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Human immunodeficiency virus type 1 (HIV-1)-infected T cells form a virological synapse with noninfected CD4(+) T cells in order to efficiently transfer HIV-1 virions from cell to cell. The virological synapse is a specialized cellular junction that is similar in some respects to the immunological synapse involved in T-cell activation and effector functions mediated by the T-cell antigen receptor. The immunological synapse stops T-cell migration to allow a sustained interaction between T-cells and antigen-presenting cells. Here, we have asked whether HIV-1 envelope gp120 presented on a surface to mimic an HIV-1-infected cell also delivers a stop signal and if this is sufficient to induce a virological synapse. We demonstrate that HIV-1 gp120-presenting surfaces arrested the migration of primary activated CD4 T cells that occurs spontaneously in the presence of ICAM-1 and induced the formation of a virological synapse, which was characterized by segregated supramolecular structures with a central cluster of envelope surrounded by a ring of ICAM-1. The virological synapse was formed transiently, with the initiation of migration within 30 min. Thus, HIV-1 gp120-presenting surfaces induce a transient stop signal and supramolecular segregation in noninfected CD4(+) T cells.

Original publication

DOI

10.1128/jvi.00835-08

Type

Journal article

Journal

Journal of Virology

Publication Date

10/2008

Volume

82

Pages

9445 - 9457

Addresses

VA Medical Center, 423 E. 23rd St., Room 18-124 North, New York, NY 10010, USA.

Keywords

Leukocytes, Mononuclear, CD4-Positive T-Lymphocytes, Immune System, Animals, Humans, Mice, HIV-1, Lipid Bilayers, Intercellular Adhesion Molecule-1, HIV Envelope Protein gp120, Cell Adhesion, Signal Transduction, Cell Movement, Gene Expression Regulation, Viral, Image Processing, Computer-Assisted