Nakai Madoka, Kinjo Hirotoshi, Takatsuka Jun, Shiotsuki Takahiro, Kamita Shizuo G, Kunimi Yasuhisa
Tokyo University of Agriculture and Technology, Saiwai, , Fuchu, Tokyo 183-8509, Japan.
Forestry and Forest Products Research Institute, Matsunosato, Tsukuba, Ibaraki 305-8687, Japan.
J Gen Virol. 2016 Jan;97(1):225-232. doi: 10.1099/jgv.0.000325. Epub 2015 Oct 23.
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.
昆虫病毒是鳞翅目昆虫最重要的病原体之一。受病毒感染的幼虫通常会出现发育缺陷,包括幼虫期延长和无法化蛹,但昆虫病毒调节宿主发育的机制仍需进一步研究。在本研究中,对一种鳞翅目昆虫痘病毒(EPV),即粘虫痘病毒(MySEV)对宿主内分泌的调节作用进行了研究。用MySEV包涵体接种四龄粘虫后,昆虫无法化蛹,并在最后(第六)龄幼虫期死亡。液相色谱-质谱分析显示,感染MySEV的六龄幼虫血淋巴中的保幼激素(JH)滴度高于模拟感染的幼虫。还使用比色底物通过动力学测定法检测了JH酯酶(JHE)活性。感染MySEV的幼虫血淋巴中的JHE活性水平通常低于模拟感染的幼虫。相比之下,通过放射免疫测定法测量时,感染MySEV的末龄幼虫血淋巴中的蜕皮甾类滴度低于模拟感染的幼虫。在暴露于促前胸腺激素(PTTH)后,未发现从感染MySEV或模拟感染的六龄第三天幼虫解剖得到的前胸腺(PGs)释放蜕皮甾类有统计学上的显著差异。我们的结果表明,蜕皮甾类的释放减少不是因为MySEV感染了PGs,而是因为大脑产生的PTTH减少。综合来看,我们的研究表明,昆虫痘病毒通过降低蜕皮激素滴度和通过阻止其代谢来维持保幼激素的现状水平,从而延缓宿主发育。