Manly K F, Buffett R F
J Virol. 1979 Apr;30(1):232-40. doi: 10.1128/JVI.30.1.232-240.1979.
Five clones of the lymphatic leukemia virus 334C were isolated by a procedure designed to maintain homogeneity of the clones. Three of these induced leukemia in mice with the time course of the uncloned parental virus, one induced leukemia with a delayed time course, and one seemed to be biologically inactive. When the clone inducing leukemia most rapidly and the clone inducing leukemia least rapidly were subcloned, the subclones retained the leukemogenicity of the parental clones. The electrophoretic patterns of purified virion proteins and hybridization of viral RNAs with virus-specific DNA suggest that these clones are two closely related variants, not unrelated viruses. Furthermore, in mice infected with these two clones, viral RNA appears in thymuses and spleens at the same time after infection and at nearly the same concentrations. Thus, variations in leukemogenicity can be determined by a genetic property of an ecotropic leukemia virus, and this property is expressed in some manner more subtle than simple control of replication.
通过一种旨在保持克隆同质性的程序,分离出了淋巴白血病病毒334C的五个克隆。其中三个在小鼠中诱发白血病,其病程与未克隆的亲代病毒相同,一个诱发白血病的病程延迟,还有一个似乎没有生物学活性。当最快速诱发白血病的克隆和最缓慢诱发白血病的克隆进行亚克隆时,亚克隆保留了亲代克隆的致白血病性。纯化病毒粒子蛋白的电泳图谱以及病毒RNA与病毒特异性DNA的杂交表明,这些克隆是两个密切相关的变体,而非无关的病毒。此外,在感染这两个克隆的小鼠中,感染后病毒RNA在胸腺和脾脏中同时出现,且浓度几乎相同。因此,致白血病性的差异可由嗜亲性白血病病毒的遗传特性决定,并且这种特性以比简单的复制控制更为微妙的方式表现出来。