Proteomic remodeling of the chicken spleen during astrovirus infection reveals coordinated interferon activation and stromal restructuring

Chicken astrovirus (CAstV) is associated with white chick syndrome (WCS), characterized by reduced hatchability, hypopigmentation, developmental delay, and increased early mortality. Although transcriptomic studies have provided insight into host responses to CAstV infection, protein-level mechanisms remain poorly understood. Here, we performed label-free quantitative proteomic profiling of spleens from CAstV-infected SPF White Leghorn chickens to characterize systemic host responses. Spleens collected at 4 days post-infection were analyzed by nanoLC–MS/MS. Among 1,118 quantified proteins, 34 showed significant differential abundance (q ≤ 0.05). Proteins with increased abundance formed a type I interferon–associated antiviral module, including IFI27L1 (ISG12), OASL, STAT1, MOV10, and IFITM1, consistent with innate antiviral activation. Proteins with reduced abundance were enriched for extracellular matrix and cytoskeletal regulators, including decorin, lumican, mimecan, and actin-associated proteins, suggesting remodeling of the splenic stromal microenvironment. Integration with previously generated RNA-seq data demonstrated concordant transcript–protein induction of interferon-stimulated genes alongside discordant regulation of extracellular matrix, cytoskeletal, and metabolic proteins, suggesting the involvement of post-transcriptional regulatory mechanisms. Together, these findings reveal coordinated antiviral, stromal, and metabolic responses in the spleen during CAstV infection and provide a proteomic framework for understanding systemic host responses associated with white chick syndrome.