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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
Pollution in our environment—from plastics to chemicals to heavy metals—can weaken animals' immune systems and make them more vulnerable to viral infections, which could then spread to humans. This review of over 160 studies shows that contaminants are actively making disease outbreaks worse in wildlife, and in some cases may even be creating viruses that resist our medicines. Understanding these pollution-disease connections matters because animals are often where new diseases start before jumping to people, so controlling pollution could help prevent the next pandemic.
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.