Abstract
Chicken anemia virus (CAV), when primarily transmitted through the vertical route, could result in a significant global prevalence. Specifically, vertical CAV transmission, especially in newly-hatched chicks, may cause anemia and immunosuppression, leading to significant losses in the global poultry industry. Although CAV infection of chick embryos is critical in its vertical transmission, the pathogenicity of CAV in these embryos remains unclear. Herein, CAV-infected chick embryos exhibited a reduced hatchability rate, decreased embryo weight, and anemia. Furthermore, histopathological findings revealed reduced hematopoietic foci in the yolk sac and spleen, as well as pancytopenia and cortical lymphopenia in the bone marrow and thymus, respectively. Additionally, an analysis of the relative expression of transcription factors (TFs) and cell markers demonstrated that CAV inhibited hematopoiesis and T-lymphocyte development. Moreover, the high viral loads and strong immunolabelling highlighted the hematopoietic cells of the yolk sac and bone marrow as the primary target tissues for CAV. It is also noteworthy that the detection of CAV load showed active CAV replication from Embryo Day 15 (ED15) to ED18, implying that CAV replication was activated before hatching. These findings collectively suggest that CAV inhibited hematopoiesis and development in embryos, with its replication activated before hatching. In addition to illuminating CAV pathogenesis, our findings on CAV pathogenicity and tissue tropism in embryos could also guide its prevention and control.