none Heliothis virescens; PROTEINS-; HORMONES-; Hymenopteran parasite development regulation; LARVAL-DEVELOPMENT; Hymenopteran parasite regulation; HYMENOPTERAN-PARASITES; Cardiochiles nigriceps; Host parasite biochemical & developmental relationships Cardiochiles nigriceps; TOXINS-AND-VENOMS; Venom regulatory factors effect on lepidopteran host physiology; EGG-; Teratocyte regulatory factors effect on lepidopteran host physiology; DUCTS-OF-FEMALE; Calyx fluid regulatory factors effect on lepidopteran host physiology; LARVAL-DEVELOPMENT; ECDYSIS-; GROWTH-; Lepidopteran host biochemistry & development relationships; LEPIDOPTERAN-HOSTS; Heliothis virescens; Host parasite biochemical & developmental relationships All larval stages of Heliothis virescens (F.) parasitized by the endophagous larval parasitoid Cardiochiles nigriceps Viereck, a braconid species belonging to the subfamily Microgasterinae, exhibit developmental arrest at last instar and fail to pupate. The major part of larval development of the parasitoid is synchronized with the arrested host last larval instar and the parasitoid first molt is never observed before the host attains the late digging stage. At this time, the total ecdysteroid titer of the hemolymph of parasitized hosts is very low and subsequently shows a slow and gradual increase, characterized by a low titer of 20-hydroxyecdysone (20-HE) associated with consistent amounts of inactive ecdysteroid polar metabolites. Juvenile hormone esterase (JHE) activity is high in both control and parasitized host larvae at the early digging stage of development, and juvenile hormone analogs (JHA) applied to parasitized host last instar larvae appear to suppress the parasitoid molt. Concurrent with these changes was an increase in the hemolymph titer of proteins which was maintained at a high level in parasitized larvae in contrast to the observed decrease in control larvae at the cell formation stage of development. Neck-ligation of newly molted host 5th instar parasitized larvae, prior to both JHE release and the increase in protein titers, inhibited growth and molting of the parasitoid. In contrast, ligation after JHE release and with high hemolymph protein titers resulted in parasitoid molting and growth. These data suggest that the host ecdysteroid hormones are not directly involved in the regulation of the parasitoid molt, although high juvenile hormone (JH) levels probably prevent it. More likely, molting is triggered by other biochemical changes, such as proteins or other factors occurring in the hemolymph. Molting of C. nigriceps larvae in vitro into an ecdysone-free semidefined medium further supported the view that host ecdysone is not necessary for the molt. Teratocytes of C. nigriceps seem to play an important role in the inactivation of 20-HE through its conversion to inactive polar metabolites, and along with female calyx fluid and venom which depress the secretory activity of the host prothoracic glands, they are the most important sources of host regulatory factors.