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Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
Published on: September 1, 2015
CCL2 increases X4-tropic HIV-1 entry into resting CD4+ T cells
Grant R Campbell1, Stephen A Spector
1Department of Pediatrics, University of California San Diego, La Jolla, California 92093-0672, USA.
The Journal of Biological Chemistry
|September 12, 2008
Summary
Chemokine ligand 2 (CCL2) increases susceptibility to human immunodeficiency virus type 1 (HIV-1) infection in CD4(+) T cells. CCL2 up-regulates CXCR4, enhancing viral entry and infection late in HIV-1 disease.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Elevated levels of chemokine ligand 2 (CCL2) correlate with higher human immunodeficiency virus type 1 (HIV-1) viral load.
- The role of CCL2 in the direct infection of resting CD4(+) T cells by HIV-1 requires further elucidation.
Purpose of the Study:
- To investigate whether CCL2 influences HIV-1 infection in resting CD4(+) T cells.
- To determine the mechanism by which CCL2 might affect HIV-1 susceptibility.
Main Methods:
- Purified resting CD4(+) T cells were incubated with CCL2.
- Cells were subsequently infected with HIV-1.
- Expression of CXCR4 and CCR2 was analyzed.
- Chemoattraction assays using gp120 were performed.
Main Results:
- CCL2 up-regulates CXCR4 expression on resting CD4(+) T cells via a CCR2-dependent pathway.
- Increased CXCR4 expression enhances chemoattraction to gp120.
- CCL2 treatment renders CD4(+) T cells more permissive to X4-tropic HIV-1 infection.
Conclusions:
- CCL2 plays a critical role in increasing the susceptibility of resting CD4(+) T cells to HIV-1 infection.
- This effect is mediated by CCL2-induced upregulation of CXCR4, facilitating viral entry.
- CCL2 may contribute to increased HIV-1 permissiveness in lymphocytes during later stages of infection.
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