Virus encoded tumor necrosis factor receptor (TNFR) homologues are usually involved in immune evasion by regulating host immune response or cell death. Singapore grouper iridovirus (SGIV) is a novel ranavirus which causes great economic losses in aquaculture industry. Previous studies demonstrated that SGIV VP51, a TNFR-like protein regulated apoptotic process in VP51 overexpression cells. Here, we developed a VP51-deleted recombinant virus Δ51-SGIV by replacing VP51 with puro^R-GFP. Deletion of VP51 resulted in the decrease of SGIV virulence, evidenced by the reduced replication in vitro and the decreased cumulative mortalities in Δ51-SGIV challenged grouper compared to WT-SGIV. Moreover, VP51 deletion significantly increased virus induced apoptosis, and reduced the expression of pro-inflammatory cytokines in vitro. In addition, the expression of several pro-inflammatory genes were decreased in Δ51-SGIV infected grouper compared to WT-SGIV. Thus, we speculate that SGIV VP51 functions as a critical virulence factor via regulating host cell apoptosis and inflammation response.

病毒编码的肿瘤坏死因子受体（TNFR）同源物通常通过调节宿主的免疫反应或细胞死亡而参与免疫逃逸。新加坡石斑鱼iridovirus（SGIV）是一种新型的鼻病毒，在水产养殖业中造成巨大的经济损失。先前的研究表明，SGIV VP51是一种TNFR样蛋白，可调节VP51过表达细胞的凋亡过程。在这里，我们通过用puro ^R -GFP替代VP51，开发了缺失VP51的重组病毒Δ51- SGIV。VP51的缺失导致SGIV毒力的降低，这在体外复制减少中得到了证明。与WT-SGIV相比，Δ51-SGIV攻击石斑鱼的累积死亡率降低。此外，VP51缺失显著增加病毒诱导的细胞凋亡，并减少促炎细胞因子的表达在体外。另外，与WT-SGIV相比，Δ51-SGIV感染的石斑鱼中几种促炎基因的表达降低。因此，我们推测SGIV VP51通过调节宿主细胞的凋亡和炎症反应起着关键的毒力因子的作用。