Abstract

Sir, Multiple multicenter, prospective, randomized, double-blind, placebo-controlled studies have shown the eVectiveness of topical imiquimod 5% cream, an immune response modiŽ er, for the treatment of anogenital warts in otherwise healthy individuals (1–3). Analysis of wart skin biopsies has been conducted to determine the molecular mechanisms contributing to the eVectiveness of imiquimod (4,5). These studies indicated that imiquimod increases the local production of multiple interferon mRNAs, including interferon-alpha, interferon-gamma, interleukin-12 and tumor necrosis factor-alpha. Increases in CD4 mRNA were also seen, suggesting an activation of the cellmediated immune response. Furthermore, it was seen that imiquimod decreases the local viral load and human papillomavirus (HPV) DNA and mRNA for HPV proteins. Because the mechanism of the eVectiveness of imiquimod seems to be directly related to its local upregulation of the immune response, it was previously questionable as to whether imiquimod would be eVective in the setting of immunosuppresFig. 1. Perianal condyloma prior to treatment. sion, as is seen in human immunodeŽ ciency virus (HIV )positive patients. It has been determined that the pathogenesis of HPV in HIV-infected individuals is diVerent, either directly through interactions between viral proteins or indirectly through altered immune functions (6, 7). HIV is thought to in uence the expression of HPV genes, resulting in local immune suppression leading ultimately to decreased immune surveillance of viral infection. Consequently, HIV would be expected to directly oppose the action of imiquimod. We describe here successful treatment of HPV with imiquimod in a patient with HIV, and discuss the literature regarding treatment with imiquimod in this population.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call