Ploss Martin, Berdel Bianca, Heber Ricarda, Reuss Frank U
Deutsches Krebsforschungszentrum (DKFZ), Angewandte Tumorvirologie F0400, Heidelberg, Germany.
J Med Virol. 2003 Feb;69(2):267-72. doi: 10.1002/jmv.10274.
Amphotropic murine leukemia virus (MLV) replicates in cells from various mammalian species including humans and is a potential contaminant in MLV vector preparations for human gene transfer studies. Because MLV replication proceeds through an RNA genome that is generated under the control of viral enhancer and promoter elements, vectors were developed that delete such elements during transduction to reduce the generation of replication-competent virus. It was shown recently that replication of amphotropic MLV in certain human cells is possible without the 75 bp transcription enhancers. It is now demonstrated that enhancer-independent replication requires functional elements within U3 and is repressed by an extended deletion in the U3 region comprising enhancers, promoter and flanking sequences. It is concluded that the transcriptional inactivation of amphotropic MLV in human cells requires the combined deletion of enhancers and of additional elements in U3.
嗜双性鼠白血病病毒（MLV）可在包括人类在内的各种哺乳动物细胞中复制，并且是用于人类基因转移研究的MLV载体制剂中的潜在污染物。由于MLV的复制通过在病毒增强子和启动子元件控制下产生的RNA基因组进行，因此开发了在转导过程中删除此类元件的载体，以减少具有复制能力的病毒的产生。最近研究表明，嗜双性MLV在某些人类细胞中无需75bp转录增强子即可复制。现已证明，不依赖增强子的复制需要U3内的功能元件，并且会被U3区域中包括增强子、启动子和侧翼序列的延伸缺失所抑制。得出的结论是，人类细胞中嗜双性MLV的转录失活需要增强子和U3中其他元件的联合缺失。
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