Data for: Genomic heterozygosity is associated with parasite abundance, but the effects are not mediated by host condition

Whether, when, and how genetic diversity buffers individuals and
populations against infectious disease risk is a critical and open
question for understanding wildlife disease and zoonotic disease risk.
Several, but not all, studies have found negative relationships between
infection and heterozygosity in wildlife. Since they can host multiple
zoonotic infections, we sampled a population of wild deer mice (Peromyscus
maniculatus), sequenced their genomes, and examined their fecal samples
for coccidia and nematode eggs. We analyzed coccidia infection status,
abundance, and coinfection status in relation to per-locus and
per-individual measures of heterozygosity, as well as identified SNPs
associated with infection status. Since heterozygosity might affect host
condition, and condition is known to affect immunity, it was included as a
co-variate in the per-individual analyses and as response variable in
relation to heterozygosity. Not only did coccidia-infected individuals
have lower levels of genome-wide per-locus diversity across all metrics,
but we found an inverse relationship between genomic diversity and
severity of coccidia infection. We also found weaker evidence that
coinfected individuals had lower levels of private allelic variation than
all other groups. In the per-individual analyses, relationships between
heterozygosity and infection were marginal but followed the same negative
trends. Condition was negatively correlated with infection, but was not
associated with heterozygosity, suggesting that effects of heterozygosity
on infection were not mediated by host condition in this system.
Association tests identified multiple loci involved in the inflammatory
response, with a particular role for NF-κB signaling, supporting previous
work on the genetic basis of coccidia resistance. Taken together, we find
that increased genome-wide neutral diversity, the presence of specific
genetic variants, and improved condition positively impact infection
status. Our results underscore the importance of considering host genomic
variation as a buffer against infection, especially in systems that can
harbor zoonotic diseases.

遗传多样性能否、何时以及如何缓冲个体和种群免受传染病风险，是理解野生动物疾病和人畜共患病（zoonotic disease）风险的关键且悬而未决的问题。已有若干研究（但非全部）发现野生动物中感染与杂合度（heterozygosity）之间存在负相关关系。鉴于野生鹿鼠（Peromyscus maniculatus）可携带多种人畜共患病感染，我们对一个野生鹿鼠种群进行了采样，对其基因组进行了测序，并检测了其粪便样本中的球虫（coccidia）和线虫卵（nematode eggs）。我们分析了球虫感染状态、丰度及共感染（coinfection）状态与位点水平和个体水平杂合度指标的关系，并鉴定了与感染状态相关的单核苷酸多态性（SNPs）。鉴于杂合度可能影响宿主状态，且已知宿主状态会影响免疫力，我们将其作为协变量纳入个体水平分析，并作为与杂合度相关的响应变量。感染球虫的个体不仅在所有指标上的全基因组位点水平多样性较低，而且基因组多样性与球虫感染严重程度之间存在负相关关系。我们还发现较弱的证据表明，共感染个体的私有等位基因变异水平低于其他所有群体。在个体水平分析中，杂合度与感染之间的关系虽不显著，但呈现相同的负向趋势。宿主状态与感染呈负相关，但与杂合度无关，这表明在该系统中杂合度对感染的影响并非通过宿主状态介导。关联测试鉴定出多个参与炎症反应的基因座，其中NF-κB信号通路发挥特殊作用，这支持了此前关于球虫抗性遗传基础的研究。综上，我们发现全基因组中性多样性的增加、特定遗传变异的存在以及宿主状态的改善均对感染状态产生积极影响。我们的结果强调了将宿主基因组变异视为抵御感染的缓冲因素的重要性，尤其是在可携带人畜共患病的系统中。