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dc.contributor.author
Schelhaas, Mario
dc.contributor.author
Shah, Bhavin
dc.contributor.author
Holzer, Michael
dc.contributor.author
Blattmann, Peter
dc.contributor.author
Kühling, Lena
dc.contributor.author
Day, Patricia M.
dc.contributor.author
Schiller, John T.
dc.contributor.author
Helenius, Ari
dc.date.accessioned
2018-11-06T17:38:12Z
dc.date.available
2017-06-09T23:40:48Z
dc.date.available
2018-11-06T17:38:12Z
dc.date.issued
2012-04-19
dc.identifier.issn
1553-7374
dc.identifier.issn
1553-7366
dc.identifier.other
10.1371/journal.ppat.1002657
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/48621
dc.identifier.doi
10.3929/ethz-b-000048621
dc.description.abstract
Infectious endocytosis of incoming human papillomavirus type 16 (HPV-16), the main etiological agent of cervical cancer, is poorly characterized in terms of cellular requirements and pathways. Conflicting reports attribute HPV-16 entry to clathrin-dependent and -independent mechanisms. To comprehensively describe the cell biological features of HPV-16 entry into human epithelial cells, we compared HPV-16 pseudovirion (PsV) infection in the context of cell perturbations (drug inhibition, siRNA silencing, overexpression of dominant mutants) to five other viruses (influenza A virus, Semliki Forest virus, simian virus 40, vesicular stomatitis virus, and vaccinia virus) with defined endocytic requirements. Our analysis included infection data, i.e. GFP expression after plasmid delivery by HPV-16 PsV, and endocytosis assays in combination with electron, immunofluorescence, and video microscopy. The results indicated that HPV-16 entry into HeLa and HaCaT cells was clathrin-, caveolin-, cholesterol- and dynamin-independent. The virus made use of a potentially novel ligand-induced endocytic pathway related to macropinocytosis. This pathway was distinct from classical macropinocytosis in regards to vesicle size, cholesterol-sensitivity, and GTPase requirements, but similar in respect to the need for tyrosine kinase signaling, actin dynamics, Na+/H+ exchangers, PAK-1 and PKC. After internalization the virus was transported to late endosomes and/or endolysosomes, and activated through exposure to low pH.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
PLOS
dc.rights.uri
http://creativecommons.org/publicdomain/zero/1.0/
dc.title
Entry of Human Papillomavirus Type 16 by Actin-Dependent, Clathrin- and Lipid Raft-Independent Endocytosis
en_US
dc.type
Journal Article
dc.rights.license
CC0 1.0 Universal
ethz.journal.title
PLoS Pathogens
ethz.journal.volume
8
en_US
ethz.journal.issue
4
en_US
ethz.journal.abbreviated
PLoS Pathog
ethz.pages.start
e1002657
en_US
ethz.size
21 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.publication.place
Lawrence, KS
ethz.publication.status
published
en_US
ethz.leitzahl
03495 - Helenius, Ari
en_US
ethz.leitzahl.certified
03495 - Helenius, Ari
ethz.date.deposited
2017-06-09T23:41:13Z
ethz.source
ECIT
ethz.identifier.importid
imp59364f2d585b160080
ethz.ecitpid
pub:80027
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-13T08:06:22Z
ethz.rosetta.lastUpdated
2024-02-02T06:33:40Z
ethz.rosetta.versionExported
true
ethz.COinS
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