Pathogenicity of duck hepatitis A virus type 3 and innate immune responses of the ducklings to virulent DHAV-3
Pathogenicity of duck hepatitis A virus type 3 and innate immune responses of the ducklings to virulent DHAV-3
复制标题
鸭甲型肝炎3型病毒的致病性及雏鸭对强毒DHAV-3的先天免疫反应
DOI：
10.1016/j.molimm.2018.01.007
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发表时间：
2018-03-01
影响因子：
3.6
通讯作者：
Ma, Bo
中科院分区：
文献类型：
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作者：
Zhang, Xuelian;Cao, Chong;Ma, Bo
鸭病毒性肝炎是由鸭甲型肝炎病毒（DHAV）引起的一种急性、接触性传染病。为了更好地了解DHAV-3在雏鸭体内的致病机制，进行了感染实验。我们的结果表明，在受感染的雏鸭中观察到了典型的症状。 DHAV-3可以感染多种组织，导致病理病变，尤其是肝脏和脾脏，感染时宿主免疫反应被激活。实时定量PCR表明，许多先天免疫相关基因的表达大多在肝脏和脾脏中上调，并建立了抗病毒先天免疫反应，但不足以限制致死剂量的病毒复制。许多主要模式识别受体 (PRR)（RIG-1、MDA5 和 TLR7）参与宿主对 DHAV-3 的免疫反应，并且肝脏和脾脏中干扰素（IFN α、IFN β 和 IFN γ）和抗病毒蛋白（MX、OAS 和 PKR）的表达也上调。大多数细胞因子（IL-1β、IL-2和IL-6）的表达也有不同程度的上调，且表达量不等；肝脏中IL-2的表达增加最为显着。我们的数据为进一步研究鸭病毒性肝炎的致病性提供了基础，并扩展了我们对鸭子对DHAV-3感染的免疫反应的理解。
Duck virus hepatitis caused by duck hepatitis A virus (DHAV) is an acute and contagious disease. To better understand the pathogenic mechanism of DHAV-3 in ducklings, an infection experiment was performed. Our results showed that typical symptoms were observed in the infected ducklings. DHAV-3 could infect many tissues, leading to pathological lesions, especially on the livers and spleen, and the host immune responses are activated in infection. Real-time quantitative PCR demonstrated that expression of many innate immune-related genes was mostly up-regulated in the livers and spleen, and antiviral innate immune response was established, but not sufficient to restrict the virus replication of lethal dose. Many major pattern recognition receptors (PRRs) (RIG-1, MDA5, and TLR7) are involved in the host immune response to DHAV-3, and the expression of interferon (IFN alpha, IFN beta and IFN gamma) and antiviral proteins (MX, OAS and PKR) are also up-regulated in the liver and spleen. The expression of most cytokines (IL-1 beta, IL-2 and IL-6) was also up-regulated to different degrees and was various; the expression of IL-2 increased most significantly in liver. Our data provide a foundation for further study of the pathogenicity of duck virus hepatitis and extend our understanding of the immune responses of ducklings to DHAV-3 infection.