In HIV infection there is persistent systemic inflammation (attributed to low-level virus replication, coinfections, microbial translocation, and a proinflammatory lipid environment, among others) [63–65] that leads to EC activation and dysfunction, creating a microenvironment rich with CX3CL1, which attracts CX3CR1+ CD8 T cells to the endothelium. Here, CD8A is linked to HIV infectious disease.