Boonrat TassaneetrithepTimothy H. BurgessAngela Granelli-PipernoChristine TrumpfhellerJennifer FinkeWellington SunMichael A. EllerKovit PattanapanyasatSuttipant SarasombathDeborah L. BirxRalph M. SteinmanSarah SchlesingerMary A. MarovichWalter Reed Army Institute of ResearchNaval Medical Research CenterRockefeller UniversityMahidol University2018-07-242018-07-242003-04-01Journal of Experimental Medicine. Vol.197, No.7 (2003), 823-829002210072-s2.0-0344642934https://repository.li.mahidol.ac.th/handle/20.500.14594/20911Dengue 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.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1084/jem.20021840