An agent-based model to simulate virus-based biocontrol for the soybean cyst nematode, Heterodera glycines

soybean cyst nematode;biocontrol;virulence;evolution;agent-based model;ecoimmunology;quasispecies

Anderson, Safyre ; Bhalerao ; Kaustubh

关键词: soybean cyst nematode;    biocontrol;    virulence;    evolution;    agent-based model;    ecoimmunology;    quasispecies;   

Others  :  https://www.ideals.illinois.edu/bitstream/handle/2142/50643/Safyre_Anderson.pdf?sequence=1&isAllowed=y

美国|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

Plant parasitic nematodes are responsible for food losses worth 78 billion dollars worldwide. The damage caused by Heterodera glycines, or soybean cyst nematode (SCN), to the US soybean crop is estimated up to 2 billion dollars annually making it the most destructive soybean pathogen. SCN is a microscopic obligate endoparasite with an entirely belowground life history that includes a robust dormant phase. These aspects of SCN biology make it nearly impossible to eradicate and expensive to manage. The most widely deployed strategy to manage SCN is an integrated management plan (IPM) that combines non-host crop rotations (frequently with corn) and planting SCN-resistant cultivars. SCN cyst diapause–which allows SCN to persist in the soil for several years–limits the effectiveness of alterate-year crop rotations. Furthermore, evidence that the most widely used resistant lines are losing their effectiveness is mounting. Additionally, nematicides are increasingly unavailable due to environmental regulations and also have the disadvantages of being prohibitively expensive, and performing inconsistently.Biological control (biocontrol) has recently been seen as a promising addition to IPM. Viruses are relatively more stable and therefore more persistent in soil, they do not need to form complicated infection structures, they can be cultured on a commercial scale, and they have simpler genomes which are amenable to genetic engineering. Furthermore, viruses exhibit higher host and tissue-specificity, decreasing the risk for non-target effects seen in other non-virus-based biocontrol cases. Though these properties of viruses have been demonstrated in insect pests with favorable results, viruses have not been investigated for nematode biocontrol. This is because infectious virus in nematodes had gone unnoticed until a couple of recent discoveries. At the University of Illinois, five SCN ssRNA viruses were discovered in 2011 giving us ample opportunity–paving the way to explore their potential as biocontrol agents. While empirical data on the pathologies of these viruses emerges, we opted to use a computational approach to investigate pathotypic factors needed for desirable nematode suppression, the epizootiology of within-nematode evolution, and the long-term population-level behavior. This study used an agent-based model, SCNSim, to simulate a virus-nematode-soybean system to investigate within-host virulence evolution. The nematode-agent recapitulates the nematode life cycle and uses purely stochastic events to advance each transition in the model. SCNSim was used to test a range of mutation rates, initial virulences, and release strategies. This investigation uses weather data and soybean planting and harvesting patterns in Champaign, IL. Where empirical data is lacking dimensionless parameters and probabilities were used.Results of the simulation showed viruses inoculated at 80% prevalence caused significantly more mortalities than those inoculated at 20% prevalence. Further investigation revealed the low mortality under lower prevalence was likely due to high horizontal and vertical transmission leading to rapid thinning of the overall viral burden as the disease spread to nearly 100% of the population. Mortality rate was found to be dependent on virulence and fidelity. Pathotypes with high starting virulence resulted in premature peaked mortalities which suggested shorter lifetime transmission. Furthermore, virulence and fidelity were inversely related in pathotypes with the highest mortalities. Further, these pathotypes had population-level fitnesses near the error threshold between persistence or extinction. Qualitative stability analysis revealed medial pathotypes exhibited stable long-term behavior reminiscent of a spiral sink in the mortality and transmissibility phase space.That intermediately virulent and transmissible viruses lead to the most damaging epizootics is in agreement with the generally accepted trade-off theory in virulence evolution. However, the evolution of the transmissibility and prevalence curves through time reveal some inconsistencies in the mechanisms of disease spread with respect to theory that require further testing. Testing combinations of varying levels of transmission rates, and virus loads for instance can provide insight on how different transmission modes impact virulence evolution and the efficacy of nematode suppression. There are still many areas where SCNSim can be improved–particularly when the transmission rates and dominant transmission modes of the SCN RNA viruses becomes known. In its present state, SCNSim has predicted the attenuation of nematode mortalities within the first four crop seasons due to either a dilution of virus particles thoughout the population or the insulation of the infected population resulting from mortality rates exceeding transmission rates. The goal for the near future is to apply SCNSim alongside genetic engineering and experimental testing of the SCN viruses, in a decision-making framework for virus-agent deployment strategies and improving virus-agent efficacy within an evolutionary timescale for nematode biocontrol.