Infectious Bronchitis Coronavirus Inhibits STAT1 Signaling and Requires Accessory Proteins for Resistance to Type I Interferon Activity
| Autor: | Jasmin Kutter, Geert F. Wiegertjes, Joeri Kint, Helena J. Maier, Jelke J. Fros, Gorben P. Pijlman, Joseph Koumans, Maria Forlenza, Annemiek Dickhout, Paul Britton |
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| Přispěvatelé: | Promovendi CD, Biochemie, RS: CARIM - R1 - Thrombosis and haemostasis |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
animal structures
Blotting Western Infectious bronchitis virus Immunology Laboratory of Virology Celbiologie en Immunologie Chick Embryo medicine.disease_cause Microbiology Laboratorium voor Virologie Interferon Virology Chlorocebus aethiops medicine Life Science Animals Humans Viral Regulatory and Accessory Proteins STAT1 Luciferases Vero Cells Cells Cultured DNA Primers Coronavirus Analysis of Variance Innate immune system biology PE&RC Immunohistochemistry Virus-Cell Interactions HEK293 Cells STAT1 Transcription Factor Cell Biology and Immunology Insect Science Interferon Type I embryonic structures WIAS biology.protein Vero cell Signal transduction Interferon type I Signal Transduction medicine.drug |
| Zdroj: | Journal of Virology Journal of Virology, 89(23), 12047-12057 Journal of Virology 89 (2015) 23 Journal of Virology, 89(23), 12047-12057. American Society for Microbiology |
| ISSN: | 0022-538X |
| DOI: | 10.1128/jvi.01057-15 |
| Popis: | 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. IMPORTANCE In the present study, we show that infectious bronchitis virus (IBV) is resistant to IFN treatment and identify a role for accessory protein 3a in the resistance against the type I IFN response. We also demonstrate that, in a time-dependent manner, IBV effectively interferes with IFN signaling and that its accessory proteins are dispensable for this activity. This study demonstrates that the gammacoronavirus IBV, similar to its mammalian counterparts, has evolved multiple strategies to efficiently counteract the IFN response of its avian host, and it identifies accessory protein 3a as multifaceted antagonist of the avian IFN system. |
| Databáze: | OpenAIRE |
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