Neonicotinoid-based real control of aphids in sugar beet permitted the effective management of associated phytoviruses. However, the prohibition on their usage has prompted an urgent search for viable replacements. The development of sugar beet varieties with aphid and/or virus resistance and/or tolerance has a huge potential to reduce aphids and the harm caused by transmitted viruses. Semiochemicals also play a significant part in determining intra- and inter-specific interactions, which directly affect aphid fitness, feeding activity, and ultimately their capacity to spread viruses. Another method of aphid management involves the use of plant volatile organic compounds (VOCs) in conjunction with an attract and kill strategy. Entomopathogenic fungi could also be used to manage aphids without endangering helpful entomofauna. Finally, soil bacteria are particularly effective biocontrol agents because they induce systemic resistance (ISR) as plant growth promoting rhizobacteria (PGPR). The sugar beet-aphid virus model would be a perfect place to test these microbial players. The adoption of complementing eco-compatible techniques in the sugar beet crop will be ensured by the application of a variety of biocontrol opportunities connected to creative aphid control strategies. This should make it possible to create technical itineraries for a comprehensive approach to controlling aphids and related viruses depending on the situation.

Alighting aphids probe a new host plant by intracellular test punctures for suitability. These induce immediate calcium signals that emanate from the punctured sites and might be the first step in plant recognition of aphid feeding and the subsequent elicitation of plant defence responses. Calcium is also involved in the transmission of non-persistent plant viruses that are acquired by aphids during test punctures. Therefore, we wanted to determine whether viral infection alters calcium signalling. For this, calcium signals triggered by aphids were imaged on transgenic Arabidopsis plants expressing the cytosolic FRET-based calcium reporter YC3.6-NES and infected with the non-persistent viruses cauliflower mosaic (CaMV) and turnip mosaic (TuMV), or the persistent virus, turnip yellows (TuYV). Aphids were placed on infected leaves and calcium elevations were recorded by time-lapse fluorescence microscopy. Calcium signal velocities were significantly slower in plants infected with CaMV or TuMV and signal areas were smaller in CaMV-infected plants. Transmission tests using CaMV-infected Arabidopsis mutants impaired in pathogen perception or in the generation of calcium signals revealed no differences in transmission efficiency. A transcriptomic meta-analysis indicated significant changes in expression of receptor-like kinases in the BAK1 pathway as well as of calcium channels in CaMV- and TuMV-infected plants. Taken together, infection with CaMV and TuMV, but not with TuYV, impacts aphid-induced calcium signalling. This suggests that viruses can modify plant responses to aphids from the very first vector/host contact.