Aboud M, Hassan Y
J Virol. 1983 Feb;45(2):489-95. doi: 10.1128/JVI.45.2.489-495.1983.
Interferon treatment of NIH 3T3 cells chronically infected with Moloney murine leukemia virus inhibited about 95% of virus release. This inhibition was accompanied by a three- to twofold accumulation of intracellular virions. However, this accumulation could be demonstrated only be exogenous reverse transcriptase reaction assay or radioactive labeling of the assembled viral proteins. It could not be shown by the endogenous reverse transcriptase reaction assay, which depended on endogenous viral RNA, or by labeling the encapsidated viral RNA. It was therefore evident that most of the intracellular virions accumulated in interferon-treated cells were RNA deficient. Hybridization analysis revealed that these virions were deficient of genomic viral RNA, whereas size analysis by gel electrophoresis suggested that the deficiency of 4S RNA normally packaged in Moloney murine leukemia virus was even stronger. Our data also suggested that this RNA deficiency was not due to degradation of the encapsidated RNA, but more likely to a defect in virus assembly. RNA-lacking intracellular virions were unstable; they were found to collapse before being released.
用干扰素处理长期感染莫洛尼鼠白血病病毒的NIH 3T3细胞,可抑制约95%的病毒释放。这种抑制伴随着细胞内病毒粒子积累三到两倍。然而,这种积累只能通过外源性逆转录酶反应测定或对组装好的病毒蛋白进行放射性标记来证明。通过依赖内源性病毒RNA的内源性逆转录酶反应测定或对衣壳化病毒RNA进行标记则无法显示这种积累。因此很明显,在干扰素处理的细胞中积累的大多数细胞内病毒粒子缺乏RNA。杂交分析表明,这些病毒粒子缺乏基因组病毒RNA,而通过凝胶电泳进行的大小分析表明,通常包装在莫洛尼鼠白血病病毒中的4S RNA的缺乏更为明显。我们的数据还表明,这种RNA缺乏不是由于衣壳化RNA的降解,而更可能是病毒组装缺陷。缺乏RNA的细胞内病毒粒子不稳定;它们在释放前就被发现解体了。