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T Cell Complicity in HIV Spread
Retrovirology volume 2, Article number: S139 (2005)
Background
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.
Materials and methods
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.
Results
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.
Conclusion
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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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 ( https://creativecommons.org/licenses/by/2.0 ), 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). https://doi.org/10.1186/1742-4690-2-S1-S139
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DOI: https://doi.org/10.1186/1742-4690-2-S1-S139
Keywords
- Human Immunodeficiency Virus
- Effector Cell
- Lipid Raft
- Virus Assembly
- Molecule Interaction