Document Detail

Mechanisms of enhanced HIV spread through T-cell virological synapses.
MedLine Citation:
PMID:  23278744     Owner:  NLM     Status:  In-Data-Review    
An elaborate network of cell-cell interactions in the immune system is essential for vertebrates to mount adaptive immune responses against invading pathogens. For lymphotropic viruses such as the human immunodeficiency virus type 1 (HIV-1), these immune cell interactions can also promote the spread of the virus within the host. The main target of HIV-1 infection is the CD4(+) helper T lymphocyte, a cell type that is responsible for coordinating immune responses and modulating effector responses to foreign antigens. As part of their normal immune surveillance duties, these cells migrate actively within lymphoid tissues and can travel from inductive sites to effector sites in search of their cognate antigen. For CD4(+) T cells, there is an ongoing search for a unique peptide antigen presented in the context of class II MHC that can activate a proliferative or tolerogenic response. This iterative and continual probing and interrogation of other cells determine the outcome of immune responses. Recent studies in vitro have revealed that the viral infection program induces cell-cell interactions called virological synapses between infected and uninfected CD4(+) T cells. These long-lived, virally induced adhesive contacts greatly enhance the rate of productive infection and may be central to the spread of the virus in vivo. Here, we review aspects of this efficient mode of cell-to-cell infection and the implications for our understanding of HIV-1 pathogenesis.
Benjamin M Dale; Raymond A Alvarez; Benjamin K Chen
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Immunological reviews     Volume:  251     ISSN:  1600-065X     ISO Abbreviation:  Immunol. Rev.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7702118     Medline TA:  Immunol Rev     Country:  England    
Other Details:
Languages:  eng     Pagination:  113-24     Citation Subset:  IM    
Copyright Information:
© 2012 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.
Division of Infectious Disease, Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, New York, NY, USA.
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