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Immunol Res. 2012 Dec;54(1-3):133-9. doi: 10.1007/s12026-012-8320-8.

T cell virological synapses and HIV-1 pathogenesis.

Author information

1
Division of Infectious Disease, Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1630, New York, NY 10029, USA. ben.chen@mssm.edu

Abstract

Human immunodeficiency virus type 1 is the cause of a modern global pandemic associated with progressive acquired immune deficiency. The infection is characterized by the loss of the primary target of viral infection, the CD4+ T cell. The measurement of plasma viremia in patients can predict the rate of CD4+ cell decline; however, it is not clear whether this cell-free plasma virus represents the engine that drives viral spread. Active viral replication is mainly observed within lymphoid tissues that are hotbeds of cell-cell interactions that initiate and organize immune responses. It is well established that cell-cell interactions enhance viral spread in vitro. Dendritic cell-T cell interactions, which lie at the heart of adaptive immune responses, enhance viral infection in vitro. Interactions between infected and uninfected CD4+ T cells are a dominant route of viral spread in vitro and are likely to play a central role in viral dissemination in vivo. Future studies will test existing paradigms of HIV-1 dissemination to determine whether virus-transmitting contacts between infected and uninfected T cells called virological synapses are the dominant mode of viral spread in vivo. Here, we review the status of our understanding of this mode of infection with a focus on T cell-T cell interactions and examine how it may explain resistance to neutralizing antibodies and or the generation of genetic diversity of HIV.

PMID:
22477441
DOI:
10.1007/s12026-012-8320-8
[Indexed for MEDLINE]

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