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Oncogenic Viruses and Inhaled Microplastics: A Double Hit Hypothesis for Asthma Progression and Lung Cancer
Jiacheng Yin1, Muzhe Su1, Minhao Xu1
1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Airborne microplastics (MPs) may worsen chronic lung diseases and cancer by increasing susceptibility to oncogenic viruses. This review proposes MPs act as cofactors, impairing immune defenses and creating a permissive environment for persistent viral infections.
Area of Science:
- Environmental Science
- Virology
- Pulmonology
Background:
- Oncogenic viruses contribute to lung cancer and chronic airway diseases.
- Environmental factors significantly influence virus-host interactions in the respiratory tract.
- Airborne microplastics (MPs) accumulate in the lungs, disrupt barriers, and induce inflammation.
Purpose of the Study:
- To review the potential role of airborne MPs as cofactors in oncogenic virus-associated pulmonary pathology.
- To propose a 'double-hit' hypothesis linking MPs and viral carcinogenesis.
- To identify knowledge gaps in understanding MP-virus interactions in lung disease.
Main Methods:
- Literature review of environmental factors, oncogenic viruses, and respiratory diseases.
- Analysis of mechanisms by which MPs affect viral persistence and host immunity.
- Synthesis of evidence supporting a link between MPs, viral infections, and lung carcinogenesis.
Main Results:
- MPs may enhance susceptibility to oncogenic viruses (e.g., HPV, EBV) by affecting viral adsorption, persistence, and immune evasion.
- MPs impair antiviral defenses, including mucosal immunity and interferon responses.
- MPs promote chronic inflammation, oxidative stress, and pathways linked to malignant transformation.
Conclusions:
- Airborne MPs may act as environmental cofactors facilitating oncogenic virus-associated lung diseases.
- Further research is needed on MP-virus interactions, immune modulation, and biomarkers.
- Understanding these interactions is crucial for insights into viral carcinogenesis and chronic airway diseases.
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