Host interaction and regulation in parasitoid wasps  (Page 6/7)

The venom secreted by Nasonia vitripennis is lethal to a wide range of manure-breeding flies and the common house fly , Musca domestica , which is a major vector of human disease. The venom is also toxic to multiple developmental stages of several mosquitoes that are vectors of diseases such as malaria, encephalitis, yellow fever and West Nile fever (Rivers 2004). The evenomation of the host fly results in a number of changes in the fly’s physiology that leads to cell death. David B. Rivers and his colleagues performed bio-assays of Nasonia venom and found that the venom operates by nonparalytic means to induce arrested development in evenomated hosts. The venom was found to alter the fly’s lipid metabolism, leading to lipid accumulation in the host fat body, and change plasma membrane permeability leading to an increase in sodium influx. Venom also suppressed the host fly’s immune response and was essential for successful parasitization by the developing wasp larvae (Rivers et al 2002).

A powerful weapon of parasitization, venom has evolved to produce both immunosuppressive and stimulatory properties to create the optimal host environment for parasitoid offspring. In order to maximize progeny production, female parasitoids must regulate the host without totally suppressing the host’s physiology and creating an unregulated host environment. Should the host become immune-compromised, the parasitoid’s progeny is subjected to unregulated microbrial attack and invasion. Thus, the female wasp must evade the host immune response without compromising the host’s immune system. To accomplish this difficult task, parasitoid wasps use a venomous mixture that includes virus-like particles, such as the polydnavirus , at the time of oviposition to subdue the host (Danneels et al 2010).