Equine arteritis virus long-term persistence is orchestrated by CD8+ T lymphocyte transcription factors, inhibitory receptors, and the CXCL16/CXCR6 axis.

摘要: Equine arteritis virus (EAV) has the unique ability to establish long-term persistent infection in reproductive tract of stallions and be sexually transmitted. Previous studies showed that is associated with a specific allele CXCL16 gene (CXCL16S) persistence maintained despite presence local inflammatory humoral mucosal antibody responses. Here, we performed transcriptomic analysis ampullae, primary site EAV carrier stallions, understand molecular signatures viral persistence. We demonstrated CD8+ T lymphocyte response predominantly orchestrated by transcription factors eomesodermin (EOMES) nuclear factor activated T-cells cytoplasmic 2 (NFATC2), which likely modulated upregulation inhibitory receptors. Most importantly, an enhanced expression CXCR6 infiltrating lymphocytes, providing evidence implication this chemokine axis pathogenesis stallion tract. Furthermore, have established link between genotype profile ampullae Specifically, acts as "hub" driving transcriptional network. The findings herein are novel strongly suggest RNA viruses such could exploit CXCL16/CXCR6 order modulate immune responses male inducing dysfunctional homing