SAMHD1公司
转导(生物物理学)
生物
病毒载体
小发夹RNA
基因敲除
病毒学
感染的多重性
髓样
遗传增强
慢病毒
RNA干扰
分子生物学
细胞培养
基因
核糖核酸
癌症研究
病毒
逆转录酶
遗传学
重组DNA
生物化学
病毒性疾病
作者
Selene Bobadilla,Nicole Sunseri,Nathaniel R. Landau
出处
期刊:Gene Therapy
[Springer Nature]
日期:2012-08-16
卷期号:20 (5): 514-520
被引量:84
摘要
Lentiviral vectors are widely used for the stable expression of genes and small hairpin RNA (shRNA)-mediated knockdown and are currently under development for clinical use in gene therapy. Pseudotyping of the vectors with VSV-G allows them to infect a wide range of cell types. However, myeloid cells, such as dendritic cells and macrophages, are relatively refractory to lentiviral vector transduction as a result of the myeloid-specific restriction factor, SAMHD1. SIVmac/HIV-2 and related viruses relieve the SAMHD1-mediated restriction by encoding Vpx, a virion-packaged accessory protein that induces the degradation of SAMHD1 upon infection. HIV-1 does not encode Vpx and cannot package the protein. We report the development of an HIV-1-based lentiviral vector in which the Vpx packaging motif has been placed in the p6 region of the Gag/Pol expression vector that is used to generate the lentiviral vector virions. The virions package Vpx in high copy number and infect myeloid cells with a two-log increase in titer. Transduction of dendritic cells with an shRNA against transportin-3 resulted in >90% knockdown of the encoding mRNA. The system can be applied to any HIV-based lentiviral vector and is useful for laboratory and clinical applications where the efficient transduction of myeloid cells is required.
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