Abstract
Herpes simplex virus type 2 (HSV-2) genes expressed in neuronal cells in response to stress stimuli that trigger latency reactivation are largely unknown. Using a chloramphenicol acetyltransferase (CAT) reporter assay we found that stress caused a significant (P < .001) increase in ICP10 expression in neuronal cells. Up-regulation correlated with activator protein (AP)-1 activation, notably c-Jun and c-Fos that bind cognate elements in the ICP10 promoter. It was blocked by mutation of the AP-1 motifs in the ICP10 promoter. ICP10 expression protected neuronal cells from stress-induced apoptosis. The data suggest that ICP10 may contribute to HSV-2 reactivation by increasing neuronal survival.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Cell Survival
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Gene Expression Regulation, Viral
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Genes, Reporter
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Heat-Shock Response
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Herpes Genitalis / virology*
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Herpesvirus 2, Human / genetics*
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Herpesvirus 2, Human / growth & development
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Molecular Sequence Data
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Neurons / cytology
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Neurons / physiology
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Neurons / virology*
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PC12 Cells
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Promoter Regions, Genetic / physiology
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Protein Serine-Threonine Kinases / genetics*
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Rats
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Ribonucleotide Reductases / genetics*
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Transcription Factor AP-1 / metabolism*
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Up-Regulation
Substances
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Transcription Factor AP-1
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ICP10 protein, herpes simplex virus type 2
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Ribonucleotide Reductases
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Protein Serine-Threonine Kinases