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Editorial Kaposi's sarcoma (KS) is a distinctive neoplasm that differs in many respects from most solid tumors. This low grade malig-nancy contains many foci of inflammatory and endothelial cell origins. The dominant partially transformed cell type is the spindle cell, which produces a cornucopia of proinflammatory and angiogenic factors believed to play an important role in the recruitment of additional cells to the sarcoma. More than four years have passed since Chang and colleagues discovered a novel viral genome in KS specimens (1), identifying it as a member of the gamma herpes family. The KS-associated herpesvirus (KSHV, also known as human her-pesvirus 8 or HHV8) is believed to play a crucial role in the development of KS neoplasia. The discovery of KSHV led to the identification of a number of viral ORFs which corresponded to known cellular homologues, including chemokines and their receptors (2, 3). This is in keeping with research over the past fifteen years that has identified numerous viral ORFs with sequence homology to cellular genes. Many of these genes vary only slightly from their cellular counterparts, and are putative mediators of viral pathogenesis, including viral entry and immune disregulation, as demonstrated most elegantly by the identification of chemokine receptors as coreceptors required for entry and infection of cells by HIV-1 (4). At least 15 accessory genes of KSHV have been identified, some of which regulate cell cycle and extracellular signaling. For example, ORF 16, the viral bcl-2 analogue, can block apop-tosis; and ORF 72, the viral cyclin D, can play a role in cell cycle progression. Among the viral growth ligands is ORF K2, the IL-6 homologue, which can act in a paracrine or possibly autocrine manner to stimulate cell growth. ORFs K4 and K6 encode viral chemokine analogues (virokines). Among the accessory genes identified to date, one has become a major focus of the investigations into the KS oncogenic/ pathogenic process. ORF 74, named KSHV G protein–cou-pled receptor (KSHV-GPCR), encodes a chemokine receptor homologue. In late 1997, Cesarman and colleagues (5) showed that KSHV-GPCR encoded a constitutively active G protein– coupled receptor that stimulated the phosphoinositide-protein kinase C pathway, resulting in the proliferation of transfected NRK-49F cells. Almost simultaneously, Mesri and colleagues (6) found that KSHV-GPCR activated two other protein ki-nase pathways, JNK/SAPK and p38MAPK. Further, Mesri's group found that in addition to the oncogenic proliferative signal mediated by KSHV-GPCR, this viral-encoded receptor-like gene also supported …

The chemokine kidnapping receptor of HHV8.