Host immune response induced by endoparasitic wasps

The insect immune system serves as a key defense against attack by parasitoids. Incompatible hosts eliminate parasitoids by encapsulation, a process in which hemocytes form a multilayered coating around the invader. Capsule formation involves cooperation between several classes of hemocytes and is mediated by molecules (e.g. cytokines) that induce a change in hemocyte behavior from a non-adhesive to a strongly adhesive state. Conversely, parasitic wasps that develop inside a living host have evolved sophisticated strategies of interacting with their host`s immune system in order to survive and reproduce successfully. Many endoparasitic wasps of the superfamily Ichneumonidae are protected from the immune defense reaction of their host by polydisperse DNA viruses (PDVs) which are integrated into the wasp`s genome. At oviposition, virus particles and venom proteins are co-injected with the parasitoid eggs into the host. The primary function of these factors is a knock-out effect on the host`s immune system by triggering apoptosis of hemocytes and altering their ability to adhere to foreign surfaces and one another. PDVs do not replicate within the host, but invade specific tissues, and especially hemocytes, where viral genes are expressed and some of the resulting proteins are involved in immune disruption. This study will focus on the gregarious, endoparasitic, PDV-carrying braconid wasp Glyptapanteles liparidis and its interactions with two economically important insect pests, Lymantria dispar and Lymantria monacha. The hosts are taxonomically closely related and phenologically very similar, but differ in their ability to serve as hosts for G. liparidis; while L. dispar larvae are permissive for the parasitoid, no development is possible in L. monacha larvae because the eggs are recognized as foreign bodies and encapsulated. The general scientific object is to study host immune responses in a permissive versus a non-permissive host on a cellular, molecular and genetic level with special emphasis on the early phase of parasitism as the crucial period for parasitoid survival. Specifically, we will monitor the effect of PDV and associated proteins on the progression of encapsulation, the types of hemocytes involved in the process, and their cytoskeletal changes. Additionally, we will study the temporal pattern of PDV-infection and PDV gene expression in host hemocytes and host gene activation or silencing by molecular biological methods. The proposed experiments will enable us to characterize the immunological basis for compatibility/ incompatibility in the host-parasitoid relationships L. dispar/L. monacha - G. liparidis. Detailed knowledge of the effect and specificity of PDVs in the wasp`s host may be of significant importance for future insect pest management programs.