Infectious spleen and kidney necrosis virus (ISKNV) has caused significant economic losses in the cultured Mandarin fish (Siniperca chuatsi) industry. The molecular mechanisms that underlie the pathogenesis of the
viral infection remain poorly understood. In this study, deep
RNA sequencing technique was used to analyze the transcriptomic profiles of Mandarin fish brain cells (CPB) at progressive time points after ISKNV
infection. A total of 96,206,040 clean data from 98,235,240 sequence reads were obtained. These raw data were assembled into 66,787 unigenes. Among these unigenes, 33,225 and 29,210 had significant hit the Nr and SwissProt databases where they matched 27,537and 19,638 unique
protein accessions, respectively. In the samples harvested at 24 or 72 h post of the
infection, a total of 10,834 or 7584 genes were differentially expressed in infected CPB cells compared to non-infected cells, including 5445 or 3766 up-regulated genes and 5389 or 3818 down-regulated genes, respectively. In addition, 12 differentially expressed genes (DEGs) were validated by quantitative PCR. These DEGs were involved in many pathways of viral pathogenesis. Further analysis of the major DEGs genes involved in the RLRs and apoptosis pathways revealed some interesting findings. In the RLRs pathway, ISKNV
infection inhibited the activation of NF-κB via over expression of the IKKB-α and IKKB-β and lessened expression of
interleukin-1 receptor-associated kinase 4 (IRAK4). In the apoptosis pathway, ISKNV
infection could induce apoptosis mainly via
tumor necrosis factor (TNF) mediated extrinsic pathway. The cellular apoptosis induced by ISKNV
infection was confirmed using annexinV-
FITC/PI and
DAPI staining methods.