Soil-transmitted helminths infect billions of people globally, particularly those residing in low- and middle-income regions with poor environmental sanitation and high levels of air and water pollution. Helminths display potent immunomodulatory activity by activating T helper type 2 (Th2) anti-inflammatory and Th3 regulatory immune responses. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the virus that causes Coronavirus disease 2019 (COVID-19), can exacerbate Th1/Th17 pro-inflammatory cytokine production in humans, leading to a cytokine storm. Air pollutants (particulate matter, oxygen radicals, hydrocarbons and volatile organic compounds) and water pollutants (metals and organic chemicals) can also intensify Th1/Th17 immune response and could exacerbate SARS-CoV-2 related respiratory distress and failure. The present review focused on the epidemiology of SARS-CoV-2, helminths and fine particulate matter 2.5 µm or less in diameter (PM_2.5) air pollution exposure in helminth endemic regions, the possible immunomodulatory activity of helminths against SARS-CoV-2 hyper-inflammatory immune response, and whether air and water pollutants can further exacerbate SARS-CoV-2 related cytokine storm and in the process hinder helminths immunomodulatory functionality. Helminth Th2/Th3 immune response is associated with reductions in lung inflammation and damage, and decreased expression levels of angiotensin-converting enzyme 2 (ACE2) receptors (SARS-CoV-2 uses the ACE2 receptors to infect cells and associated with extensive lung damage). However, air pollutants are associated with overexpression of ACE2 receptors in the epithelial cell surface of the respiratory tract and exhaustion of Th2 immune response. Helminth-induced immunosuppression activity reduces vaccination efficacy, and diminishes vital Th1 cytokine production immune responses that are crucial for combating early stage infections. This could be reversed by continuous air pollution exposure which is known to intensify Th1 pro-inflammatory cytokine production to a point where the immunosuppressive activities of helminths could be hindered. Again, suppressed activities of helminths can also be disadvantageous against SARS-CoV-2 inflammatory response. This “yin and yang” approach seems complex and requires more understanding. Further studies are warranted in a cohort of SARS-CoV-2 infected individuals residing in helminths and air pollution endemic regions to offer more insights, and to impact mass periodic deworming programmes and environmental health policies.

土源性蠕虫感染了全球数十亿人，特别是居住在环境卫生条件差、空气和水污染严重的低收入和中等收入地区的人们。蠕虫通过激活 2 型辅助性 T (Th2) 抗炎和 Th3 调节性免疫反应，表现出强大的免疫调节活性。严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 是导致 2019 年冠状病毒病 (COVID-19) 的病毒，可加剧人类 Th1/Th17 促炎细胞因子的产生，导致细胞因子风暴。空气污染物（颗粒物、氧自由基、碳氢化合物和挥发性有机化合物）和水污染物（金属和有机化学品）也会增强 Th1/Th17 免疫反应，并可能加剧 SARS-CoV-2 相关的呼吸窘迫和衰竭。本综述重点关注蠕虫流行地区 SARS-CoV-2、蠕虫和直径 2.5 µm 或更小细颗粒物 (PM _2.5 ) 空气污染暴露的流行病学、蠕虫对 SARS-CoV-2 的可能免疫调节活性。 -炎症免疫反应，以及空气和水污染物是否会进一步加剧 SARS-CoV-2 相关的细胞因子风暴，并在此过程中阻碍蠕虫的免疫调节功能。蠕虫 Th2/Th3 免疫反应与肺部炎症和损伤的减少以及血管紧张素转换酶 2 (ACE2) 受体的表达水平降低相关（SARS-CoV-2 使用 ACE2 受体感染细胞并与广泛的肺部损伤相关） 。然而，空气污染物与呼吸道上皮细胞表面 ACE2 受体过度表达和 Th2 免疫反应耗竭有关。蠕虫诱导的免疫抑制活性会降低疫苗接种效果，并削弱重要的 Th1 细胞因子产生免疫反应，而这些免疫反应对于对抗早期感染至关重要。这种情况可以通过持续接触空气污染来逆转，众所周知，空气污染会增强 Th1 促炎细胞因子的产生，达到阻碍蠕虫免疫抑制活性的程度。同样，蠕虫活动受到抑制也不利于 SARS-CoV-2 炎症反应。这种“阴阳”的方法看起来很复杂，需要更多的理解。需要对居住在蠕虫和空气污染流行地区的 SARS-CoV-2 感染者进行进一步研究，以提供更多见解，并影响大规模定期驱虫计划和环境卫生政策。