Journal
CELL HOST & MICROBE
Volume 12, Issue 4, Pages 544-557Publisher
CELL PRESS
DOI: 10.1016/j.chom.2012.08.009
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Funding
- Conseil Regional d'Ile-de-France
- Ministere de la Recherche
- Fondation pour la Recherche Medicale
- Pediatric Dengue Vaccine Initiative
- Institut Universitaire d'Hematologie
- Institut National de la Recherche Medicale (INSERM)
- ANR DENtry
- ANR
- Institut Pasteur
- National Institutes of Health [R01 AI077058, R01 AI101400]
- Marie Curie (EU program CARMUSYS)
- TOTAL Oil and Gas Venezuela
- Instituto Venezolano de Investigaciones Cientificas (IVIC)
- Leukemia and Lymphoma Society
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Dengue viruses (DVs) are responsible for the most medically relevant arboviral diseases. However, the molecular interactions mediating DV entry are poorly understood. We determined that TIM and TAM proteins, two receptor families that mediate the phosphatidylserine (PtdSer)-dependent phagocytic removal of apoptotic cells, serve as DV entry factors. Cells poorly susceptible to DV are robustly infected after ectopic expression of TIM or TAM receptors. Conversely, DV infection of susceptible cells is inhibited by anti-TIM or anti-TAM antibodies or knockdown of TIM and TAM expression. TIM receptors facilitate DV entry by directly interacting with virion-associated PtdSer. TAM-mediated infection relies on indirect DV recognition, in which the TAM ligand Gas6 acts as a bridging molecule by binding to PtdSer within the virion. This dual mode of virus recognition by TIM and TAM receptors reveals how DVs usurp the apoptotic cell clearance pathway for infectious entry.
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