Taken together, our data support a model for generation of memory-like NK cells by influenza virus involving upregulation of CD25 by virus-induced IFN-α; selective, IL-2–driven expansion of less differentiated (CD57−) NK cells; rapid and enhanced responsiveness of these cells to subsequent cytokine stimulation; and, in the absence of further boosting or infection, a resting or reversion phase (Supplemental Fig. 4). Here, B3GAT1 is linked to infection.