Solar Ultraviolet Radiation and Vitamin D Deficiency on Epstein-Barr Virus Reactivation: Observational and Genetic Evidence From a Nasopharyngeal Carcinoma-Endemic Population.

Solar Ultraviolet Radiation and Vitamin D Deficiency on Epstein-Barr Virus Reactivation: Observational and Genetic Evidence From a Nasopharyngeal Carcinoma-Endemic Population.
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DOI:
10.1093/ofid/ofaa426
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发表时间:
2020-10
影响因子:
4.2
通讯作者:
Lam TH
Lam TH
中科院分区:
医学3区
文献类型:
--
作者:
Mai ZM;Lin JH;Ngan RK;Kwong DL;Ng WT;Ng AW;Ip KM;Chan YH;Lee AW;Ho SY;Lung ML;Lam TH

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我们调查了EB病毒病毒衣壳抗原(EBV VCA-IgA)血清状态与环境和个人紫外线辐射(UVR)和维生素D暴露的关系。使用多中心病例对照研究的数据,我们纳入了2014-2017年中国香港的1026例对照受试者。采用校正潜在混杂因素的非条件logistic回归模型计算UVR暴露与EBV VCA-IgA(血清阳性vs血清阴性)之间相关性的比值比(OR)和95%置信区间(CI)。我们观察到,在招募前10年和19-30岁时,EBV VCA-IgA血清阳性率大幅增加与日光暴露时间相关(≥8小时/天vs <2小时/天,校正OR= 3.59,95%CI = 1.46-8.77;校正OR = 2.44,95%CI =1.04-5.73;趋势P值分别为0.005和0.048)。          然而,未发现EBV VCA-IgA血清状态与UVR暴露的其他指标相关。此外,循环25-羟基维生素D(25 OHD)和遗传预测的25 OHD与EBV VCA-IgA血清状态无关。我们的研究结果表明,个人UVR暴露可能与EBV再激活的风险较高,但我们没有发现明确的证据维生素D暴露(观察或遗传),UVR暴露的分子介质。需要在其他人群中进行进一步的前瞻性研究来证实这一发现并探索潜在的生物学机制。应收集有关光敏剂、EBV血清学标志物以及与全身免疫和炎症相关的生物标志物的信息,这些信息在未来的研究中也具有高度相关性。
We investigated the relationship of Epstein-Barr virus viral capsid antigen (EBV VCA-IgA) serostatus with ambient and personal ultraviolet radiation (UVR) and vitamin D exposure. Using data from a multicenter case-control study, we included 1026 controls subjects in 2014–2017 in Hong Kong, China. Odds ratios (ORs) and 95% confidence intervals (CIs) of the association between UVR exposure and EBV VCA-IgA (seropositivity vs seronegativity) were calculated using unconditional logistic regression models adjusted for potential confounders. We observed a large increase in seropositivity of EBV VCA-IgA in association with duration of sunlight exposures at both 10 years before recruitment and age 19–30 years (adjusted OR = 3.59, 95% CI = 1.46–8.77; and adjusted OR = 2.44, 95% CI = 1.04–5.73 for ≥8 vs <2 hours/day; P for trend = .005 and .048, respectively). However, no association of EBV VCA-IgA serostatus with other indicators of UVR exposure was found. In addition, both circulating 25-hydroxyvitamin D (25OHD) and genetic predicted 25OHD were not associated with EBV VCA-IgA serostatus. Our results suggest that personal UVR exposure may be associated with higher risk of EBV reactivation, but we did not find clear evidence of vitamin D exposure (observational or genetic), a molecular mediator of UVR exposure. Further prospective studies in other populations are needed to confirm this finding and to explore the underlying biological mechanisms. Information on photosensitizing agents, and serological markers of EBV, and biomarkers related to systemic immunity and inflammation should be collected and are also highly relevant in future studies.
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