DC-SIGN and DC-SIGNR Interact with the Glycoprotein of Marburg Virus and the S Protein of Severe Acute Respiratory Syndrome Coronavirus
Andrea Marzi, Thomas Gramberg, Graham Simmons(University of Pennsylvania), Peggy Möller(Philipps University of Marburg), Andrew J. Rennekamp(University of Pennsylvania), Mandy Krumbiegel, Martina Geier, Jutta Eisemann(Friedrich-Alexander-Universität Erlangen-Nürnberg), Nadine M. Turza(Friedrich-Alexander-Universität Erlangen-Nürnberg), Bertrand Saunier(Ohio University), Alexander Steinkasserer(Friedrich-Alexander-Universität Erlangen-Nürnberg), Stephan Becker(Philipps University of Marburg), Paul Bates(University of Pennsylvania), Heike Hofmann, Stefan Pöhlmann
Cited by 397Open Access
Abstract
The lectins DC-SIGN and DC-SIGNR can augment viral infection; however, the range of pathogens interacting with these attachment factors is incompletely defined. Here we show that DC-SIGN and DC-SIGNR enhance infection mediated by the glycoprotein (GP) of Marburg virus (MARV) and the S protein of severe acute respiratory syndrome coronavirus and might promote viral dissemination. SIGNR1, a murine DC-SIGN homologue, also enhanced infection driven by MARV and Ebola virus GP and could be targeted to assess the role of attachment factors in filovirus infection in vivo.
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