Data from: Critical disease windows shaped by stress exposure alter allocation trade-offs between development and immunity

1. Ubiquitous environmental stressors are often thought to alter animal susceptibility to pathogens and contribute to disease emergence. However, duration of exposure to a stressor is likely critical, because while chronic stress is often immunosuppressive, acute stress can temporarily enhance immune function. Furthermore, host susceptibility to stress and disease often varies with ontogeny; increasing during critical developmental windows. How the duration and timing of exposure to stressors interact to shape critical windows and influence disease processes is not well tested. 2. We used ranaviruses and larval amphibians as a model system to investigate how physiological stress and pathogenic infection shape development and disease dynamics in vertebrates. Based on a resource allocation model, we designed experiments to test how exposure to stressors may induce resource trade-offs that shape critical windows and disease processes because the neuroendocrine stress axis coordinates developmental remodeling, immune function, and energy allocation in larval amphibians. 3. We used wood frog larvae (Lithobates sylvaticus) to investigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid hormone, mediates development and immune function via splenocyte immunohistochemistry analysis in association with ranavirus infection. 4. Corticosterone treatments affected immune function, as both chronic and acute exposure suppressed splenocyte proliferation, although viral replication rate increased only in the chronic corticosterone treatment. 5. Time to metamorphosis and survival depended on both corticosterone treatment and infection status. In the control and chronic corticosterone treatments, ranavirus infection decreased survival and delayed metamorphosis, although chronic corticosterone exposure accelerated time to metamorphosis in uninfected larvae. Acute corticosterone exposure accelerated metamorphosis increased survival in infected larvae. 6. Interactions between stress exposure (via glucocorticoid actions) and infection impose resource trade-offs that shape optimal allocation between development and somatic function. As a result, critical disease windows are likely shaped by stress exposure because any conditions that induce changes in differentiation rates will alter the duration and susceptibility of organisms to stressors or disease.1. 普遍存在的环境胁迫因子（environmental stressors）通常被认为会改变动物对病原体（pathogens）的易感性，并推动疾病暴发。然而，胁迫暴露的时长可能是关键因素：慢性应激（chronic stress）往往具有免疫抑制作用，而急性应激（acute stress）则可暂时性增强免疫功能。此外，宿主对应激和疾病的易感性常随个体发育（ontogeny）发生变化，在关键发育窗口（critical developmental windows）期间会上升。目前尚缺乏对胁迫暴露时长与时机如何共同塑造关键发育窗口、进而影响疾病进程的充分检验。 2. 本研究以蛙病毒（ranaviruses）和两栖动物幼体（larval amphibians）为模型系统，探究生理应激（physiological stress）与病原体感染（pathogenic infection）如何塑造脊椎动物的发育与疾病动态。基于资源分配模型（resource allocation model），我们设计实验以检验胁迫暴露如何诱发资源权衡（resource trade-offs），进而塑造关键发育窗口与疾病进程——这是因为神经内分泌应激轴（neuroendocrine stress axis）可协调两栖动物幼体的发育重塑、免疫功能与能量分配。 3. 本研究使用林蛙幼体（Lithobates sylvaticus），结合蛙病毒感染实验，通过脾细胞免疫组化分析（splenocyte immunohistochemistry analysis），探究两栖动物主要糖皮质激素（glucocorticoid hormone）皮质酮（corticosterone）的慢性与急性暴露如何调控发育与免疫功能。 4. 皮质酮处理对免疫功能产生影响：慢性与急性暴露均会抑制脾细胞增殖（splenocyte proliferation），但仅在慢性皮质酮处理组中，病毒复制率（viral replication rate）出现上升。 5. 变态时间与存活情况同时受皮质酮处理与感染状态（infection status）影响。在对照组（control）与慢性皮质酮处理组中，蛙病毒感染会降低存活率并延缓变态；但在未感染幼体中，慢性皮质酮暴露可加速变态进程。而急性皮质酮暴露则可加速变态，并提升感染幼体的存活率。 6. 应激暴露（通过糖皮质激素作用）与感染之间的相互作用会引发资源权衡，进而塑造发育与体细胞功能（somatic function）间的最优分配。由此，关键疾病窗口可能由应激暴露塑造：任何能诱导分化速率（differentiation rates）改变的条件，都会改变生物体对应激或疾病的暴露时长与易感性。