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在存在反式激活转录蛋白（Tat）的情况下，人类免疫缺陷病毒1型启动子的快速激活及随后的下调：对潜伏感染可能的作用机制

Rapid activation and subsequent down-regulation of the human immunodeficiency virus type 1 promoter in the presence of Tat: possible mechanisms contributing to latency.

作者信息

Drysdale C M, Pavlakis G N

机构信息

National Cancer Institute-Frederick Cancer Research and Development Center, ABL-Basic Research Program, Maryland 21702-1201.

出版信息

J Virol. 1991 Jun;65(6):3044-51. doi: 10.1128/JVI.65.6.3044-3051.1991.

DOI:10.1128/JVI.65.6.3044-3051.1991
PMID:2033665
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC240959/
Abstract

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.

摘要

在细胞融合试验中研究了人免疫缺陷病毒1型长末端重复序列（LTR）的基因表达由Tat反式激活蛋白诱导的机制。Tat可迅速激活LTR的转录以及杂种LTR-氯霉素乙酰转移酶mRNA的积累。在由Tat诱导后约4小时，LTR启动子的表达被下调，导致LTR mRNA积累减少。这种表达下调发生在Tat持续存在的情况下。蛋白质合成抑制剂可阻断这种下调；因此，诱导后表达的抑制依赖于从头合成蛋白质。我们提出一种不稳定的细胞蛋白负责低水平的人免疫缺陷病毒1型表达，可能有助于建立病毒表达的潜伏状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/b77693ff72b8/jvirol00049-0298-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/a29fdae55fbe/jvirol00049-0296-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/b77693ff72b8/jvirol00049-0298-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/a29fdae55fbe/jvirol00049-0296-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/5c5474fcc775/jvirol00049-0297-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/c7d8d54b416a/jvirol00049-0297-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/8fe78e386f29/jvirol00049-0298-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d4/240959/b77693ff72b8/jvirol00049-0298-b.jpg

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