Data from: Reciprocal interaction matrix reveals complex genetic and dose-dependent specificity among coinfecting parasites

Understanding genetic specificity in factors determining the outcome of host-parasite interactions is especially important as it contributes to parasite epidemiology, virulence, and maintenance of genetic variation. Such specificity, however, is still generally poorly understood. We examined genetic specificity in interactions among coinfecting parasites. In natural populations, individual hosts are often simultaneously infected by multiple parasite species and genotypes that interact. Such interactions could maintain genetic variation in parasite populations if they are genetically specific so that the relative fitness of parasite genotypes varies across host individuals depending on (1) the presence/absence of coinfections and/or (2) the genetic composition of the coinfecting parasite community. We tested these predictions using clones of fish eye flukes Diplostomum pseudospathaceum and Diplostomum gasterostei. We found that interactions among parasites had a strong genetic basis and that this modified genetic variation in infection success of D. pseudospathaceum between single and multiple infections as well as across multiply infected host individuals depending on the genetic identity of the coinfecting D. gasterostei. The relative magnitude of these effects, however, depended on the exposure dose, suggesting that ecological factors can modify genetic interactions between parasites.

解析宿主-寄生虫互作结局决定因子中的遗传特异性，对于寄生虫流行病学、毒力以及遗传变异维持均具有重要意义。然而目前学界对这类遗传特异性的认知仍普遍较为匮乏。本研究针对共感染寄生虫之间的互作展开遗传特异性分析。在自然种群中，单个宿主通常会同时被多种存在互作关系的寄生虫物种与基因型感染。若这类互作具有遗传特异性，则寄生虫基因型的相对适合度会随宿主个体差异发生变化，具体取决于两点：一是是否存在共感染，二是共感染寄生虫群落的遗传组成（或两者兼具）；此类遗传特异性互作或可维持寄生虫种群的遗传变异。本研究以复口吸虫属（Diplostomum）的两种鱼类眼吸虫——假叶复口吸虫（Diplostomum pseudospathaceum）与加斯泰复口吸虫（Diplostomum gasterostei）的克隆株为实验材料，对上述预测进行验证。研究结果显示，寄生虫间的互作具有极强的遗传基础，且该遗传基础会改变假叶复口吸虫（D. pseudospathaceum）在单一感染与多重感染情境下的感染成功率遗传变异，同时也会随共感染的加斯泰复口吸虫（D. gasterostei）的遗传特征，在多重感染宿主个体间产生差异。但上述效应的相对强度取决于暴露剂量，这表明生态因子可调控寄生虫间的遗传互作。