Aoki H, Nishiyama Y, Tsurumi T, Shibata M, Ito Y, Seo H, Yoshii S, Maeno K
J Gen Virol. 1984 Aug;65 ( Pt 8):1385-93. doi: 10.1099/0022-1317-65-8-1385.
Simultaneous infection of MDCK cells with influenza viruses A/WSN and B/Kanagawa resulted in mutual interference with virus protein synthesis and in significant suppression of A/WSN growth. When infection by one virus preceded the other by 1 or 2 h, growth of the superinfecting virus was selectively inhibited at the level of transcription. Interference by the pre-infecting virus was strongly dependent on the expression of the viral genome but not on haemagglutinin activity. When the replication of both virus types was restricted to primary transcription by cycloheximide, the only translation products following removal of the drug were those of the preinfecting virus. This result was not affected by blocking secondary transcription by actinomycin D. These findings suggest that intertypic interference occurs at the level of primary transcription. This concept was supported further by the observation that a ts mutant of A/WSN (ts-65) with a defect in primary transcription interfered only with superinfection by B/Kanagawa at the permissive temperature.
用甲型流感病毒A/WSN和乙型流感病毒B/神奈川同时感染犬肾传代细胞（MDCK细胞），会导致病毒蛋白合成相互干扰，并显著抑制A/WSN的生长。当一种病毒的感染比另一种病毒提前1或2小时进行时，超感染病毒的生长在转录水平上受到选择性抑制。先感染病毒的干扰强烈依赖于病毒基因组的表达，而不依赖于血凝素活性。当两种病毒类型的复制都通过环己酰亚胺限制在初级转录时，去除药物后唯一的翻译产物是先感染病毒的产物。用放线菌素D阻断二级转录不会影响这一结果。这些发现表明，不同型别之间的干扰发生在初级转录水平。A/WSN的一个初级转录有缺陷的温度敏感突变体（ts-65）在允许温度下仅干扰B/神奈川的超感染，这一观察结果进一步支持了这一概念。
