Trim2b mediates protection against SVCV infection by degrading NLRP12-like and viral SVCV-N/SVCV-G proteins
In the present study, we report the functional characterization of zebrafish trim2b. we show that zebrafish trim2b plays a protective role in the host defense against SVCV infection. During SVCV infection, the in vivo studies revealed that trim2b overexpression led to the decreased virus loads and increased survival rate. Zebrafish trim2b deficiency led to the increased virus loads and decreased survival rate. In addition, Zebrafish trim2b deficiency leads higher numbers of immune related DEGs and signaling pathways enriched during the SVCV infection or uninfection. Among them, NOD-like receptor signaling pathway was significantly enriched. The present study characterized two NLRs degraded by trim2b plays a negative role in the host defense against SVCV infection. Overall design: We then performed gene expression profiling analysis using data obtained from RNA-seq of  WT and trim2b-/- zebrafish larvae at  6 days post fertilization and 48 hours post SVCV infection