Selective Defect in Plasmacyoid Dendritic Cell Function in a Patient with AIDS-Associated Atypical Genital Herpes Simplex Vegetans Treated with Imiquimod

We report a case of acquired immunodeficiency syndrome (AIDS)‐associated, acyclovir-refractory genital herpes infection treated with topical imidazoquinoline therapy. The patient’s plasmacytoid dendritic cells made a robust interferon-a response following in vitro stimulation with imidazoquinoline but not with herpes simplex virus. We hypothesize that disease resulting from defective herpes simplex virus‐stimulated interferon-a may be overcome by stimulating intact alternative pathways. In patients with advanced HIV-1 infection, unusual and severe manifestations of herpes simplex virus (HSV) infection are common and are included among the opportunistic processes that define AIDS [1]. The use of long-term immunosuppressive therapy to control recurrent HSV episodes may lead to drug resistance in these patients. Immune system‐stimulating agents that promote IFN-a production may represent an alternative or adjunct approach to treatment with antiviral agents. IFN-a is a key component of the innate immune response, which plays a critical role in the control of viral infections, including HSV infection. Recently, a specialized cell, the plasmacytoid dendritic cell (pDC), was shown to be the principal producer of IFN-a in peripheral blood [2]. However, this function is deficient in patients with AIDS, a deficiency that may predispose them to opportunistic infections [3]. IFN-a production by pDCs occurs in response to ligation of pathogen-recognition