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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2170-2179. Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-09-3129. This Article Full Text (PDF) All Versions of this Article: 2003-09-3129v1 103/6/2170    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Turville, S. G Articles by Cunningham, A. L Search for Related Content PubMed PubMed Citation Articles by Turville, S. G Articles by Cunningham, A. L Social Bookmarking                   What's this? Submitted September 15, 2003 Accepted October 17, 2003 Immunodeficiency virus uptake, turnover, and two-phase transfer in human dendritic cells Stuart G Turville, John J Santos, Ines Frank, Paul U Cameron, John Wilkinson, Monica Miranda-Saksena, Joanne Dable, Hella Stossel, Nikolaus Romani, Michael Piatak, Jeffrey D Lifson, Melissa Pope, and Anthony L Cunningham* Centre For Virus Research, Westmead Millennium Institute, Sydney, NSW, Australia Centre for Biomedical Research, Population Council, New York, NY, USA Department of Microbiology and Immunology, University of Melbourne, Melbourne, VIC, Australia Department of Dermatology and Venereology, University of Innsbruck, Innsbruck, Austria AIDS Vaccine Program, National Cancer Institute at Frederick, Frederick, MD, USA * Corresponding author; email: tony_cunningham{at}mail.wmi.usyd.edu.au. HIV-1 subverts antigen processing in dendritic cells (DCs) resulting in viral uptake, infection, and transfer to T-cells. Although DCs bound monomeric gp120 and HIV-1 similarly, virus rarely co-localized with endolysosomal markers, unlike gp120, suggesting HIV-1 alters endolysosomal trafficking. Virus within DC intracellular compartments rapidly moved to DC-CD4+ lymphocyte synapses when introduced to CD4+ lymphocyte cultures. Although viral harboring and transfer from non-lysosomal compartments was transient, given DC-associated virus protein, nucleic acids, and infectious HIV-1 transfer to CD4+ lymphocytes decayed within 24 hours. However a second long term transfer phase was apparent in immature DCs after 48 hours as a zidovudine-sensitive rise in proviral DNA. Therefore, DCs transfer HIV-1 to CD4+ lymphocytes in two distinct phases. Immature and mature DCs first divert virus from the endolysosomal pathway to the DC-T-cell synapse. Secondly, the later transfer phase from immature DCs is through de novo HIV-1 production. Thus the controversy of DCs being infected or not infected for the mechanics of viral transfer to CD4+ lymphocytes can be addressed as a function of time. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Muratori, E. Ruggiero, A. Sistigu, R. Bona, and M. Federico Human immunodeficiency virus type 1 (HIV-1) protease inhibitors block cell-to-cell HIV-1 endocytosis in dendritic cells J. Gen. Virol., November 1, 2009; 90(11): 2777 - 2787. [Abstract] [Full Text] [PDF] M. R. Tardif, C. Gilbert, S. Thibault, J.-F. Fortin, and M. J. Tremblay LFA-1 Antagonists as Agents Limiting Human Immunodeficiency Virus Type 1 Infection and Transmission and Potentiating the Effect of the Fusion Inhibitor T-20 Antimicrob. Agents Chemother., November 1, 2009; 53(11): 4656 - 4666. [Abstract] [Full Text] [PDF] A. R. Anand, A. Prasad, R. R. Bradley, Y. S. Deol, T. Nagaraja, X. Ren, E. F. Terwilliger, and R. K. 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