The latency-associated promoter of herpes simplex virus type 1 requires a region downstream of the transcription start site for long-term expression during latency
| Autor: | Herve Berthomme, J. R. Lokensgard, Lawrence T. Feldman |
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| Rok vydání: | 1997 |
| Předmět: |
Gene Expression Regulation
Viral Time Factors viruses Immunology Response element Gene Expression Herpesvirus 1 Human Biology medicine.disease_cause Microbiology Mice Ganglia Spinal Virology Gene expression Virus latency medicine Animals Humans Binding site Peptide Chain Initiation Translational Promoter Regions Genetic Gene Binding Sites Chromosome Mapping Promoter biochemical phenomena metabolism and nutrition medicine.disease Molecular biology Virus Latency Mice Inbred C57BL DNA binding site Herpes simplex virus Lac Operon Insect Science Female Research Article |
| Zdroj: | Journal of Virology. 71:6714-6719 |
| ISSN: | 1098-5514 0022-538X |
| DOI: | 10.1128/jvi.71.9.6714-6719.1997 |
| Popis: | The latency-associated transcript (LAT) promoter of herpes simplex virus type 1 (HSV-1) is unique among the many promoters on the viral genome in that it remains active during the latent state. We have previously shown that a DNA fragment comprising the LAT promoter element through the cap site, when moved from the LAT locus to the glycoprotein C gene, is capable of only short-term expression. These and other data suggested that an HSV DNA element from the repeat region, not included in the LAT promoter itself, might be needed to preserve long-term expression. Based on a number of recombinant viruses, we narrowed our search for this putative element to a region 3' of the LAT transcription start site. In the present study, we have shown that a 1.1-kb DNA fragment containing the putative long-term expression element (LTE) is able to restore latent-phase gene expression to the LAT promoter. The element appeared to function best when it was placed in its natural location, which is 3' of the LAT promoter; however, partial function was obtained when the LTE was inserted upstream of the LAT promoter in the reverse direction. These data indicate that the LAT promoter region is more complex than originally anticipated and that in addition to requiring both core promoter and neuronal transcription factor binding sites, the promoter requires a specific region of DNA to prevent its shutoff during a latent infection. |
| Databáze: | OpenAIRE |
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