Inhibition of Superinfection and the Evolution of Viral Latency
Inhibition of Superinfection and the Evolution of Viral Latency
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DOI：
10.1128/jvi.00865-10
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发表时间：
2010-10-01
影响因子：
5.4
通讯作者：
Gandon, Sylvain
中科院分区：
文献类型：
--
作者：
Berngruber, Thomas W.;Weissing, Franz J.;Gandon, Sylvain
潜伏病毒通常会保护宿主细胞免受可能破坏宿主细胞的非潜伏毒力突变体的重复感染。因此，重复感染抑制似乎是维持病毒潜伏期的先决条件。然而，当出现对重复感染抑制（称为超毒力）的抵抗时，病毒潜伏期可能会被打破。为了了解病毒潜伏期的演变，我们开发了一个模型来分析超毒力下潜伏感染的流行病学。我们表明，当重复感染抑制和抵抗力在军备竞赛中共同进化时，潜伏期可以维持，这可能导致毒力的大幅波动。一个例子是噬菌体 lambda (cI) 的毒力和双重感染抑制蛋白及其结合靶标 lambda oLoR 操纵子的共同进化。我们表明，这种抑制子/操纵子协同进化是重复感染免疫群体进化的驱动力。除了潜伏噬菌体之外，我们预测任何使用单一阻遏物同时控制毒力和重复感染的潜伏病毒也会出现类似的动力学。
Latent viruses generally defend their host cell against superinfection by nonlatent virulent mutants that could destroy the host cell. Superinfection inhibition thus seems to be a prerequisite for the maintenance of viral latency. Yet viral latency can break down when resistance to superinfection inhibition, known as ultravirulence, occurs. To understand the evolution of viral latency, we have developed a model that analyzes the epidemiology of latent infection in the face of ultravirulence. We show that latency can be maintained when superinfection inhibition and resistance against it coevolve in an arms race, which can result in large fluctuations in virulence. An example is the coevolution of the virulence and superinfection repressor protein of phage lambda (cI) and its binding target, the lambda oLoR operator. We show that this repressor/operator coevolution is the driving force for the evolution of superinfection immunity groups. Beyond latent phages, we predict analogous dynamics for any latent virus that uses a single repressor for the simultaneous control of virulence and superinfection.