Sugita K
J Gen Virol. 1981 Jul;55(Pt 1):95-107. doi: 10.1099/0022-1317-55-1-95.
Interference between a virulent and an avirulent strain of Sendai virus was studied by plaque morphology and analysis of viral protein and RNA. On simultaneous infection a virulent, large plaque-forming strain (RL) was inhibited by an avirulent, small plaque-forming strain (RS). The interference was dose-dependent and decreased with u.v. irradiation of RS. One infectious particle was sufficient to induce the interference. SDS-polyacrylamide gel electrophoresis showed that interference was detectable in the synthesis of viral P protein; this was abolished when RS was u.v.-irradiated. Both growth and P protein synthesis of RL was restricted by superinfection with RS when this was done within 4 h after infection of RL, but the interference decreased gradually after this period and was not detectable after 8 h. Cycloheximide prolonged the period susceptible to superinfection by RS.
通过蚀斑形态以及病毒蛋白和RNA分析，对仙台病毒的强毒株和无毒株之间的干扰作用进行了研究。同时感染时，强毒的大蚀斑形成毒株（RL）受到无毒的小蚀斑形成毒株（RS）的抑制。这种干扰具有剂量依赖性，且随着RS经紫外线照射而减弱。一个感染性颗粒就足以引发干扰。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳显示，在病毒P蛋白合成中可检测到干扰；当RS经紫外线照射后，这种干扰就消失了。当在RL感染后4小时内进行RS的超感染时，RL的生长和P蛋白合成均受到限制，但在此之后干扰逐渐减弱，8小时后则检测不到。环己酰亚胺延长了对RS超感染敏感的时期。
