| Summary: | The interactions between <i>Drosophila melanogaster</i> and the parasitoid wasps that infect <i>Drosophila</i> species provide an important model for understanding host–parasite relationships. Following parasitoid infection, <i>D. melanogaster</i> larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes, leading to death of the parasitoid. Previous studies have found that host hemocyte load; the number of hemocytes available for the encapsulation response; and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the <i>D. melanogaster</i> host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We identified a previously undescribed parasitoid species, <i>Asobara</i> sp. <i>AsDen</i>, which utilizes an active virulence mechanism to infect <i>D. melanogaster</i> hosts. <i>Asobara</i> sp. <i>AsDen</i> infection inhibits host hemocyte expression of <i>msn</i>, a member of the JNK signaling pathway, which plays a role in lamellocyte production. <i>Asobara</i> sp. <i>AsDen</i> infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered <i>msn</i> expression. Our findings suggest that <i>Asobara</i> sp. <i>AsDen</i> infection alters host signaling to suppress immunity.
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