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      C-type lectins DC-SIGN and L-SIGN mediate cellular entry by Ebola virus in cis and in trans.

      Journal of Biology
      Cell Adhesion Molecules, Dendritic Cells, metabolism, Ebolavirus, pathogenicity, Humans, Jurkat Cells, Lectins, Lectins, C-Type, Monocytes, Receptors, Antigen, Receptors, Cell Surface, Receptors, Virus, Tumor Cells, Cultured, Virion

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          Abstract

          Ebola virus is a highly lethal pathogen responsible for several outbreaks of hemorrhagic fever. Here we show that the primate lentiviral binding C-type lectins DC-SIGN and L-SIGN act as cofactors for cellular entry by Ebola virus. Furthermore, DC-SIGN on the surface of dendritic cells is able to function as a trans receptor, binding Ebola virus-pseudotyped lentiviral particles and transmitting infection to susceptible cells. Our data underscore a role for DC-SIGN and L-SIGN in the infective process and pathogenicity of Ebola virus infection.

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