shown). Similarly, the majority ($90%) of CD8 + T cells elicited by HKNPN3A infection bound the D b NP 366 tetramer and produced IFN-c (data not shown) at levels equivalent to those seen for the response to NPN3A, indicating a high level of cross-reactivity between the D b NP 366 + CD8 + and NPN3A + CD8 + T cell responses. Staining with the D b PA 224 tetramer was included to establish that the NPN3A mutation neither diminished nor enhanced other influenza-specific CD8 + T cell responses (Fig 2) .