Abstract

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.

Author affiliations

1. Oliver T. Fackler is at the Department of Virology, University of Heidelberg, D-69120 Heidelberg, Germany.
2. Andres Alcover is at the Unité de Biologie Cellulaire des Lymphocytes, Institut Pasteur, 75724 Paris Cedex 15, France.
3. Olivier Schwartz is at the Groupe Virus et Immunité, Institut Pasteur.

Correspondence to: Oliver T. Fackler¹ Email: oliver_fackler@med.uni-heidelberg.de

Correspondence to: Olivier Schwartz³ Email: schwartz@pasteur.fr

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