Aphid density and community composition differentially affect apterous aphid movement and plant virus transmission

2017 ◽  
Vol 42 (3) ◽  
pp. 245-254 ◽  
Author(s):  
SUZI B. CLAFLIN ◽  
ALISON G. POWER ◽  
JENNIFER S. THALER
Plants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 304 ◽  
Author(s):  
Nuria Montes ◽  
Israel Pagán

Increased light intensity has been predicted as a major consequence of climate change. Light intensity is a critical resource involved in many plant processes, including the interaction with viruses. A central question to plant–virus interactions is understanding the determinants of virus dispersal among plants. However, very little is known on the effect of environmental factors on virus transmission, particularly through seeds. The fitness of seed-transmitted viruses is highly dependent on host reproductive potential, and requires higher virus multiplication in reproductive organs. Thus, environmental conditions that favor reduced virus virulence without controlling its level of within-plant multiplication (i.e., tolerance) may enhance seed transmission. We tested the hypothesis that light intensity conditions that enhance plant tolerance promote virus seed transmission. To do so, we challenged 18 Arabidopsis thaliana accessions with Turnip mosaic virus (TuMV) and Cucumber mosaic virus (CMV) under high and low light intensity. Results indicated that higher light intensity increased TuMV multiplication and/or plant tolerance, which was associated with more efficient seed transmission. Conversely, higher light intensity reduced plant tolerance and CMV multiplication, and had no effect on seed transmission. This work provides novel insights on how environmental factors modulate plant virus transmission and contributes to understand the underlying processes.


2007 ◽  
Vol 104 (46) ◽  
pp. 17959-17964 ◽  
Author(s):  
M. Uzest ◽  
D. Gargani ◽  
M. Drucker ◽  
E. Hebrard ◽  
E. Garzo ◽  
...  

2021 ◽  
Author(s):  
Nik J. Cunniffe ◽  
Nick P. Taylor ◽  
Frédéric M. Hamelin ◽  
Michael J. Jeger

ABSTRACTMany 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.


2021 ◽  
Author(s):  
Benjamin W. Lee ◽  
Robert E. Clark ◽  
Saumik Basu ◽  
David W. Crowder

AbstractArthropods that vector plant pathogens often interact with predators within food webs. Predators affect vectors by eating them (consumptive effects) and by inducing antipredator behaviors (non-consumptive effects), and these interactions may affect transmission of vector-borne pathogens. However, it has proven difficult to experimentally tease apart the effects of predators on vector fitness and behavior as they are often correlated. We addressed this problem by assessing how both aphids and an aphid-borne pathogen were affected by variable predation risk. Specifically, we experimentally manipulated ladybeetle predators’ mouthparts to isolate consumptive, and non-consumptive, effects of predators on aphid fitness, movement, and virus transmission. We show that although lethal predators decreased aphid vector abundance, they increased pathogen transmission by increasing aphid movement among hosts. Moreover, aphids responded to risk of predation by moving to younger plant tissue that was more susceptible to the pathogen. Aphids also responded to predator risk through compensatory reproduction, which offset direct consumptive effects. Our results support predictions of disease models showing alterations of vector movement due to predators can have greater effects on transmission of pathogens than vector consumption. Broadly, our study shows isolating direct and indirect predation effects can reveal novel pathways by which predators affect vector-borne pathogens.


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