ICAR-National Bureau of Fish Genetic Resources, Canal Ring Road, P.O. Dilkusha, Lucknow, 226002, Uttar Pradesh, India.
ICAR-Central Institute of Fisheries Education, Versova, Andheri (W), Mumbai, 400 061, Maharashtra, India.
Fish Shellfish Immunol. 2021 Apr;111:208-219. doi: 10.1016/j.fsi.2021.02.005. Epub 2021 Feb 10.
Nile tilapia (Oreochromis niloticus) is one of the most important aquaculture species farmed worldwide. However, the recent emergence of tilapia lake virus (TiLV) disease, also known as syncytial hepatitis of tilapia, has threatened the global tilapia industry. To gain more insight regarding the host response against the disease, the transcriptional profiles of liver in experimentally-infected and control tilapia were compared. Analysis of RNA-Seq data identified 4640 differentially expressed genes (DEGs), which were involved among others in antigen processing and presentation, MAPK, apoptosis, necroptosis, chemokine signaling, interferon, NF-kB, acute phase response and JAK-STAT pathways. Enhanced expression of most of the DEGs in the above pathways suggests an attempt by tilapia to resist TiLV infection. However, upregulation of some of the key genes such as BCL2L1 in apoptosis pathway; NFKBIA in NF-kB pathway; TRFC in acute phase response; and SOCS, EPOR, PI3K and AKT in JAK-STAT pathway and downregulation of the genes, namely MAP3K7 in MAPK pathway; IFIT1 in interferon; and TRIM25 in NF-kB pathway suggested that TiLV was able to subvert the host immune response to successfully establish the infection. The study offers novel insights into the cellular functions that are affected following TiLV infection and will serve as a valuable genomic resource towards our understanding of susceptibility of tilapia to TiLV infection.
尼罗罗非鱼（Oreochromis niloticus）是全球最重要的水产养殖物种之一。然而，最近出现的罗非鱼湖病毒（TiLV）病，也称为罗非鱼合胞体肝炎，已经威胁到了全球罗非鱼产业。为了更深入地了解宿主对这种疾病的反应，我们比较了实验感染和对照罗非鱼肝组织的转录谱。RNA-Seq 数据分析鉴定了 4640 个差异表达基因（DEGs），这些基因参与抗原加工和呈递、MAPK、凋亡、坏死性凋亡、趋化因子信号转导、干扰素、NF-kB、急性期反应和 JAK-STAT 途径等。上述途径中大多数 DEGs 的表达增强表明罗非鱼试图抵抗 TiLV 感染。然而，一些关键基因的上调，如凋亡途径中的 BCL2L1；NF-kB 途径中的 NFKBIA；急性期反应中的 TRFC；以及 JAK-STAT 途径中的 SOCS、EPOR、PI3K 和 AKT，以及 MAPK 途径中的 MAP3K7；干扰素中的 IFIT1；和 NF-kB 途径中的 TRIM25 的下调表明，TiLV 能够颠覆宿主免疫反应，成功建立感染。该研究为 TiLV 感染后受影响的细胞功能提供了新的见解，并为我们理解罗非鱼对 TiLV 感染的易感性提供了有价值的基因组资源。
