Potts T V, Christensen J R
J Virol. 1974 Dec;14(6):1319-25. doi: 10.1128/JVI.14.6.1319-1325.1974.
The ability of certain phages to successfully infect a restricting host at a high multiplicity of infection is known as cooperative infection or cooperation. We have examined the ability of unmodified T1 (T1.0) to participate in cooperative infection in cells possessing the P1 restriction system. We have found that cooperation is dependent upon protein synthesis during the first few minutes after phage infection. However, we have been unable to attribute the necessary protein to a known T1 cistron. Degradation of the restricted T1 genome is approximately equally extensive whether cooperative infection occurs or whether it is blocked by chloramphenicol. It is postulated that an inducible host repair mechanism may be responsible for the phenomenon of cooperative infection.
某些噬菌体在高感染复数下成功感染限制宿主的能力被称为协同感染或合作。我们研究了未修饰的T1(T1.0)在具有P1限制系统的细胞中参与协同感染的能力。我们发现,合作依赖于噬菌体感染后最初几分钟内的蛋白质合成。然而,我们无法将所需蛋白质归因于已知的T1顺反子。无论是否发生协同感染,或者是否被氯霉素阻断,受限制的T1基因组的降解程度大致相同。据推测,一种可诱导的宿主修复机制可能是协同感染现象的原因。