To test whether this local reduction in NK cells impairs the control of viral replication, we performed plaque assays on control-and anti-IL-15 treated mice to quantify viral load in the lungs of animals with intact or diminished IL-15 and NK cell responses. Viral load was quantified on days 1-5 and 7-8 p.i. to specifically look at control during the time frame of NK cell entry and accumulation in the lung airways and the kinetics of subsequent viral clearance. In IL-15 blocked animals, differences in viral load were apparent as early as d2 p.i. where viral titers were about 36 higher through day 3 p.i. ( Figure 2E) ; however, these animals seemed to regain control of viral replication by day 4 p.i., which perhaps corresponds with the early entry of cells of the adaptive immune response as anti-influenza specific CD8 T cells are first detectable in the lung airways by d6 post infection by flow cytometry ( [34] and data not shown). Thus, while viral elimination is not ultimately dependent on IL-15, early control of the virus is impaired in the absence of IL-15, which correlates with the arrival of a significant number of NK cells in the lung airways. We thus hypothesized that IL-15 was important for the migration of NK cells in the lung airways following influenza infection.