Abstract
Several Ebola viruses cause outbreaks of lethal haemorrhagic fever in humans, but developing therapies tackle only Zaire Ebola virus. Dendritic cells (DCs) are targets of this infection in vivo. Here, we found that Ebola virus entry into activated DCs requires the sialic acid-binding Ig-like lectin 1 (Siglec-1/CD169), which recognizes sialylated gangliosides anchored to viral membranes. Blockage of the Siglec-1 receptor by anti-Siglec-1 monoclonal antibodies halted Ebola viral uptake and cytoplasmic entry, offering cross-protection against other ganglioside-containing viruses such as human immunodeficiency virus type 1.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies, Monoclonal / pharmacology*
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Cytoplasm / virology*
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Dendritic Cells / drug effects
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Dendritic Cells / metabolism
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Dendritic Cells / virology
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Ebolavirus / physiology*
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Gangliosides / metabolism
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HIV-1 / physiology
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Hemorrhagic Fever, Ebola / virology
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Host-Pathogen Interactions / drug effects
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Humans
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Interferon-alpha / pharmacology
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Lipopolysaccharides / pharmacology
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Sialic Acid Binding Ig-like Lectin 1 / antagonists & inhibitors*
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Sialic Acid Binding Ig-like Lectin 1 / immunology
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Sialic Acid Binding Ig-like Lectin 1 / metabolism
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Virion / metabolism
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Virus Attachment / drug effects*
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Virus Internalization / drug effects*
Substances
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Antibodies, Monoclonal
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Gangliosides
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Interferon-alpha
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Lipopolysaccharides
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SIGLEC1 protein, human
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Sialic Acid Binding Ig-like Lectin 1