INTRODUCTION

Kaposi's Sarcoma (KS) is an angioproliferative condition, the precise nature of which has been long debated. It is still usually classified as a cancer, although with recent advances in virology, it can also be considered to be an opportunistic infection. Classical KS was first described in 1872 in elderly men of Mediterranean origin. An endemic form was subsequently reported in young men in Africa. The epidemic form, described during the early 1980's in AIDS patients, affects homosexual men more often than drug abusers (or hemophilic patients). The iatrogenic form, observed after organ transplantation, differs with respect to clinical presentation, demographics, therapeutic options based on considerations involving immunosuppressive drugs and the specific transplanted allograft.

PATHOGENESIS

It has been clearly shown that all forms of KS are associated with a herpes virus discovered in 1994, called KS-associated herpesvirus or Human Herpes Virus 8 (HHV8). HHV8 is an oncogenic gamma2-herpesvirus (rhadinovirus) encoding cytokines and regulatory factors involved in malignant transformation of B-cells and endothelial cells, such as K1, vGPCR, kaposin (A, B, C), LANA, vIL-6, and vMIP/vCCLs. HHV8 DNA is present within nearly all KS tissues and occasionally in normal skin of KS patients; however, evidence of HHV8 DNA disappears from scar tissue remaining after the regression of KS lesions. Quantification of HHV8 load within peripheral blood mononuclear cells has been shown to be useful in following disease progression. Persistent viremia may long precede the development of clinical disease.