Journal
PATHOGENS
Volume 10, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/pathogens10010049
Keywords
parasitoid wasp; virulence strategy; venom; immune cell; Drosophila
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Funding
- National Institute of General Medical Sciences of the National Institutes of Health [R35GM133760]
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The interaction between Drosophila melanogaster and parasitoid wasps provides an important model for understanding host-parasite relationships. Parasitoids have evolved various virulence mechanisms to overcome the immune response of D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. The newly identified parasitoid species, Asobara sp. AsDen, utilizes an active virulence mechanism to infect D. melanogaster hosts by altering host signaling to suppress immunity.
The interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host-parasite relationships. Following parasitoid infection, D. melanogaster 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 D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We identified a previously undescribed parasitoid species, Asobara sp. AsDen, which utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen infection alters host signaling to suppress immunity.
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