Modelling and manipulation of aphid-mediated spread of non-persistently transmitted viruses.
Watt, Lewis G
Pate, Adrienne E
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Carr, J., Tungadi, T., Donnelly, R., Bravo-Cazar, A., Rhee, S., Watt, L. G., Mutuku, J. M., et al. (2020). Modelling and manipulation of aphid-mediated spread of non-persistently transmitted viruses.. Virus research, 277 197845. https://doi.org/10.1016/j.virusres.2019.197845
Aphids vector many plant viruses in a non-persistent manner i.e., virus particles bind loosely to the insect mouthparts (stylet). This means that acquisition of virus particles from infected plants, and inoculation of uninfected plants by viruliferous aphids, are rapid processes that require only brief probes of the plant’s epidermal cells. Virus infection alters plant biochemistry, which causes changes in emission of volatile organic compounds and altered accumulation of nutrients and defence compounds in host tissues. These virus-induced biochemical changes can influence the migration, settling and feeding behaviours of aphids. Working mainly with cucumber mosaic virus and several potyviruses, a number of research groups have noted that in some plants, virus infection engenders resistance to aphid settling (sometimes accompanied by emission of deceptively attractive volatiles, that can lead to exploratory penetration by aphids without settling). However, in certain other hosts, virus infection renders plants more susceptible to aphid colonisation. It has been suggested that induction of resistance to aphid settling encourages transmission of non-persistently transmitted viruses, while induction of susceptibility to settling retards transmission. However, recent mathematical modelling indicates that both virus-induced effects contribute to epidemic development at different scales. We have also investigated at the molecular level the processes leading to induction, by cucumber mosaic virus, of feeding deterrence versus susceptibility to aphid infestation. Both processes involve complex interactions between specific viral proteins and host factors, resulting in manipulation or suppression of the plant’s immune networks.
JPC gratefully acknowledges funding from the U.K. Biotechnological and Biological Sciences Research Council (BBSRC: SCPRID Grant Number BB/J011762/1; GCRF Grant Number BB/P023223/1). JMM receives support from the BBSRC BB/R005397/1 GCRF-CONNECTED Network (https://www.connectedvirus.net/). RD and CAG are funded by the Bill and Melinda Gates Foundation. LGW is supported by a PhD studentship from the BBSRC-Cambridge University Doctoral Training Programme (BB/M011194/1). AB-C was funded by a PhD studentship from the Secretaria Nacional de Educación Superior, Ciencia y Technologí e Innovación, Republic of Ecuador. WA is supported by a Cambridge-Africa PhD studentship. SJR was funded by a Postdoctoral Fellowship from the National Research Foundation of the Republic of Korea. FOW is funded by a Royal Society-FLAIR Fellowship (Grant number FLR\R1\190462).
BBSRC (via University of Bristol) (BB/R005397/1)
External DOI: https://doi.org/10.1016/j.virusres.2019.197845
This record's URL: https://www.repository.cam.ac.uk/handle/1810/300208
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