Abstract
Host heterogeneity in disease transmission is widespread but precisely how different host traits drive this heterogeneity remains poorly understood. Part of the difficulty in linking individual variation to population-scale outcomes is that individual hosts can differ on multiple behavioral, physiological and immunological axes, which will together impact their transmission potential. Moreover, we lack well-characterized, empirical systems that enable the quantification of individual variation in key host traits, while also characterizing genetic or sex-based sources of such variation. Here we used Drosophila melanogaster and Drosophila C Virus as a host-pathogen model system to dissect the genetic and sex-specific sources of variation in multiple host traits that are central to pathogen transmission. Our findings show complex interactions between genetic background, sex, and female mating status accounting for a substantial proportion of variance in lifespan following infection, viral load, virus shedding, and viral load at death. Two notable findings include the interaction between genetic background and sex accounting for nearly 20% of the variance in viral load, and genetic background alone accounting for ~10% of the variance in viral shedding and in lifespan following infection. To understand how variation in these traits could generate heterogeneity in individual pathogen transmission potential, we combined measures of lifespan following infection, virus shedding, and previously published data on fly social aggregation. We found that the interaction between genetic background and sex explained ~12% of the variance in individual transmission potential. Our results highlight the importance of characterising the sources of variation in multiple host traits to understand the drivers of heterogeneity in disease transmission.
Highlights
Individual host heterogeneity in pathogen transmission is a pervasive feature of all host-pathogen systems [1,2,3,4,5]
To begin our characterization of host heterogeneity in pathogen spread we measured fly lifespan following septic infection with Drosophila C Virus (DCV). This allowed us to confirm that the lines we chose showed a range of continuous variation in susceptibility[57], but infected lifespan is directly relevant to the individual transmission potential V [12], by determining the full extent of the infectious period
We found no evidence that mating affected the lifespan of females following DCV infection (Fig 1A and Table 1)
Summary
Individual host heterogeneity in pathogen transmission is a pervasive feature of all host-pathogen systems [1,2,3,4,5]. Mary Mallon, who became known as ‘Typhoid Mary’, was a superspreader of particular infamy, infecting over 50 people with Salmonella typhi while working as a cook in New York during the early 20th century [8]. Beyond this anecdotal example, the 2003 outbreaks of SARS in Singapore and Hong Kong were greatly accelerated by a few superspreading individuals who caused over 70% of all SARS transmission [9]. Similar levels of individual heterogeneity in transmission were recorded and are thought to have accelerated the spread of MERS, Ebola and most recently, SARS-CoV2 [10, 11]
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