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

J Virol. 2002 Jul;76(13):6841-4. doi: 10.1128/jvi.76.13.6841-6844.2002.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion Molecules*
  • Dendritic Cells / metabolism
  • Ebolavirus / metabolism
  • Ebolavirus / pathogenicity*
  • Humans
  • Jurkat Cells
  • Lectins / metabolism*
  • Lectins, C-Type*
  • Monocytes
  • Receptors, Antigen / metabolism*
  • Receptors, Cell Surface / metabolism*
  • Receptors, Virus / metabolism*
  • Tumor Cells, Cultured
  • Virion / metabolism


  • CLEC4M protein, human
  • Cell Adhesion Molecules
  • DC-specific ICAM-3 grabbing nonintegrin
  • Lectins
  • Lectins, C-Type
  • Receptors, Antigen
  • Receptors, Cell Surface
  • Receptors, Virus