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In the March issue of the ARCHIVES, de Villiers and Ruhland¹ reported that the proinflammatory cytokines interleukin 17 and interferon- activate in vitro the promoter of human papillomavirus (HPV) 20, a human papillomavirus associated with epidermodysplasia verruciformis (EV), which may induce replication of this virus. They conclude that EV-HPV infection (eg, HPV-5) does not play an active role in the pathogenesis of psoriasis, but that the virus, present latently in the skin, could become activated by cytokines.

The cytokines are indeed an important stimulus for keratinocyte proliferation, which is a prerequisite for activation of latent HPV infection. It is generally accepted that early (guttate) psoriatic lesions are induced by an influx of proinflammatory cytokines (ie, interferon-, interleukin 17, and others) produced by CD4⁺ lymphocytes activated polyclonally by microbial superantigens. The authors¹ demonstrated in vitro an interesting mechanism of direct stimulation of the EV-HPV promoter by proinflammatory cytokines, and it . . . [Full Text of this Article]

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