Transcriptiomics analysis reveals immue regulation and cell death of in Pelodiscus sinensis STA cells

Our previous study showed that overexpression interferon gamma (IFNg) in soft-shelled turtle (Pelodiscus sinensis) artery cell line (STA cells) could induce soft-shelled turtle iridovirus (STIV)-infected cell death and inhibit STIV replication. To understand the molecular basis, four samples (named as Ctrl, Ctrl_STIV, IFNg and IFNg_STIV) including cells treatment with recombinant IFNg (rIFNg) or not, and infected or mock-infected with STIV were used to transcriptome analysis. A total of 77.18 Gb clean data were obtained and the clean data of each sample was over 5.97 Gb. Compared to the Ctrl group, there are 2172, 1192 and 2638 DEGs were detected, with 1127, 580 and 1349 up-regulated genes and 1045, 612, and 1259 down-regulated genes, in STA cells after treatment with IFNg, Ctrl_STIV and IFNg_STIV respectively. Subsequently, DEGs were annotated and enriched to GO items and the KEGG pathway, the result showed that immune activation of rIFNg in STA cells including JakSTAT signaling activation, pattern recognition receptor (PRR) mediated innate immunity activation and cell death regulation etc. The activation of PRR mediated innate immunity may contribute to antiviral activity of IFNg, and it was not affected by STIV infection. From the aspect of cell death, rIFNg could regulated a series of cell death associated Go items including positive regulation and negative regulation, however some GO items including negative regulation of cell death were no longer enriched after STIV infection. The enriched deathrelated KEGG pathways including "Apoptosis" and "Necroptosis" were enriched in STA cells after rIFNg treatment, and however, besides "Necroptosis", "Cellular senescence", "p53 signaling pathway" were enriched after STIV infection. All of these indicate that rIFNg could build an antiviral activity in STA cells and may induce STIVinfected cell death through limiting the negative regulation of cell death and inducing necroptosis, apoptosis and cellular senescence.