Consideration of host-viral interactions in the pathogenesis of Kaposi's sarcoma.

Human herpesvirus type 8 (HHV-8) is a recently identified gamma herpesvirus that is associated with and most likely the etiologic agent of Kaposi's sarcoma (KS). Both monocytes and B lymphocytes appear to serve as reservoirs for HHV-8 in asymptomatic individuals, whereas HHV-8 is present in both spindle cells and microvascular endothelial cells within KS lesions. This suggests that a necessary event for the development of KS is infection of endothelial cells with HHV-8. This paper proposes a model for KS in which cellular adhesion molecules are involved in the recruitment of HHV-8-infected leukocytes into KS-prone areas and in which HHV-8-infected cells overcome the antiviral machinery present in endothelial cells. Mechanisms employed by endothelial cells to recognize and contain viral infections are discussed and possible mechanisms employed by HHV-8 to overcome the endothelial antiviral response.