Ma Jie, Xu Chen, Jiang Nan, Meng Yan, Zhou Yong, Xue Mingyang, Liu Wenzhi, Li Yiqun, Fan Yuding
Yangtze River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Wuhan 430223, China.
National Demonstration Center for Experimental Fisheries Science Education, Shanghai Ocean University, Shanghai 201306, China.
Animals (Basel). 2023 Jun 4;13(11):1870. doi: 10.3390/ani13111870.
Grass carp reovirus genotype Ⅱ (GCRV Ⅱ) causes a variety of fish hemorrhagic disease, which seriously affects the sustainable development of grass carp aquaculture in China. Rare minnow () is an ideal model fish to study the pathogenesis of GCRV Ⅱ. To investigate the involved molecular responses against the GCRV Ⅱ infection, we performed comparative transcriptomic analysis in the spleen and liver of rare minnow injected with virulent strain DY197 and attenuated strain QJ205. Results showed that the virulent DY197 strain induced more differently expressed genes (DEGs) than the attenuated QJ205 strain, and tissue-specific responses were induced. In the spleen, the attenuated and virulent strains induced different DEGs; the attenuated QJ205 infection activated steroid synthesis pathway that involved in membrane formation; however, virulent DY197 infection activated innate immunity and apoptosis related pathways while suppressing cell proliferation and migration related pathways that are important for damage tissue repair, as well as hemorrhage related pathways. In the liver, the attenuated and virulent strains infection induced similar DEGs; both strains infection activated immunity and apoptosis related pathways but suppressed metabolism-related pathways; virulent DY197 infection especially activated protein digestion and absorption-related pathways and suppressed steroid synthesis pathway. To conclude, virulent strain infection especially induced tissue-specific alterations and caused severe suppression of hemorrhage-related pathways in spleen. Our findings will contribute to better understanding of the interactions between host and GCRV II.
草鱼呼肠孤病毒Ⅱ型（GCRVⅡ）可引发多种鱼类出血性疾病，严重影响我国草鱼养殖业的可持续发展。稀有鮈鲫（）是研究GCRVⅡ发病机制的理想模式鱼类。为探究稀有鮈鲫针对GCRVⅡ感染的分子应答，我们对注射强毒株DY197和弱毒株QJ205的稀有鮈鲫的脾脏和肝脏进行了比较转录组分析。结果显示，强毒株DY197诱导产生的差异表达基因（DEGs）比弱毒株QJ205更多，且诱导了组织特异性应答。在脾脏中，弱毒株和强毒株诱导产生了不同的DEGs；弱毒株QJ205感染激活了参与膜形成的类固醇合成途径；然而，强毒株DY197感染激活了先天免疫和凋亡相关途径，同时抑制了对损伤组织修复很重要的细胞增殖和迁移相关途径以及出血相关途径。在肝脏中，弱毒株和强毒株感染诱导产生了相似的DEGs；两种毒株感染均激活了免疫和凋亡相关途径，但抑制了代谢相关途径；强毒株DY197感染尤其激活了蛋白质消化和吸收相关途径并抑制了类固醇合成途径。总之，强毒株感染尤其诱导了组织特异性改变，并导致脾脏中出血相关途径受到严重抑制。我们的研究结果将有助于更好地理解宿主与GCRV II之间的相互作用。
