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Human Immunodeficiency Virus and the Skin: Selected Controversies

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      Acquired immunodeficiency syndrome was first recognized as a new disease in 1981 because of the unusual association of Kaposi's sarcoma and Pneumocystis carinii pneumonia in young men. The skin remains one of the most important clinical markers for acquired immunodeficiency syndrome, now recognized as the end stage of infection with the human immunodeficiency virus (HIV). Indeed, an urticarial viral exanthem appearing during seroconversion may allow early identification of newly infected individuals who might benefit from administration of antiviral therapy during plasma viremia. The “asymptomatic HIV infection” is often accompanied by multiple skin complaints, which commonly include xerosis, pruritus, psoriasis/seborrheic dermatitis, and pruritic papular eruptions, the cause of which remains controversial. Psoriasis and Kaposi's sarcoma lesions share features including angiogenesis, dermal dendrocytes infected with HIV, and epidermal hyperproliferation, and are manifested by mice trans-genic for HIV provirus or Tat-ltr. Changes in the immune system including T-cell function, antigen response, and shifting cytokine expression as well as a propensity for autoimmune reactions must underlie the skin immunodysfunction occurring in the setting of HIV infection. One of the most unsettling controversies suggested by in vitro data is that ultraviolet light, an effective therapy for HIV-related skin disorders, may actually activate the virus. J Invest Dermatol 105-117S-121S, 1995

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