The review, authored by Diana Maryory Gómez-Gallego and Juan C. Hernandez at Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia in Medellín, synthesizes recent toxicological and immunological data to delineate how MP/NPs act as biological Trojan horses. By forming a complex chemical corona on their surfaces, these particles stabilize viral particles, enhance their persistence in the environment, and facilitate their translocation across compromised mucosal barriers. At the cellular level, internalized MP/NPs trigger chronic immune dysfunction by overactivating the NLRP3 inflammasome and inducing mitochondrial oxidative stress, while paradoxically suppressing essential antiviral signaling pathways such as the type I interferon response. The authors argue that this dual mechanism—simultaneously amplifying inflammatory damage and weakening antiviral defenses—creates a synergistic scenario in which microplastics function as powerful amplifiers of immunopathology during viral infection.

Microplastics are defined as synthetic particles with a diameter of less than 5 millimeters, while nanoplastics range from 1 to 1000 nanometers. They originate either as primary particles intentionally manufactured for industrial and consumer applications, such as cosmetic microbeads and synthetic textiles, or as secondary particles arising from the environmental fragmentation of larger plastic debris through sunlight radiation, mechanical weathering, and wave action. Among the most commonly used polymers are polypropylene, polyethylene, polyethylene terephthalate, polycarbonate, polyvinyl chloride, polystyrene, and nylon. Humans are exposed to these particles primarily through ingestion, inhalation, and dermal contact. Ingestion is the most well-documented pathway, given the presence of microplastics in marine products, drinking water, processed foods, table salt, and honey. Inhalation constitutes another critical route, especially in urban and industrial environments where airborne microplastics derived from synthetic textiles and tire erosion can reach the pulmonary alveoli and trigger inflammatory effects.

Recent evidence has demonstrated the ability of these particles to cross physiological barriers and accumulate in human tissues. Microplastics have been identified in the lungs, feces, the large and small intestine, placenta, blood, liver, urine, ovarian follicular fluid, and semen, indicating systemic distribution and bioaccumulation. A particularly alarming finding is the recent detection of microplastics in human brain tissue, providing compelling evidence that these particles can access the central nervous system. While this finding raises the possibility of blood-brain barrier translocation, the precise mechanisms remain to be elucidated. A critical structural attribute of microplastics is their high surface adsorption capacity, which facilitates the formation of a chemical corona that enables them to serve as vectors for a wide array of hazardous xenobiotics, including environmental pollutants and viral particles.

The interaction between microplastics and viruses extends beyond simple co-occurrence in contaminated environments. The physicochemical characteristics of microplastics, including polymer type, surface charge, and hydrophobicity, govern viral adsorption and retention primarily through electrostatic, hydrophobic, and van der Waals interactions. Environmental aging induced by ultraviolet radiation introduces polar functional groups on the plastic surface, strengthening hydrophobic interactions and hydrogen bonding between the viral capsid and aged particles. Experimental evidence highlights the efficiency of this Trojan horse mechanism: up to 98.6 percent of bacteriophage T4 particles adsorb onto polystyrene microplastics, driven primarily by electrostatic complementarity. Similarly, the sorption of SARS-CoV-2 onto laundry-derived microfibers is governed by a synergy of electrostatic and hydrophobic forces, which provides mechanical protection to the virion and reduces its degradation rate, thereby increasing the likelihood of indirect transmission.

Viral stability on plastic surfaces has been confirmed across diverse experimental models. Avian influenza virus H9N2 remained detectable for up to 14 days on polyethylene, polystyrene, and polyethylene terephthalate surfaces. Hepatitis E virus retains infectivity for up to 8 weeks on plastic surfaces, significantly longer than on natural materials like wood or ceramic. Human coronavirus 229E preserved its infectivity for at least 5 days on polytetrafluoroethylene and polyvinyl chloride surfaces. More recently, it was demonstrated that microplastics not only allow SARS-CoV-2 adsorption but also increase its infectivity in vitro in human cells, an effect associated with the activation of inflammatory markers including TNF-α, IL-8, and caspase-3. Beyond simple adsorption, microplastics may act as delivery platforms that concentrate virions on their surface, protect them from environmental stressors including dilution, enzymatic degradation, temperature shifts, and UV-mediated inactivation, and function as mobile carriers supporting viral transport across environmental compartments.

