Giant viruses can control their eukaryotic host populations, shaping the ecology and evolution of aquatic microbial communities. Understanding the impact of the viruses’ own parasites, the virophages, on the control of microbial communities remains a challenge. Most virophages have two modes of infection. They can exist as free particles coinfecting host cells together with the virus, where they replicate while inhibiting viral replication. Virophages can also integrate into the host genome, replicate through host cell division and remain dormant until the host is infected with a virus, leading to virophage reactivation and replication without inhibiting viral replication. Both infection modes (reactivation vs. coinfection) occur within host-virus-virophage communities, and their relative contributions are expected to be dynamic and context dependent. The consequences of this dynamic regime for ecological and evolutionary dynamics remain unexplored. Here, we test whether and how the relative contribution of virophage infection modes influences the ecological dynamics of an experimental host-virus-virophage system and the evolutionary responses of the virophage. We indirectly manipulated the level of virophage (Mavirus) integration into the host (Cafeteria burkhardae) in the presence of the giant Cafeteria roenbergensis virus. Communities with higher virophage integration were characterised by lower population densities and reduced fluctuations in host and virus populations, whereas virophage fluctuations were increased. The virophage evolved toward lower inhibition and higher replication, but the evolution of these traits was weaker with higher virophage integration. Our study shows that differences in the virophage infection modes contributes to the complex interplay between virophages, viruses and hosts.

中文翻译：

---

噬菌体感染模式决定了宿主-病毒-噬菌体系统的生态和进化变化


巨型病毒可以控制其真核宿主种群，塑造水生微生物群落的生态和进化。了解病毒自身的寄生虫（病毒噬菌体）对微生物群落控制的影响仍然是一个挑战。大多数噬菌体有两种感染方式。它们可以以自由颗粒的形式存在，与病毒共感染宿主细胞，在那里它们复制，同时抑制病毒复制。噬菌体还可以整合到宿主基因组中，通过宿主细胞分裂进行复制并保持休眠状态，直到宿主感染病毒，导致病毒噬菌体重新激活和复制，而不会抑制病毒复制。两种感染模式（再激活与混合感染）都发生在宿主病毒-病毒噬菌体群落内，预计它们的相对贡献是动态的和依赖于环境的。这种动态机制对生态和进化动力学的影响仍有待探索。在这里，我们测试了病毒噬菌体感染模式的相对贡献是否以及如何影响实验宿主-病毒-噬菌体系统的生态动力学和病毒噬菌体的进化反应。在巨大的 Cafeteria roenbergensis 病毒存在下，我们间接操纵了病毒噬菌体 （Mavirus） 整合到宿主 （Cafeteria burkhardae） 中的水平。病毒噬菌体整合度较高的群落的特点是种群密度较低，宿主和病毒种群的波动较小，而病毒噬菌体波动增加。病毒噬菌体向较低的抑制和较高的复制方向进化，但这些性状的进化随着病毒噬菌体整合度的增加而较弱。 我们的研究表明，病毒噬菌体感染模式的差异有助于病毒噬菌体、病毒和宿主之间复杂的相互作用。