PRJNA669241
Understanding molecular  basis of host-pathogen-environment interaction of Tilapia Lake Virus Disease
Nile tilapia (Oreochromis niloticus) is one of the most important aquaculture species cultured worldwide. However, the recent emergence of tilapia lake virus (TiLV) has threatened the global tilapia industry. To increase our knowledge particularly with regards to host response against TiLV infection, the transcriptional profile of liver of TiLV-infected and control tilapia was investigated. Analysis of RNA-Seq data identified 4640 differentially expressed genes (DEGs), which were involved among others in Antigen processing and presentation, MAPK, Apoptosis, Chemokine signaling, Interferon, NF-kB, Acute phase response and JAK-STAT pathways. Although there was upregulation of most of the DEGs in the above pathways suggesting an attempt by tilapia to resist TiLV infection, but modulation of some of the key genes, namely upregulation of BCLX1 in apoptosis pathway; NFKBIA in NF-kB pathway; TRFC in acute phase response; and SOCS, EPOR, PI3K and AKT in JAK-STAT pathway as well as downregulation of the genes, namely MAP3K7 in MAPK pathway; IFIT1 in interferons; 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.