State Key Laboratory of Veterinary Biotechnology, Heilongjiang Provincial Key Laboratory of Laboratory Animal and Comparative Medicine, Harbin Veterinary Research Institute, the Chinese Academy of Agriculture Sciences, 678 Haping Road, Harbin, 150069, PR China.
State Key Laboratory of Veterinary Biotechnology, Heilongjiang Provincial Key Laboratory of Laboratory Animal and Comparative Medicine, Harbin Veterinary Research Institute, the Chinese Academy of Agriculture Sciences, 678 Haping Road, Harbin, 150069, PR China.
Vet Microbiol. 2019 Mar;230:78-85. doi: 10.1016/j.vetmic.2019.01.014. Epub 2019 Jan 15.
Retinoic acid-inducible gene I (RIG-I) is a nucleic acid sensor that plays a key role in host antiviral defenses. Duck viral enteritis (DEV) is a DNA virus that causes significant economic losses to the poultry industry worldwide. Although RIG-I is known to be involved in a common antiviral signaling pathway triggered by RNA viruses, its role in DEV infection remains unclear. In this study, we demonstrated that DEV infection increased the expression levels of interferon β (IFN-β) and RIG-I in ducks both in vivo and in vitro. Furthermore, overexpression of duck RIG-I significantly upregulated the expression of interferon-stimulated genes, including myxovirus resistance protein (Mx), Interferon-induced oligodenylate synthetase-like (OASL) and IFN-β. We therefore used overexpression and knockdown methods to determine if RIG-I affected DEV infection in ducks. Viral infection was inhibited by RIG-I, and enhanced by knockdown of RIG-I expression using small interfering RNA. RIG-I overexpression also activated signal transducer and activator of transcription 1 (STAT1), as a member of the JAK-STAT family. The combined results following STAT1 knockdown and RIG-I overexpression suggested that the antiviral activity of RIG-I was STAT1-dependent. Overall, these findings indicate that RIG-I effectively restricts DEV replication and may play a vital role in the host immune response to DEV infection in ducks.
视黄酸诱导基因 I（RIG-I）是一种核酸传感器，在宿主抗病毒防御中发挥关键作用。鸭病毒性肠炎（DEV）是一种 DNA 病毒，它会给全球家禽业造成巨大的经济损失。尽管 RIG-I 已知参与了由 RNA 病毒触发的常见抗病毒信号通路，但它在 DEV 感染中的作用尚不清楚。在本研究中，我们证明 DEV 感染会在体内和体外增加鸭干扰素 β（IFN-β）和 RIG-I 的表达水平。此外，鸭 RIG-I 的过表达还显著上调了干扰素刺激基因的表达，包括抗粘病毒蛋白（Mx）、干扰素诱导寡核苷酸合成酶样（OASL）和 IFN-β。因此，我们使用过表达和敲低方法来确定 RIG-I 是否会影响鸭的 DEV 感染。RIG-I 抑制了病毒感染，而使用小干扰 RNA 敲低 RIG-I 表达则增强了病毒感染。RIG-I 的过表达还激活了信号转导和转录激活因子 1（STAT1），作为 JAK-STAT 家族的一员。在 STAT1 敲低和 RIG-I 过表达后联合观察到的结果表明，RIG-I 的抗病毒活性依赖于 STAT1。总的来说，这些发现表明 RIG-I 可有效抑制 DEV 的复制，并且在鸭对 DEV 感染的宿主免疫反应中可能发挥重要作用。
