Sakuragi A L, Simon E H
Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907.
J Gen Virol. 1988 Feb;69 ( Pt 2):275-83. doi: 10.1099/0022-1317-69-2-275.
Interferon (IFN) response mutants were selected from mouse L929 fibroblast cells and their specific resistance to is-1, an IFN-sensitive mutant of mengovirus, was studied. The standard L cell subline used in our laboratory (G3), is resistant to is-1 infection after pretreatment with low levels of IFN. Two clonal sublines that support the growth of is-1 in the presence of IFN (AS-4 and TA-6) were isolated from it, and two revertant lines (AS-4R1 and TA-6R1) were subsequently selected from AS-4 and TA-6. The kinetics of is-1 growth in the presence of IFN were found to vary in each of these sublines. Specific resistance to is-1 cannot be accounted for by enhanced induction of IFN, ability to bind IFN, or increased 2'-5'-oligo(A)-dependent endonuclease activity. AS-4 and TA-6 appear to have arisen through loss of one or more whole chromosomes. The origin of TA-6R1 is unclear.
从小鼠L929成纤维细胞中筛选出干扰素(IFN)反应突变体,并研究了它们对脑心肌炎病毒的IFN敏感突变体is -1的特异性抗性。我们实验室使用的标准L细胞亚系(G3),在经过低水平IFN预处理后对is -1感染具有抗性。从该亚系中分离出了两个在IFN存在下支持is -1生长的克隆亚系(AS -4和TA -6),随后又从AS -4和TA -6中筛选出了两个回复系(AS -4R1和TA -6R1)。发现在IFN存在下is -1在这些亚系中的生长动力学各不相同。对is -1的特异性抗性不能通过IFN诱导增强、结合IFN的能力或2'-5'-寡聚腺苷酸依赖性核酸内切酶活性增加来解释。AS -4和TA -6似乎是由于一条或多条整条染色体的丢失而产生的。TA -6R1的起源尚不清楚。