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Journal of Virology, December 2007, p. 13916-13921, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.01585-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Adhesion Molecule Interactions Facilitate Human Immunodeficiency Virus Type 1-Induced Virological Synapse Formation between T Cells{triangledown}

Clare Jolly,* Ivonne Mitar, and Quentin J. Sattentau

The Sir William Dunn School of Pathology, The University of Oxford, Oxford OX1 3RE, United Kingdom

Received 20 July 2007/ Accepted 24 September 2007

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.

* Corresponding author. Mailing address: The Sir William Dunn School of Pathology, The University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom. Phone: 44 1865 275510. Fax: 44 1865 275511. E-mail: clare.jolly{at}path.ox.ac.uk

{triangledown} Published ahead of print on 3 October 2007.

Journal of Virology, December 2007, p. 13916-13921, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.01585-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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