Modeling nutrient and disease dynamics in a plant-pathogen system

Pell, Bruce; Kendig, Amy E.; Borer, Elizabeth T.; Kuang, Yang

doi:10.3934/mbe.2019013

Cited by 9 publications

(19 citation statements)

References 65 publications

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“…Two models differing in the way nutrient supply affects disease dynamics were developed and tested against data on virus accumulation of cereal yellow dwarf virus and number of infected phloem cells from stems of Avena sativa [85]. Uniquely for models of plant virus dynamics, a basic reproduction number was derived depending in part on nutrient-mediated virus production parameters.…”

Section: Environmental Driversmentioning

confidence: 99%

The Epidemiology of Plant Virus Disease: Towards a New Synthesis

Jeger

2020

Plants

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Epidemiology is the science of how disease develops in populations, with applications in human, animal and plant diseases. For plant diseases, epidemiology has developed as a quantitative science with the aims of describing, understanding and predicting epidemics, and intervening to mitigate their consequences in plant populations. Although the central focus of epidemiology is at the population level, it is often necessary to recognise the system hierarchies present by scaling down to the individual plant/cellular level and scaling up to the community/landscape level. This is particularly important for diseases caused by plant viruses, which in most cases are transmitted by arthropod vectors. This leads to range of virus-plant, virus-vector and vector-plant interactions giving a distinctive character to plant virus epidemiology (whilst recognising that some fungal, oomycete and bacterial pathogens are also vector-borne). These interactions have epidemiological, ecological and evolutionary consequences with implications for agronomic practices, pest and disease management, host resistance deployment, and the health of wild plant communities. Over the last two decades, there have been attempts to bring together these differing standpoints into a new synthesis, although this is more apparent for evolutionary and ecological approaches, perhaps reflecting the greater emphasis on shorter often annual time scales in epidemiological studies. It is argued here that incorporating an epidemiological perspective, specifically quantitative, into this developing synthesis will lead to new directions in plant virus research and disease management. This synthesis can serve to further consolidate and transform epidemiology as a key element in plant virus research.

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Section: Environmental Driversmentioning

confidence: 99%

The Epidemiology of Plant Virus Disease: Towards a New Synthesis

Jeger

2020

Plants

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“…Together, viral replication and transmission between cells can describe the population density of viruses within plants [34,37]. In general, viral infection of a cell only leads to the production of new virus particles after a delay in time [1,22].…”

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confidence: 99%

“…In general, viral infection of a cell only leads to the production of new virus particles after a delay in time [1,22]. Delayed differential equations can explain empirical patterns of animal [17,45] and plant [37] viruses. Time delays in animal virus models that assume cell-to-cell virus transmission can induce oscillations that are absent from models that assume cellto-free virus transmission [14].…”

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confidence: 99%

“…Time delays in animal virus models that assume cell-to-cell virus transmission can induce oscillations that are absent from models that assume cellto-free virus transmission [14]. Including cell-to-cell virus transmission in a model with a time delay provides additional biological realism that may improve the model fit to plant virus observations demonstrating non-linear dynamics [37].…”

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confidence: 99%

“…On the other hand, while the dynamics of vector-host for plant virus has been studied using delay differential equations [25], within-host dynamics of plant viruses are much less explored. For this study, we modified the model by Pell et al [37] to assume cell-to-cell transmission rather than cell-to-free virus transmission. By assuming that transmission is ratio-dependent rather than mass action, we approximate the rigid cell configuration of plants.…”

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confidence: 99%

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Rich dynamics of a simple delay host-pathogen model of cell-to-cell infection for plant virus

Phan

Pell

Kendig

et al. 2021

Discrete &Amp; Continuous Dynamical Systems - B

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Viral dynamics within plant hosts can be important for understanding plant disease prevalence and impacts. However, few mathematical modeling efforts aim to characterize within-plant viral dynamics. In this paper, we derive a simple system of delay differential equations that describes the spread of infection throughout the plant by barley and cereal yellow dwarf viruses via the cell-to-cell mechanism. By incorporating ratio-dependent incidence function and logistic growth of the healthy cells, the model can capture a wide range of biologically relevant phenomena via the disease-free, endemic, mutual extinction steady states, and a stable periodic orbit. We show that when the basic reproduction number is less than 1 (R 0 < 1), the disease-free steady state is asymptotically stable. When R 0 > 1, the dynamics either converge to the endemic equilibrium or enter a periodic orbit. Using a ratiodependent transformation, we show that if the infection rate is very high relative to the growth rate of healthy cells, then the system collapses to the mutual extinction steady state. Numerical and bifurcation simulations are provided to demonstrate our theoretical results. Finally, we carry out parameter estimation using experimental data to characterize the effects of varying nutrients on the dynamics of the system. Our parameter estimates suggest that varying the nutrient supply of nitrogen and phosphorous can alter the dynamics of the infection in plants, specifically reducing the rate of viral production and the rate of infection in certain cases.

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