期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2016
卷号：113
期号：48
页码：13780-13784
DOI：10.1073/pnas.1613843113
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceReproduction and growth of viruses depend on successful encounters with appropriate hosts. However, some hosts are difficult to encounter. In particular, chloroviruses cannot reach their target zoochlorellae hosts, because zoochlorellae are endosymbionts, living inside the cell of a protist that protects the zoochlorellae from the chlorovirus. The protist host is subject to predation, and we show that copepods foraging on zoochlorellae-bearing protists can disrupt the mutualism and pass endosymbiontic zoochlorellae through their guts, exposing them to chloroviruses. In this way, predators can catalyze the virus population growth by breaking down physical barriers between viruses and their endosymbiont hosts. Virus population growth depends on contacts between viruses and their hosts. It is often unclear how sufficient contacts are made between viruses and their specific hosts to generate spikes in viral abundance. Here, we show that copepods, acting as predators, can bring aquatic viruses and their algal hosts into contact. Specifically, predation of the protist Paramecium bursaria by copepods resulted in a >100-fold increase in the number of chloroviruses in 1 d. Copepod predation can be seen as an ecological "catalyst" by increasing contacts between chloroviruses and their hosts, zoochlorellae (endosymbiotic algae that live within paramecia), thereby facilitating viral population growth. When feeding, copepods passed P. bursaria through their digestive tract only partially digested, releasing endosymbiotic algae that still supported viral reproduction and resulting in a virus population spike. A simple predator-prey model parameterized for copepods consuming protists generates cycle periods for viruses consistent with those observed in natural ponds. Food webs are replete with similar symbiotic organisms, and we suspect the predator catalyst mechanism is capable of generating blooms for other endosymbiont-targeting viruses.
