GCRV-II Triggers B and T Lymphocyte Apoptosis via Mitochondrial ROS Pathway

文献类型： 外文期刊

第一作者： Wang, Jie

作者： Wang, Jie;Dong, Wen-Jing;Wu, Chang-Song;Tian, Tian-Tian;Zhang, Xu-Jie;Zhang, Yong-An;Zhang, Xu-Jie;Zhang, Xu-Jie

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关键词： GCRV-II; apoptosis; Caspase-3; B and T lymphocytes; reactive oxygen species

期刊名称：VIRUSES-BASEL （ 影响因子：3.5； 五年影响因子：3.7 ）

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年卷期： 2025 年 17 卷 7 期

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收录情况： SCI

摘要： Grass carp reovirus (GCRV), particularly the highly prevalent genotype II (GCRV-II), is known to infect peripheral blood leukocytes (PBLs) of grass carp. However, it is unclear whether GCRV-II can induce apoptosis in bystander lymphocytes within infected PBLs. Here, we have shown that GCRV-II infection induces apoptosis via the mitochondria-dependent caspase-3 pathway in infected PBLs. GCRV-II infection was also found to induce a significant increase in reactive oxygen species (ROS) accumulation in leukocytes and lymphocytes, accompanied by increased apoptosis in IgM+ B and CD4+ T lymphocyte subsets. Further studies have demonstrated that the targeted inhibition of mitochondrial ROS production can effectively attenuate apoptosis in neighboring B and T lymphocytes within infected PBLs, suggesting that GCRV-II-induced pro-apoptotic effects on bystander lymphocytes largely require the involvement of the mitochondrial-dependent ROS pathway. Taken together, our study reveals the underlying mechanism by which GCRV-II induces apoptosis in bystander B and T lymphocytes through ROS production, providing new insights into understanding the virus-induced pro-apoptotic mechanism in specific immune cells and a potential strategy for viral immune escape.

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