A novel avian origin A/H7N9 influenza virus causes high admissions rates (>99%) and mortality (>30%), with ultimately favorable outcomes ranging from rapid recovery to prolonged hospitalisation. The absence of pre-existing neutralizing antibodies specific for the novel A (H7N9) influenza virus indicates a lack of prior human exposure. As influenza A virus-specific CD8+ cytotoxic T lymphocytes (CTLs) can be broadly cross-reactive, we tested whether H7N9-infected cells might be recognized by memory CTLs established following infection with other influenza strains. Protective HLA alleles (A*0201, A*0301, B*5701, B*1801and B*0801) elicit robust CTL responses against any human influenza A virus, including H7N9, while ethnicities where HLA-A*0101, A*6801, B*1501 and A*2402 are prominent show limited CTL response profiles. By this criterion, some groups, especially the Alaskan and Australian Indigenous peoples, would be particularly vulnerable to H7N9 infection. Using a novel multi-colour assay for monitoring adaptive and innate immunity, we further dissected the kinetic emergence of different effector mechanisms across the spectrum of H7N9 disease and recovery, to find that a diversity of response mechanisms contribute to resolution and survival. Patients discharged within 2-3 weeks had an early peak in H7N9-specific CD8+ T-cell responses, while individuals with prolonged hospital stays had late recruitment of CD8+/CD4+ T cells and antibodies simultaneously (recover by week 4), augmented even later by prominent NK cell responses (recovery >30 days). In contrast, those who succumbed had minimal influenza-specific immunity and little evidence of T-cell activation. Our study illustrates the importance of robust CD8+ T-cell memory for protection against severe influenza disease caused by newly-emerging influenza A viruses.