Novel approaches to manage the virus complex present in sweet potato virus disease (SPVD)

The cotton aphid, Aphis gossypii Glover (Hemiptera: Aphididae), is an efficient vector of plant viruses that results in significant economic losses. For example, the sweet potato feathery mottle virus (SPFMV) is a non-persistent virus that forms a synergistic interaction with the persistent whitefly-vectored virus sweet potato chlorotic stunt virus (SPCSV) to cause sweet potato virus disease (SPVD). This synergistic interaction can result in yield losses of 90%. Therefore, we aimed to test the ability of small-molecule inhibitor of inward rectifier potassium (Kir) channels VU041 alongside commercialized aphicides to prevent SPFMV-infected aphids from inoculating plants. A foliar application of VU041 reduced SPFMV transmission (P < 0.01) by 68% compared to the untreated control (93%). For comparison, commercialized aphicides containing flonicamid and flupyradifurone, reduced horizontal transmission of SPFMV by 60% and 12%, respectively. To further define the mechanism of VU041 mediated inhibition to non-persistent virus inoculation, aphid feeding behavior after exposure to the different aphicides was assessed using the electrical penetration graph technique. Inoculation of non-persistent plant viruses occurs during the cell sampling of plant mesophyll tissue and is visualized in EPG recordings as a potential drop subphase II-1. Only VU041 significantly reduced the duration of subphase II-1 (P < 0.001), suggesting Kir inhibition is correlated to a lack of saliva secretion during cell sampling and subsequent reduction of SPFMV inoculation. Pairing these results with our previous findings that VU041 application eliminated phloem feeding, suggests that Kir channels represent a novel target to reduce feeding and transmission of non-persistent and persistent viruses.