Autophagy-Associated Proteins Control Ebola Virus Internalization into Host Cells
JournalJournal of Infectious Diseases
PublisherOxford University Press
MetadataShow full item record
AbstractEbola virus (EBOV) enters host cells by macropinocytosis, a poorly understood process. Recent studies have suggested that cell factors involved in autophagy, an evolutionally conserved pathway leading to the lysosomal degradation of protein aggregates and organelles during cellular stress, also have roles in macropinocytosis. Here, we demonstrate that autophagy-associated proteins are required for trafficking of EBOV into the cell body. Depleting cells of beclin 1, autophagy-related protein 7, or microtubule-associated protein 1A/B light chain 3B (LC3B) abolished EBOV uptake, owing to a block in vesicle formation at the cell surface. Both LC3B-I and LC3B-II interacted with macropinocytic structures. Our work indicates that, although various forms of LC3B possess an inherent ability to associate with forming macropinosomes, LC3B-II is critical for internalization of macropinocytic vesicles and, therefore, EBOV from the cell surface. Copyright 2018. This article contains public sector information licensed under the Open Government Licence v3.0.
SponsorsThis work was supported by the National Institute of Allergy and Infectious Diseases (grant R01AI063513), the Defense Threat Reduction Agency (grant HDTRA1-12-1-0002), and the Douglass and Ewing Halsell Foundations
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85057178406&doi=10.1093%2finfdis%2fjiy294&partnerID=40&md5=f6e38036010a3661d0ac672ac28c3073; http://hdl.handle.net/10713/8916
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