Ebola virus entry requires the cholesterol transporter Niemann–Pick C1

Jan E. Carette, Matthijs Raaben, Anthony C. Wong, Andrew S. Herbert, Gregor Obernosterer, Nirupama Mulherkar, Ana I. Kuehne, Philip J. Kranzusch, April M. Griffin, Gordon Ruthel, Paola Dal Cin, John M. Dye (), Sean P. Whelan (), Kartik Chandran () and Thijn R. Brummelkamp ()
Additional contact information
Jan E. Carette: Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA
Matthijs Raaben: Harvard Medical School, Boston, Massachusetts 02115, USA
Anthony C. Wong: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Andrew S. Herbert: US Army Medical Research Institute of Infectious Diseases, 1425 Porter St, Fort Detrick, Maryland 21702-5011, USA
Gregor Obernosterer: Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA
Nirupama Mulherkar: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Ana I. Kuehne: US Army Medical Research Institute of Infectious Diseases, 1425 Porter St, Fort Detrick, Maryland 21702-5011, USA
Philip J. Kranzusch: Harvard Medical School, Boston, Massachusetts 02115, USA
April M. Griffin: Harvard Medical School, Boston, Massachusetts 02115, USA
Gordon Ruthel: US Army Medical Research Institute of Infectious Diseases, 1425 Porter St, Fort Detrick, Maryland 21702-5011, USA
Paola Dal Cin: Center for Advanced Molecular Diagnostics, Shapiro 5-058, 70 Francis Street, Boston, Massachusetts 02115, USA
John M. Dye: US Army Medical Research Institute of Infectious Diseases, 1425 Porter St, Fort Detrick, Maryland 21702-5011, USA
Sean P. Whelan: Harvard Medical School, Boston, Massachusetts 02115, USA
Kartik Chandran: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Thijn R. Brummelkamp: Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA

Nature, 2011, vol. 477, issue 7364, 340-343

Abstract: Filovirus infectivity factors The extraordinary virulence of the Ebola and Marburg filoviruses has spurred intensive research into the molecular mechanisms by which they multiply and cause disease. Carette et al. use a genome-wide genetic screen in human cells to identify factors required for entry of Ebola virus. The screen uncovered 67 mutations disrupting all six members of the homotypic fusion and vacuole protein-sorting (HOPS) multisubunit tethering complex, which is involved in the fusion of endosomes to lysosomes, and 39 independent mutations that disrupt the endo/lysosomal cholesterol transporter protein Niemann–Pick C1 (NPC1). Côté et al. report the identification of a novel benzylpiperazine adamantane diamide-derived compound that inhibits EboV infection in cell culture, with NPC1 being the target. The unexpected role for the hereditary disease gene NPC1 in Ebola virus infection may facilitate the development of antifilovirus therapeutics.

Date: 2011
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DOI: 10.1038/nature10348

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