%0 Journal Article %A Nakai, Madoka %A Kinjo, Hirotoshi %A Takatsuka, Jun %A Shiotsuki, Takahiro %A Kamita, Shizuo G. %A Kunimi, Yasuhisa %T Entomopoxvirus infection induces changes in both juvenile hormone and ecdysteroid levels in larval Mythimna separata %D 2016 %J Journal of General Virology, %V 97 %N 1 %P 225-232 %@ 1465-2099 %R https://doi.org/10.1099/jgv.0.000325 %I Microbiology Society, %X Insect viruses are among the most important pathogens of lepidopteran insects. Virus-infected larvae often show developmental defects including a prolonged larval period and a failure to pupate, but the mechanisms by which insect viruses regulate host development need further investigation. In this study, the regulation of host endocrinology by a lepidopteran entomopoxvirus (EPV), Mythimna separata EPV (MySEV), was examined. When fourth instar M. separata were inoculated with MySEV occlusion bodies, pupation was prevented and the insects died during the final (sixth) larval instar. Liquid chromatography–MS analysis revealed that juvenile hormone (JH) titres in the haemolymph of MySEV-infected sixth instars were higher than those in mock-infected larvae. JH esterase (JHE) activity was also examined by kinetic assay using a colorimetric substrate. The level of JHE activity in the haemolymph of MySEV-infected larvae was generally lower than that found in mock-infected larvae. In contrast, ecdysteroid titre in the haemolymph of final-instar MySEV-infected larvae was lower than that found in mock-infected larvae when measured by radioimmunoassay. A statistically significant difference in the release of ecdysteroids from prothoracic glands (PGs) that were dissected from MySEV- or mock-infected sixth instar Day 3 larvae was not found following prothoracicotropic hormone (PTTH) exposure. Our results indicate that the release of ecdysteroids was reduced not by infection of the PGs by MySEV, but by reduced PTTH production from the brain. Taken together our study suggests that EPVs retard host development by both reducing ecdysone titre and maintaining status quo levels of JH by preventing its metabolism. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.000325