Despite the fact that all classes of herpesviruses downregulate MHC I [61], licensed iKIR+ NK cells specifically expand in response to CMV infection in comparison to Epstein-Barr virus (EBV), Herpes simplex virus (HSV)-1, HSV-2, or Varicella zoster virus (VZV) infection [62], resulting in long-term CMV-associated imprints on the human KIR repertoire. Here, KIR3DL1 is linked to infection.