Comparative transcriptome analysis of rainbow trout gonadal cells (RTG-2) infected with U and J genogroup infectious hematopoietic necrosis virus
文献类型: 外文期刊
第一作者: Zhao, Jing-Zhuang
作者: Zhao, Jing-Zhuang;Teng, Chun-Bo;Zhao, Jing-Zhuang;Xu, Li-Ming;Ren, Guang-Ming;Shao, Yi-Zhi;Liu, Qi;Lu, Tong-Yan;Zhao, Jing-Zhuang
作者机构:
关键词: rainbow trout gonadal cells; infectious hematopoietic necrosis virus; transcriptome analysis (RNAseq); U genogroup; J genogroup
期刊名称:FRONTIERS IN MICROBIOLOGY ( 影响因子:5.2; 五年影响因子:6.2 )
ISSN:
年卷期: 2023 年 13 卷
页码:
收录情况: SCI
摘要: Infectious hematopoietic necrosis virus (IHNV) is the causative pathogen of infectious hematopoietic necrosis, outbreaks of which are responsible for significant losses in rainbow trout aquaculture. Strains of IHNV isolated worldwide have been classified into five major genogroups, J, E, L, M, and U. To date, comparative transcriptomic analysis has only been conducted individually for the J and M genogroups. In this study, we compared the transcriptome profiles in U genogroup and J genogroup IHNV-infected RTG-2 cells with mock-infected RTG-2 cells. The RNA-seq results revealed 17,064 new genes, of which 7,390 genes were functionally annotated. Differentially expressed gene (DEG) analysis between U and J IHNV-infected cells revealed 2,238 DEGs, including 1,011 downregulated genes and 1,227 upregulated genes. Among the 2,238 DEGs, 345 new genes were discovered. The DEGs related to immune responses, cellular signal transduction, and viral diseases were further analyzed. RT-qPCR validation confirmed that the changes in expression of the immune response-related genes trpm2, sting, itgb7, ripk2, and irf1, cellular signal transduction-related genes irl, cacnb2, bmp2l, gadd45 alpha, and plk2, and viral disease-related genes mlf1, mtor, armc5, pik3r1, and c-myc were consistent with the results of transcriptome analysis. Taken together, our findings provide a comprehensive transcriptional analysis of the differential virulence of the U and J genogroups of IHNV, and shed new light on the pathogenic mechanisms of IHNV strains.
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