Abstract

Abstract Keratinocyte carcinoma (KC), comprised of squamous cell carcinoma and basal cell carcinoma, is the most common cancer in the United States. The effects of ultraviolet radiation (UVR), an established risk factor for KC, on cutaneous human papillomavirus (HPV) infection, a suggested risk factor currently under investigation, are not well established. We assessed cross sectional associations between UVR exposure and cutaneous beta HPV infection, using data obtained from the Viruses in Skin Cancer Study (VIRUSCAN), a prospective cohort study conducted at the Moffitt Cancer Center and the University of South Florida. Methods: Eyebrow hairs (EBH), skin swabs (SSW) and spectrophotometer-based measurements of recent UVR exposure were obtained from 1,179 skin cancer screening patients enrolled in the VIRUSCAN study. Viral DNA was measured using a multiplex PCR assay for 46 beta HPV types in both skin swab samples and eyebrow hair follicles. Logistic regression was used to examine the association between UVR exposure and cutaneous HPV infection in individual sites. Ordinal logistic regression was used to examine the effect of UVR exposure on the trend of having the same HPV infection across two sites, adjusted for age and sex. Results: Patients with higher UVR exposure were more likely to test positive for beta HPV 19, 47, 100 and 145 in EBH. In SSW, beta 38, 49, 76, 100, 124 were positively associated with UVR exposure. When considering viral infection across two sites, we found UVR exposure to be significantly associated with the odds of having infection in both EBH and SSW for beta HPV 19 (OR = 1.12, 95% CI: 1.03–1.23, p-trend = 0.04), 38 (OR = 1.08, 95% CI: 1.04–1.13, p-trend < 0.01), 76 (OR = 1.06, 95% CI: 1.00–1.12, p-trend = 0.01), and 100 (OR = 1.10, 95% CI: 1.04–1.17, p-trend = 0.01). Conclusions: UVR exposure is positively associated with beta cutaneous HPV at the type level, in both individual sites and across skin swab and eyebrow hair. Future research is needed to better understand the biological mechanisms mediating the associations between UVR and cutaneous HPV infection.

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