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Abstract:
To explain the epidemiology of Kaposi's sarcoma, including its predominance in men, I present a theory based on three concurrent factors: immunodeficiency, exposure to a specific viral agent, and a recessive, highly prevalent X-linked regulatory gene. The X-linked locus is inferred from comparing the aberrant lymphaticovenous nature of immature lesions with absence of lymphaticovenous connections in XO karyotypes. The theory predicts that for heterosexual populations without sex differences in viral exposure or degree of immunodeficiency, the male-to-female ratio of Kaposi's sarcoma will equal the inverse of the lesion's frequency causative virus. In addition, an increased incidence of Kaposi's sarcoma is expected outside of the context of the acquired immunodeficiency syndrome as the causative virus is transmitted separately from the human immunodeficiency virus.