Microplastics and BPA Quietly Rewire Fish Immunity, Raising Viral Disease Risk in Aquaculture

Viral outbreaks in fish farms have long been blamed on the usual suspects: highly virulent pathogens, susceptible host genetics, and the relentless intensification of farming practices. But a growing body of evidence, synthesized in an editorial published in Advanced Biotechnology by Shaoping Weng, Liqing Wu, and Changjun Guo of Sun Yat-sen University, points to a quieter and more insidious driver of disease. In waters laced with microplastics and the endocrine-disrupting chemical bisphenol A, farmed fish and shellfish may fall ill not because the viruses have grown stronger, but because the environment has systematically dismantled the animals’ antiviral defenses. The authors argue that these mixed contaminants should be understood as non-traditional ecological determinants of viral susceptibility, repositioning aquatic virology within an environmentally mediated framework.

The scale of the exposure problem is difficult to overstate. Microplastics are now ubiquitous in marine and freshwater systems, and coastal aquaculture often operates in waters already receiving diffuse plastic pollution from urban, industrial, and riverine sources. Farming itself adds to the burden: plastic ropes, nets, buoys, cages, and feeding devices gradually weather and abrade, shedding particles that can be ingested and retained by cultured species. Bisphenol A, a plasticizer and industrial chemical that leaches from plastics, is equally widespread. Once in the water, these pollutants do not simply coexist; they interact, with microplastic surfaces adsorbing dissolved chemicals and concentrating co-pollutants into complex exposures that cultured animals encounter continuously through rearing water and feed.

One of the most consequential shifts in thinking concerns the role of plastic particles as biological interfaces rather than inert debris. Microplastics in aquatic environments rapidly acquire a coating of microorganisms known as the Plastisphere, and these biofilms can be loaded with Vibrio species and antimicrobial-resistant bacteria. Crucially for virologists, plastic surfaces can also stabilize viral particles, modify waterborne transmission routes, and act as non-host reservoirs that co-transport microbial hazards through the water column. In polluted farming environments, a virus may therefore encounter not only a susceptible host but also a durable plastic platform that concentrates and disperses infectious particles, potentially amplifying transmission opportunities in ways that classical epidemiological models of aquaculture disease have not accounted for.

The physiological mechanism linking pollution to viral susceptibility is increasingly well characterized, and it centers on a reprogramming of immune baselines rather than acute lethal toxicity. Across teleost models, dietary exposure to polyvinyl chloride, polyethylene, or polypropylene microplastics has been shown to induce histopathological lesions, redox imbalance, and disturbances of immune regulation, while suppressing antiviral responses and increasing viral replication in immune organs. In European sea bass, for example, dietary PVC and polyethylene produced measurable histological damage, oxidative stress, and immunoregulatory disruption. These findings indicate that plastic particles can markedly alter the basal physiological status of fish even at exposures that do not cause overt mortality, quietly lowering the threshold at which an otherwise manageable infection becomes a disease outbreak.

Recent experimental work in largemouth bass provides perhaps the clearest demonstration of how mixed contaminant exposure translates into viral susceptibility. Under environmentally realistic co-exposure to microplastics and bisphenol A, the fish exhibited inhibition of NRF2-driven antioxidant signaling, a master regulatory pathway that normally mobilizes cellular defenses against oxidative damage. Hepatic activities of the antioxidant enzymes superoxide dismutase 1, catalase, and glutathione peroxidase declined, while reactive oxygen species and lipid peroxidation rose. Mitochondrial function was disrupted and cellular ATP was depleted, ultimately activating caspase-dependent apoptosis. The resulting biochemical milieu proved favorable to replication of nervous necrosis virus, a devastating pathogen of farmed marine fish, illustrating how sublethal pollutant stress can create conditions that a virus exploits.

