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J Exp Med. 2014 Aug 25;211(9):1707-14. doi: 10.1084/jem.20140488. Epub 2014 Aug 18.

Long-term survival of influenza virus infected club cells drives immunopathology.

Author information

1
Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
2
Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029 Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
3
Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029 peter.palese@mssm.edu benjamin.tenOever@mssm.edu.
4
Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029 Department of Microbiology, Global Health and Emerging Pathogens Institute, and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029 peter.palese@mssm.edu benjamin.tenOever@mssm.edu.

Abstract

Respiratory infection of influenza A virus (IAV) is frequently characterized by extensive immunopathology and proinflammatory signaling that can persist after virus clearance. In this report, we identify cells that become infected, but survive, acute influenza virus infection. We demonstrate that these cells, known as club cells, elicit a robust transcriptional response to virus infection, show increased interferon stimulation, and induce high levels of proinflammatory cytokines after successful viral clearance. Specific depletion of these surviving cells leads to a reduction in lung tissue damage associated with IAV infection. We propose a model in which infected, surviving club cells establish a proinflammatory environment aimed at controlling virus levels, but at the same time contribute to lung pathology.

PMID:
25135297
PMCID:
PMC4144728
DOI:
10.1084/jem.20140488
[Indexed for MEDLINE]
Free PMC Article

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