Abstract
Accumulating evidence suggests that cutaneous human papillomavirus (HPV) infection is associated with non-melanoma skin cancer (NMSC). Little is known about the natural history of cutaneous HPV. A sub-cohort of 209 men with no NMSC history, initially enrolled in the HPV infection in men (HIM) study, were followed for a median of 12.6 months. Epidemiological data were collected through self-administered questionnaires. Cutaneous HPV DNA was measured in normal skin swabs (SS) and eyebrow hairs (EB) for 25 and 16 HPV types in genera β and γ, respectively. Any β HPV infection was more prevalent in SS (67.3%) compared to EB (56.5%, p = 0.04). Incidence in SS was higher than 20 per 1,000 person-months for HPV types 4, 5, 23, 38 and 76. Median duration of persistence of β and γ HPV infection was 8.6 and 6.1 months in EB, respectively, and 11.3 months and 6.3 months, in SS, respectively. Older age (>44 years vs. 18-30 years) was significantly associated with prevalent (SS OR = 3.0, 95% CI = 1.2–7.0) and persistent β HPV infection (EB OR = 6.1, 95% CI = 2.6–14.1). History of blistering sunburn was associated with prevalent (OR = 2.8, 95% CI = 1.3–5.8) and persistent (OR = 2.3, 95% CI = 1.2–4.6) β HPV infection in SS. Cutaneous HPV is highly prevalent in men, with age and blistering sunburn being significant risk factors for cutaneous β HPV infection.
Highlights
Human papillomavirus (HPV) is a non-enveloped DNA virus, primarily infecting stratified epithelium [1,2]
Accumulating evidence suggests that, infection with cutaneous HPV types is associated with increased risk of nonmelanoma skin cancer (NMSC), in both immunocompetent and immunocompromised individuals [10,11,12], perhaps through an indirect mechanism
We evaluated a spectrum of epidemiological measures including risk factors associated with prevalence, persistence and incidence across two genera of cutaneous HPV infection
Summary
Human papillomavirus (HPV) is a non-enveloped DNA virus, primarily infecting stratified epithelium [1,2]. HPV infections are broadly classified as mucosal (a genus) or cutaneous (a, b, c, m, Nv genera) [3]. An etiologic role for mucosal HPV infection has been established for several cancers, including penile [4] and cervical [5,6] as well as a subset of head and neck cancers [7]. Accumulating evidence suggests that, infection with cutaneous HPV types is associated with increased risk of nonmelanoma skin cancer (NMSC), in both immunocompetent and immunocompromised individuals [10,11,12], perhaps through an indirect mechanism. Inhibition of ultraviolet radiation induced apoptosis has been suggested as a potential mechanism of carcinogenic activity of cutaneous HPV [13,14]
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