Characterization of HIV-1 integrase N-terminal mutant viruses.

Characterization of HIV-1 integrase N-terminal mutant viruses.
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HIV-1 整合酶 N 末端突变病毒的表征。

DOI:
10.1016/j.virol.2006.10.007
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发表时间:
2007
期刊:
影响因子:
3.7
通讯作者:
Mulder,LubbertusCF
Mulder,LubbertusCF
中科院分区:
医学3区
文献类型:
--
作者:
Lloyd,AlizaG;Ng,YenShing;Muesing,MarkA;Simon,Viviana;Mulder,LubbertusCF

文献摘要

被引文献

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在感染过程中,人类免疫缺陷病毒1型整合酶参与许多病毒和细胞来源的分子和机制。在其中一种情况下,整合酶被认为是通过N-末端规则蛋白酶体途径降解的,这是一种靶向其底物的N-末端残基的过程。在这里,我们描述了HIV-1病毒的特性,其中整合酶的第一个氨基酸残基已被取代,使其耐N-末端规则途径。由于这种交换,我们观察到一组I类和II类缺陷,导致病毒复制效率大幅降低。具体而言,逆转录和整合是似乎受到影响的步骤。我们建议,这些突变体的严重缺陷施加强大的选择压力,导致在HIV-1,HIV-2和SIV的整合酶的N-末端残基的几乎完全保守。
During infection, human immunodeficiency virus type 1 integrase engages a number of molecules and mechanisms, both of viral and cellular origin. In one of such instances, integrase is thought to be degraded by the N-end rule proteasome pathway a process that targets the N-terminal residue of its substrates. Here we describe the properties of HIV-1 viruses in which the first amino acid residue of integrase has been substituted to render it resistant to the N-end rule pathway. As result of this exchange, we observe a set of class I and class II defects that result in a large decrease of viral replication efficiency. Specifically, reverse transcription and integration are the steps that appear to be affected. We propose that the severe deficiency of these mutants exert a strong selective pressure that leads to the near total conservation of the N-terminal residue of integrase in HIV-1, HIV-2 and SIV.