Involvement of Surfactant Protein D in Ebola Virus Infection Enhancement via Glycoprotein Interaction
Anne-Laure Favier,
Olivier Reynard,
Evelyne Gout,
Martin van Eijk,
Henk P. Haagsman,
Erika Crouch,
Viktor Volchkov,
Christophe Peyrefitte,
Nicole M. Thielens
Affiliations
Anne-Laure Favier
Unité de Virologie, Institut de Recherche Biomédicale des Armées, 91220 Brétigny-sur-Orge, France
Olivier Reynard
Molecular basis of viral pathogenicity, Centre International de Recherche en Infectiologie (CIRI), INSERMU1111—CNRS UMR5308, Université Lyon 1, ENS de Lyon, 69365 LYON cedex 07, France
Evelyne Gout
Université de Grenoble Alpes, CNRS, CEA, IBS, F-38000 Grenoble, France
Martin van Eijk
Division of Molecular Host Defence, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3512 The Netherlands
Henk P. Haagsman
Division of Molecular Host Defence, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3512 The Netherlands
Erika Crouch
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA
Viktor Volchkov
Molecular basis of viral pathogenicity, Centre International de Recherche en Infectiologie (CIRI), INSERMU1111—CNRS UMR5308, Université Lyon 1, ENS de Lyon, 69365 LYON cedex 07, France
Christophe Peyrefitte
Unité de Virologie, Institut de Recherche Biomédicale des Armées, 91220 Brétigny-sur-Orge, France
Nicole M. Thielens
Université de Grenoble Alpes, CNRS, CEA, IBS, F-38000 Grenoble, France
Since the largest 2014–2016 Ebola virus disease outbreak in West Africa, understanding of Ebola virus infection has improved, notably the involvement of innate immune mediators. Amongst them, collectins are important players in the antiviral innate immune defense. A screening of Ebola glycoprotein (GP)-collectins interactions revealed the specific interaction of human surfactant protein D (hSP-D), a lectin expressed in lung and liver, two compartments where Ebola was found in vivo. Further analyses have demonstrated an involvement of hSP-D in the enhancement of virus infection in several in vitro models. Similar effects were observed for porcine SP-D (pSP-D). In addition, both hSP-D and pSP-D interacted with Reston virus (RESTV) GP and enhanced pseudoviral infection in pulmonary cells. Thus, our study reveals a novel partner of Ebola GP that may participate to enhance viral spread.
