Abstract
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.
Highlights
IntroductionVirus progression within multi-cellular hosts operates via two distinct mechanisms: cell-to-cell proximal contamination and longdistance migration (either as free infectious units or in circulating cells) to colonize new organs and/or tissues
Virus progression within multi-cellular hosts operates via two distinct mechanisms: cell-to-cell proximal contamination and longdistance migration to colonize new organs and/or tissues
It seems intuitively obvious that the number of initially infected cells, the number of viral genomes entering each of these cells, and the number of founders of new viral ‘‘colonies’’, will depend on the concentration of infectious units transported in the plasma or sap flooding the vasculature
Summary
Virus progression within multi-cellular hosts operates via two distinct mechanisms: cell-to-cell proximal contamination and longdistance migration (either as free infectious units or in circulating cells) to colonize new organs and/or tissues. One could speculate that the number of ‘‘entry points’’ into various organs of the host might sometimes be extremely limited, and the number of founder viral genomes in such territories may always be low or constant, regardless of the circulating virus load For both animal and plant viruses, experimental data supporting one or the other of these contrasting scenarios are extremely rare and only fragmentary at best
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