Invertebrates mount a sophisticated immune response with the potential to exhibit a form of immune memory through ‘priming’. Increased immune protection following early exposure to bacteria has been found both later in life (within generation priming) and in the next generation (transgeneration priming) in a number of invertebrates. However, it is unclear how general immune priming is and whether immune priming occurs in response to different parasites, including viruses. Here, using Plodia interpuctella (Lepidoptera) and its natural DNA virus, Plodia interpunctella granulosis virus, we find evidence for both within generation and transgeneration immune priming. Individuals previously exposed to low doses of virus, as well as the offspring of exposed individuals, are subsequently less susceptible to viral challenge. Relatively little is known about the mechanisms that underpin viral immunity but it is probable that the viral immune response is somewhat different to that of bacteria. We show that immune priming may, however, be a characteristic of both responses, mediated through different mechanisms, suggesting that immune memory may be a general phenomenon of insect immunity. This is important because immune priming may influence both host–parasite population and evolutionary dynamics.

The expansion of invasive non-indigenous species in the Mediterranean is generating an increasing concern about biodiversity protection and human health, with European countries being solicited to apply early warning measures in such circumstances. The recent expansion of the hazardous fish Lagocephalus sceleratus in the Straits of Sicily, the subsequent actions adopted to manage the risk and the feedback received from the public are herein presented, as an example of the interaction between experts and the public in promoting scientific citizenship through an ad hoc action. A rapid increase in media reports related to L. sceleratus had been registered after the launch of the early warning campaign as part of a scientific and health risk communication strategy, and seven new records of this species have emerged shortly after. This study represents a useful contribution to the further bridging of the science-policy gap.

Exposure to low doses of pathogens that do not result in the host becoming infectious may 'prime' the immune response and increase protection to subsequent challenge. There is increasing evidence that such immune priming is a widespread and important feature of invertebrate host-pathogen interactions. Immune priming clearly has implications for individual hosts but will also have population-level implications. We present a susceptible-primed-infectious model-in contrast to the classic susceptibleinfectious-recovered framework-to investigate the impacts of immune priming on pathogen persistence and population stability. We describe impacts of immune priming on the epidemiology of the disease in both constant and seasonal environments. A key result is that immune priming may act to destabilize population dynamics. In particular, when the proportion of individuals becoming primed rather than infected is high, but this priming does not confer full immunity, the population may be strongly destabilized through the generation of limit cycles. We discuss the implications of our model both in the context of invertebrate immunity and more widely.

While invertebrates lack the machinery necessary for 'acquired immunity', there is increasing empirical evidence that exposure to low levels of disease may 'prime' an invertebrate's immune response, increasing its defence to subsequent exposure. Despite this increasing empirical data, there has been little theoretical attention paid to immune priming. Here, we investigate the evolution of immune priming, focusing on the role of the unique feedbacks generated by a newly developed susceptible -primed -infected epidemiological model. Contrasting our results with previous models on the evolution of acquired immunity, we highlight that there are important implications to the evolution of immunity through priming owing to these different epidemiological feedbacks. In particular, we find that in contrast to acquired immunity, priming is strongly selected for at high as well as intermediate pathogen virulence. We also find that priming may be greatest at either intermediate or high host lifespans depending on the severity of disease. Furthermore, hosts faced with more severe pathogens are more likely to evolve diversity in priming. Finally, we show when the evolution of priming leads to the exclusion of the pathogens or hosts experiencing population cycles. Overall the model acts as a baseline for understanding the evolution of priming in host -pathogen systems.

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