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Journal of Virology, April 2003, p. 4070-4080, Vol. 77, No. 7
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.7.4070-4080.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Hepatitis C Virus Glycoproteins Interact with DC-SIGN and DC-SIGNR

Stefan Pöhlmann,1 Jie Zhang,2 Frédéric Baribaud,1 Zhiwei Chen,3 George J. Leslie,1 George Lin,4 Angela Granelli-Piperno,4 Robert W. Doms,1 Charles M. Rice,2 and Jane A. McKeating2*

Department of Microbiology and Department of Medicine, Hematology-Oncology Division, University of Pennsylvania, Philadelphia, Pennsylvania 19104,1 Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease,2 Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, New York 10021,4 Aaron Diamond AIDS Research Center, New York, New York 100163

Received 19 July 2002/ Accepted 12 December 2002

DC-SIGN and DC-SIGNR are two closely related membrane-associated C-type lectins that bind human immunodeficiency virus (HIV) envelope glycoprotein with high affinity. Binding of HIV to cells expressing DC-SIGN or DC-SIGNR can enhance the efficiency of infection of cells coexpressing the specific HIV receptors. DC-SIGN is expressed on some dendritic cells, while DC-SIGNR is localized to certain endothelial cell populations, including hepatic sinusoidal endothelial cells. We found that soluble versions of the hepatitis C virus (HCV) E2 glycoprotein and retrovirus pseudotypes expressing chimeric forms of both HCV E1 and E2 glycoproteins bound efficiently to DC-SIGN and DC-SIGNR expressed on cell lines and primary human endothelial cells but not to other C-type lectins tested. Soluble E2 bound to immature and mature human monocyte-derived dendritic cells (MDDCs). Binding of E2 to immature MDDCs was dependent on DC-SIGN interactions, while binding to mature MDDCs was partly independent of DC-SIGN, suggesting that other cell surface molecules may mediate HCV glycoprotein interactions. HCV interactions with DC-SIGN and DC-SIGNR may contribute to the establishment or persistence of infection both by the capture and delivery of virus to the liver and by modulating dendritic cell function.

* Corresponding author. Mailing address: Center for the Study of Hepatitis, The Rockefeller University, 1230 York Ave., New York, NY 10021. Phone: (212) 327-7066. Fax: (212) 327-7048. E-mail: mckeatj{at}mail.rockefeller.edu.

Journal of Virology, April 2003, p. 4070-4080, Vol. 77, No. 7
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.7.4070-4080.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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