Gyrovirus 3 (GyV3) has been identified in humans and other hosts, suggesting its cross-species pathogenicity, which poses an increased public health risk. In the current study, we established chicken and mouse models of GyV3 infection. We found that GyV3 induced persistent infections, characterized by viremia, aplastic anemia, immunosuppression, and systematic lymphocytic inflammation, in both species. Kinetic viral loads and antigen expression demonstrated rapid viral replication and broad tissue tropism of GyV3 in both models. The highest viral loads and the strongest antigen immunostaining were present in bone marrow and cerebrum in both chickens and mice, indicating that these are target tissues for GyV3. Genetic diversity analysis of VP1 in infected chickens and mice showed that GyV3 adapts to new hosts via rapid evolution of the hypervariable region of the gene encoding the structural protein VP1. Overall, our results indicate that GyV3 is a cross-species pathogenic virus; therefore, more attention needs to be paid to high levels of GyV3-induced neurotropism and aplastic anemia as a public health risk.

已经在人类和其他宿主中发现了 Gyrovirus 3 (GyV3)，表明其具有跨物种致病性，从而增加了公共卫生风险。在目前的研究中，我们建立了 GyV3 感染的鸡和小鼠模型。我们发现 GyV3 在两个物种中都诱导了持续感染，其特征是病毒血症、再生障碍性贫血、免疫抑制和系统性淋巴细胞炎症。动力学病毒载量和抗原表达证明了两种模型中 GyV3 的快速病毒复制和广泛的组织趋向性。鸡和小鼠的骨髓和大脑中存在最高的病毒载量和最强的抗原免疫染色，表明这些是 GyV3 的靶组织。受感染的鸡和小鼠中 VP1 的遗传多样性分析表明，GyV3 通过编码结构蛋白 VP1 的基因的高变区的快速进化来适应新宿主。总的来说，我们的结果表明 GyV3 是一种跨物种的致病病毒；因此，需要更多地关注高水平的 GyV3 诱导的神经性和再生障碍性贫血作为公共健康风险。