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Mapping the impact of prolonged microplastics exposure on enteric viral infections using human intestinal organoids

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Using human intestinal organoids exposed to micro- and nanoplastics over extended periods, researchers found that chronic exposure disrupted mitochondrial function and reprogrammed antiviral immune responses, reducing the effectiveness of antiviral treatments against echovirus and rotavirus. This reveals a previously underappreciated way that microplastic accumulation in the gut may worsen infectious disease outcomes and impair therapeutic responsiveness.

Micro- and nanoplastic particles (MNPs) are pervasive environmental pollutants increasingly detected in the human body, yet the health consequences of chronic exposure remain poorly defined. Human intestinal organoids (HIO) have emerged as superior platforms for modelling intestinal diseases including enteric viral infections. In this study, we established a chronic MNPs exposure model using HIO. Long-term MNPs exposure elicited transcriptomic signatures of mitochondrial stress and broad metabolic disruption without inducing overt epithelial cell death. Using this system, we modeled enteric viral infection with echovirus and rotavirus, and demonstrated that prolonged MNPs exposure reprogrammed epithelial antiviral responses, altered viral infection capability, and diminished the efficacy of antiviral treatment. Together, these findings suggest that chronic microplastic exposure can reshape mucosal physiology, modulate virus-host interactions, and impair therapeutic responsiveness, highlighting an under recognized dimension of MNPs impact on infectious disease outcomes.

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