Clinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Anzio Rd, Observatory, 7925, Western Cape, South Africa.
Photochem Photobiol Sci. 2017 Mar 16;16(3):314-338. doi: 10.1039/c6pp00355a.
The seasonality of infectious disease outbreaks suggests that environmental conditions have a significant effect on disease risk. One of the major environmental factors that can affect this is solar radiation, primarily acting through ultraviolet radiation (UVR), and its subsequent control of vitamin D production. Here we show how UVR and vitamin D, which are modified by latitude and season, can affect host and pathogen fitness and relate them to the outcomes of bacterial, viral and vector-borne infections. We conducted a thorough comparison of the molecular and cellular mechanisms of action of UVR and vitamin D on pathogen fitness and host immunity and related these to the effects observed in animal models and clinical trials to understand their independent and complementary effects on infectious disease outcome. UVR and vitamin D share common pathways of innate immune activation primarily via antimicrobial peptide production, and adaptive immune suppression. Whilst UVR can induce vitamin D-independent effects in the skin, such as the generation of photoproducts activating interferon signaling, vitamin D has a larger systemic effect due to its autocrine and paracrine modulation of cellular responses in a range of tissues. However, the seasonal patterns in infectious disease prevalence are not solely driven by variation in UVR and vitamin D levels across latitudes. Vector-borne pathogens show a strong seasonality of infection correlated to climatic conditions favoring their replication. Conversely, pathogens, such as influenza A virus, Mycobacterium tuberculosis and human immunodeficiency virus type 1, have strong evidence to support their interaction with vitamin D. Thus, UVR has both vitamin D-dependent and independent effects on infectious diseases; these effects vary depending on the pathogen of interest and the effects can be complementary or antagonistic.
传染病暴发的季节性表明，环境条件对疾病风险有重大影响。其中一个主要的环境因素是太阳辐射，它主要通过紫外线辐射（UVR）及其随后对维生素 D 生成的控制来影响疾病风险。在这里，我们展示了 UVR 和维生素 D 如何受纬度和季节的影响，从而影响宿主和病原体的适应性，并将其与细菌、病毒和媒介传播感染的结果联系起来。我们对 UVR 和维生素 D 对病原体适应性和宿主免疫的分子和细胞作用机制进行了彻底比较，并将这些机制与在动物模型和临床试验中观察到的结果联系起来，以了解它们对传染病结果的独立和互补作用。UVR 和维生素 D 通过抗菌肽产生和适应性免疫抑制等途径共享先天免疫激活的共同途径。虽然 UVR 可以在皮肤中诱导维生素 D 非依赖性效应，例如产生激活干扰素信号的光产物，但由于维生素 D 对多种组织中细胞反应的自分泌和旁分泌调节，其具有更大的系统效应。然而，传染病流行的季节性模式并不仅仅是由纬度之间 UVR 和维生素 D 水平的变化驱动的。媒介传播病原体的感染具有很强的季节性，与有利于其复制的气候条件有关。相反，流感 A 病毒、结核分枝杆菌和人类免疫缺陷病毒 1 等病原体有强有力的证据支持它们与维生素 D 的相互作用。因此，UVR 对传染病既有维生素 D 依赖性效应，也有非依赖性效应；这些效应取决于相关病原体，其效应可以是互补的，也可以是拮抗的。
