion / immunology*
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Trigeminal Ganglion / virology*
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Vero Cells
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Virus Replication / genetics
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Virus Replication / immunology*
Substances
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Antiviral Agents
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Interferon-beta
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Endoribonucleases
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2-5A-dependent ribonuclease