Wang X S, Khuntirat B, Qing K, Ponnazhagan S, Kube D M, Zhou S, Dwarki V J, Srivastava A
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
J Virol. 1998 Jul;72(7):5472-80. doi: 10.1128/JVI.72.7.5472-5480.1998.
The pSub201-pAAV/Ad plasmid cotransfection system was developed to eliminate homologous recombination which leads to generation of the wild-type (wt) adeno-associated virus type 2 (AAV) during recombinant vector production. The extent of contamination with wt AAV has been documented to range between 0.01 and 10%. However, the precise mechanism of generation of the contaminating wt AAV remains unclear. To characterize the wt AAV genomes, recombinant viral stocks were used to infect human 293 cells in the presence of adenovirus. Southern blot analyses of viral replicative DNA intermediates revealed that the contaminating AAV genomes were not authentic wt but rather wt AAV-like sequences derived from recombination between (i) AAV inverted terminal repeats (ITRs) in the recombinant plasmid and (ii) AAV sequences in the helper plasmid. Replicative AAV DNA fragments, isolated following amplification through four successive rounds of amplification in adenovirus-infected 293 cells, were molecularly cloned and subjected to nucleotide sequencing to identify the recombinant junctions. Following sequence analyses of 31 different ends of AAV-like genomes derived from two different recombinant vector stocks, we observed that all recombination events involved 10 nucleotides in the AAV D sequence distal to viral hairpin structures. We have recently documented that the first 10 nucleotides in the D sequence proximal to the AAV hairpin structures are essential for successful replication and encapsidation of the viral genome (X.-S. Wang et al., J. Virol. 71:3077-3082, 1997), and it was noteworthy that in each recombinant junction sequenced, the same 10 nucleotides were retained. We also observed that adenovirus ITRs in the helper plasmid were involved in illegitimate recombination with AAV ITRs, deletions of which significantly reduced the extent of wt AAV-like particles. Furthermore, the combined use of recombinant AAV plasmids lacking the distal 10 nucleotides in the D sequence and helper plasmids lacking the adenovirus ITRs led to complete elimination of replication-competent wt AAV-like particles in recombinant vector stocks. These strategies should be useful in producing clinical-grade AAV vectors suitable for human gene therapy.
开发pSub201-pAAV/Ad质粒共转染系统是为了消除同源重组,这种重组在重组载体生产过程中会导致野生型2型腺相关病毒(AAV)的产生。据记载,野生型AAV的污染程度在0.01%至10%之间。然而,污染性野生型AAV产生的确切机制仍不清楚。为了表征野生型AAV基因组,在腺病毒存在的情况下,使用重组病毒株感染人293细胞。对病毒复制性DNA中间体的Southern印迹分析表明,污染性AAV基因组并非真正的野生型,而是源自于(i)重组质粒中的AAV反向末端重复序列(ITR)与(ii)辅助质粒中的AAV序列之间重组的野生型AAV样序列。在腺病毒感染的293细胞中经过四轮连续扩增后分离得到的复制性AAV DNA片段,进行分子克隆并进行核苷酸测序以鉴定重组连接点。在对源自两种不同重组载体株的31个不同的AAV样基因组末端进行序列分析后,我们观察到所有重组事件都涉及病毒发夹结构远端AAV D序列中的10个核苷酸。我们最近记录到,AAV发夹结构近端D序列中的前10个核苷酸对于病毒基因组的成功复制和包装至关重要(X.-S. Wang等人,《病毒学杂志》71:3077 - 3082,1997),值得注意的是,在每个测序的重组连接点中,相同的10个核苷酸被保留下来。我们还观察到辅助质粒中的腺病毒ITR与AAV ITR发生了非法重组,删除这些ITR会显著降低野生型AAV样颗粒的程度。此外,联合使用在D序列中缺少远端10个核苷酸的重组AAV质粒和缺少腺病毒ITR的辅助质粒,可导致重组载体株中具有复制能力的野生型AAV样颗粒完全消除。这些策略对于生产适用于人类基因治疗的临床级AAV载体应该是有用的。