Equine arteritis virus long-term persistence is orchestrated by CD8+ T lymphocyte transcription factors, inhibitory receptors, and the CXCL16/CXCR6 axis
Fig 5
Gene expression analysis of selected genes, transcription factor enrichment analysis and molecular networks associated with long-term EAV persistence.
(A) Heatmap depicting gene expression profiling by RT-qPCR of selected genes. Upregulation of specific chemokines/cytokines and chemokine receptors (including CXCL16 and CXCR6), selected transcription factors and inhibitory receptors was observed. The heatmap was generated using -ΔCt values. (B) Analysis of putative transcription factor site enrichment in DEGs between long-term and short-term carrier stallions using CiiiDER. Color and size of circles reflect p-value of enrichment. Over-represented transcription factors of potential interest are depicted. Those differentially expressed in long-term carrier stallions are depicted in bold. (C) Molecular network associated with DEGs observed between long-term and short-term carrier stallions. The network is driven by specific transcription factors, some of which were over-represented as determined by transcription factor binding site enrichment analysis. Upregulated and downregulated genes (log2 fold-change compared to short-term carrier stallions) are depicted in red and green color, respectively. The degree in color intensity reflects the magnitude of the fold-change, where intense red or green indicate a higher or lower fold-change, respectively. Only direct relationships are shown.