Air pollutants are a major source of increased risk of disease, hospitalization, morbidity, and mortality worldwide. The respiratory tract is a primary target of potential concurrent exposure to both inhaled pollutants and pathogens, including viruses. Although there are various associative studies linking adverse outcomes to co- or subsequent exposures to inhaled pollutants and viruses, knowledge about causal linkages and mechanisms by which pollutant exposure may alter human respiratory responses to viral infection is more limited. In this article, we review what is known about the impact of pollutant exposure on antiviral host defense responses and describe potential mechanisms by which pollutants can alter the viral infection cycle. This review focuses on evidence from human observational and controlled exposure, ex vivo, and in vitro studies. Overall, there are a myriad of points throughout the viral infection cycle that inhaled pollutants can alter to modulate appropriate host defense responses. These alterations may contribute to observed increases in rates of viral infection and associated morbidity and mortality in areas of the world with high ambient pollution levels or in people using tobacco products. Although the understanding of mechanisms of interaction is advancing through controlled in vivo and in vitro exposure models, more studies are needed because emerging infectious pathogens, such as severe acute respiratory syndrome coronavirus 2, present a significant threat to public health.

空气污染物是全球疾病、住院、发病和死亡风险增加的主要来源。呼吸道是潜在同时接触吸入污染物和病原体（包括病毒）的主要目标。尽管有各种关联研究将不良后果与同时或随后接触吸入污染物和病毒联系起来，但对污染物接触可能改变人类呼吸道对病毒感染反应的因果关系和机制的了解更为有限。在本文中，我们回顾了污染物暴露对抗病毒宿主防御反应的影响的已知信息，并描述了污染物改变病毒感染周期的潜在机制。本综述重点关注来自人类观察和受控暴露、离体和体外研究的证据。总体而言，在整个病毒感染周期中有无数的点，吸入的污染物可以改变这些点以调节适当的宿主防御反应。这些变化可能导致世界上环境污染水平较高的地区或使用烟草产品的人群中病毒感染率以及相关发病率和死亡率的增加。尽管通过受控的体内和体外暴露模型正在推进对相互作用机制的理解，但还需要更多的研究，因为新出现的传染性病原体，如严重急性呼吸综合征冠状病毒2，对公众健康构成重大威胁。