BACKGROUND Parasites may mediate the success of biological invasions through their effect on host fitness and thus, on host population growth and stability. However, a release from the pressure of parasites is strongly related to the genetic differentiation of the host. In invasive host populations, the number of available genetic variants, allowing them to 'fight' the infection, are likely to be influenced by founder events and genetic drift. The level standing genetic variation of invasive populations may be crucial in successfully adapting to new environments and resisting diseases. We studied invasive populations of raccoon that experienced a random reduction in genetic diversity during the establishment and evaluated the relationship between host immune genetic diversity and intestinal parasites infection. RESULTS We distinguished two different genetic clusters that are characterized by different sets of functionally relevant MHC-DRB alleles. Both clusters were characterized by considerably different allele-parasite associations and different levels of parasite infection. The specific resistance MHC-DRB alleles explained the lower prevalence of Digenea parasites. An increased infection intensity was related to the presence of two MHC-DRB alleles. One of these alleles significantly decreased in frequency over time, causing a decrease of Digenea abundance in raccoons in consecutive years. CONCLUSIONS Our findings suggest that intestinal parasites can exert selective pressure on an invasive host with lowered levels of immune genetic diversity and contribute to promoting local adaptation over time. The random genetic drift that created the two different genetic clusters in the invasive raccoon range imposed completely different MHC-parasite associations, strongly associated with the infection status of populations. Our findings underline the role of standing genetic variation in shaping host-parasite relationships and provide empirical support that functional genetic variation may be, at least partly, responsible for differences in the success of invasive populations.

中文翻译：

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非本地入侵物种中的宿主-寄生虫相互作用取决于免疫基因座上常设遗传变异的水平。

背景技术寄生虫可通过其对宿主适应性的影响并因此对宿主种群的生长和稳定性的影响来介导生物入侵的成功。但是，寄生虫压力的释放与宿主的遗传分化密切相关。在侵入性宿主种群中，可能的遗传变异数量（使它们能够“抵抗”感染）很可能会受到创始人事件和遗传漂移的影响。入侵人群的水平遗传变异对于成功适应新环境和抵抗疾病可能至关重要。我们研究了在建立过程中经历了遗传多样性随机减少的浣熊入侵种群，并评估了宿主免疫遗传多样性与肠道寄生虫感染之间的关系。结果我们区分了两个不同的基因簇，其特征在于功能相关的MHC-DRB等位基因的不同集合。这两个簇的特征是等位基因-寄生虫的关联大大不同，寄生虫感染的水平也不同。MHC-DRB等抗性的等位基因解释了Digenea寄生虫的患病率较低。感染强度增加与两个MHC-DRB等位基因的存在有关。这些等位基因之一的频率随着时间的推移而显着下降，从而导致浣熊中的Digenea丰度连续几年下降。结论我们的研究结果表明，肠道寄生虫可以对入侵宿主施加选择性压力，使免疫遗传多样性水平降低，并随着时间的推移促进局部适应。在侵入性浣熊范围内产生两个不同遗传簇的随机遗传漂移施加了完全不同的MHC-寄生虫关联，与人群的感染状况密切相关。我们的发现强调了遗传变异在塑造宿主-寄生虫关系中的作用，并提供了经验支持，即功能遗传变异可能至少部分是造成入侵人群成功的差异的原因。