Host regulation has been described as the many effects-- mostly physiological changes--that parasitoids cause in their host which benefit their own development (Vinson and Iwantsch, 1980). It evokes developmental disruption usually via hormonal or neurohormonal pathways, like the endocrine signaling which coordinates development of the parasitoid with that of the host so that the two partners molt in synchrony (Beckage and Gelman, 2004). It also includes all the effects on the host immune system (Strand and Pech, 1995; Schmidt et al., 2001; Pennacchio and Strand, 2006; Carton et al., 2008; Eslin et al., 2009), the first physiological barrier that endophagous parasitoids encounter after they enter the hemocoel of their host. In order to regulate their host's immunity and physiology, parasitoids produce and release active factors in the host hemocoel. These factors may come from either the female wasp's reproductive apparatus and its associated glands, or the parasitic egg or larva itself. In many species of the ichneumonid and braconid families (Ichneumonoidea), symbiotic polydnaviruses (PDVs) or virus-like particles (VLPs) (Schmidt and Schumann-Feddersen, 1989; Strand and Pech, 1995; Beckage, 1998; Drezen et al., 2003; Beckage and Gelman, 2004; Pennacchio and Strand, 2006; Bézier et al., 2009) can act as infecting agents. PDVs multiply in the calyx cells of the female wasp's ovaries while