Duck enteritis virus (DEV) can successfully evade the host innate immune responses and establish a lifelong latent infection in the infected host. However, the study about how DEV escapes host innate immunity is still deficient up to now. In this study, for the first time, we identified a viral protein VP16 by which DEV can obviously downregulate the production of IFN-β in duck embryo fibroblast (DEF). Our results showed that ectopic expression of VP16 decreased duck IFN-β (duIFN-β) promoter activation and significantly inhibited the mRNA transcription of IFN-β. Further study showed that VP16 can also obviously inhibit the mRNA transcription of interferon-stimulated genes (ISGs), such as myxovirus resistance protein (Mx) and interferon-induced oligoadenylate synthetase-like (OASL). Furthermore, we found that this anti-interferon activity of VP16 depended on its N-terminus (aa1-200). Coexpression analysis revealed that VP16 selectively blocked duIFN-β promoter activity at the duIRF7 level rather than duIRF1. Based on the results of coimmunoprecipitation analysis (co-IP) and indirect immunofluorescence assay (IFA), VP16 was able to bind to duck IRF7 (duIRF7) directly, but did not interact with duck IRF1 (duIRF1) in vitro.

中文翻译：

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鸭肠炎病毒VP16拮抗IFN-β介导的抗病毒先天免疫力。

鸭肠炎病毒（DEV）可以成功规避宿主的先天免疫反应，并在受感染的宿主中建立终身潜伏感染。但是，到目前为止，关于DEV如何逃避宿主固有免疫的研究仍然缺乏。在本研究中，我们首次鉴定了一种病毒蛋白VP16，DEV可通过该蛋白明显下调鸭胚胎成纤维细胞（DEF）中IFN- β的产生。我们的研究结果表明，异位表达VP16可降低鸭IFN- β（duIFN - β）启动子的激活，并显着抑制IFN- β的mRNA转录。。进一步的研究表明，VP16还可以明显抑制干扰素刺激基因（ISG）的mRNA转录，例如粘液病毒抗性蛋白（Mx）和干扰素诱导的寡腺苷酸合成酶样（OASL）。此外，我们发现VP16的这种抗干扰素活性取决于其N末端（aa1-200）。共表达分析表明，VP16在duIRF7水平而非duIRF1选择性地阻断了duIFN- β启动子的活性。根据免疫共沉淀分析（co-IP）和间接免疫荧光分析（IFA）的结果，VP16能够直接结合鸭IRF7（duIRF7），但在体外不与鸭IRF1（duIRF1）相互作用。