Abstract

Funding sources None. Conflicts of interest None declared. For many years, a search for a viral trigger or cofactor for psoriasis has failed to give any clear pathogenetic lead. Among the candidates for disease‐influencing infectious agents are the cutaneous papillomaviruses, especially the betapapillomaviruses, the genotypes originally described in epidermodysplasia verruciformis. They are found commonly in the skin and skin cancers of the immunosuppressed and are not uncommon in normal individuals. With the ability to remain latent or as subclinical commensals on the skin, but with known epidermal proliferative effects, this virus group fulfils some of the possible requirements to influence development of psoriasis lesions on the skin. It is over a decade since the first report suggested a possible link between psoriasis and papillomavirus infection, when both anti‐papillomavirus antibodies and human papillomavirus (HPV) detection in patients with psoriasis were found to be higher than in normal individuals and patients with atopic dermatitis.1 de Koning et al.,2 in this issue, compare patients with psoriasis and with atopic dermatitis, using both the detection of betapapillomavirus DNA in eyebrow hair bulbs and the level of antibodies to the viral capsid coat protein, the L1 protein, in 15 β‐HPVs.

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