Mixed pollution amplifies these effects well beyond what microplastics alone can achieve. In crustaceans and fish, combinations of microplastics with dissolved pollutants disrupt innate immune signaling and alter gut microbiota, the microbial communities that contribute to immune priming and barrier defense. Hydrophobic contaminants such as polybrominated diphenyl ethers effectively hitchhike on microplastic particles, accumulate in host tissues, and initiate ferroptosis-related immune impairment, a form of regulated cell death driven by lipid peroxidation. In the swimming crab Portunus trituberculatus, combined microplastic and bisphenol A exposure perturbed both innate immune responses and intestinal microflora. Even at the earliest life stages, combined polystyrene microplastic and bisphenol A exposure alters oxidative and metabolic biomarkers in embryos, suggesting that developmental windows of immune programming may be particularly vulnerable.

The chemistry governing these interactions at the environmental interface is itself complex. Microplastic–bisphenol A interactions are shaped by surface aging, functionalization, and water chemistry, all of which influence sorption–desorption dynamics and therefore the bioavailability of the leached chemical. In coastal aquaculture waters, bisphenol A undergoes phototransformation whose rate and products depend on salinity and dissolved organic matter, generating additional reactive metabolites whose toxicity remains incompletely understood. This means that the effective dose and composition of a contaminant mixture can vary substantially between farms, seasons, and salinity regimes, complicating both risk assessment and the design of monitoring programs intended to predict when environmental conditions favor disease emergence.

From the perspective of farm management, these findings reveal an additional layer of risk that overlays traditional biosecurity concerns. Contaminants enter culture systems through seawater intake, riverine inputs, resuspension of legacy plastics from sediments, and contaminated feeds or additives. Once present, microplastics and associated pollutants interact with dissolved organic matter and microbiota, favoring the formation of Plastisphere biofilms that host bacteria and adsorb viruses. For farmed fish and shellfish, routine exposure to rearing water may therefore be accompanied by chronic intake of contaminant–pathogen complexes that induce subclinical immunosuppression. Viral susceptibility, in this framing, emerges from environmental pollution pressure acting on cultured animals rather than from any intrinsic weakness of aquaculture itself.

The practical implication is that pollution monitoring and control must become an integral complement to classical disease control. Even when vaccines, husbandry, and genetic selection are optimized, elevated burdens of microplastics and bisphenol A in the farming environment may lower the threshold for viral infection by driving oxidative stress, disrupting immune signaling, and altering host–microbiota relationships. The authors point to a suite of mitigating measures: improving water quality protection in surrounding catchments, reducing external plastic inputs, selecting rearing materials that are less prone to shedding or adsorbing contaminants, and augmenting antioxidant and immune defenses in cultured species. Each of these interventions addresses a different node in the chain that connects pollutant source, environmental persistence, host uptake, and immune erosion.

Taken together, the evidence assembled by Weng and colleagues indicates that microplastic- and bisphenol A-driven susceptibility represents an emerging challenge for otherwise sustainable aquaculture systems, with implications that extend to human health through seafood safety, food-borne exposure, and the disruption of coastal ecosystems under a One Health perspective. Integrating strategies that mitigate contaminant sources and reduce bioaccumulation with measures that support the antioxidant and immune competence of cultured species will complement conventional approaches based on selective breeding, vaccination, and improved husbandry. As aquaculture continues to expand to meet global protein demand, the invisible chemistry of polluted water may prove as decisive for disease outcomes as any pathogen, and recognizing mixed contaminants as hidden determinants of viral susceptibility is a first step toward managing that risk.

Subject of Research: How mixed aquatic pollutants such as microplastics and bisphenol A increase viral susceptibility in farmed fish and shellfish

Article Title: Pollution-driven viral susceptibility: mixed contaminants as hidden determinants of aquaculture disease

Article References: Weng, S., Wu, L., & Guo, C. (2025). Pollution-driven viral susceptibility: mixed contaminants as hidden determinants of aquaculture disease. Advanced Biotechnology, 3(4), Article 33. https://doi.org/10.1007/s44307-025-00091-7

Image Credits: AI Generated

DOI: 10.1007/s44307-025-00091-7

Keywords: aquaculture, microplastics, bisphenol A, viral susceptibility, oxidative stress, nervous necrosis virus, Plastisphere, immune suppression, fish health, environmental pollution, One Health, aquatic virology