Circulating virus load determines the size of bottlenecks in viral populations progressing within a host.
Circulating virus load determines the size of bottlenecks in viral populations progressing within a host.
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DOI：
10.1371/journal.ppat.1003009
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发表时间：
2012
期刊：
影响因子：
6.7
通讯作者：
Blanc S
中科院分区：
文献类型：
--
作者：
Gutiérrez S;Yvon M;Pirolles E;Garzo E;Fereres A;Michalakis Y;Blanc S
对于任何生物体，种群规模及其波动在决定其进化动力方面具有首要意义。对于病毒快速进化的实体来说尤其如此，这些实体形成的种群具有短暂和爆炸性的扩张，并与迁移阶段交替，导致强大的种群瓶颈和相关的创始人效应，从而增加遗传漂变。这种模式的一个典型例证是真核宿主内病毒疾病的进展，其中这种人口统计学波动是出现具有改变的毒力的新变体的关键因素。病毒在一个或仅几个感染灶中开始复制，然后通过脉管系统移动到种子继发感染部位，从而侵入远处器官和组织。在宿主内定植期间的创始人效应可能取决于在脉管系统中积累和循环的感染单位的浓度，因为这代表了到达新器官或“领土”的感染剂量。令人惊讶的是，是否容易测量的循环（血浆）病毒载量直接驱动宿主定殖过程中的人口瓶颈的大小还没有记录在动物病毒，而在植物中的汁液中的病毒载量从来没有估计。在这里，我们通过监测宿主植物汁液中流动的病毒浓度和在每个连续的新叶中建立种群的病毒基因组的数量来解决这个重要问题。我们的研究结果清楚地表明，循环病毒的浓度直接决定了瓶颈的大小，从而控制了宿主疾病进展期间的创始人效应和有效群体大小。感染病毒通过两种不同的机制在多细胞宿主中进展：细胞间近端污染和通过脉管系统长距离迁移到远端器官。在远距离易感器官中，最初感染细胞的数量、进入这些细胞中的每一个的病毒基因组的数量以及因此新病毒“菌落”的创建者的数量取决于在脉管系统中转运的感染单位的浓度，这似乎是合乎逻辑的。对于任何生物体来说，殖民“处女地”的创始人数量在决定推动其进化的力量方面至关重要。对于病毒来说尤其如此，所谓的创始人效应是出现毒力改变的新变体的关键因素。然而，令人惊讶地注意到，在宿主定殖期间，循环病毒载量是否直接驱动病毒群体的大小仍然难以捉摸。通过第一次监测宿主植物汁液中的病毒浓度，与每个连续叶片中病毒基因组创始人的数量平行，我们提供了明确的证据，即循环病毒的浓度可以直接决定在真核宿主疾病进展期间的创始人效应和有效群体大小。
For any organism, population size, and fluctuations thereof, are of primary importance in determining the forces driving its evolution. This is particularly true for viruses—rapidly evolving entities that form populations with transient and explosive expansions alternating with phases of migration, resulting in strong population bottlenecks and associated founder effects that increase genetic drift. A typical illustration of this pattern is the progression of viral disease within a eukaryotic host, where such demographic fluctuations are a key factor in the emergence of new variants with altered virulence. Viruses initiate replication in one or only a few infection foci, then move through the vasculature to seed secondary infection sites and so invade distant organs and tissues. Founder effects during this within-host colonization might depend on the concentration of infectious units accumulating and circulating in the vasculature, as this represents the infection dose reaching new organs or “territories”. Surprisingly, whether or not the easily measurable circulating (plasma) virus load directly drives the size of population bottlenecks during host colonization has not been documented in animal viruses, while in plants the virus load within the sap has never been estimated. Here, we address this important question by monitoring both the virus concentration flowing in host plant sap, and the number of viral genomes founding the population in each successive new leaf. Our results clearly indicate that the concentration of circulating viruses directly determines the size of bottlenecks, which hence controls founder effects and effective population size during disease progression within a host. Infecting viruses progress within multi-cellular hosts via two distinct mechanisms: cell-to-cell proximal contamination and long-distance migration to remote organs through the vasculature. In distant susceptible organs, it seems logical that the number of initially infected cells, the number of viral genomes entering each of these cells, and thus the number of founders of new viral “colonies”, depends on the concentration of infectious units transported in the vasculature. For any organism, the number of founders colonizing a “virgin territory”, is of prime importance in determining the forces driving its evolution. This is particularly true for viruses where the so-called founder effect is a key factor in the emergence of new variants with altered virulence. It is surprising to note, however, that whether the circulating virus load directly drives the size of viral populations during host colonization remains elusive. By monitoring for the first time the virus concentration flowing in host plant sap, in parallel with the number of viral genome founders in each successive leaf, we provide unequivocal evidence that the concentration of circulating viruses can directly determine the founder effect and effective population size during disease progression in a eucaryotic host.
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