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

Author:

Mai Zhi-Ming12ORCID,Lin Jia-Huang12,Ngan Roger Kai-Cheong234,Kwong Dora Lai-Wan23,Ng Wai-Tong25,Ng Alice Wan-Ying26,Ip Kai-Ming12,Chan Yap-Hang27,Lee Anne Wing-Mui23,Ho Sai-Yin1,Lung Maria Li23,Lam Tai-Hing12

Affiliation:

1. School of Public Health, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), China

2. Centre for Nasopharyngeal Carcinoma Research, Research Grants Council Area of Excellence Scheme, The University of Hong Kong, Hong Kong SAR, China

3. Department of Clinical Oncology, The University of Hong Kong, Hong Kong SAR, China

4. Department of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong SAR, China

5. Department of Clinical Oncology, Pamela Youde Nethersole Eastern Hospital, Hong Kong SAR, China

6. Department of Clinical Oncology, Tuen Mun Hospital, Hong Kong SAR, China

7. Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China

Abstract

Abstract Background 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. Methods 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. Results 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. Conclusions 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.

Funder

Hong Kong RGC Area of Excellence Scheme

World Cancer Research Fund

Wereld Kanker Onderzoek Fonds

WCRF International Grant Programme

Publisher

Oxford University Press (OUP)

Subject

Infectious Diseases,Oncology

Reference42 articles.

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