Department of Aquatic Animal Medicine, College of Fisheries, Hubei Provincial Engineering Laboratory for Pond Aquaculture, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei, 430070, China; Guangzhou Key Laboratory of Aquatic Animal Diseases and Waterfowl Breeding, Guangdong Provincial Key Laboratory of Waterfowl Healthy Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangzhou, Guangdong, 510225, China.
Department of Aquatic Animal Medicine, College of Fisheries, Hubei Provincial Engineering Laboratory for Pond Aquaculture, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei, 430070, China; School of Animal Sciences and Nutritional Engineering, Wuhan Polytechnic University, Wuhan, Hubei, 430023, China.
Fish Shellfish Immunol. 2017 Dec;71:58-68. doi: 10.1016/j.fsi.2017.09.070. Epub 2017 Sep 29.
The channel catfish virus (CCV) can cause lethal hemorrhagic infection in juvenile channel catfish, thereby resulting in a huge economic loss to the fish industry. The genome of the CCV has been fully sequenced, and its prevalence is well documented. However, less is known about the molecular mechanisms and pathogenesis of the CCV. Herein, the channel catfish ovary cells (CCO) were infected with CCV and their transcriptomic sketches were analyzed using an RNA sequencing technique. In total, 72,686,438 clean reads were obtained from 73,231,128 sequence reads, which were further grouped into 747,168 contigs. These contigs were assembled into 49,119 unigenes, of which 20,912 and 18,333 unigenes were found in Nr and SwissProt databases and matched 15,911 and 14,625 distinctive proteins, respectively. From these, 3641 differentially expressed genes (DEGs), comprising 260 up-regulated and 3381 down-regulated genes, were found compared with the control (non-infected) cells. For verification, 16 DEGs were analyzed using qRT-PCR. The analysis of the DEGs and their related cellular signaling pathways revealed a substantial number of DEGs that were involved in the apoptosis pathway induced by CCV infection. The apoptosis pathways were further elucidated using standard apoptosis assays. The results showed that CCV could induce extrinsic apoptosis pathway (instead of a mitochondrial intrinsic apoptosis pathway) in CCO cells. This study helps our understanding of the pathogenesis of CCV and contributes to the prevention of CCV infection in channel catfish.
斑点叉尾鮰病毒(CCV)可引起幼龄斑点叉尾鮰的致命性出血性感染,从而给鱼类养殖业造成巨大的经济损失。CCV 的基因组已被完全测序,其流行情况已有详细记录。然而,对于 CCV 的分子机制和发病机制知之甚少。在此,使用 RNA 测序技术分析了 CCV 感染的斑点叉尾鮰卵巢细胞(CCO)的转录组草图。从 73,231,128 个序列读取中,共获得了 72,686,438 个清洁读取,进一步将其分为 747,168 个 contigs。这些 contigs 组装成 49,119 个 unigenes,其中 20,912 和 18,333 个 unigenes分别在 Nr 和 SwissProt 数据库中被找到,并分别匹配了 15,911 和 14,625 个独特的蛋白质。其中,与对照组(未感染)细胞相比,发现了 3641 个差异表达基因(DEGs),包括 260 个上调基因和 3381 个下调基因。为了验证,使用 qRT-PCR 分析了 16 个 DEGs。对 DEGs 及其相关细胞信号通路的分析表明,大量 DEGs 参与了 CCV 感染诱导的细胞凋亡途径。使用标准的细胞凋亡检测进一步阐明了凋亡途径。结果表明,CCV 可以在 CCO 细胞中诱导细胞外凋亡途径(而不是线粒体内在的凋亡途径)。这项研究有助于我们了解 CCV 的发病机制,并有助于预防斑点叉尾鮰感染 CCV。