KIR3DL1 and Epstein-Barr virus infection: These results confirmed and extended a previous study in a humanized mouse model in which EBV infection induced expansion of NKG2A+KIR− NK cells with antiviral activity before initiation of CD8 T-cell responses; most importantly, upon depletion of NK cells, infected mice showed higher viral titers, more severe IM symptoms (e.g., lymphocytosis, high INF-γ levels), and higher incidence of EBV-induced malignancies, indicating that early differentiated NK cells crucially restrict EBV infection and prevent disease progression [61].