Population viability in a host-parasitoid system is mediated by interactions between population stage structure and life stage differential susceptibility to toxicants.

The effects of toxicants, such as pesticides, may be more severe for some life stages of an organism than others. However, in most toxicity studies, data is developed for only one life stage, which may lead to misleading interpretations. Furthermore, population stage-structure may interact with differential susceptibility, especially when populations consist of higher proportions of individuals in more susceptible stages at the time of toxicant exposure. We explore the interaction of differential stage susceptibility and stage distribution using a stage-structured Lefkovitch matrix model. We incorporate lab-derived toxicity data for a common parasitoid, the braconid Diaeretiella rapae (M'Intosh), a common natural enemy of the cabbage aphid (Brevicoryne brassicae L.), exposed to the pesticide imidacloprid. We compare population outcomes of simulations in which we vary both the population stage structure along with the susceptibility of each stage to toxicants. Our results illustrate an interaction between differential susceptibility and initial stage distribution, highlighting the fact that both of these demographic features should be considered in interpreting toxicity data and the development of ecological risk assessments.

Exogenous JH and ecdysteroid applications alter initiation of polydnaviral replication in an endoparasitoid wasp, Cotesia plutellae (Braconidae: Hymenoptera).

Polydnaviruses are a group of double-stranded DNA viruses and are symbiotically associated with some ichneumonoid wasps. As proviruses, the replication of polydnaviruses occurs in the female reproductive organ at the pupal stage. This study analyzed the effects of two developmental hormones, juvenile hormone (JH) and ecdysteroid, on the viral replication of Cotesia plutellae bracovirus (CpBV). All 23 CpBV segments identified contained a conserved excision/rejoining site ('AGCTTT') from their proviral segments. Using quantitative real-time PCR based on this excision/rejoining site marker, initiation of CpBV replication was determined to have occurred on day 4 on the pupal stage. Pyriproxyfen, a JH agonist, significantly inhibited adult emergence of C. plutellae, whereas RH5992, an ecdysteroid agonist, had no inhibitory effect. Although RH5992 had no effect dose on adult development, it significantly accelerated viral replication. The results of immunoblotting assays against viral coat proteins support the effects of the hormone agonists on viral replication.

Exposure of ichnovirus particles to digitonin leads to enhanced infectivity and induces fusion from without in an in vitro model system.

Unlike most viruses, the mature ichnovirus particle possesses two unit membrane envelopes. Following loss of the outer membrane in vivo, nucleocapsids are believed to gain entry into the cytosol via a membrane fusion event involving the inner membrane and the plasma membrane of susceptible host cells; accordingly, experimentally induced damage to the outer membrane might be expected to increase infectivity. Here, in an attempt to develop an in vitro model system for studying ichnovirus infection, we show that digitonin-induced disruption of the virion outer membrane not only increases infectivity, but also uncovers an activity not previously associated with any polydnavirus: fusion from without.