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            <funder>Supported by National Center for Research Resources and National Center for Advancing Translational Sciences grant 8UL1TR000043; NIH grants 5R01NS072381 (J.-L.C. and L.D.N.), 5R01AI100887 (L.D.N.), and 1U19AI109945 (C.F.B.); the Rockefeller University, the St. Giles Foundation, the French National Research Agency under the “Investments for the Future” program grant ANR-10-IAHU-01, the Laboratoire d’Excellence Integrative Biology of Emerging Infectious Diseases (ANR-10-LABX-62-IBEID), INSERM, Paris Descartes University, and ERC grant 2010-StG‐261299 (F.G.); and Center for Research on Influenza Pathogenesis and the NIAID-funded Center of Excellence for Influenza Research and Surveillance contract HHSN272201400008C (A.G.-S.)</funder>
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              <p>Severe influenza disease strikes otherwise healthy children and remains unexplained. We report compound heterozygous null mutations in IRF7, which encodes the transcription factor interferon regulatory factor 7, in an otherwise healthy child who suffered life-threatening influenza during primary infection. In response to influenza virus, the patient's leukocytes and plasmacytoid dendritic cells produced very little type I and III interferons (IFNs). Moreover, the patient's dermal fibroblasts and induced pluripotent stem cell (iPSC)-derived pulmonary epithelial cells produced reduced amounts of type I IFN and displayed increased influenza virus replication. These findings suggest that IRF7-dependent amplification of type I and III IFNs is required for protection against primary infection by influenza virus in humans. They also show that severe influenza may result from single-gene inborn errors of immunity.</p>
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          <desc>Institut Hospitalo-Universitaire Imagine</desc>
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