To V, R0 to V ?
Siva-Jothy, Jonathon Arumugam
Outbreaks of infectious disease can be caused by only a few highly infectious individuals. These individuals are produced by variation in traits affecting contact between infected and susceptible individuals, the likelihood that contact results in infection and the duration of infection. High-risk individuals are difficult to predict because traditional assessments of disease transmission, such as R0, rely on population averages that conceal the variation that produces high transmission-risk phenotypes. Contact rate between infected and susceptible individuals, is primarily determined by behaviour whereas physiological immunity is the main determinant of the likelihood that contact causes infection and infection duration. I characterise variation in traits affecting the determinants of disease transmission and use this to predict individual variation in disease transmission, V. Using the fruit fly, Drosophila melanogaster, and its viral pathogen Drosophila C Virus, I have found pervasive and complex effects of genetic and sex-specific variation, mating, and infection on suites of behaviours, physiological traits and outcomes of infection. Many of my results point to an individual’s disease transmission potential being determined by genetic background and sex. Males, for example, typically survive DCV infection longer than females, however the amount of virus they shed is also determined by their genetic background. To predict how this variation could affect disease transmission dynamics, I simulated outbreaks of DCV in theoretical populations. These populations exhibited genetic and sex-specific variation based on my experiments and significantly affected population-level outbreak dynamics. Differences in these dynamics highlight potentially high-risk transmission classes of individuals, defined by their genetic background and sex.