Little is known about the composition or mode of action of venoms from parasitic Hymenoptera. Among the ectoparasitic wasps, venoms are thought to paralyze the host prior to oviposition. Such wasp species generally attack mobile hosts, like lepidopteran larvae, and thus, it is highly advantageous for the host to be paralyzed for sometime in order for the ectoparasite to oviposit without disturbance. A paralytic mode of action seems unnecessary for the venoms of parasitoids that utilize an egg or pupal host because these stages are already immobile. Our studies on the mode of action of the venom from Nasonia vitripennis reveal that this pupal ectoparasitoid does not induce paralysis in its fly hosts, and in fact, dramatically alters host development and physiology by nonparalytic mechanisms. Upon encountering a host, N. vitripennis drills through the hardened fly puparium, injects venom, and then deposits eggs. The host immune response appears to be disabled almost immediately following envenomation, thereby allowing female wasps to host feed without interruption caused by a host wound-healing response. Prior to parasitoid egg hatch, fly development ceases and a series of changes is induced in host metabolism that seems to facilitate parasitoid growth. Ultimately the fly host dies either indirectly due to the feeding action of developing wasp larvae or directly by venom action. Venom-induced death is oncotic through a colloidal osmotic mechanism of cell death. The suitability of a fly host for the development of N. vitripennis progeny can be predicted by the response of the fly species to envenomation. In this review, we will discuss the importance of venom to the reproductive success of N. vitripennis and other ectoparasitic wasps, offer insight into venom mode of action, and propose that the venom system of this wasp serve as model for the study of ectoparasitic wasp venoms.
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