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Literature detail

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

Carmen P Alvarez1 Fátima Lasala Jaime Carrillo Oscar Muñiz Angel L Corbí Rafael Delgado
Affiliations 1 institutions
  1. Laboratory of Molecular Microbiology, Dept. of Microbiology, Hospital 12 de Octubre, 28041 Madrid, Spain.
PMID 12050398 2002 J Virol eng ppublish
PubMed DOI Browse context

Article

Publication summary

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.

Cell Adhesion Molecules Lectins, C-Type DC-Specific ICAM-3 Grabbing Nonintegrin Dendritic Cells Ebolavirus Humans Jurkat Cells Lectins Monocytes Receptors, Antigen Receptors, Cell Surface Receptors, Virus Tumor Cells, Cultured Virion CLEC4M protein, human

Structured evidence records

Evidence records

1 total
Receptor Usage 1 records
Receptor Usage Extraction confidence 0.98
Key finding

Ebola virus entry is mediated by the C-type lectins DC-SIGN and L-SIGN, with DC-SIGN functioning as a trans receptor on dendritic cells to facilitate infection.

Virus
EBOV
Location
Not specified
Supporting text

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.

Method
pseudovirus assay; cell-entry assay
Receptors
DC-SIGN
Host factors
L-SIGN