|Title||Infectious bronchitis coronavirus inhibits STAT1 signaling and requires accessory proteins for resistance to type I interferon activity|
|Author(s)||Kint, Joeri; Dickhout, Annemiek; Kutter, Jasmin; Maier, H.J.; Britton, Paul; Koumans, Joseph; Pijlman, G.P.; Fros, J.J.; Wiegertjes, G.F.; Forlenza, Maria|
|Source||Journal of Virology 89 (2015)23. - ISSN 0022-538X - p. 12047 - 12057.|
Cell Biology and Immunology
Laboratory of Virology
|Publication type||Refereed Article in a scientific journal|
The innate immune response is the first line of defense against viruses, and type I interferon (IFN) is a critical component of this response. Similar to other viruses, the gammacoronavirus infectious bronchitis virus (IBV) has evolved under evolutionary pressure to evade and counteract the IFN response to enable its survival. Previously, we reported that IBV induces a delayed activation of the IFN response. In the present work, we describe the resistance of IBV to IFN and the potential role of accessory proteins herein. We show that IBV is fairly resistant to the antiviral state induced by IFN and identify that viral accessory protein 3a is involved in resistance to IFN, as its absence renders IBV less resistant to IFN treatment. In addition to this, we found that independently of its accessory proteins, IBV inhibits IFN-mediated phosphorylation and translocation of STAT1. In summary, we show that IBV uses multiple strategies to counteract the IFN response.