Inhibition of endocytic pathways impacts cytomegalovirus maturation
Author
Archer, Madeline A.Brechtel, Teal M.
Davis, Leslie E.
Parmar, Rinkuben C.
Hasan, Mohammad H.
Tandon, Ritesh
Affiliation
Univ Arizona, Dept Mol & Cellular BiolIssue Date
2017-04-13
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Show full item recordPublisher
NATURE PUBLISHING GROUPCitation
Inhibition of endocytic pathways impacts cytomegalovirus maturation 2017, 7:46069 Scientific ReportsJournal
Scientific ReportsRights
© The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Endocytic processes are critical for cellular entry of several viruses; however, the role of endocytosis in cellular trafficking of viruses beyond virus entry is only partially understood. Here, we utilized two laboratory strains (AD169 and Towne) of human cytomegalovirus (HCMV), which are known to use cell membrane fusion rather than endocytosis to enter fibroblasts, in order to study a post-entry role of endocytosis in HCMV life cycle. Upon pharmacological inhibition of dynamin-2 or clathrin terminal domain (TD) ligand association, these strains entered the cells successfully based on the expression of immediate early viral protein. However, both the inhibitors significantly reduced the growth rates and final virus yields of viruses without inhibiting the expression of early to late viral proteins. Clathrin accumulated in the cytoplasmic virus assembly compartment (vAC) of infected cells co-localizing with virus tegument protein pp150 and the formation of vAC was compromised upon endocytic inhibition. Transmission electron micrographs (TEM) of infected cells treated with endocytosis inhibitors showed intact nuclear stages of nucleocapsid assembly but the cytoplasmic virus maturation was greatly compromised. Thus, the data presented here implicate endocytic pathways in HCMV maturation and egress.ISSN
2045-2322PubMed ID
28406138Version
Final published versionSponsors
American Heart Association Scientist Development Grant [14SDG20390009]Additional Links
http://www.nature.com/articles/srep46069ae974a485f413a2113503eed53cd6c53
10.1038/srep46069
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