Abstract

With recently discovered soybean cyst nematode (SCN) viruses, biological control of the nematodes is a theoretical possibility. This study explores the question of what kinds of viruses would make useful biocontrol agents, taking into account evolutionary and population dynamics. An agent-based model, Soybean Cyst Nematode Simulation (SCNSim), was developed to simulate within-host virulence evolution in a virus-nematode-soybean ecosystem. SCNSim was used to predict nematode suppression under a range of viral mutation rates, initial virulences, and release strategies. The simulation model suggested that virus-based biocontrol worked best when the nematodes were inundated with the viruses. Under lower infection prevalence, the viral burden thinned out rapidly due to the limited mobility and high reproductive rate of the SCN. In accordance with the generally accepted trade-off theory, SCNSim predicted the optimal initial virulence for the maximum nematode suppression. Higher initial virulence resulted in shorter lifetime transmission, whereas viruses with lower initial virulence values evolved toward avirulence. SCNSim also indicated that a greater viral mutation rate reinforced the virulence pathotype, suggesting the presence of a virulence threshold necessary to achieve biocontrol against SCN.

Highlights

  • Soybean Cyst Nematode Simulation Framework (SCNSim) to expect that the virus and the nematode could both evolve in potentially unpredictable ways

  • This study documents the development of Soybean Cyst Nematode Simulation Framework (SCNSim), an agent-based simulation engine designed to explore the biocontrol outcomes of a range of hypothetical viruses interacting with the soybean cyst nematode (SCN)

  • SCNSim represents the first attempt at capturing the evolutionary dynamics of host–pathogen interaction in the context of biocontrol of SCNs with viruses

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Summary

Introduction

SCNSim to expect that the virus and the nematode could both evolve in potentially unpredictable ways. The virulence–transmissibility tradeoff has been demonstrated empirically in malaria models where transmission and virulence are positively correlated until the benefit of increased transmission no longer outweighs the concomitant increase in host mortality (Mackinnon and Read, 2004b; Alizon et al, 2009; Rabergand Stjernman, 2012). Another example is the canonical study of the myxoma virus in invasive European rabbit (Oryctolagus cuniculus) populations in Australia (Fenner and Ratcliffe, 1965). Within 2 years, the myxoma virus fatality cases caused by the most prevalent strains dropped from 90% to 99% to between 70% and 95% over 30 years. (Fenner and Ratcliffe, 1965; Kerr et al, 2012)

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