In plant–virus–vector tripartite relationships, viral infection has been reported to alter the host plant’s physiological state to change the vector's performance, further facilitating virus transmission to other plants. However, in natural plant populations, where infected host plants maintain their perennial lifespan and vegetative spread, the tripartite system is assumed to persist over extended period. Here we hypothesise that viruses alter vector's performance to reduce virus transmission, mitigating their detrimental impact on the host. To verify this, we investigated whether viral infection reduces vector density and alters the plant transcriptome in the natural system of Arabidopsis halleri–turnip mosaic virus (TuMV)–aphid.
  First, field surveys were conducted once a week from 19 Apr to 7 Jun 2022. Aphids were observed less frequently on TuMV-infected plants, and aphid numbers tended to be lower throughout the survey period, with significant differences detected around the peak of aphid abundance in the study site. Bioassays revealed that aphid fecundity, but not preference, was reduced on the TuMV-infected leaves than on the uninfected leaves. Subsequently, we compared the host transcriptomes of intact, aphid-infested, TuMV-infected, and aphid-infested TuMV-infected plants collected from the natural habitat in April. Both aphid infestation and TuMV infection caused significant transcriptomic changes in intact hosts; however, host responses to aphids were markedly weakened in the TuMV-infected plants. This attenuation of the host response to aphids occurred in the form of a counter-response, in which host genes responded in opposite directions to viruses and aphids. Among the host genes known to increase aphid fecundity, we identified three genes exhibiting counter-responses that were activated by aphids but suppressed by TuMV. Additionally, four genes were identified as candidate aphid defence genes encoding the phloem proteins and callose synthases that were activated by TuMV, but not by aphids.
  In conclusion, our findings suggest that viral infections simultaneously suppress aphid fecundity and aphid-triggered host plant responses, thereby preventing the collapse of the host plant population and supporting plant–virus–vector coexistence in natural environments