The Antiviral Drug Docosanol as a Treatment for Kaposi's Sarcoma Lesions in HIV Type 1-Infected Patients: A Pilot Clinical Study

2001 ◽  
Vol 17 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Michael J. Scolaro ◽  
Lucy B. Gunnill ◽  
Laura E. Pope ◽  
M.H. Khalil ◽  
David H. Katz ◽  
...  
Keyword(s):  
Clinical Study ◽  
Kaposi's Sarcoma ◽  
Antiviral Drug ◽  
Kaposi’S Sarcoma ◽  
Pilot Clinical Study ◽  
Hiv Type 1

HIV Type 1 Tat Protein Is a Survival Factor for Kaposi's Sarcoma and Endothelial Cells

2001 ◽  
Vol 17 (10) ◽  
pp. 965-976 ◽  
Author(s):  
Vincenzo Cantaluppi ◽  
Luigi Biancone ◽  
Mariarosaria Boccellino ◽  
Sophie Doublier ◽  
Roberto Benelli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Tat Protein ◽  
Survival Factor ◽  
Hiv Type 1

scholarly journals Interleukin-8 and Growth-Regulated Oncogene Alpha Mediate Angiogenesis in Kaposi's Sarcoma

2002 ◽  
Vol 76 (22) ◽  
pp. 11570-11583 ◽  
Author(s):  
Brian R. Lane ◽  
Jianguo Liu ◽  
Paul J. Bock ◽  
Dominique Schols ◽  
Michael J. Coffey ◽  
...  
Keyword(s):  
Cell Culture ◽  
Endothelial Cells ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Interleukin 8 ◽  
Cellular Growth ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Stimulation Of

ABSTRACT The development of the complex neoplasm Kaposi's sarcoma is dependent on infection with the Kaposi's sarcoma-associated herpesvirus (KSHV) and appears to be greatly enhanced by cytokines and human immunodeficiency virus type 1 (HIV-1) Tat. Interleukin-8 (IL-8) and growth-regulated oncogene alpha (GRO-α) are chemokines involved in chemoattraction, neovascularization, and stimulation of HIV-1 replication. We have previously demonstrated that production of GRO-α is stimulated by exposure of monocyte-derived macrophages (MDM) to HIV-1. Here we show that exposure of MDM to HIV-1, viral Tat, or viral gp120 leads to a substantial increase in IL-8 production. We also demonstrate that IL-8 and GRO-α are induced by KSHV infection of endothelial cells and are crucial to the angiogenic phenotype developed by KSHV-infected endothelial cells in cell culture and upon implantation into SCID mice. Thus, the three known etiological factors in Kaposi's sarcoma pathogenesis—KSHV, HIV-1 Tat, and cellular growth factors—might be linked, in part, through induction of IL-8 and GRO-α.

scholarly journals Angiogenic Effects of Extracellular Human Immunodeficiency Virus Type 1 Tat Protein and Its Role in the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

2002 ◽  
Vol 15 (2) ◽  
pp. 310-326 ◽  
Author(s):  
Giovanni Barillari ◽  
Barbara Ensoli
Keyword(s):  
Human Immunodeficiency Virus ◽  
Kaposi's Sarcoma ◽  
Secretory Pathway ◽  
Active Form ◽  
Kaposi’S Sarcoma ◽  
Biologically Active ◽  
Viral Gene ◽  
Tat Protein ◽  
Immunodeficiency Virus

SUMMARY The Tat protein of human immunodeficiency virus (HIV) type 1 is a transactivator of viral gene expression that is required for virus replication and spread. Moreover, Tat is released by acutely HIV-infected cells via a leaderless secretory pathway and in a biologically active form that exerts effects on both HIV-infected and uninfected cells from different organs and systems. This review focuses on the activities of extracellular Tat protein on endothelial cells, on angiogenesis, and on the pathogenesis of AIDS-associated angioproliferative diseases such as Kaposi's sarcoma. In particular, we discuss results from different groups indicating that Tat mimics the proangiogenic activities of extracellular matrix molecules and that it enhances the effects of angiogenic factors.

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