Abstract

HIV-related immunosuppression is a well-accepted, strong biological risk factor for two virus-associated cancers: Kaposi’s sarcoma, which is associated with Kaposi’s sarcoma – associated herpesvirus, and non-Hodgkin lymphoma, which is associated with Epstein – Barr virus. In fact, recognition of an extraordinarily high rate of Kaposi’s sarcoma among men who have sex with men in New York and California during the early 1980s was one of the first indications of the existence of a human immunodeficiency virus ( 1 – 3 ). Soon thereafter, high rates of non-Hodgkin lymphoma in men who have sex with men were also recognized ( 4 , 5 ), and both Kaposi’s sarcoma and non-Hodgkin lymphoma became designated as AIDS-defining malignancies in HIV-positive patients ( 6 – 8 ). It was not until the 1990s though that formal linkages between population-based AIDS registries and cancer registries were initiated ( 9 , 10 ). The AIDS – cancer match registry study in the United States ( 11 , 12 ), and similar studies in other countries ( 13 – 15 ), found that the risks for both Kaposi’s sarcoma and non-Hodgkin lymphoma were increased by at least 100-fold in persons who developed AIDS compared with the general population ( 11 , 12 ). Furthermore, there were indications of a biological gradient—one of several criteria used to assess a possible causal relationship. Specifically, the risks for both Kaposi’s sarcoma and non-Hodgkin lymphoma increased, and with lower CD4 T-cell count at time of AIDS onset ( 16 ) with increasing time after AIDS diagnosis (which is thought to be a surrogate indicator

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