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.
Offermann
M K
MK
Winship Cancer Center, Department of Medicine, Emory University, Atlanta, Georgia 30322, USA. mofferm@emory.edu
D000818:Animals; D004727:Endothelium / Q000821:virology; D019288:Herpesvirus 8, Human; D006801:Humans; D008954:Models, Biological; D011494:Protein Kinases / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012514:Sarcoma, Kaposi / Q000209:etiology* / Q000821:virology; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics
D012333:RNA, Messenger; D019010:Vascular Cell Adhesion Molecule-1; D011494:Protein Kinases