High frequency of detection of human papillomaviruses associated with epidermodysplasia verruciformis in children with psoriasis

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Abstract
Background Psoriasis is a T‐cell‐mediated immunological disease characterized by epidermal proliferation. The nature of the antigen(s) responsible for T‐cell activation is still unknown. It has been suggested that the human papillomaviruses (HPVs) associated with epidermodysplasia verruciformis (EV), including the oncogenic HPV5, may contribute to the pathogenesis of psoriasis. Objectives To determine whether EV‐HPVs may play a role early in the disease, we searched for these viruses in children with psoriasis. The influence of clinical data on EV‐HPV infection was investigated. Methods We studied scrapings of involved skin from 26 children aged 1·5–13 years with psoriasis. As controls, we analysed scrapings from 28 adults with psoriasis and 15 children with atopic dermatitis, as well as scrapings from normal skin of 28 adults with no known history of HPV infection. We searched for EV‐HPV DNA sequences with a nested polymerase chain reaction method using degenerate primers specific for EV‐HPVs and primers specific for HPV5 and HPV36, two EV‐HPVs frequently detected in adults with psoriasis. Results Similar high prevalences were observed in children and adults with psoriasis for EV‐HPVs (38·5% vs. 35·7%), HPV5 (46·2% vs. 46·4%) and HPV36 (15·4% vs. 25·0%). As in adults, we found several EV‐HPV genotypes and HPV5 and HPV36 variants. A novel HPV36 subtype, HPV36b, was identified. Lower prevalences were observed in children with atopic dermatitis and in adults from the general population (6·7–10·1%). No correlation was observed between frequency of detection of HPVs and clinical data. It is noteworthy that HPV5 was identified in an 18‐month‐old girl and in a boy with psoriasis developing for only 1 week. Conclusions The early detection of several EV‐HPV genotypes in children further supports the link between psoriasis and EV‐HPVs and suggests a putative role for these viruses in the pathogenesis of psoriasis.