Lundquist R E, Sullivan M, Maizel J V
Cell. 1979 Nov;18(3):759-69. doi: 10.1016/0092-8674(79)90129-6.
An independent isolate of poliovirus defective interfering particles has been analyzed. These particles, designated DI(A), are apparently analogous to the DI particles described by Baltimore and co-investigators. Electron microscopic heteroduplex analysis reveals that the DI(A) isolate is a mixture of deletion mutants which changes with passage level. The DI(A) population consists of at least five distinct deletion mutants, including one double deletion. Electron microscopic mapping of the deleted regions indicates that most, if not all, of the viral capsid region can be deleted. Despite this heterogeneity, the mutant genomes are quite similar in physical size. We propose a model which suggests that the observed properties of poliovirus DI genomes reflect selective pressures extant during the amplification of the mutant genome. According to this model, only those deleted genomes which retain a minimal size and the capacity to synthesize a functional viral polymerase will replicate successfully in a mixed infection. Furthermore, this model proposes a mechanism for the enrichment of poliovirus DI genomes and an explanation for the low level of complementation observed in mixed infections of picornaviruses.
已对一株独立的脊髓灰质炎病毒缺陷干扰颗粒进行了分析。这些颗粒被命名为DI(A)，显然类似于巴尔的摩及其共同研究者所描述的DI颗粒。电子显微镜异源双链分析表明，DI(A)分离株是缺失突变体的混合物，其会随传代水平而变化。DI(A)群体至少由五个不同的缺失突变体组成，包括一个双重缺失突变体。对缺失区域的电子显微镜定位表明，病毒衣壳区域的大部分（如果不是全部的话）都可以被删除。尽管存在这种异质性，但突变基因组在物理大小上相当相似。我们提出了一个模型，该模型表明脊髓灰质炎病毒DI基因组的观察到的特性反映了突变基因组扩增过程中存在的选择压力。根据这个模型，只有那些保留最小大小且具有合成功能性病毒聚合酶能力的缺失基因组才能在混合感染中成功复制。此外，该模型提出了一种脊髓灰质炎病毒DI基因组富集的机制，并解释了在微小核糖核酸病毒混合感染中观察到的低水平互补现象。
