CCL2 increases X4-tropic HIV-1 entry into resting CD4+ T cells.
During human immunodeficiency virus type 1 (HIV-1) infection, there is a strong positive correlation between CCL2 levels and HIV viral load. To determine whether CCL2 alters HIV-1 infection of resting CD4(+) T cells, we infected purified resting CD4(+) T cells after incubation with CCL2. We show that CCL2 up-regulates CXCR4 on resting CD4(+) T cells in a CCR2-dependent mechanism, and that this augmentation of CXCR4 expression by CCL2 increases the ability of these cells to be chemoattracted to CXCR4 using gp120 and renders them more permissive to X4-tropic HIV-1 infection. Thus, CCL2 has the capacity to render a large population of lymphocytes more susceptible to HIV-1 late in the course of infection.
Campbell
Grant R
GR
Department of Pediatrics, University of California San Diego, La Jolla, California 92093-0672, USA.
Spector
Stephen A
SA
D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism* / Q000821:virology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism* / Q000494:pharmacology; D015658:HIV Infections / Q000378:metabolism*; D015497:HIV-1 / Q000378:metabolism*; D006801:Humans; D019718:Receptors, CXCR4 / Q000096:biosynthesis*; D015854:Up-Regulation / Q000187:drug effects; D053586:Virus Internalization / Q000187:drug effects
C111835:CCL2 protein, human; C527276:CXCR4 protein, human; D018932:Chemokine CCL2; D019718:Receptors, CXCR4
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