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

Jolly C, Mitar I, Sattentau QJ

The Sir William Dunn School of Pathology, The University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom. clare.jolly@path.ox.ac.uk

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.

Published 26 November 2007 in J Virol, 81(24): 13916-21.
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