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Environmental virotoxicology: how pollutant exposure modulates viral infections – a systematic review of wildlife-associated evidence
Original title: Environmental virotoxicology: how pollutant exposure modulates viral infections – a systematic review of wildlife-associated evidence
Summary
This review of over 160 studies shows that pollution—including plastics, metals, and chemicals—weakens animals' immune systems and makes them more susceptible to viral infections, which could create bigger disease outbreaks in wildlife. Since viruses can spread from animals to humans and pollutants are everywhere in our environment, understanding how pollution worsens viral infections in nature helps us predict and prevent the next pandemic. Scientists are calling for doctors and environmental experts to work together to track both pollution and disease spread in wildlife as an early warning system for human health threats.
Within a One Health framework, pollution is no longer a passive backdrop to host-virus interactions but actively reshapes disease dynamics across humans, animals, and ecosystems. The aim of this review was to synthesize evidence across free-ranging wildlife and wild-derived models to define environmental virotoxicology, which is the study of how environmental contaminants alter susceptibility, replication, shedding, transmission, pathogenesis, persistence, and viral evolution in hosts. A systematic search of PubMed, Scopus, and Web of Science (26 Oct 2025), augmented by citation-chasing, yielded 162 eligible studies spanning more than 100 taxa (marine mammals, birds, amphibians, reptiles, fish, invertebrates) and major DNA/RNA virus families. Across 9 contaminant classes (>180 chemicals), including legacy persistent organic pollutants, petroleum hydrocarbons/polycyclic aromatic hydrocarbons (PAHs), metals, agrochemicals, pharmaceuticals, per- and polyfluoroalkyl substances (PFAS), and micro/nanoplastics, recurrent patterns emerge: (1) suppression or dysregulation of antiviral immunity, (2) reactivation of latent infections, and (3) increases in viral load, severity, and epizootic magnitude. Effects are context-dependent, with documented null or mixed outcomes shaped by dose, timing, life stage, immune compartment, and host ecology. Two broad implications follow: 1) contaminants might amplify wildlife epizootics and reshape reservoir competence, and in at least one well-supported case (2) low, environmentally realistic exposure to antiviral residues in wild waterfowl may impose selective pressure on viral populations and select for antiviral resistance. It is recommended to integrate contaminant surveillance with viral infectious disease monitoring and prioritizing multifactor, mechanistic designs that couple exposure history, immune phenotype, and virological endpoints.