Review

KSHV/HHV-8 and HIV infection in Kaposi's sarcoma development

Pawan Pyakurel¹ , Fatemeh Pak¹ , Amos R Mwakigonja^1,2 , Ephata Kaaya^1,2 and Peter Biberfeld¹

¹  Immunopathology Lab., Department of Pathology and Oncology, Karolinska Institutet, 171-76 Solna, Stockholm, Sweden

²  Muhimbili University College of Health Sciences, P. O. Box 65023, Dar-Es-Salaam, Tanzania

author email corresponding author email

Infectious Agents and Cancer 2007, 2:4doi:10.1186/1750-9378-2-4

Published:	2 February 2007

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.