CCR7 ligands CCL19 and CCL21 increase permissiveness of resting memory CD4+ T cells to HIV-1 infection: a novel model of HIV-1 latency

Blood. 2007 Dec 15;110(13):4161-4. doi: 10.1182/blood-2007-06-097907. Epub 2007 Sep 19.

Abstract

Latent HIV-1 infection of resting memory CD4(+) T cells represents the major barrier to HIV-1 eradication. To determine whether the CCR7 ligands involved in lymphocyte migration can alter HIV-1 infection of resting CD4(+) T cells, we infected purified resting CD4(+) T cells after incubation with the chemokines CCL19 and CCL21. Incubation with CCL19 or CCL21 did not alter markers of T-cell activation or proliferation. However, after HIV-1 infection of CCL19- or CCL21-treated CD4(+) T-cells, we observed low-level HIV-1 production but high concentrations of integrated HIV-1 DNA, approaching that seen in mitogen-stimulated T-cell blasts. Restimulation of CCL19-treated infected CD4(+) T cells resulted in virus production consistent with establishment of postintegration latency. CCR7 ligands facilitate efficient entry of HIV-1 into resting CD4(+) T cells. These studies demonstrate a unique action of the chemokines CCL19 and CCL21 and provide a novel model with which to study HIV-1 latency in vitro.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / virology*
  • Chemokine CCL19 / pharmacology*
  • Chemokine CCL21 / pharmacology*
  • HIV Infections / etiology
  • HIV-1 / pathogenicity*
  • Humans
  • Immunologic Memory*
  • Receptors, CCR7
  • Virus Latency*

Substances

  • Chemokine CCL19
  • Chemokine CCL21
  • Receptors, CCR7