Previous studies have indicated that white spot syndrome virus (WSSV) infection induces apoptosis in many shrimp organs. However, the mechanism by which WSSV causes host apoptosis remains largely unknown. In this study, we demonstrated the function of wsv152, the first mitochondrial protein identified as encoded by WSSV. Glutathione S-transferase pulldown and co-immunoprecipitation analysis revealed that wsv152 interacts with the shrimp mitochondrial protein cytochrome c oxidase 5a (COX5a), a subunit of the COX complex. We also found that wsv152 expression significantly increased the rate of apoptosis, suggesting a role of wsv152 in WSSV-induced apoptosis in shrimp. Knockdown of wsv152 in vivo led to downregulation of several apoptosis-related shrimp genes, including cytochrome c, apoptosis-inducing factor and caspase-3. Suppression of wsv152 also resulted in significant reductions in the number of WSSV genome copies in tissues and in the mortality of WSSV-infected shrimp. Together, these results suggest that wsv152 targets host COX5a and is associated with the expression profiles of apoptosis-related shrimp genes. Wsv152 is likely also involved in WSSV-induced apoptosis, thereby facilitating virus infection and playing a complex role in WSSV pathogenesis.

中文翻译：

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WSV152诱导凡纳滨对虾中的细胞凋亡并促进病毒复制。

先前的研究表明，白斑综合症病毒（WSSV）感染在许多虾器官中诱导凋亡。但是，WSSV导致宿主凋亡的机制仍然未知。在这项研究中，我们证明了wsv152的功能，wsv152是第一个被WSSV编码的线粒体蛋白。谷胱甘肽S-转移酶的下拉和共同免疫沉淀分析表明，wsv152与虾线粒体蛋白细胞色素c氧化酶5a（COX5a）相互作用，这是COX复合物的一个亚基。我们还发现，wsv152的表达显着提高了细胞凋亡的速率，表明wsv152在WSSV诱导的虾的细胞凋亡中发挥了作用。体内敲低wsv152导致下调一些与凋亡相关的虾基因，包括细胞色素c，细胞凋亡诱导因子和caspase-3。wsv152的抑制还导致组织中WSSV基因组拷贝数的大幅减少以及WSSV感染虾的死亡率的降低。总之，这些结果表明wsv152靶向宿主COX5a，并与凋亡相关虾基因的表达谱有关。Wsv152也可能参与WSSV诱导的凋亡，从而促进病毒感染并在WSSV发病机理中发挥复杂作用。