The epidemiology of KS suggested an infectious etiology for this disease. As a consequence of its close association with the AIDS epidemic, initial research focus was concentrated on a newly identified virus, HIV, as the KS etiologic agent. Early work suggested that the potent transactivator HIV-1 protein, Tat, plays a major role in the pathogenesis of AIDS-related KS. Among many of its KS-promoting activities, the Tat protein augments the angiogenic activities of basic fibroblast growth factor (bFGF), interferon gamma, and vascular endothelial growth factor (VEGF); mimics the effects of the extramedullary matrix proteins fibronectin and vitronectin; and increases the expression of matrix metalloproteinases .
However, as KS is found in only a subpopulation of HIV-infected individuals, HIV did not appear to be sufficient for KS development. Moreover, the cause of KS in HIV-
negative individuals remained unexplained. This suggested that a second etiologic agent or cofactor might be involved in KS pathogenesis.
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