<b>Fruit flies fight low dose infections by having more offspring</b>
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Innate immune defences exhibit variable effectiveness, a phenomenon not yet fully understood. Recent research indicates that organisms may employ fundamentally different mechanisms to combat low-dose topical infections common in nature than severe infections. Here, we show that insects respond to low-dose topical infections by triggering terminal investment. Using simple methods for topical inoculations, we find that exposing fruit flies, <i>Drosophila melanogaster</i>, to low or sexually transmitted doses of the indigenous fungus <i>Aspergillus austwickii</i> boosts egg-to-adult viability, thereby maintaining lifetime reproductive output. By varying infection doses, we describe a pattern of correlations between reproductive success and mortality rate consistent with the threshold model of terminal investment. Quantitative analysis of age-dependent reproductive and mortality patterns reveals a misunderstanding of fundamental assumptions in life history theory: theories of senescence inadequately explain life history trade-offs induced by infections. Residual Reproductive Value may not necessarily be the evolutionary rationale underlying terminal investment. Our study shows that terminal investment involves an immediate trade-off between egg-to-adult viability and survival post-infection, rather than being driven by age-dependent trade-offs. The plasticity of life history traits in response to low-dose infections constrains the evolution of immunity, maintaining negative phenotypic correlations. Using the Gal4/UAS RNAi candidate gene knockdown approach, we compare the life history consequences of a canonical innate immune gene,<i> Dorsal</i>-related immunity factor. This comparison confirms that immune gene-mediated antagonistic pleiotropy drives insects to shift from reproductive to survival mechanisms of protection, depending on the mode of infection. Furthermore, we characterise a novel terminal investment mechanism encoded by <i>Turandot</i> C gene, which helps females minimise the costs of defence against the entomopathogenic fungus <i>Metarhizium robertsii</i> by shifting reproductive output post-infection. Our findings highlight the need for more research on common infections in nature to inform important non-immunological defences in a broader ecological context.<br>
固有免疫防御（Innate immune defences）的防御效能存在显著差异，这一现象迄今尚未得到完全阐明。近期研究显示，相较于重症感染，生物体或采用截然不同的机制来对抗自然界中常见的低剂量局部感染。本研究证实，昆虫可通过激活终末投资（terminal investment）机制应对低剂量局部感染。我们通过简便的局部接种方法，将黑腹果蝇（Drosophila melanogaster）暴露于低剂量或性传播剂量的本土真菌<i>Aspergillus austwickii</i>后，发现其卵至成虫存活率显著提升，进而维持了终生繁殖产出。通过调控感染剂量，我们观测到繁殖成功率与死亡率间的关联模式，该模式与终末投资的阈值模型相符。对年龄依赖性繁殖与死亡模式的定量分析揭示，现有生活史理论（life history theory）的核心假设存在认知偏差：衰老理论无法充分解释感染引发的生活史权衡（trade-offs）。残差繁殖价值（Residual Reproductive Value）未必是驱动终末投资的进化逻辑。本研究表明，终末投资实则涉及卵至成虫存活率与感染后存活之间的直接权衡，而非由年龄依赖性权衡所驱动。低剂量感染诱导的生活史性状可塑性会限制免疫的演化进程，维持负表型关联。我们借助Gal4/UAS RNAi候选基因敲低技术，对比了经典固有免疫基因<i>Dorsal</i>相关免疫因子对生活史的影响。该对比证实，由免疫基因介导的拮抗多效性（antagonistic pleiotropy）会驱使昆虫根据感染模式，在繁殖保护与存活保护机制之间进行切换。此外，我们还解析了由<i>Turandot</i> C基因编码的新型终末投资机制：该机制可通过调整感染后的繁殖产出，帮助雌性个体降低抵御昆虫病原真菌<i>Metarhizium robertsii</i>的防御成本。本研究结果凸显，为在更广泛的生态背景下阐释关键的非免疫防御机制，亟需针对自然界常见感染开展更多研究。
