Holmes-Son M L, Chow S A
Department of Molecular and Medical Pharmacology, UCLA AIDS Institute, and Molecular Biology Institute, UCLA School of Medicine, Los Angeles, California 90095, USA.
J Virol. 2000 Dec;74(24):11548-56. doi: 10.1128/jvi.74.24.11548-11556.2000.
Purified fusion proteins made up of a retroviral integrase and a sequence-specific DNA-binding protein have been tested in in vitro assays for their ability to direct integration into specific target sites. To determine whether these fusion proteins can be incorporated into human immunodeficiency virus type 1 (HIV-1) and are functional to mediate integration, we used an in trans approach to deliver various integrase-LexA proteins to an integrase-defective virus containing an integrase mutation at aspartate residue 64. Integrase-LexA, integrase-LexA DNA-binding domain, or N- or C-terminally truncated integrase-LexA proteins were fused to the HIV-1 accessory protein, Vpr. Coexpression of the Vpr fusion proteins and an integrase-defective HIV-1 molecular clone by a producer cell line resulted in efficient incorporation of the fusion protein into the integrase-mutated virus. In addition, each of these viruses was infectious and capable of performing integration, as determined by two independent cellular assays that measure reporter gene expression. With the exception of the N-terminally truncated integrase fused to LexA, which was at about 1%, all of the fusion proteins restored integration to a similar level, at 17 to 24% of that of the wild-type virus. The low level observed with the N-terminally truncated integrase fused to LexA is consistent with previous results implying that the N terminus of integrase is involved in multiple steps of the retroviral life cycle. These data indicate that the integrase-fusion proteins retain catalytic function in the integrase-mutated viruses and demonstrate the feasibility of incorporating integrase fusion proteins into HIV-1 for the development of site-directed retroviral vectors.
由逆转录病毒整合酶和序列特异性DNA结合蛋白组成的纯化融合蛋白已在体外试验中测试其直接整合到特定靶位点的能力。为了确定这些融合蛋白是否能整合到人免疫缺陷病毒1型(HIV-1)中并具有介导整合的功能,我们采用反式方法将各种整合酶-LexA蛋白递送至在天冬氨酸残基64处含有整合酶突变的整合酶缺陷型病毒。整合酶-LexA、整合酶-LexA DNA结合结构域或N端或C端截短的整合酶-LexA蛋白与HIV-1辅助蛋白Vpr融合。通过生产细胞系共表达Vpr融合蛋白和整合酶缺陷型HIV-1分子克隆,导致融合蛋白有效整合到整合酶突变型病毒中。此外,通过两种测量报告基因表达的独立细胞试验确定,这些病毒中的每一种都具有感染性且能够进行整合。除了与LexA融合的N端截短的整合酶,其活性约为1%外,所有融合蛋白都将整合恢复到相似水平,为野生型病毒的17%至24%。与LexA融合的N端截短的整合酶观察到的低水平与先前的结果一致,这表明整合酶的N端参与逆转录病毒生命周期的多个步骤。这些数据表明,整合酶融合蛋白在整合酶突变型病毒中保留催化功能,并证明了将整合酶融合蛋白整合到HIV-1中以开发定点逆转录病毒载体的可行性。