Introduction

In 1872, Moritz Kaposi, a Hungarian dermatologist, described six patients with multifocal brown–red or blue–red nodules or plaques on the feet and hands (Kaposi, 1872). Initially called “Idiopathisches multiples Pigmentsarcoma der Haut” (multiple idiopathic sarcoma of the skin) by Kaposi, the condition later became known as Kaposi's sarcoma (KS). Decades later, after the epidemiology of KS began to be investigated, its uneven geographic distribution suggested that exogenous factors were etiologically important. Subsequently, as the AIDS epidemic unfolded in the early 1980s, homosexual men were found to be up to 20 times more likely than other risk groups to develop KS, a markedly disproportionate risk that led to the hypothesis that the exogenous factor was a sexually transmitted infectious agent (Beral et al., 1990). Numerous microbial candidates were proposed (Drew et al., 1982; Huang et al., 1992; Wang et al., 1993) but for none was convincing evidence demonstrated until Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8 (HHV-8), was discovered in 1994 (Table 54.1) (Chang et al., 1994). In a short period following the discovery of KSHV, consensus rapidly developed that it is a necessary, albeit not sufficient, causal agent of KS (Whitby et al., 1995; Gao et al., 1996a, b; Martin et al., 1998; Renwick et al.,1998; O'Brien et al., 1999). This discovery was more than academic in that, because of the AIDS epidemic, KS is now worldwide the fourth most common cancer caused by an infectious agent, following gastric, cervical, and hepatic cancer.