Abstract
The spread of epidemics not only depends on the average number of parasites produced per host, but also on the existence of highly infectious individuals. It is widely accepted that infectiousness depends on genetic and environmental determinants. However, even in clonal populations of host and viruses growing in homogeneous conditions, high variability can exist. Here we show that Escherichia coli cells commonly display high differentials in viral burst size, and address the kinetics of emergence of such variability with the non-lytic filamentous virus M13. By single-cell imaging of a virally-encoded fluorescent reporter, we monitor the viral charge distribution in infected bacterial populations at different time following infection. A mathematical model assuming autocatalytic virus replication and inheritance of bacterial growth rates quantitatively reproduces the experimental distributions, demonstrating that deterministic amplification of small host inhomogeneities is a mechanism sufficient to explain large and highly skewed distributions. This mechanism of amplification is general and may occur whenever a parasite has an initial phase of exponential growth within its host. Moreover, it naturally reproduces the shift towards higher virulence when the host is experimenting poor conditions, as observed commonly in host-parasite systems.
Highlights
In the development of epidemics it is the average parasite production that matters, and the distribution of secondary cases infected by single individuals
Far from being an unusual property of the phage a studied by Max Delbruck, the high heterogeneity in virus production per cell is a common characteristic of several phages, in spite of marked differences in their infection strategy and impact on the host
For all the four viruses studied, PFU distributions have a larger coefficient of variation than any other phenotypic trait measured in a bacterial population, as cell size [4,8] or cell elongation rate [11]
Summary
In the development of epidemics it is the average parasite production that matters, and the distribution of secondary cases infected by single individuals. The spread of a disease can be deeply affected by heterogeneities in infectiousness, with high viral charge ‘superspreader’ individuals triggering stronger epidemic events [1]. For better data interpretation and disease control, it is of primary importance to understand how the distribution of virus production is shaped by the underlying host-parasite interactions. Strong differences in virus production exist even among cells of a clonal bacterial population growing in a homogeneous environment. Several studies pointed out the existence of nongenetic large differences between clonal subpopulations in the response to stresses [5,6] or following viral infection [7,8]. The mechanisms behind the origin and maintenance of such large differentials are still unknown
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