Polystyrene nanoplastics promote fish iridovirus replication via inducing inflammatory response, antioxidant damage...

Nanoplastics (NPs) are widespread in aquatic environments and pose potential risks to aquatic organisms. In this study, a novel fin-derived cell line from sea perch (LJFin) has been established to evaluate the size-dependent toxicity of polystyrene nanoplastics (PS-NPs) and the potential mechanism underlying their actions on sea perch iridovirus (SPIV) infection. The cell viability assay showed that the particle size, concentration of PS-NPs, and the exposure time directly determined their cytotoxicity on LJFin cells. Exposure to 80 nm PS-NPs (PS-80) at 100 μg/mL for 96 h significantly reduced cell viability, whereas 500 nm PS-NPs (PS-500) were nontoxic to LJFin cells. Moreover, PS-NPs were internalized into LJFin cells in a time-dependent manner. PS-80 entered the cytoplasm more efficiently, but the majority of PS-500 were intercepted on the membrane. Both PS-80 and PS-500 were capable of inducing inflammatory response and antioxidant damage in LJFin cells. In addition, PS-NPs exposure increased SPIV replication, even promoting viral entry at the early stage of SPIV infection. Furthermore, sucrose treatment not only significantly inhibited PS-NPs internalization but also reduced the pro-viral effect of PS-NPs during SPIV infection. In contrast, methyl-β-cyclodextrin and ethyl-isopropyl amiloride treatment exhibited no regulatory effects, suggesting that PS-NPs internalization and promoted SPIV replication via the clathrin-mediated endocytosis in vitro. Overall, our findings offer new insights into the pro-viral actions of PS-NPs on fish iridovirus infection in vitro, which highlights a potential threat of NPs to aquatic viral diseases.