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T Cell Complicity in HIV Spread


The human immunodeficiency virus type-1 (HIV-1) can spread between target cells via release of cell-free virions or by direct cell-cell transmission across a virological synapse. Virus is released from T cells in a polarized manner from regions of the plasma membrane rich in raft-associated lipids and proteins.

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We have established a model system in which conjugate formation between HIV-1-infected (effector) and unifected (target) T cells results in the assembly of a virological synapse (VS) at the intercellular interface.


Env-receptor and adhesion molecule interactions are required for functional VS formation. Gag transits to the plasma membrane in a CD63/CD81+ compartment. Polarization of HIV-1 Env and Gag on effector cells and subsequent viral release depends on actin and tubulin remodelling and lipid raft and PIP2 integrity.


We hypothesize that viral infection triggers pre-existing T cell programs that activate elements of the T cell secretory apparatus to deliver Gag, allowing efficient virus assembly.

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Correspondence to Quentin Sattentau.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Jolly, C., Mitar, I. & Sattentau, Q. T Cell Complicity in HIV Spread. Retrovirology 2 (Suppl 1), S139 (2005).

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