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dc.contributor.authorArcher, Madeline A.
dc.contributor.authorBrechtel, Teal M.
dc.contributor.authorDavis, Leslie E.
dc.contributor.authorParmar, Rinkuben C.
dc.contributor.authorHasan, Mohammad H.
dc.contributor.authorTandon, Ritesh
dc.date.accessioned2017-06-05T21:34:32Z
dc.date.available2017-06-05T21:34:32Z
dc.date.issued2017-04-13
dc.identifier.citationInhibition of endocytic pathways impacts cytomegalovirus maturation 2017, 7:46069 Scientific Reportsen
dc.identifier.issn2045-2322
dc.identifier.pmid28406138
dc.identifier.doi10.1038/srep46069
dc.identifier.urihttp://hdl.handle.net/10150/623928
dc.description.abstractEndocytic 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.
dc.description.sponsorshipAmerican Heart Association Scientist Development Grant [14SDG20390009]en
dc.language.isoenen
dc.publisherNATURE PUBLISHING GROUPen
dc.relation.urlhttp://www.nature.com/articles/srep46069en
dc.rights© The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License.en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleInhibition of endocytic pathways impacts cytomegalovirus maturationen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Dept Mol & Cellular Biolen
dc.identifier.journalScientific Reportsen
dc.description.collectioninformationThis 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.en
dc.eprint.versionFinal published versionen
refterms.dateFOA2018-07-01T13:25:35Z
html.description.abstractEndocytic 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.


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© The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License.
Except where otherwise noted, this item's license is described as © The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License.