Induction and suppression of type I interferon responses by mink enteritis virus in CRFK cells

•MEV neither induced nor was sensitive to the effects of type I interferon.•The nonstructural protein (NS1) of MEV inhibits IFN induction.•The ORI-binding domain of NS1 protein suppresses IFNβ expression. Mink enteritis virus (MEV) is one of the most important viral pathogens causing serious disease...

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Veröffentlicht in:Veterinary microbiology 2017-02, Vol.199, p.8-14
Hauptverfasser: Zhang, Xiaomei, Wang, Jigui, Mao, Yaping, Xi, Ji, Yu, Yongle, Liu, Weiquan
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Sprache:eng
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Zusammenfassung:•MEV neither induced nor was sensitive to the effects of type I interferon.•The nonstructural protein (NS1) of MEV inhibits IFN induction.•The ORI-binding domain of NS1 protein suppresses IFNβ expression. Mink enteritis virus (MEV) is one of the most important viral pathogens causing serious disease in mink. Type I interferon (IFN) plays a critical role in antiviral innate immunity and, for successful infection, many viruses have evolved evasive strategies against it. Here, we show that MEV infection does not evoke IFN or interferon-stimulated genes (ISGs) responses in feline kidney (CRFK) cells, and that MEV suppresses IFN production in both poly I:C-stimulated and untreated cells. In CRFK cells pre-exposure to IFN, show that infection with, and replication of, MEV remain unaffected. This inhibition appears to be mediated by the MEV nonstructural protein (NS1) with its ORI-binding domain playing a major role.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2016.12.002