Abstract:
Kaposi's sarcoma (KS) is a highly and abnormally vascularized tumor-like lesion affecting the skin,
lymphnodes and viscera, which develops from early inflammatory stages of patch/plaque to late,
nodular tumors composed predominant of spindle cells (SC). These SC are infected with the
Kaposi's sarcoma-associated herpesvirus or human herpesvirus-8 (KSHV/HHV-8). KS is promoted
during HIV infection by various angiogenic and pro-inflammatory factors including HIV-Tat. The
latency associated nuclear antigen type 1 (LANA-1) protein is well expressed in SC, highly
immunogenic and considered important in the generation and maintenance of HHV-8 associated
malignancies. Various studies favour an endothelial origin of the KS SC, expressing "mixed"
lymphatic and vascular endothelial cell markers, possibly representing hybrid phenotypes of
endothelial cells (EC). A significant number of SC during KS development are apparently not HHV8
infected, which heterogeneity in viral permissiveness may indicate that non-infected SC may
continuously be recruited in to the lesion from progenitor cells and locally triggered to develop
permissiveness to HHV8 infection. In the present study various aspects of KS pathogenesis are
discussed, focusing on the histopathological as well as cytogenetic and molecular genetic changes
in KS
