DC-SIGN Interactions with Human Immunodeficiency Virus Type 1 and 2 and Simian Immunodeficiency Virus

doi:10.1128/JVI.75.10.4664-4672.2001

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Journal of Virology, May 2001, p. 4664-4672, Vol. 75, No. 10
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.10.4664-4672.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

DC-SIGN Interactions with Human Immunodeficiency Virus Type 1 and 2 and Simian Immunodeficiency Virus

Stefan Pöhlmann,¹ Frédéric Baribaud,¹ Benhur Lee,¹ George J. Leslie,¹ Melissa D. Sanchez,¹ Kirsten Hiebenthal-Millow,² Jan Münch,²^, Frank Kirchhoff,²^, and Robert W. Doms¹^,^*

Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104,¹ and Institute for Clinical and Molecular Virology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany²

Received 30 November 2000/Accepted 21 February 2001

Dendritic cells (DCs) efficiently bind and transmit human immunodeficiency virus (HIV) to cocultured T cells and so may playan important role in HIV transmission. DC-SIGN, a novel C-typelectin that is expressed in DCs, has recently been shown to bindR5 HIV type 1 (HIV-1) strains and a laboratory-adapted X4 strain.To characterize the interaction of DC-SIGN with primate lentiviruses,we investigated the structural determinants of DC-SIGN requiredfor virus binding and transmission to permissive cells. We constructeda panel of DC-SIGN mutants and established conditions which allowedcomparable cell surface expression of all mutants. We found thatR5, X4, and R5X4 HIV-1 isolates as well as simian immunodeficiencyand HIV-2 strains bound to DC-SIGN and could be transmitted toCD4/coreceptor-positive cell types. DC-SIGN contains a singleN-linked carbohydrate chain that is important for efficient cellsurface expression but is not required for DC-SIGN-mediated virusbinding and transmission. In contrast, C-terminal deletions removingeither the lectin binding domain or the repeat region abrogatedDC-SIGN function. Trypsin-EDTA treatment inhibited DC-SIGN mediatedinfection, indicating that virus was maintained at the surfaceof the DC-SIGN-expressing cells used in this study. Finally, quantitativefluorescence-activated cell sorting analysis of AU1-tagged DC-SIGNrevealed that the efficiency of virus transmission was stronglyaffected by variations in DC-SIGN expression levels. Thus, variationsin DC-SIGN expression levels on DCs could greatly affect the susceptibilityof human individuals to HIVinfection.

^* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, University of Pennsylvania, 806 Abramson,Philadelphia, PA 19104. Phone: (215) 898-0890. Fax: (215) 573-2883.E-mail: doms{at}mail.med.upenn.edu.

Present address: Abteilung Virologie, Institut für Mikrobiologie und Immunologie, Universitätsklinikum Ulm, 89081 Ulm,Germany.

Journal of Virology, May 2001, p. 4664-4672, Vol. 75, No. 10
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.10.4664-4672.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

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