Abstract
Gamma interferon (IFN-gamma)-mediated indoleamine-2,3-dioxygenase (IDO) activity in human astrocytoma cells and in native astrocytes was found to be responsible for the inhibition of herpes simplex virus replication. The effect is abolished in the presence of excess amounts of L-tryptophan. Both IFN-alpha and IFN-beta restricted herpes simplex virus replication in both cell types, but (in contrast to the results seen with IFN-gamma) the addition of an excess amount of L-tryptophan did not inhibit the induced antiviral effect.
MeSH terms
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Antiviral Agents / pharmacology*
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Astrocytoma / enzymology
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Astrocytoma / virology
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Cell Line, Tumor
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Enzyme Induction / drug effects
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Humans
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Indoleamine-Pyrrole 2,3,-Dioxygenase
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Interferon-alpha / pharmacology
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Interferon-beta / pharmacology
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Interferon-gamma / pharmacology
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Interferons / pharmacology*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Simplexvirus / drug effects*
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Simplexvirus / physiology
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Tryptophan / pharmacology
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Tryptophan Oxygenase / genetics
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Tryptophan Oxygenase / metabolism*
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Virus Replication / drug effects
Substances
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Antiviral Agents
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Indoleamine-Pyrrole 2,3,-Dioxygenase
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Interferon-alpha
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RNA, Messenger
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Interferon-beta
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Interferon-gamma
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Tryptophan
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Interferons
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Tryptophan Oxygenase