CD4- and dynamin-dependent endocytosis of HIV-1 into plasmacytoid dendritic cells

Journal Article · Mon Feb 20 00:00:00 EST 2012 · Virology

DOI:https://doi.org/10.1016/J.VIROL.2011.11.026· OSTI ID:22149259

Pritschet, Kathrin; Donhauser, Norbert; Schuster, Philipp; Ries, Moritz; Haupt, Sabrina; Kittan, Nicolai A.; Korn, Klaus ^[1]; Poehlmann, Stefan ^[2]; Holland, Gudrun; Bannert, Norbert ^[3]; Bogner, Elke ^[4]; Schmidt, Barbara ^[1]

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1. Institute of Clinical and Molecular Virology, National Reference Centre for Retroviruses, Friedrich-Alexander-Universitaet Erlangen-Nuernberg, 91054 Erlangen (Germany)
2. Institute of Virology, Hannover Medical School, 30625 Hannover (Germany)
3. Robert Koch-Institute, Center for Biological Security 4, 13353 Berlin (Germany)
4. Institute of Virology, Charite University Hospital, 10117 Berlin (Germany)

Chronic immune activation, triggered by plasmacytoid dendritic cell (PDC) interferon (IFN)-alpha production, plays an important role in HIV-1 pathogenesis. As the entry of HIV-1 seems to be important for the activation of PDC, we directly characterized the viral entry into these cells using immuno-electron microscopy, cellular fractionation, confocal imaging, and functional experiments. After attachment to PDC, viruses were taken up in an energy-dependent manner. The virions were located in compartments positive for caveolin; early endosomal antigen 1; Rab GTPases 5, 7 and 9; lysosomal-associated membrane protein 1. PDC harbored more virus in endocytic vesicles than CD4+ T cells (p < 0.05). Blocking CD4 inhibited the uptake of virions into cytosolic and endosomal compartments. Dynasore, an inhibitor of dynamin-dependent endocytosis, not the fusion inhibitor T-20, reduced the HIV-1 induced IFN-alpha production. Altogether, our morphological and functional data support the role of endocytosis for the entry and IFN-alpha induction of HIV-1 in PDC.

• OSTI ID: 22149259
• Journal Information: Virology, Vol. 423, Issue 2; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
• Country of Publication: United States
• Language: English

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