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- Title
Influenza A virus abrogates IFN-γ response in respiratory epithelial cells by disruption of the Jak/Stat pathway.
- Authors
Uetani, Kohsaku; Hiroi, Miki; Meguro, Tadamichi; Ogawa, Hiroshi; Kamisako, Toshinori; Ohmori, Yoshihiro; Erzurum, Serpil C.
- Abstract
The innate immunity to viral infections induces a potent antiviral response mediated by interferons (IFN). Although IFN-γ is detected during the acute stages of illness in the upper respiratory tract secretions and in the serum of influenza A virus-infected individuals, control of influenza A virus is not dependent upon IFN-γ as evidenced by studies using anti-IFN-γ Ab and IFN-γ mice. Thus, we hypothesized that IFN-γ is not critical in host survival because influenza A virus has mechanisms to evade the antiviral activity of IFN-γ. To test this, A549 cells, an epithelial cell line derived from lung adenocarcinoma, were infected with influenza virus strain A/Aichi/2/68 (H3N2) (Aichi) and/or stimulated with IFN-γ to detect IFN-γ-stimulated MHC class II expression. Influenza A virus infection inhibited IFN-γ-induced up-regulation of HLA-DRα mRNA and the IFN-γ induction of class II transactivator (CIITA), an obligate mediator of MHC class II expression. Nuclear translocation of Stat1α upon IFN-γ stimulation was significantly inhibited in influenza A virus-infected cells and this was associated with a decrease in Tyr701 and Ser727 phosphorylation of Stat1α. Thus, influenza A virus subverts antiviral host defense mediated by IFN-γ through effects on the intracellular signaling pathways.
- Publication
European Journal of Immunology, 2008, Vol 38, Issue 6, p1559
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.200737045