Transcriptional analysis of host responses related to immunity in chicken spleen tissues infected with reticuloendotheliosis virus strain SNV.

In avian species, the Reticuloendotheliosis virus (REV) causes severe immunosuppression and other symptoms, including avian dwarfing syndrome, and chronic tumors in lymphoid and other tissues. The pathogenesis of REV and its interaction with the host have yet to be fully elucidated with transcriptional studies on the changes in host gene expression after REV infection at the body level. In this study, the Spleen Necrosis Virus (SNV) was used to inoculate the one-day-old specific pathogen free (SPF) chicken to simulate congenital infection. We identified 1507 differentially expressed genes (DEGs) at 7, 14 and 21 dpi using Next Generation Sequencing (NGS) technology. Through the Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of these DEGs, it was found that DEGs were mainly involved in the categories of signal transduction, immune system and signaling molecules and interaction. Among them, Pattern recognition receptors (PRRs), chemokine, T cell receptor, JAK-STAT, TNF, and NF-kappa B signaling pathway, and the Hematopoietic cell lineage play an important role in the tumorigenic and immunosuppressive regulation of REV. In addition, a series of DEGs associated with inflammatory factors (CCL4, TNFRSF18, CDKN2), apoptosis (IRF1, PDCD1, WNT5A), innate immunity (TLR, MAD5, TRIM25), and adaptive immunity (LY6E, CD36, LAG3) were also discovered. We further verified 33 selected immune- relevant DEGs using quantitative RT-PCR (qRT-PCR). These findings provide new insights and research directions for revealing the pathogenesis of REV infection and the interaction between REV and the chicken immune system.