Transcriptome analysis reveals the host immune response upon LMBV infection in largemouth bass (Micropterus salmoides)

Largemouth bass (Micropterus salmoides) is one of the important economical freshwater aquaculture species in China. However, the outbreak of viral diseases always caused great economic losses in the largemouth bass aquaculture industry. Largemouth bass virus (LMBV), a double-stranded DNA (dsDNA) virus belonging to genus Ranavirus, family Iridoviridae causes high mortality in cultivated largemouth bass. However, host responses, especially the molecular events involved in LMBV infection still remained largely uncertain. Here, we established an in vivo model of LMBV infection, and systematically investigated the mRNA expression profiles of host genes in liver and spleen from infected largemouth bass using RNA sequencing (RNA-seq). Histopathological analysis indicated that necrotic cells and the formed necrotic focus were present in spleen, while numerous basophilic cells, hepatocytes volume shrinkage, nucleus pyknosis, and the disappeared boundary of hepatocytes were observed in the liver of infected largemouth bass. Transcriptomic analysis showed that transcription levels of 5128 genes (2804 up-regulated genes and 2324 down-regulated) in liver and 7008 genes (2603 up-regulated and 4405 down-regulated) in spleen were altered significantly. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that numerous co-regulated differentially expressed genes (DEGs) in liver and spleen were enriched in the pathways related to cell death and immune signaling, such as apoptosis, necroptosis, cytokine-cytokine receptor interaction and JAK-STAT signaling. Moreover, the DEGs specially regulated by LMBV infection in liver were significantly enriched in the KEGG pathways related to metabolism and cell death, while those in spleen were enriched in the immune related pathways. In addition, the expression changes of several randomly selected genes, such as SOCS1, IL-6, CXCL2, CASP8, CYC and TNF from qPCR were consistent with the transcriptomic data. Taken together, our findings will provide new insights into the fundamental patterns of molecular responses induced by LMBV in vivo, but also contribute greatly to understanding the host defense mechanisms against iridoviral pathogens.