HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

Budding of Ebola Virus Particles Requires the Rab11-Dependent Endocytic Recycling Pathway

Files in This Item:
Ebora_Rab11_AN_Fig_071818.pdf6.84 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/76317

Title: Budding of Ebola Virus Particles Requires the Rab11-Dependent Endocytic Recycling Pathway
Authors: Nanbo, Asuka Browse this author →KAKEN DB
Ohba, Yusuke Browse this author →KAKEN DB
Keywords: Ebola virus
Rab11
recycling endosome
viral-like particles
virus egress
VP40
Issue Date: 15-Dec-2018
Publisher: Oxford University Press
Journal Title: Journal of Infectious Diseases
Volume: 218
Start Page: S388
End Page: S396
Publisher DOI: 10.1093/infdis/jiy460
PMID: 30476249
Abstract: The Ebola virus-encoded major matrix protein VP40 traffics to the plasma membrane, which leads to the formation of filamentous viral particles and subsequent viral egress. However, the cellular machineries underlying this process are not fully understood. In the present study, we have assessed the role of host endocytic recycling in Ebola virus particle formation. We found that a small GTPase Rab11, which regulates recycling of molecules among the trans-Golgi network, recycling endosomes, and the plasma membrane, was incorporated in Ebola virus-like particles. Although Rab11 predominantly localized in the perinuclear region, it distributed diffusely in the cytoplasm and partly localized in the periphery of the cells transiently expressing VP40. In contrast, Rab11 exhibited a perinuclear distribution when 2 VP40 derivatives that lack ability to traffic to the plasma membrane were expressed. Finally, expression of a dominant-negative form of Rab11 or knockdown of Rab11 inhibited both VP40-induced clusters at the plasma membrane and release of viral-like particles. Taken together, our findings demonstrate that Ebola virus exploits host endocytic recycling machinery to facilitate the trafficking of VP40 to the cell surface and the subsequent release of viral-like particles for its establishment of efficient viral egress.
Rights: This is a pre-copyedited, author-produced version of an article accepted for publication in The Journal of Infectious Diseases following peer review. The version of record Volume 218, Issue suppl_5, S388-S396, 2018 is available online at: https://doi.org/10.1093/infdis/jiy460.
Type: article (author version)
URI: http://hdl.handle.net/2115/76317
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 南保 明日香

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 

 - Hokkaido University