Epidemiological and ecological consequences of virus manipulation of host and vector in plant virus transmission.

Many plant viruses are transmitted by insect vectors. Transmission can be described as persistent or non-persistent depending on rates of acquisition, retention, and inoculation of virus. Much experimental evidence has accumulated indicating vectors can prefer to settle and/or feed on infected versus noninfected host plants. For persistent transmission, vector preference can also be conditional, depending on the vector's own infection status. Since viruses can alter host plant quality as a resource for feeding, infection potentially also affects vector population dynamics. Here we use mathematical modelling to develop a theoretical framework addressing the effects of vector preferences for landing, settling and feeding-as well as potential effects of infection on vector population density-on plant virus epidemics. We explore the consequences of preferences that depend on the host (infected or healthy) and vector (viruliferous or nonviruliferous) phenotypes, and how this is affected by the form of transmission, persistent or non-persistent. We show how different components of vector preference have characteristic effects on both the basic reproduction number and the final incidence of disease. We also show how vector preference can induce bistability, in which the virus is able to persist even when it cannot invade from very low densities. Feedbacks between plant infection status, vector population dynamics and virus transmission potentially lead to very complex dynamics, including sustained oscillations. Our work is supported by an interactive interface https://plantdiseasevectorpreference.herokuapp.com/. Our model reiterates the importance of coupling virus infection to vector behaviour, life history and population dynamics to fully understand plant virus epidemics

Modelling Vector Transmission and Epidemiology of Co-Infecting Plant Viruses.

Co-infection of plant hosts by two or more viruses is common in agricultural crops and natural plant communities. A variety of models have been used to investigate the dynamics of co-infection which track only the disease status of infected and co-infected plants, and which do not explicitly track the density of inoculative vectors. Much less attention has been paid to the role of vector transmission in co-infection, that is, acquisition and inoculation and their synergistic and antagonistic interactions. In this investigation, a general epidemiological model is formulated for one vector species and one plant species with potential co-infection in the host plant by two viruses. The basic reproduction number provides conditions for successful invasion of a single virus. We derive a new invasion threshold which provides conditions for successful invasion of a second virus. These two thresholds highlight some key epidemiological parameters important in vector transmission. To illustrate the flexibility of our model, we examine numerically two special cases of viral invasion. In the first case, one virus species depends on an autonomous virus for its successful transmission and in the second case, both viruses are unable to invade alone but can co-infect the host plant when prevalence is high

Coinfections by noninteracting pathogens are not independent and require new tests of interaction.

If pathogen species, strains, or clones do not interact, intuition suggests the proportion of coinfected hosts should be the product of the individual prevalences. Independence consequently underpins the wide range of methods for detecting pathogen interactions from cross-sectional survey data. However, the very simplest of epidemiological models challenge the underlying assumption of statistical independence. Even if pathogens do not interact, death of coinfected hosts causes net prevalences of individual pathogens to decrease simultaneously. The induced positive correlation between prevalences means the proportion of coinfected hosts is expected to be higher than multiplication would suggest. By modelling the dynamics of multiple noninteracting pathogens causing chronic infections, we develop a pair of novel tests of interaction that properly account for nonindependence between pathogens causing lifelong infection. Our tests allow us to reinterpret data from previous studies including pathogens of humans, plants, and animals. Our work demonstrates how methods to identify interactions between pathogens can be updated using simple epidemic models

Immune priming and the limited diversity of resistance genes in host mixtures

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Immune priming and the limited diversity of resistance genes in host mixtures

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Spatial spread of infectious diseases with conditional vector preferences

International audienceWe explore the spatial spread of vector-borne infections with conditional vector preferences, meaning that vectors do not visit hosts at random. Vectors may be differentially attracted toward infected and uninfected hosts depending on whether they carry the pathogen or not. The model is expressed as a system of partial differential equations with vector diffusion. We first study the diffusion-less model. We show that conditional vector preferences alone (in the absence of any epidemiological feedback on their population dynamics) may result in bistability between the disease-free equilibrium and an endemic equilibrium. A backward bifurcation may allow the disease to persist even though its basic reproductive number is less than one. Bistability can occur only if both infected and uninfected vectors prefer uninfected hosts. Back to the model with diffusion, we show that bistability in the local dynamics may generate travelling waves with either positive or negative spreading speeds, meaning that the disease either invades or retreats into space. In the monostable case, we show that the disease spreading speed depends on the preference of uninfected vectors for infected hosts but not on the preference of infected vectors for uninfected hosts. We discuss the implications of our results for vector-borne plant diseases, which are the main source of evidence for conditional vector preferences so far

Emerging Themes and Approaches in Plant Virus Epidemiology

International audiencePlant diseases caused by viruses share many common features with those caused by other pathogen taxa in terms of the host-pathogen interaction, but there are also distinctive features in epidemiology, most apparent where transmission is by vectors. Consequently, the host-virus-vector-environment interaction presents a continuing challenge in attempts to understand and predict the course of plant virus epidemics. Theoretical concepts, based on the underlying biology, can be expressed in mathematical models and tested through quantitative assessments of epidemics in the field; this remains a goal in understanding why plant virus epidemics occur and how they can be controlled. To this end, this review identifies recent emerging themes and approaches to fill in knowledge gaps in plant virus epidemiology. We review quantitative work on the impact of climatic fluctuations and change on plants, viruses, and vectors under different scenarios where impacts on the individual components of the plant-virus-vector interaction may vary disproportionately; there is a continuing, sometimes discordant, debate on host resistance and tolerance as plant defense mechanisms, including aspects of farmer behavior and attitudes toward disease management that may affect deployment in crops; disentangling host-virus-vector-environment interactions, as these contribute to temporal and spatial disease progress in field populations; computational techniques for estimating epidemiological parameters from field observations; and the use of optimal control analysis to assess disease control options. We end by proposing new challenges and questions in plant virus epidemiology

Spatial spread of infectious diseases with conditional vector preferences

International audienceWe explore the spatial spread of vector-borne infections with conditional vector preferences, meaning that vectors do not visit hosts at random. Vectors may be differentially attracted toward infected and uninfected hosts depending on whether they carry the pathogen or not. The model is expressed as a system of partial differential equations with vector diffusion. We first study the diffusion-less model. We show that conditional vector preferences alone (in the absence of any epidemiological feedback on their population dynamics) may result in bistability between the disease-free equilibrium and an endemic equilibrium. A backward bifurcation may allow the disease to persist even though its basic reproductive number is less than one. Bistability can occur only if both infected and uninfected vectors prefer uninfected hosts. Back to the model with diffusion, we show that bistability in the local dynamics may generate travelling waves with either positive or negative spreading speeds, meaning that the disease either invades or retreats into space. In the monostable case, we show that the disease spreading speed depends on the preference of uninfected vectors for infected hosts but not on the preference of infected vectors for uninfected hosts. We discuss the implications of our results for vector-borne plant diseases, which are the main source of evidence for conditional vector preferences so far

The proportion of resistant hosts in mixtures should be biased towards the resistance with the lowest breaking cost

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