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Abstract

Polydnaviruses (PDVs) are obligate symbionts of endoparasitoid wasps, which
exclusively attack the larval stages of their lepidopteran hosts. The Polydnavirus is
injected by the parasitoid female during oviposition to selectively infect host tissues
by the expression of viral genes without undergoing replication. Toxoneuron nigriceps
bracovirus (TnBV) is associated with Toxoneuron nigriceps (Hymenoptera: Braconidae)
wasp, 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 of ecdysteroidogenesis is the main alteration
which occurs in last (fifth) instar larvae and, as a consequence, prevents pupation.
TnBV induces the functional inactivation of H. virescens prothoracic glands (PGs),
resulting in decreased protein synthesis and phosphorylation. 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 enzyme immunoassay (EIA) showed that parasitism
inhibits ecdysteroidogenesis and the phosphorylation of the two targets of TOR
(4E-BP and S6K), despite the stimulation of PTTH contained in the brain extract.
Using a transcriptomic approach, we identified viral genes selectively expressed in
last instar H. virescens PGs, 48 h after parasitization, and evaluated expression
levels of PI3K/Akt/TOR pathway genes in these tissues. The relative expression of
selected genes belonging to the TOR pathway (tor, 4e-bp, and s6k) in PGs of
parasitized larvae was further confirmed by qRT-PCR. The down-regulation of these
genes in PGs of parasitized larvae supports the hypothesis of TnBV involvement in
blocking ecdysteroidogenesis, through alterations of the PI3K/Akt/TOR pathway at the transcriptional level.