Expression of the viral virulence protein PB1-F2 during infection has been linked to NLRP3-inflammasome complex activation in macrophages and induction of early inflammatory events enhancing immunopathology during influenza disease. We sought to determine whether PB1-F2-specific NLRP3-inflammasome activation influenced the magnitude and/or robustness of the CD8(+) T cell responses specific for conserved viral antigens and subsequent virus elimination. Using murine heterosubtypic viral infection models we showed that mice infected with virus unable to produce PB1-F2 protein showed no deficit in the overall magnitude and functional memory responses of CD8(+) T cells established during the effector phase compared to those infected with wild-type PB1-F2-expressing virus and were equally capable of mounting robust recall responses. These data indicate that while expression of PB1-F2 protein can induce inflammatory events, the capacity to generate memory CD8(+) T cells specific for immunodominant viral epitopes remains uncompromised.Immunology and Cell Biology accepted article preview online, 15 December 2015. doi:10.1038/icb.2015.115.