DC-SIGN (CD209) Mediates Dengue Virus Infection of Human Dendritic Cells

Boonrat Tassaneetrithep(Henry M. Jackson Foundation), Timothy H. Burgess(Naval Medical Research Command), Angela Granelli‐Piperno(Rockefeller University), Christine Trumpfheller(Rockefeller University), Jennifer Finke(Rockefeller University), Wellington Sun(Walter Reed Army Institute of Research), Michael A. Eller(Henry M. Jackson Foundation), Kovit Pattanapanyasat(Siriraj Hospital), S Sarasombath(Siriraj Hospital), Deborah L. Birx(Henry M. Jackson Foundation), Ralph M. Steinman(Rockefeller University), Sarah J. Schlesinger(Rockefeller University), Mary Marovich(Henry M. Jackson Foundation)
The Journal of Experimental Medicine
April 7, 2003
Cited by 890Open Access
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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.


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