中文摘要：

鸟的传染支气管炎病毒(IBV ) 是在家庭 Coronaviridae 的 Gammacoronavirus 并且在鸡引起高度传染的呼吸疾病。天生的免疫对 IBV 在主人防卫起重要作用。这里，我们探索了在 IBV 和主人之间的相互作用天生的免疫系统。严重组织病理学说的损害分别地在 8 dpi 在 3-5 天驿站接种(dpi ) 并且在肾在气管的 mucosa 被观察，与在 1-11 和 1-28 dpi 的重病毒的精液。编码像使用费的受体(TLR ) 的 mRNAs 的表示 3 并且 TLR7 是在 3-8 dpi 的 upregulated，并且 TIR-domain-containing 导致改编者的干扰素(IFN )(TRIF ) 的是在在气管和肾的 21 dpi 的 upregulated。Myeloid 区别(MyD88 ) 主要反应蛋白质 88 在早感染期间是在气管的 upregulated。肿瘤坏死因素联系受体的因素(TRAF ) 3 并且 TRAF6 是在两件织物的 upregulated 表示。而且，黑瘤联系区别的蛋白质 5 ( MDA5 )，遗传和生理学的实验室 2 ( LGP2 )， IFN 基因(圈套)的激发器，和 mitochondrial 抗病毒的发信号蛋白质( MAVS )，以及坦克有约束力的 kinase 1 ( TBK1 )， kappaB kinase ( IKK )的禁止者， IKK ， IKK ， IFN 规章的因素( IRF ) 7 ， kappaB ( NF-B )的原子因素，IFN-，IFN-，各种各样的 interleukins ( IL )，和煽动性的 protein-1 ( MIP-1 )是的巨噬细胞显著地在气管的 upregulated 和在 kidne 的 downregulated 这些结果建议表明小径和天生的有免疫力的 cytokine 的 TLR 和 MDA5 在 IBV 感染以后被导致。另外，对 IBV 感染的一致回答在早感染期间被观察，与在肾的微分、复杂的回答。

英文摘要：

Avian infectious bronchitis virus（IBV） is a Gammacoronavirus in the family Coronaviridae and causes highly contagious respiratory disease in chickens. Innate immunity plays significant roles in host defense against IBV. Here, we explored the interaction between IBV and the host innate immune system. Severe histopathological lesions were observed in the tracheal mucosa at 3–5days post inoculation（dpi） and in the kidney at 8 dpi, with heavy viral loads at 1–11 and 1–28 dpi,respectively. The expression of m RNAs encoding Toll-like receptor（TLR） 3 and TLR7 were upregulated at 3–8 dpi, and that of TIR-domain-containing adapter-inducing interferon（IFN） β（TRIF） was upregulated at 21 dpi in the trachea and kidney. Myeloid differentiation primary response protein 88（My D88） was upregulated in the trachea during early infection. Tumor necrosis factor receptor-associated factor（TRAF） 3 and TRAF6 were upregulated expression in both tissues.Moreover, melanoma differentiation-associated protein 5（MDA5）, laboratory of genetics and physiology 2（LGP2）, stimulator of IFN genes（STING）, and mitochondrial antiviral signaling protein（MAVS）, as well as TANK binding kinase 1（TBK1）, inhibitor of kappa B kinase（IKK） ？, IKKα, IKKβ,IFN regulatory factor（IRF） 7, nuclear factor of kappa B（NF-κB）, IFN-α, IFN-β, various interleukins（ILs）, and macrophage inflammatory protein-1β（MIP-1β） were significantly upregulated in the trachea and downregulated in the kidney. These results suggested that the TLR and MDA5 signaling pathways and innate immune cytokine were induced after IBV infection. Additionally,consistent responses to IBV infection were observed during early infection, with differential and complicated responses in the kidney.