An entomopoxvirus and a granulovirus have different impacts on Adoxophyes honmai (Tortricidae, Lepidoptera) simultaneously parasitized by Ascogaster reticulatus (Braconidae: Hymenoptera)

Abstract

Abstract Development of the endoparasitoid Ascogaster reticulatus is adversely affected when its host, Adoxophyes honmai, is simultaneously infected with either an entomopoxvirus (AdhoEPV) or a granulovirus (AdhoGV). The two viruses, however, have different effects on the survival of A. reticulatus: AdhoEPV infection prevents parasitoid emergence, whereas parasitoid larvae emerge from AdhoGV-infected hosts but die before pupation. Prevention of emergence of the parasitoid from AdhoEPV-infected hosts seems to be due to earlier death of the host during head capsule slippage in the 4th instar, which did not occur in AdhoGV-infected larvae. Previous studies showed that healthy A. honmai larvae have peaks of juvenile hormone esterase (JHE) and 20-hydroxyecdysone (20E) during the 5th instar before pupation. AdhoEPV-infected (non-parasitized) larvae do not pupate, because no peak of 20E appears in AdhoEPV-infected larvae. AdhoGV-infected larvae also do not pupate, in this case because ecdysteroid UDP-glucosyltransferase (EGT) is expressed by AdhoGV and inactivates 20E. In this study, we measured JHE and 20E levels in parasitized A. honmai larvae simultaneously infected with either AdhoEPV or AdhoGV to explain their different metamorphosis. Parasitized larvae infected with either virus alone had no JHE peak during the 4th instar. In AdhoGV-infected and parasitized larvae, however, a large peak of ecdysteroid was observed during the 4th instar, which may be abolished by EGT, whereas AdhoEPV-infected and parasitized larvae showed a small ecdysteroid peak which allows larval–larval molting. These endocrinological results are consistent with the morphology of parasitized and infected larvae, and consequently explain the fate of parasitoid larvae in virus-infected hosts.