| Literature DB >> 21767814 |
Pierre-Yves Lozach1, Andreas Kühbacher, Roger Meier, Roberta Mancini, David Bitto, Michèle Bouloy, Ari Helenius.
Abstract
During natural transmission, bunyaviruses are introduced into the skin through arthropod bites, and dermal dendritic cells (DCs) are the first to encounter incoming viruses. DC-SIGN is a C-type lectin highly expressed on the surface of dermal DCs. We found that several arthropod-borne phleboviruses (Bunyaviridae), including Rift Valley fever and Uukuniemi viruses, exploit DC-SIGN to infect DCs and other DC-SIGN-expressing cells. DC-SIGN binds the virus directly via interactions with high-mannose N-glycans on the viral glycoproteins and is required for virus internalization and infection. In live cells, virus-induced clustering of cell surface DC-SIGN could be visualized. An endocytosis-defective mutant of DC-SIGN was unable to mediate virus uptake, indicating that DC-SIGN is an authentic receptor required for both attachment and endocytosis. After internalization, viruses separated from DC-SIGN and underwent trafficking to late endosomes. Our study provides real-time visualization of virus-receptor interactions on the cell surface and establishes DC-SIGN as a phlebovirus entry receptor.Entities:
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Year: 2011 PMID: 21767814 DOI: 10.1016/j.chom.2011.06.007
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023