Polystyrene nanoplastics promote fish iridovirus replication via inducing inflammatory response, antioxidant damage and enhancing viral entry.

Abstract

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.