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鸡hnRNPK抑制干扰素产生,从而增强传染性法氏囊病病毒的复制。

Chicken hnRNPK suppresses interferon production, thereby enhancing IBDV replication.

作者信息

Wang Ke, Hu Ying, Nie Jiangjiang, Zeng Qinghua, Hu Yu, Wu Huansheng

机构信息

Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Zhimin Street, Qingshan Lake, Nanchang 330045, PR China.

Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Zhimin Street, Qingshan Lake, Nanchang 330045, PR China.

出版信息

Res Vet Sci. 2025 Mar;184:105527. doi: 10.1016/j.rvsc.2025.105527. Epub 2025 Jan 3.

Abstract

Heterogeneous ribonucleoprotein K (hnRNPK) is a well-known RNA-binding protein initially identified for its role in inhibiting the growth of various human tumors. Members of the hnRNP family have also been implicated in both interferon production and RNA virus replication. However, the role of chicken hnRNPK (chhnRNPK) in the replication of Infectious Bursal Disease Virus (IBDV) remains unclear. In this study, we identified chhnRNPK as a protein that interacts with genomic double-stranded RNA (dsRNA). Following IBDV infection, chhnRNPK was recruited to the virus replication complex in the cytoplasm. Furthermore, chhnRNPK expression inhibited dsRNA-induced interferon production, specifically at the mitochondrial antiviral signaling protein (MAVS) step. Overexpression of chhnRNPK significantly enhanced virus replication, while knockdown of chhnRNPK increased dsRNA-induced interferon production and subsequently disrupted IBDV replication. Collectively, these findings suggest that chhnRNPK promotes IBDV replication by interacting with genomic dsRNA, highlighting a novel host factor that regulates viral replication.

摘要

异质性核糖核蛋白K(hnRNPK)是一种著名的RNA结合蛋白,最初因其在抑制多种人类肿瘤生长中的作用而被发现。hnRNP家族的成员也与干扰素产生和RNA病毒复制有关。然而,鸡hnRNPK(chhnRNPK)在传染性法氏囊病病毒(IBDV)复制中的作用仍不清楚。在本研究中,我们鉴定出chhnRNPK是一种与基因组双链RNA(dsRNA)相互作用的蛋白。IBDV感染后,chhnRNPK被招募到细胞质中的病毒复制复合体。此外,chhnRNPK的表达抑制了dsRNA诱导的干扰素产生,特别是在线粒体抗病毒信号蛋白(MAVS)步骤。chhnRNPK的过表达显著增强了病毒复制,而chhnRNPK的敲低增加了dsRNA诱导的干扰素产生,并随后破坏了IBDV复制。总的来说,这些发现表明chhnRNPK通过与基因组dsRNA相互作用促进IBDV复制,突出了一种调节病毒复制的新型宿主因子。

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