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

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.

B and T lymphocytes; Caspase-3; GCRV-II; apoptosis; reactive oxygen species.