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Viral Transmission Dynamics at Single-Cell Resolution Reveal Transiently Immune Subpopulations Caused by a Carrier State Association

机译:在单细胞分辨率下的病毒传播动力学揭示了由携带者状态协会引起的暂时性免疫亚群。

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摘要

Monitoring the complex transmission dynamics of a bacterial virus (temperate phage P22) throughout a population of its host (Salmonella Typhimurium) at single cell resolution revealed the unexpected existence of a transiently immune subpopulation of host cells that emerged from peculiarities preceding the process of lysogenization. More specifically, an infection event ultimately leading to a lysogen first yielded a phage carrier cell harboring a polarly tethered P22 episome. Upon subsequent division, the daughter cell inheriting this episome became lysogenized by an integration event yielding a prophage, while the other daughter cell became P22-free. However, since the phage carrier cell was shown to overproduce immunity factors that are cytoplasmically inherited by the P22-free daughter cell and further passed down to its siblings, a transiently resistant subpopulation was generated that upon dilution of these immunity factors again became susceptible to P22 infection. The iterative emergence and infection of transiently resistant subpopulations suggests a new bet-hedging strategy by which viruses could manage to sustain both vertical and horizontal transmission routes throughout an infected population without compromising a stable co-existence with their host.
机译:以单细胞分辨率监测细菌病毒(温带噬菌体P22)在其宿主(鼠伤寒沙门氏菌)整个种群中的复杂传播动力学,发现宿主细胞瞬时免疫亚群的意外存在,该亚群是由溶菌作用之前的特殊性产生的。更具体地说,最终导致溶原的感染事件首先产生了噬菌体载体细胞,该细胞带有极性束缚的P22附加体。在随后的分裂中,继承该附加体的子代细胞因整合事件而发生溶原,产生噬菌体,而另一个子代细胞则不含P22。但是,由于噬菌体载体细胞显示出过量产生的免疫因子,这些免疫因子是无P22子代细胞胞质遗传并进一步传给其同胞的,因此产生了短暂耐药的亚群,这些免疫因子稀释后又变得对P22敏感感染。短暂出现抗性亚群的反复出现和感染表明一种新的对冲策略,通过这种策略,病毒可以设法在整个感染人群中维持垂直和水平传播途径,而又不损害与宿主的稳定共存。

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