African Swine Fever (ASF) is a highly contagious viral pathology in suids, precipitating profound global economic disruptions. In the absence of efficacious vaccines, elucidating the molecular determinants of ASF virus (ASFV) pathogenesis is imperative for advancing targeted mitigation and therapeutic strategies. This study utilized high-throughput RNA-sequencing to characterize the systemic host immune architecture in infected Bama mini-pigs. Comparative transcriptomic analysis of the spleen and inguinal lymph nodes identified a conserved signature of 77 differentially expressed genes, signifying a synchronized systemic transcriptional response. Functional enrichment analysis revealed robust upregulation of critical immunomodulatory cascades, specifically cytokine-cytokine receptor interaction, Toll-like receptor signaling, MAPK signaling, and apoptosis. Significant transcriptional perturbations were observed in pivotal immune regulators, including XCL1, IFIT2, and FCGR1A. Furthermore, protein-protein interaction (PPI) network topology identified central hub genes, P4HB, EEF1A2, and DNAJC3, which orchestrate cellular stress adaptation, proteostasis, and immunomodulation during infection. Integration of transcription factor and microRNA (miRNA) regulatory mapping unveiled sophisticated, multi-layered governance of these hub nodes, suggesting their potential utility as molecular biomarkers and high-priority therapeutic targets. Collectively, these findings provide comprehensive mechanistic insights into the molecular landscape of ASFV pathogenesis and substantially enhance the current understanding of systemic host-pathogen dynamics in swine.
K et al. (Wed,) studied this question.