ArticleEnvironment & health (Washington, D.C.)2026
Polystyrene Microplastic-Induced Cellular Alterations and Their Effects on Viral Entry (RSV, HCoV-OC43, EV-A71) and Viral Persistence.
Article in Environment & health (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
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 viruseshuman 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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