Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms7833
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Funding
- NSFC [81471556, 81470094, 81430030]
- Program for Emergency Response to H7N9 Outbreak [2013QLG003]
- Shanghai Municipal Commission of Health and Family Planning
- 973 National Key Basic Research Project [2014CB542502]
- Ministry of Science and Technology of China
- NHMRC Program Grant [GNT567122]
- ACSRF Group Mission [16621]
- University of Melbourne IRRTF Grants
- University of Melbourne International Research Scholarship
- CONACyT Scholar
- NHMRC
- Australian Heart Foundation Career Development Fellowship [1061435]
- NIH grant [AI107625]
- St Jude Center of Excellence for Influenza Research and Surveillance [HHSN272201400006C]
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The avian origin A/H7N9 influenza virus causes high admission rates (>99%) and mortality (>30%), with ultimately favourable outcomes ranging from rapid recovery to prolonged hospitalization. Using a multicolour assay for monitoring adaptive and innate immunity, here we dissect the kinetic emergence of different effector mechanisms across the spectrum of H7N9 disease and recovery. We find that a diversity of response mechanisms contribute to resolution and survival. Patients discharged within 2-3 weeks have early prominent H7N9-specific CD8(+) T-cell responses, while individuals with prolonged hospital stays have late recruitment of CD8(+)/CD4(+) T cells and antibodies simultaneously (recovery by week 4), augmented even later by prominent NK cell responses (recovery >30 days). In contrast, those who succumbed have 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.
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