This review summarizes recent data on the regulation of host development by insect baculoviruses through the action of the viral egt gene. This gene was first identified in the genome of Autographa californica nuclear polyhedrosis virus (AcMNPV) and encodes the enzyme ecdysteroid UDP-glucosyl-transferase (EGT), which catalyses the conjugation of ecdysteroids with glucose or galactose. Egt genes have now been identified in 6 baculoviruses other than AcMNPV; the encoded proteins all display significant homology throughout their length. The baculovirus EGTs are also homologous to a variety of UDP-glycosyltransferases from animal, plant and bacterial species and five conserved domains have been identified that are shared by many of these proteins. Seven amino acids are absolutely conserved in all of these proteins. They all occur within domains III and IV; this region of the protein is thought to be involved in UDP-sugar binding. Comparison of insects infected by an egt-mutant of AcMNPV with those infected by wild-type virus demonstrated that EGT-catalysed conjugation of ecdysteroids causes a suppression of host moulting and pupation. Wild-type AcMNPV-infected insects do not experience the feeding arrest, normally associated with ecdysis and therefore become larger, and yield more virus, than those infected with egt-viruses. Thus, one function of egt may be to increase the yield of progeny virus by prolonging insect feeding. Other possible functions discussed in this review include the alteration of host behaviour or the suppression of adverse effects of ecdysteroids on viral replication at the cellular level. Because egt expression prolongs insect feeding, recombinant baculoviruses lacking egt appear to be more efficient biological insecticides. In addition to the reduced feeding, egt-AcMNPV-infected insects display accelerated mortality. Thus, deletion of egt represents a simple approach to the improvement of baculovirus pesticides by genetic engineering.