Anderson C W, Hardy M M, Lewis J B
Biology Department, Brookhaven National Laboratory, Upton, NY 11973.
Virus Genes. 1988 Mar;1(2):149-64. doi: 10.1007/BF00555934.
The drastically reduced virus yields obtained from monkey cells abortively infected with adenovirus 2 (Ad2) have been attributed primarily to a severe decrease in the accumulation of the virion protein fiber (IV), a product of the most pomoter distal late gene family, L5. Here we report that the accumulation of virion protein IIIa, a product of the proximal late gene family, L1, is also severely depressed. In contrast, the i-leader protein LO-13.6K and L1 protein(s) 52K/55K are expressed with the same time course and in equal amounts in monkey cells abortively infected by Ad2 or productively infected by the Ad2-simian virus 40 (SV40) hybrid Ad2+ND1 or by the host range mutant Ad2+ND3 hr602. L1-52K/55K is phosphorylated in abortively infected CV-1 or CV-C monkey cells as well as in productively infected human and monkey cells. As with fiber expression, the failure to produce IIIa appears to be due partly to reduced or delayed IIIa mRNA accumulation. The small amount of IIIa protein that is synthesized in monkey cells is stable. Since the accumulation of both IIIa and fiber protein is deficient, the mechanism of abortive infection cannot be attributed solely to the absence of the auxiliary fiber leader sequences (1).
从被腺病毒2（Ad2）感染但感染失败的猴细胞中获得的病毒产量大幅降低，这主要归因于病毒粒子蛋白纤维（IV）的积累严重减少，纤维是最靠近启动子的晚期基因家族L5的产物。在此我们报告，晚期基因家族L1近端基因产物病毒粒子蛋白IIIa的积累也严重受抑。相比之下，i-前导蛋白LO-13.6K和L1蛋白52K/55K在被Ad2感染失败的猴细胞中，以及在被Ad2-猴病毒40（SV40）杂交体Ad2+ND1或宿主范围突变体Ad2+ND3 hr602有效感染的猴细胞中，表达的时间进程相同且数量相等。L1-52K/55K在感染失败的CV-1或CV-C猴细胞以及有效感染的人和猴细胞中会发生磷酸化。与纤维蛋白的表达情况一样，IIIa蛋白无法产生似乎部分是由于IIIa mRNA积累减少或延迟。在猴细胞中合成的少量IIIa蛋白是稳定的。由于IIIa和纤维蛋白的积累均不足，感染失败的机制不能仅仅归因于缺乏辅助性纤维前导序列（1）。
