Abstract
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.
Highlights
Influenza A virus (IAV) poses a substantial threat to human health in the forms of seasonal epidemics and occasional pandemics (Reperant et al, 2014)
The innate immune system initiates host defenses against IAV infection, which is triggered by pattern recognition receptors (PRRs) that recognize viruses or their genetic material (Kawai and Akira, 2006; Wilkins and Gale, 2010)
We explored the impact of IL-17A stimulation on the expression of inflammatory response genes during IAV infection of A549 cells
Summary
Influenza A virus (IAV) poses a substantial threat to human health in the forms of seasonal epidemics and occasional pandemics (Reperant et al, 2014). The innate immune system initiates host defenses against IAV infection, which is triggered by pattern recognition receptors (PRRs) that recognize viruses or their genetic material (Kawai and Akira, 2006; Wilkins and Gale, 2010). This recognition results in appropriate antiviral responses, Differential Response to H1N1 Infection including the production of a variety of cytokines and the induction of inflammatory and adaptive immune responses (Yoneyama and Fujita, 2010). The molecular mechanisms underlying the balance between protective and pathological immune responses against IAV infection remain unclear
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