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Front Microbiol. 2019 Oct 10;10:2344. doi: 10.3389/fmicb.2019.02344. eCollection 2019.

Transcriptome Profiling Reveals Differential Effect of Interleukin-17A Upon Influenza Virus Infection in Human Cells.

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CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China.
School of Dentistry, Philips Institute for Oral Health Research, Virginia Commonwealth University, Richmond, VA, United States.
MOE Joint International Research Laboratory of Animal Immunology, Nanjing Agricultural University, Nanjing, China.
MOA Key Laboratory of Animal Virology, Department of Veterinary Medicine, Zhejiang University, Hangzhou, China.


Influenza A virus (IAV) has developed elegant strategies to utilize cellular proteins and pathways to promote replication and evade the host antiviral response. Identification of these sabotaged host factors could increase the number of potential antiviral drug targets. Here, IAV A/PR/8/34 (PR8)- and A/California/04/2009-infected A549 and 293T cells displayed differential virus replication. To determine the host cellular responses of A549 and 293T cells to IAV infection, RNA-seq was used to identify differentially expressed genes. Our data revealed that IAV-infected A549 cells activated stronger virus-sensing signals and highly expressed cytokines, which play significant roles in initiating the innate immune and inflammatory responses. In addition, IAV-infected 293T cells displayed weak immune signaling and cytokine production. Remarkably, IL-17A and associated genes were highly enriched in IAV-infected 293T cells. Furthermore, IL-17A can partially facilitate A549 cell infection by the PR8 strain and PR8-infected IL-17A knock-out mice consistently exhibited decreased weight loss and reduced lung immunopathology, as compared to controls. This work uncovered the differential responses of cells infected with two H1N1 IAV strains and the potential roles of IL-17A in modulating virus infection.


H1N1 influenza virus; IL-17A; differential replication; human cells; transcriptome analysis

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