Department of Animal and Plant Sciences, University of Sheffield, Sheffield, UK.
Proc Biol Sci. 2012 Nov 7;279(1746):4505-12. doi: 10.1098/rspb.2012.1841. Epub 2012 Sep 12.
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 susceptible-infectious-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.
暴露于不会导致宿主感染的低剂量病原体可能会“启动”免疫反应,并增加对随后挑战的保护。越来越多的证据表明,这种免疫启动是无脊椎动物宿主-病原体相互作用的一个普遍而重要的特征。免疫启动显然对个体宿主有影响,但也会对种群水平产生影响。我们提出了一个易感性-启动-感染模型——与经典的易感性-感染-恢复框架相反——来研究免疫启动对病原体持续存在和种群稳定性的影响。我们描述了免疫启动对恒态和季节性环境中疾病流行病学的影响。一个关键的结果是,免疫启动可能会破坏种群动态的稳定性。特别是,当处于启动状态而不是感染状态的个体比例较高,但这种启动并不能赋予完全免疫力时,种群可能会通过产生极限环而受到强烈的破坏。我们讨论了我们的模型在无脊椎动物免疫和更广泛范围内的意义。