Modulation of the immunological synapse: a key to HIV-1 pathogenesis?
AIDS is the result of a constant struggle between the lentivirus HIV and the immune system. Infection with HIV interferes directly with the function of CD4(+) T cells and manipulates the host immune response to the virus. Recent studies indicate that the viral protein Nef, a central player in HIV pathogenesis, impairs the ability of infected lymphocytes to form immunological synapses with antigen-presenting cells and affects T-cell-receptor-mediated stimulation. An integrative picture of the abnormal behaviour of HIV-infected lymphocytes is therefore emerging. We propose that modulating lymphocyte signalling, apoptosis and intracellular trafficking ensures efficient spread of the virus in the hostile environment of the immune system.
Fackler
Oliver T
OT
Oliver T. Fackler is at the Department of Virology, University of Heidelberg, D-69120 Heidelberg, Germany. oliver_fackler@med.uni-heidelberg.de
Alcover
Andres
A
Schwartz
Olivier
O
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology*; D015693:Gene Products, nef / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D021381:Protein Transport / Q000276:immunology; D020239:Receptor Cross-Talk / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D054311:nef Gene Products, Human Immunodeficiency Virus
D015693:Gene Products, nef; D011948:Receptors, Antigen, T-Cell; D054311:nef Gene Products, Human Immunodeficiency Virus