Rapid activation and subsequent down-regulation of the human immunodeficiency virus type 1 promoter in the presence of Tat: possible mechanisms contributing to latency
| Autor: | C M Drysdale, G N Pavlakis |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Chloramphenicol O-Acetyltransferase
Transcription Genetic viruses Immunology Down-Regulation Biology Microbiology Virus Cell Line Transactivation Transcription (biology) Virology Gene expression Protein biosynthesis Humans RNA Messenger Promoter Regions Genetic HIV Long Terminal Repeat Messenger RNA Molecular biology Long terminal repeat Kinetics Insect Science Gene Products tat HIV-1 tat Gene Products Human Immunodeficiency Virus Research Article HeLa Cells |
| Zdroj: | Journal of Virology. 65:3044-3051 |
| ISSN: | 1098-5514 0022-538X |
| DOI: | 10.1128/jvi.65.6.3044-3051.1991 |
| Popis: | The mechanism of induction of gene expression of the human immunodeficiency virus type 1 long terminal repeat (LTR) by the Tat transactivator protein was studied in a cell fusion assay. Tat causes a rapid activation of both transcription from the LTR and accumulation of hybrid LTR-chloramphenicol acetyltransferase mRNAs. Approximately 4 h after induction by Tat, expression from the LTR promoter is down-regulated, resulting in a decrease in the accumulation of LTR mRNA. This down-regulation of expression occurs in the continued presence of Tat. Protein synthesis inhibitors can block this down-regulation; therefore, the postinduction repression of expression is dependent upon de novo protein synthesis. We propose that a labile cellular protein(s) is responsible for the low levels of human immunodeficiency virus type 1 expression, possibly contributing to the establishment of a latent state of viral expression. |
| Databáze: | OpenAIRE |
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