Publication: DC-SIGN (CD209) mediates dengue virus infection of human dendritic cells
Issued Date
2003-04-01
Resource Type
ISSN
00221007
Other identifier(s)
2-s2.0-0344642934
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Experimental Medicine. Vol.197, No.7 (2003), 823-829
Suggested Citation
Boonrat Tassaneetrithep, Timothy H. Burgess, Angela Granelli-Piperno, Christine Trumpfheller, Jennifer Finke, Wellington Sun, Michael A. Eller, Kovit Pattanapanyasat, Suttipant Sarasombath, Deborah L. Birx, Ralph M. Steinman, Sarah Schlesinger, Mary A. Marovich DC-SIGN (CD209) mediates dengue virus infection of human dendritic cells. Journal of Experimental Medicine. Vol.197, No.7 (2003), 823-829. doi:10.1084/jem.20021840 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/20911
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Title
DC-SIGN (CD209) mediates dengue virus infection of human dendritic cells
Abstract
Dengue virus is a single-stranded, enveloped RNA virus that productively infects human dendritic cells (DCs) primarily at the immature stage of their differentiation. We now find that all four serotypes of dengue use DC-SIGN (CD209), a C-type lectin, to infect dendritic cells. THP-1 cells become susceptible to dengue infection after transfection of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), or its homologue L-SIGN, whereas the infection of dendritic cells is blocked by anti-DC-SIGN antibodies and not by antibodies to other molecules on these cells. Viruses produced by dendritic cells are infectious for DC-SIGN- and L-SIGN-bearing THP-1 cells and other permissive cell lines. Therefore, DC-SIGN may be considered as a new target for designing therapies that block dengue infection.