SRA

Polydnaviruses (PDVs) are obligate symbionts of endoparasitoid wasps, which exclusively attack the larval stages of theirlepidopteran hosts. The Polydnavirus is injected by the parasitoid female during oviposition to selectively infect host tissues by theexpression of viral genes without undergoing replication. Toxoneuron nigriceps bracovirus (TnBV) is associated with Toxoneuronnigriceps (Hymenoptera: Braconidae) wasps, an endoparasitoid of the tobacco budworm larval stages, Heliothis virescens(Lepidoptera: Noctuidae). Previous studies showed that TnBV is responsible for alterations in host physiology. The arrest ofecdysteroidogenesis is the main alteration which occurs in last (fifth) instar larvae and, as a consequence, prevents pupation. TnBVinduces the functional inactivation of H. virescens prothoracic glands (PGs), resulting in decreased protein synthesis andphosphorylation. Previous work showed the involvement of the PI3K/Akt/TOR pathway in H. virescens PG ecdysteroidogenesis.Here, we demonstrate that this cellular signaling is one of the targets of TnBV infection. Western blot analysis and enzymeimmunoassay (EIA) showed that parasitism inhibits ecdysteroidogenesis and the phosphorylation of the two targets of TOR (4E-BPand S6K), despite the stimulation of PTTH contained in the brain extract. Using a transcriptomic approach, we identified viralgenes selectively expressed in last instar H. virescens PGs, 48h after parasitization, and evaluated expression levels ofPI3K/Akt/TOR pathway genes in these tissues. The relative expression of selected genes belonging to the TOR pathway (tor, 4e-bpand s6k) in PGs of parasitized larvae was further confirmed by qRT-PCR. The down-regulation of these genes in PGs of parasitizedlarvae supports the hypothesis of TnBV involvement in blocking ecdysteroidogenesis, through alterations of the PI3K/Akt/TORpathway at the transcriptional level.