The factors which are driving and maintaining these large populations of effector memory CD8 T cells might differ between specific herpes viruses; while repetitive antigen exposure is believed to drive memory inflation and maintenance of effector memory cells in peripheral tissues after CMV infection, skin resident memory cells after HSV-1 infection were shown to adopt this phenotype irrespective of local antigen recognition, and lytic antigen expression seems to evoke effector memory CD8 T cells during EBV and MHV-68 infection. Here, CD8A is linked to cytomegalovirus infection.