At the cellular level, chronic exposure to microplastics leads to persistent immune stimulation, an imbalance between effector and regulatory cells, and eventually immune exhaustion. In human monocytic THP-1 cells, diverse micro- and nanoplastics induce NLRP3 activation and increased IL-1β production. Amino-modified polystyrene nanoplastics activate the NLRP3/caspase-1 pathway, promoting IL-1β maturation and gasdermin D cleavage, thereby triggering pyroptosis, a highly inflammatory form of programmed cell death. Within the intestinal epithelium, microplastics disrupt tight junctions through a reactive oxygen species to NF-κB to NLRP3 to IL-1β to MLCK axis, increasing permeability and compromising barrier integrity. In human lung epithelial A549 cells, polystyrene microplastics enhanced influenza A virus infection by inhibiting the RIG-I/IRF3 signaling pathway and reducing the expression of IFN-β and antiviral proteins such as IFITM3. This suppression of the type I interferon response, the body’s first line of antiviral defense, represents a paradoxical mechanism by which microplastics simultaneously prime inflammatory pathways while disabling the very signaling cascades designed to combat viral replication.

A novel finding reported in the review involves vaccinia virus: in cell cultures, polystyrene nanoplastics accelerated migrasome formation, a vesicular process involved in viral dissemination, thereby promoting early viral entry into cells and enhancing intracellular spread. This represents a mechanism of viral pathogenesis mediated by microplastics that has not been reported for other environmental contaminants. In aquatic models, multiple studies have shown that exposure to microplastics and nanoplastics reduces immunity and increases viral replication. In spotted sea bass, chronic exposure to polypropylene microplastics induced immunosuppression in lymphoid tissues, promoting the replication of an ulcerative virus. In juvenile European sea bass, exposure to functionalized polystyrene nanoplastics reduced the expression of inflammatory and antiviral genes, facilitating infection by nervous necrosis virus in both brain cells and live fish. In aquaculture, polyvinyl chloride microplastics enhanced both the replication and virulence of white spot syndrome virus in shrimp by suppressing the STING-mediated antiviral response.

In murine models, microplastics alter the inflammatory response during viral infection. In mice infected with chikungunya virus, microplastic consumption prolonged post-infectious joint inflammation and led to increased levels of inflammatory cells including Th1, NK, and neutrophils. In a murine model of mild COVID-19, co-exposure to inhaled microplastics and SARS-CoV-2 did not alter viral load or cause evident histopathological lesions, but it suppressed the early innate immune response at 2 days post-infection and induced a late peak of pro-inflammatory cytokines at 6 days post-infection, a profile consistent with cytokine storm. In salmon, co-exposure to microplastics and infectious hematopoietic necrosis virus was associated with increased mortality, correlating with higher viral load and greater branchial inflammation, suggesting that microplastics compromise physical barriers and increase susceptibility to infection. The authors hypothesize that persistent exposure to micro- and nanoplastics could contribute to the maintenance of low-grade inflammation and immune dysregulation, processes that are recognized hallmarks of chronic infections such as HIV, although direct experimental or epidemiological evidence linking microplastic exposure to HIV progression is currently lacking.

The review concludes that microplastics should be recognized as universal inflammatory cofactors that can potentiate the severity and duration of viral infections through conserved mechanisms across diverse biological taxa. This phenomenon is particularly critical in respiratory pathologies such as COVID-19 and influenza, where mucosal barrier integrity and innate immune fitness are primary determinants of clinical prognosis. Inhalation or systemic translocation of microplastics may drive profound immunological dysregulation, transforming localized antiviral defenses into uncontrolled systemic inflammation reminiscent of the cytokine release syndrome observed in severe viral syndromes. However, the authors emphasize that most evidence remains experimental, derived from in vitro and animal models using homogeneous particles and controlled polymer compositions that may not accurately reflect the heterogeneous and chronic nature of environmental human exposure. To date, no robust epidemiological or clinical studies have established a direct association between microplastic burden and the risk, progression, or severity of viral infections. Addressing this synergistic threat requires a transition toward a One Health framework, with future research necessitating integrated biomonitoring strategies, prospective epidemiological studies, translational research using environmentally relevant exposure conditions, and quantitative risk assessment frameworks capable of integrating exposure burden, bioavailability, and immune outcomes to define the clinical implications of microplastic-induced immune dysregulation and viral infection susceptibility.

Subject of Research: Inflammation, immune dysfunction and viral disease: could micro- and nanoplastics be the missing link?

Article Title: Inflammation, immune dysfunction and viral disease: could micro- and nanoplastics be the missing link?

Article References: Gómez-Gallego, D. M., & Hernandez, J. C. (2026). Inflammation, immune dysfunction and viral disease: could micro- and nanoplastics be the missing link?. Frontiers in Virology, 6, Article 1885812. https://doi.org/10.3389/fviro.2026.1885812

Image Credits: AI Generated

DOI: 10.3389/fviro.2026.1885812

Keywords: Inflammation, immune, dysfunction, viral, disease, micro-, nanoplastics, missing, link, scientific research