Parasitoid-induced cellular immune deficiency in Drosophila.

L. heterotoma females inject VLPs along with their eggs into the hemocoel of the Drosophila larva. The VLPs destroy lamellocytes that are potentially harmful for the parasite eggs, but the other types of host hemocytes retain their functions. The parasitized third instar Drosophila larvae continue to grow and pupariate, showing no outward adverse effects. Minimum disruption to the growth and development of the host is advantageous to the endoparasite egg, since survival of the endoparasite depends on the health of the host to the developmental stage at which the endoparasite begins feeding on host tissues. The target of the VLPs must be microtubule components, because VLP entry into the lamellocyte induces depolymerization and repolymerization of microtubules. Microtubule rearrangement changes the discoidal lamellocyte to a bipolar cell. Concomitant with the modification in cell morphology, lamellocytes lose their surface adhesivity so they cannot adhere to a foreign object or to each other to form a capsule around endoparasite eggs. VLP-affected lamellocytes continue to elongate, lose cytoplasmic contents at the poles as blebs full of microvesicles, and are eventually destroyed. The molecular nature of the L. heterotoma VLP and the mechanisms underlying its specificity for lamellocyte cytoplasm are not known. An interesting consideration is the evolution of a particle whose selectivity for a host hemocyte protects the eggs of the parasitic insect. On the basis of information available at this time, it is clear that the L. heterotoma VLP is a useful tool for studying molecular aspects of microtubules and cytoskeleton.