Purpose of review: Knowledge of the pathophysiology of Kaposi sarcoma continues to expand and influence our therapeutic approaches. This review summarizes developments within the last 18 to 24 months.
Recent findings: Pieces of the puzzle as they relate to viral factors—both human herpes virus 8 (HHV-8) and human immunodeficiency virus (HIV)—endothelial cells, host immune factors, and cytokines are described. Recent observations relating to highly active antiretroviral therapy (HAART) and agents under investigation that exploit the developments in pathophysiology are reviewed.
Summary: Advances in Kaposi sarcoma pathophysiology are leading to new therapeutic approaches. These will undoubtedly have an impact on other viral and malignant processes as well.
Abbreviations:AIDS acquired immunodeficiency syndrome, HAART highly active antiretroviral therapy, HHV-8 human herpes virus 8, HIV human immunodeficiency virus, KSHV Kaposi sarcoma herpes virus, MMP matrix metalloproteinase
Despite changes relating to highly active antiretroviral therapy (HAART), Kaposi sarcoma remains the most common neoplasm associated with acquired immunodeficiency syndrome (AIDS). Many geographic areas, such as the Mediterranean basin and sub-Saharan Africa, remain endemic for Kaposi sarcoma, with HIV–positive male homosexual people at particular risk. Kaposi sarcoma is a virally driven process that requires infection by the gammaherpes virus, human herpes virus 8 (HHV-8), also known as Kaposi sarcoma herpes virus (KSHV). This is necessary, but insufficient, for the development of Kaposi sarcoma, a complex multifactorial process. For a thorough review of the viral epidemiology, pathology and pathogenesis, and treatment of Kaposi sarcoma, the reader is referred to Scadden [1••]. The current review focuses on the developments within the last 18 to 24 months.