NK cells expand following primary EBV infection with killing of infected cells being associated with a downregulation of MHC class I and upregulation of NKG2D ligand (ULBP-1) and other costimulatory molecules (e.g., CD70) on infected cells in the viral lytic stage and the resulting shift in the NK cell signals from inactive to active [17]. This evidence concerns the gene ULBP1 and Epstein-Barr virus infection.