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Reduced inflammatory response and promoted multiciliated cell differentiation in mice protected by defective interfering influenza virus

Chang Wang, Rebekah Honce, Mirella Salvatore, Jianjun Yang, Nicholas M. Twells, Lara K. Mahal, View ORCID ProfileStacey Schultz-Cherry, View ORCID ProfileElodie Ghedin
doi: https://doi.org/10.1101/2022.01.25.477719
Chang Wang
1Center for Genomics and Systems Biology, Department of Biology, New York University, New York, NY
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Rebekah Honce
2Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN
3Integrated Program in Biomedical Sciences, Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, TN
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Mirella Salvatore
4Department of Medicine, Weill Cornell Medical College, New York, NY
5Department of Population Health Sciences, Weill Cornell Medical College, New York, NY
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Jianjun Yang
4Department of Medicine, Weill Cornell Medical College, New York, NY
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Nicholas M. Twells
6Department of Chemistry, University of Alberta, Edmonton, AB, CANADA
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Lara K. Mahal
6Department of Chemistry, University of Alberta, Edmonton, AB, CANADA
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Stacey Schultz-Cherry
2Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN
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Elodie Ghedin
1Center for Genomics and Systems Biology, Department of Biology, New York University, New York, NY
7Systems Genomics Section, Laboratory of Parasitic Diseases, NIAID, National Institutes of Health, Bethesda, MD
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  • ORCID record for Elodie Ghedin
  • For correspondence: elodie.ghedin@nih.gov
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ABSTRACT

Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and to induce antiviral immunity. However, the mechanisms underlying DI-mediated antiviral immunity have not been extensively explored. Here, we demonstrated interferon (IFN) independent protection conferred by influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. By integrating transcriptional and post-transcriptional regulatory data we identified unique host signatures in response to DI co-infection. DI-treated mice exhibited reduced viral transcription, less intense inflammatory and innate immune responses, and primed multiciliated cell differentiation in their lungs at an early stage of infection, even in the absence of type I or III IFNs. Overall, our study provides mechanistic insight into the protection mediated by DIs, implying a unifying theme involving inflammation and multiciliogenesis in maintaining respiratory homeostasis, and reveals their IFN-independent antiviral activity.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. This article is a US Government work. It is not subject to copyright under 17 USC 105 and is also made available for use under a CC0 license.
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Posted January 25, 2022.
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Reduced inflammatory response and promoted multiciliated cell differentiation in mice protected by defective interfering influenza virus
Chang Wang, Rebekah Honce, Mirella Salvatore, Jianjun Yang, Nicholas M. Twells, Lara K. Mahal, Stacey Schultz-Cherry, Elodie Ghedin
bioRxiv 2022.01.25.477719; doi: https://doi.org/10.1101/2022.01.25.477719
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Reduced inflammatory response and promoted multiciliated cell differentiation in mice protected by defective interfering influenza virus
Chang Wang, Rebekah Honce, Mirella Salvatore, Jianjun Yang, Nicholas M. Twells, Lara K. Mahal, Stacey Schultz-Cherry, Elodie Ghedin
bioRxiv 2022.01.25.477719; doi: https://doi.org/10.1101/2022.01.25.477719

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