Suppr超能文献

缺陷型和野生型人类I型T细胞白血病病毒前病毒:基因产物的特征及前病毒之间的反式相互作用

Defective and wild-type human T-cell leukemia virus type I proviruses: characterization of gene products and trans-interactions between proviruses.

作者信息

Shuh M, Hill S A, Derse D

机构信息

Division of Basic Sciences, National Cancer Institute, Frederick, Maryland, 21702-1201, USA.

出版信息

Virology. 1999 Sep 30;262(2):442-51. doi: 10.1006/viro.1999.9909.

Abstract

Defective provirus genomes of human T-cell leukemia virus type I are frequently detected in lymphocytes from infected individuals and in infected cell lines. One type of defective provirus contains internal deletions spanning gag, pol, and env genes but retains portions of open reading frames for trans-regulatory proteins. The deleted proviruses could potentially contribute to viral pathology by producing novel gene products that directly affect cell metabolism or that modulate expression of resident, wild-type proviruses. Virus gene products and the control of their expression were examined in cells transfected with defined molecular clones of wild-type and defective proviruses. Internally deleted provirus clones, which are unable to produce functional Tax and Rex proteins, were transcriptionally inactive in transfected cells. Ectopic expression of p40Tax activated transcription of the deleted provirus, resulting in the accumulation of a two-exon mRNA that yields a truncated form of Rex (p21Rex). Although this two-exon mRNA also has a potential initiation codon in the tax frame, a truncated form of Tax was not detected by immunoblotting or in transactivation assays. When complemented with p40Tax and p27Rex, cells transfected with deleted proviruses accumulated an unspliced mRNA that could potentially encode gag-pX fusion proteins. Although expression of deleted proviruses was dependent on trans-acting factors produced from intact proviruses, gene products from defective proviruses did not significantly affect expression of a cotransfected, full-length provirus.

摘要

在感染个体的淋巴细胞以及感染的细胞系中,经常能检测到I型人类T细胞白血病病毒的缺陷前病毒基因组。一种缺陷前病毒包含跨越gag、pol和env基因的内部缺失,但保留了反式调节蛋白开放阅读框的部分序列。这些缺失的前病毒可能通过产生直接影响细胞代谢或调节常驻野生型前病毒表达的新基因产物,对病毒病理学产生影响。在转染了野生型和缺陷前病毒的特定分子克隆的细胞中,研究了病毒基因产物及其表达调控。内部缺失的前病毒克隆无法产生功能性的Tax和Rex蛋白,在转染细胞中转录无活性。p40Tax的异位表达激活了缺失前病毒的转录,导致一种双外显子mRNA的积累,该mRNA产生截短形式的Rex(p21Rex)。尽管这种双外显子mRNA在tax阅读框中也有一个潜在的起始密码子,但通过免疫印迹或反式激活试验未检测到截短形式的Tax。当用p40Tax和p27Rex进行互补时,转染了缺失前病毒的细胞积累了一种未剪接的mRNA,该mRNA可能编码gag-pX融合蛋白。尽管缺失前病毒的表达依赖于完整前病毒产生的反式作用因子,但缺陷前病毒的基因产物对共转染的全长前病毒的表达没有显著影响。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验