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Polystyrene Microplastic-Induced Cellular Alterations and Their Effects on Viral Entry (RSV, HCoV-OC43, EV-A71) and Viral Persistence
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Researchers systematically investigated how polystyrene microplastics affect human cells and their interactions with three respiratory and enteric viruses. The study found that microplastic exposure caused cell damage, suppressed innate antiviral immune responses, and enhanced the persistence of enveloped viruses like coronavirus OC43 and RSV, suggesting that microplastics may create conditions favorable for viral survival.
Microplastics (MPs) are emerging environmental pollutants with biological impacts extending beyond cytotoxicity, yet their interactions with viruses remain poorly understood. This study systematically investigated the cellular and virological effects of polystyrene microplastics (PS-MPs) using three medically relevant viruses─human coronavirus OC43 (HCoV-OC43), respiratory syncytial virus (RSV), and Enterovirus A71 (EV-A71)─across multiple human cell lines under identical experimental conditions. PS-MP exposure induced dose- and time-dependent cytotoxicity, G2/M cell-cycle arrest, and early apoptosis, including effects observed at subcytotoxic concentrations. Coexposure assays revealed increased detectable infection levels and enhanced cold-temperature persistence of enveloped viruses (HCoV-OC43 and RSV), whereas no comparable effect was observed for the nonenveloped EV-A71, suggesting preferential effects on viral stability rather than intrinsic infectivity. Under coexposure conditions, PS-MPs reduced type I interferon (IFN-α/β) expression, indicating impaired innate antiviral signaling, while modulation of IFITM3 expression varied depending on viral species and host cell context. Gene-expression analyses demonstrated virus-specific antiviral modulation with attenuated interferon-mediated antiviral priming during HCoV-OC43 infection and reduced IFITM3 expression in RSV-infected cells. Collectively, these findings indicate that PS-MPs act as environmental and biological cofactors that induce cellular stress, suppress antiviral immune responses, and promote viral stability under low-temperature conditions, with implications for viral persistence in contaminated ecosystems.
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