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猿猴免疫缺陷病毒的包装信号位于主要剪接供体的上游,与1型和2型人类免疫缺陷病毒的RNA帽位点的距离相似。

The packaging signal of simian immunodeficiency virus is upstream of the major splice donor at a distance from the RNA cap site similar to that of human immunodeficiency virus types 1 and 2.

作者信息

Strappe P M, Greatorex J, Thomas J, Biswas P, McCann E, Lever A M L

机构信息

University of Cambridge Department of Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK.

出版信息

J Gen Virol. 2003 Sep;84(Pt 9):2423-2430. doi: 10.1099/vir.0.19185-0.

DOI:10.1099/vir.0.19185-0
PMID:12917463
Abstract

Deletion mutation of the RNA 5' leader sequence of simian immunodeficiency virus (SIV) was used to localize the virus packaging signal. Deletion of sequences upstream of the major splice donor (SD) site produced a phenotype most consistent with a packaging defect when analysed by both RNase protection assay and RT-PCR. Sequences downstream of the SD were deleted and produced varying effects but did not affect packaging: a large downstream deletion had little effect on function, whereas a nested deletion produced a profound replication defect characterized by reduced protein production. Secondary structure analysis provided a potential explanation for this. The major packaging signal of SIV appears to be upstream of the SD in a region similar to that of human immunodeficiency virus type 2 (HIV-2) but unlike that of HIV-1; however, the packaging signal of all three viruses are at a similar distance from their respective cap sites. This conserved positioning suggests that it is more important in the virus life cycle than the position of the signal relative to the SD.

摘要

利用猿猴免疫缺陷病毒(SIV)RNA 5'前导序列的缺失突变来定位病毒包装信号。当通过核糖核酸酶保护试验和逆转录聚合酶链反应进行分析时,主要剪接供体(SD)位点上游序列的缺失产生了一种最符合包装缺陷的表型。SD下游的序列被删除,并产生了不同的影响,但不影响包装:一个大的下游缺失对功能影响很小,而一个嵌套缺失则产生了以蛋白质产生减少为特征的严重复制缺陷。二级结构分析为此提供了一个潜在的解释。SIV的主要包装信号似乎位于SD上游,在一个与2型人类免疫缺陷病毒(HIV-2)相似但与HIV-1不同的区域;然而,所有这三种病毒的包装信号与其各自的帽位点距离相似。这种保守的定位表明,它在病毒生命周期中比信号相对于SD的位置更重要。

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