Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/170715
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dc.titleAnalysis of the endocytic pathway mediating the infectious entry of mosquito-borne flavivirus West Nile into Aedes albopictus mosquito (C6/36) cells
dc.contributor.authorChu, JJH
dc.contributor.authorLeong, PWH
dc.contributor.authorNg, ML
dc.date.accessioned2020-06-25T03:39:47Z
dc.date.available2020-06-25T03:39:47Z
dc.date.issued2006-06-05
dc.identifier.citationChu, JJH, Leong, PWH, Ng, ML (2006-06-05). Analysis of the endocytic pathway mediating the infectious entry of mosquito-borne flavivirus West Nile into Aedes albopictus mosquito (C6/36) cells. Virology 349 (2) : 463-475. ScholarBank@NUS Repository.
dc.identifier.issn00426822
dc.identifier.issn10960341
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/170715
dc.description.abstractThe initial interaction between mosquito-borne flavivirus West Nile and mosquito cells is poorly characterized. This study analyzed the endocytic and the associated signaling pathway that mediate the infectious entry of West Nile virus (WNV) into mosquito cell line (C6/36). Pretreatment of C6/36 cells with pharmacological drugs that blocks clathrin-mediated endocytosis significantly inhibited virus entry. Furthermore, the transfection of functional blocking antibody against clathrin molecules and the overexpression of dominant-negative mutants of Eps15 in C6/36 cells caused a marked reduction in WNV internalization. WNV was shown to activate focal adhesion kinase (FAK) to facilitate the endocytosis of virus but not the mitogen-activated protein kinases (ERK1 and ERK2). Subsequent to the internalization of WNV, the virus particles are translocated along the endosomal pathway as revealed by double-immunofluorescence assays with anti-WNV envelope protein and cellular markers for early and late endosomes. Specific inhibitor for protein kinase C (PKC) was shown to be highly effective in blocking WNV entry by inhibiting endosomal sorting event. The disruption of the microtubule network using nocodazole also drastically affects the entry process of WNV but not the disruption of actin filaments by cytochalasin D. Finally, a low-pH-dependent step is required for WNV infection as revealed by the resistance of C6/36 cells to WNV infection in the presence of lysosomotropic agents. © 2006 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.virol.2006.01.022
dc.publisherElsevier BV
dc.sourceElements
dc.subjectActin Cytoskeleton
dc.subjectAedes
dc.subjectAnimals
dc.subjectAntigens, Viral
dc.subjectCadaverine
dc.subjectCell Line
dc.subjectChlorpromazine
dc.subjectClathrin
dc.subjectCytochalasin D
dc.subjectEndocytosis
dc.subjectEndosomes
dc.subjectEnzyme Inhibitors
dc.subjectFilipin
dc.subjectFocal Adhesion Protein-Tyrosine Kinases
dc.subjectIntracellular Signaling Peptides and Proteins
dc.subjectMicroscopy, Confocal
dc.subjectMicroscopy, Fluorescence
dc.subjectMicrotubules
dc.subjectMitogen-Activated Protein Kinases
dc.subjectNocodazole
dc.subjectProtein Kinase C
dc.subjectSucrose
dc.subjectWest Nile virus
dc.typeArticle
dc.date.updated2020-06-23T10:20:26Z
dc.contributor.departmentMICROBIOLOGY AND IMMUNOLOGY
dc.description.sourcetitleVirology
dc.description.volume349
dc.description.issue2
dc.description.page463-475
dc.identifier.isiut000238274900020
dc.description.placeUnited States
dc.published.statePublished
dc.description.redepositCompleted
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