Abstract
Viral agents have been implicated in the development of Kaposi sarcoma (KS) and lymphoproliferative diseases; a relation between KS and human herpesvirus type 8 (HHV-8)1 has been ascertained, and Hodgkin's disease often is found in association with Epstein–Barr virus (EBV).2 The two viruses may be concomitant in some B-cell lymphomas (body cavity-based lymphomas).3 Both of these viruses belong to the gamma-herpesviridae family and have lymphotropic and oncogenic activity.4 The stimuli activating their oncogenic potential vary and often are unknown. An important factor in the case of KS is an impaired immune defense due to the aging of the immune system (Mediterranean KS),5 the onset of chronic malnutrition-induced infectious diseases (African KS), iatrogenic immunosuppression (KS in organ transplantation), or immunosuppression during the course of the acquired immunodeficiency syndrome. The triggering factors in the case of EBV remain unknown. It is unlikely that the simultaneous onset of the two pathologies is a matter of chance, although to our knowledge the stimuli activating both herpesviruses at the same time are not known.6 The genetic substrate may be of fundamental importance.7 Quantitative HHV-8 antibody serology may provide information regarding the course of KS, but not regarding the possibly associated lymphoproliferative disease6 because to our knowledge HHV-8 has never been found in the latter type of pathology other than body cavity-based lymphomas and Castleman disease. Lucia Brambilla M.D.*, Vinicio Boneschi M.D.*, Silvia Ferrucci M.D.*, Silvia Fossati M.D.*, * Institute of Dermatology, State University, IRCCS Ospedale Policlinico, Milan, Italy
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