Population biology and epidemiology of plant virus epidemics: from tripartite to tritrophic interactions

Abstract

Natural enemies have long been used in biological control programs to mitigate the damage caused by herbivory. Many herbivorous insect species also act as plant virus vectors, enabling virus transmission from plant to plant and hence disease development in a plant population. Whilst an intuitive assumption would be to expect a decrease in vector numbers to lead to subsequent reductions in virus transmission, recent evidence suggests that introduction of natural enemies (parasitoids and predators) may in some cases increase plant virus transmission while at the same time reducing vector numbers. In this paper we review the evidence for plant-virus-vector-natural enemy interactions, the signalling mechanisms involved and their implications for virus transmission, and show how a modelling approach can assist in identifying the key parameters and relationships involved in determining the disease outcome. A mathematical model linking the population dynamics of a vector-parasitoid system with virus transmission was used to investigate the effects of virus inoculation and acquisition rates, parasitoid attack rate and vector aggregation on disease dynamics across a wide range of parameter value combinations. Virus spread was found to increase with enhanced inoculation, acquisition and parasitoid attack rate but decrease with high levels of vector aggregation.