Differential gene expression and immune cell infiltration in maedi-visna virus infected lung tissues
Maedi -visna virus (MVV) is a lentivirus that infects monocyte/macrophage lineage cells in sheep, goats, and wild ruminants and causes pneumonia, mastitis, arthritis, and encephalitis. The immune response to MVV infection is complex, and a complete understanding of its infection and pathogenesis is lacking. To enhance our understanding of the genes implicated in the host reaction to MVV infection, this study investigated the in vivo transcriptomic patterns of lung tissues in sheep exposed to MVV using RNA sequencing technology. The results indicated that 2739 genes were significantly differentially expressed, with 1643 downregulated genes and 1096 upregulated genes. In addition to previously identified limiting factors for other viral infections, many variables that could be unique to MVV infections were also discovered. Gene Ontology analysis revealed that a significant proportion of the genes were enriched in terms directly related to the immune system and biological responses to viral infections, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the most enriched pathways were associated with virus-host cell interactions and inflammatory responses .Numerous immune-related genes, including those encoding a number of cytokines and interferon regulatory factors, were identified in the protein-protein interaction (PPI) network of differentially expressed genes (DEGs). The expression of DEGs was evaluated by real-time polymerase chain reaction and western blot analysis, and CXCL13, CXCL6, CXCL11, CCRL1, CXCL8, CXCL9, CXCL10, TNFSF8, IFNG, CCL2, and MMP9 were generally upregulated.Immunohistochemistry analysis was performed to identify the types of immune cells that infiltrated MVV-infected tissues. The most prevalent immune cells associated with MVV infection in the lungs were B cells, CD4+ and CD8+ T cells, and macrophages. Taken together, the findings of this study provide a better understanding of the in vivo host response to MVV infection and offer new perspectives on the gene regulatory networks that underlie pathogenesis in natural hosts.