Abstract
Red sea bream iridovirus (RSIV) belongs to the family Iridoviridae, genus Megalocytivirus, which could widely infect marine fish, causing diseases and huge economic losses. Now it has been reported that RSIV was also detected in diseased mandarin fish. Transmission electron microscopy and immunohistochemistry showed that spleen was the main target organ in mandarin fish infected with RSIV. To investigate the immune response mechanism of mandarin fish to RSIV infection, transcriptomics of RSIV-infected mandarin fish was analyzed. A total of 53,040 unigenes were obtained, and there were 21,576 and 17,904 unigenes had significant hit the Nr and SwissProt databases, respectively. In RSIV-infected and non-infected spleen tissues, there were 309 differentially expressed genes (DEGs), including 100 up-regulated genes and 209 down-regulated genes. Gene Ontology database (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis were performed to reveal the function information and give a better understanding of the signal transduction pathways of DEGs. Further analysis of the cytokine-cytokine receptor interactions pathway exhibited that the expression of cytokines was widely activated after viral infection. In addition, ten DEGs were randomly selected and verified by quantitative real-time PCR, which revealed a similar expression tendency as the high-throughput sequencing data. These findings present valuable information that will benefit for better understanding of RSIV infection in mandarin fish.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.