Mutagenesis of a cAMP Response Element within the Latency-Associated Transcript Promoter of HSV-1 Reduces Adrenergic Reactivation

Mutagenesis of a cyclic AMP response element (CRE) within the LAT promoter of HSV-1 reduces the ability of LAT expression to be induced in transient assays, but has only a minimal impact on reactivation of the virus inin vitrosystems. Here we show that a CRE mutation results in a significant reducti...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 1997-09, Vol.236 (1), p.202-207
Main Authors: Bloom, David C., Stevens, Jack G., Hill, James M., Tran, Robert K.
Format: Article
Language:English
Subjects:
Actins - biosynthesis
Animals
Base Sequence
Binding Sites
Cells, Cultured
Cyclic AMP - pharmacology
Cyclic AMP Response Element-Binding Protein - metabolism
DNA Primers
DNA, Viral - biosynthesis
DNA, Viral - chemistry
DNA, Viral - isolation & purification
Herpes Simplex
Molecular Sequence Data
Mutagenesis, Site-Directed
Polymerase Chain Reaction
Promoter Regions, Genetic
Rabbits
Simplexvirus - genetics
Simplexvirus - growth & development
Simplexvirus - isolation & purification
Skin
Transcription, Genetic
Trigeminal Ganglion - virology
Virus Activation
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Summary:Mutagenesis of a cyclic AMP response element (CRE) within the LAT promoter of HSV-1 reduces the ability of LAT expression to be induced in transient assays, but has only a minimal impact on reactivation of the virus inin vitrosystems. Here we show that a CRE mutation results in a significant reduction of adrenergically induced reactivationin vivoin the rabbit eye model. Spontaneous reactivation frequencies were also reduced. In addition, we demonstrate that this mutation has no effect on the amount of LAT expressed during latency when compared with the parent, 17syn+, and the rescuant. These results indicate a greater effect of CRE on induced reactivationin vivothan inin vitrosystems, but also suggest that the CRE in the LAT promoter is not autonomous in conducting the reactivation signal.
ISSN:0042-6822
1096-0341
DOI:10.1006/viro.1997.8723