Adhesion molecule interactions facilitate human immunodeficiency virus type 1-induced virological synapse formation between T cells.

Journal article

Human immunodeficiency virus type 1 (HIV-1) can spread between CD4+ T cells by using a virological synapse (VS). The VS assembly is a cytoskeleton-driven process dependent on HIV-1 envelope glycoprotein (Env)-receptor engagement and is hypothesized to require adhesion molecule interactions. Here we demonstrate that leukocyte function-associated antigen 1 (LFA-1), intercellular adhesion molecule 1 (ICAM-1), and ICAM-3 are enriched at the VS and that inhibition of these interactions influences conjugate formation and reduces VS assembly. Moreover, CD4+ T cells deficient in LFA-1 or with modified LFA-1 function were less able to support VS assembly and cell-cell transfer of HIV-1. Thus, cognate adhesion molecule interactions at the VS are important for HIV-1 spread between T cells.

Authors: Jolly, C; Mitar, I; Sattentau, Q

• Publication status: Published
• Journal: Journal of virology
• Volume: 81
• Issue: 24
• Pages: 13916-13921
• Publication date: 2007-12-01
• DOI: 10.1128/jvi.01585-07
• EISSN: 1098-5514
• ISSN: 0022-538X
• Language: English
• Keywords: Antigens, CD; HIV-1; Flow Cytometry; Humans; Intercellular Junctions; Jurkat Cells; Cell Adhesion Molecules; Intercellular Adhesion Molecule-1; HIV Infections; Lymphocyte Function-Associated Antigen-1; CD4-Positive T-Lymphocytes