Endothelial cells enhance human immunodeficiency virus type 1 replication in macrophages through a C/EBP-dependent mechanism.

Content Provider	Semantic Scholar
Author	Lee, Eileen S. Zhou, Haixia Henderson, Andrew J.
Copyright Year	2001
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/EBPbeta is critical for macrophages to respond to endothelial cell-derived signals. We show that endothelial cells significantly enhance C/EBPbeta 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/EBPbeta, provide a microenvironment that supports HIV-1 replication in monocytes/macrophages.
File Format	PDF HTM / HTML
DOI	10.1128/jvi.75.20.9703-9712.2001
PubMed reference number	11559803
Journal	Medline
Volume Number	75
Issue Number	20
Alternate Webpage(s)	http://europepmc.org/articles/pmc114542?pdf=render
Alternate Webpage(s)	https://doi.org/10.1128/jvi.75.20.9703-9712.2001
Journal	Journal of virology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article