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ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Emerging Pests and Pathogens Research » Research » Publications at this Location » Publication #432622

Research Project: Management and Biology of Insect and Nematode Pests and their Vectored Plant Pathogens

Location: Emerging Pests and Pathogens Research

Title: Aphid-polerovirus protein interactions couple antiviral immunity and plant virus transmission in Myzus persicae

Author
item THOMPSON, LUKE - Cornell University
item WEST-ORTIZ, MICHAEL - Cornell University
item Heck, Michelle

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2026
Publication Date: 7/6/2026
Citation: Thompson, L., West-Ortiz, M., Heck, M.L. 2026. Aphid-polerovirus protein interactions couple antiviral immunity and plant virus transmission in Myzus persicae. Meeting Abstract. Hemipteran Plant Insect Symposium, Montpellier, France. July 6-8, 2026.

Interpretive Summary:

Technical Abstract: Poleroviruses are phloem-restricted, positive-sense, RNA viruses that are transmitted by aphids in a circulative, non-propagative manner. Although these viruses do not replicate in their insect vectors, successful transmission requires coordinated trafficking of virions across aphid gut and accessory salivary gland barrier as well as persistence of the virions within the hemocoel. We recently demonstrated that acquisition of potato leafroll virus (PLRV) by Myzus persicae suppresses RNAi-mediated antiviral immunity in the aphid. PLRV acquisition resulted in elevation of titers of two insect infecting viruses: Myzus persicae densovirus (MpDNV), a DNA virus, and Myzus persicae flavivirus (MpFV), an RNA virus. PLRV-mediated suppression of aphid antiviral immunity occurs via two distinct mechanisms. Inhibition of small RNA production against MpDNV is indirect and mediated via plant expression of the PLRV silencing suppressor, P0. In contrast, the suppression of the antiviral response against MpFV occurs via a direct mechanism associated with the PLRV virion. To identify aphid proteins involved in this interaction, we performed co-immunoprecipitation experiments using anti-PLRV antibodies, followed by mass spectrometry. Analysis of the PLRV-interactome using a de novo transcriptome assembly from our M. persicae colony revealed candidate proteins directly and indirectly associated with antiviral RNAi as well as mitochondrial, cytoskeletal, and lipid-associated proteins. Notably, we identified a host factor previously implicated in flavivirus infection in mosquitoes. These findings suggest that PLRV engages a network of aphid proteins at the intersection of RNA silencing, mitochondrial function, epithelial cell cytoskeleton and lipid metabolism. Ongoing studies aim to determine how PLRV leverages these interactions to modulate aphid antiviral immunity and how such cross-virus immune modulation influences vector competence and plant virus spread.