Integrating transcriptomics and metabolomics revealed pathogenic mechanism of Chinese soft-shell turtle (Trionyx sinensis) infected with Trionyx sinensis hemorrhagic syndrome virus (TSHSV)

Trionyx sinensis Hemorrhagic Syndrome Virus(TSHSV)seriously hinders the aquaculture of Chinese soft-shell turtle (Trionyx sinensis) due to its high mortality. However, the pathogenic mechanisms of TSHSV in T. sinensis are still unclear. In present study, transcriptomic and metabolomic analyses were performed on turtle livers following TSHSV infection. 734 up-regulated and 770 down-regulated differentially expressed genes (DEGs) were identified in different TSHSV challenge groups. These DEGs were categorized into 12 pathways related to virus infection and host immunity. Moreover, 27, 2679, and 4341 differentially expressed metabolites (DEMs) were identified in the D1, D3, and D5 groups, respectively. These DEMs were mapped into the pathways of energy metabolism, amino acid metabolism and fatty acid metabolism. Association analysis revealed TSHSV induced inflammatory responses, hepatocyte apoptosis, and ultimately led to liver tissue damage. Taurine supplementation promoted the survival rate of turtle after TSHSV infection and reduced the inflammatory response of liver by regulating the production of interferons, antioxidases, and the pro-inflammatory cytokine TNF-α. Collectively, our results provide comprehensive profiles of the transcriptome and metabolome in Chinese soft-shell turtle liver after TSHSV invasion, shedding light on the underlying pathogenic mechanism. The method of taurine supplementation might be a promising therapeutic strategy for protecting turtles from TSHSV.