Effect of Extracellular Human Immunodeficiency Virus Type 1 Glycoprotein 120 on Primary Human Vascular Endothelial Cell Cultures

1999 ◽  
Vol 15 (14) ◽  
pp. 1265-1277 ◽  
Author(s):  
Ming-Bo Huang ◽  
Melissa Hunter ◽  
Vincent C. Bond
Angiogenesis ◽  
2012 ◽  
Vol 15 (1) ◽  
pp. 151-163 ◽  
Author(s):  
Martin J. Siemerink ◽  
Ingeborg Klaassen ◽  
Ilse M. C. Vogels ◽  
Arjan W. Griffioen ◽  
Cornelis J. F. Van Noorden ◽  
...  

1991 ◽  
Vol 88 (18) ◽  
pp. 7998-8002 ◽  
Author(s):  
E. Langhoff ◽  
E. F. Terwilliger ◽  
H. J. Bos ◽  
K. H. Kalland ◽  
M. C. Poznansky ◽  
...  

2001 ◽  
Vol 75 (20) ◽  
pp. 9703-9712 ◽  
Author(s):  
Eileen S. Lee ◽  
Huiyu Zhou ◽  
Andrew J. Henderson

ABSTRACT Macrophages are early targets of human immunodeficiency virus type 1 (HIV-1) infection and serve as potential reservoirs for long-term infection. Through inflammatory mediators and direct cell contact, infected macrophages interact with neighboring cell populations, such as the endothelium, which create a microenvironment favorable for HIV-1 replication. We hypothesize that the transcriptional activator C/EBPβ is critical for macrophages to respond to endothelial cell-derived signals. We show that endothelial cells significantly enhance C/EBPβ binding activity and HIV-1 replication in macrophages. This increase in HIV-1 transcription is due to cell-cell contact as well as the production of soluble factors, mediated in part by ICAM-1 and interleukin 6, respectively. Furthermore, C/EBP factors are necessary for endothelial cell-dependent activation of HIV-1 transcription in macrophages, and HIV-1 induction can be inhibited by a C/EBP dominant-negative protein. In addition, C/EBP binding sites are necessary for efficient LTR activity and HIV-1 replication in the presence of endothelial cells. Taken together, these results indicate that endothelial cells, through the activation of C/EBPβ, provide a microenvironment that supports HIV-1 replication in monocytes/macrophages.


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