CD8A and infection: Considering that aging is associated with an increase in low grade systemic inflammation even under homeostatic conditions (Goplen et al., 2021), and heightened inflammatory signaling drives memory precursors to a terminally differentiated cell fate (Joshi et al., 2007), it is likely that the enhanced inflammatory microenvironment within the aged brain, coupled with enhanced BBB leakiness, could work two‐fold to drive nonspecific recruitment of CD8+ T cells into the CNS following infection and limit establishment of TRM in this site.