ABSTRACT

In 1872, University of Vienna dermatologist Moritz Kaposi (1837-1902), who had changed his name from Moriz Kohn to resemble that of his hometown of Kaposvár, Hungary, rst described ve men with aggressive idiopathic multiple pigmented sarcomas of the skin, which became known as Kaposi sarcoma (KS) [1]. A decade later, the second report about KS was by Tommaso De Amicis, dermatologist at the University of Naples, who described 12 patients: 10 of which presented the typical classic form of the disease, with a peculiar indolent course, while two others, as well as those previously described by Kaposi, strongly resemble the clinical form of KS currently recognized as that associated to the acquired immunodeciency syndrome (AIDS) [2]. For the rst eight decades of the twentieth century, KS was generally considered to be a nonaggressive neoplasm [2]. In 1981, AIDS-associated KS was rst identied, and strong epidemiological evidence lead to speculate about an infectious cause as well as sexual transmission [3]. In 1994, using representational difference analysis (RDA) to identify two herpesvirus DNA fragments, KS330Bam and KS631Bam, in a biopsy sample from a patient with AIDS-KS, Chang and colleagues [4] described KS-associated herpesvirus (KSHV), also known as human herpesvirus-8 (HHV-8). Soon after, KSHV genomes were found to be present in two lymphoproliferative conditions known to occur more frequently

in AIDS patients: primary effusion lymphoma (PEL) and the plasma cell variant of multicentric Castleman’s disease (MCD) [5,6]. Subsequent sequencing of a 21 kb AIDS-KS genomic library fragment (KS5) hybridizing to KS330Bam evidenced that KSHV is a γ-herpesvirus related to herpesvirus saimiri belonging to the genus Rhadinovirus [7], and its genome was sequenced soon after [8].