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Characterization of dengue virus entry into HepG2 cells

BACKGROUND: Despite infections by the dengue virus being a significant problem in tropical and sub-tropical countries, the mechanism by which the dengue virus enters into mammalian cells remains poorly described. METHODS: A combination of biochemical inhibition, dominant negative transfection of Eps...

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Detalles Bibliográficos
Autores principales: Suksanpaisan, Lukkana, Susantad, Tharinee, Smith, Duncan R
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653518/
https://www.ncbi.nlm.nih.gov/pubmed/19272179
http://dx.doi.org/10.1186/1423-0127-16-17
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author Suksanpaisan, Lukkana
Susantad, Tharinee
Smith, Duncan R
author_facet Suksanpaisan, Lukkana
Susantad, Tharinee
Smith, Duncan R
author_sort Suksanpaisan, Lukkana
collection PubMed
description BACKGROUND: Despite infections by the dengue virus being a significant problem in tropical and sub-tropical countries, the mechanism by which the dengue virus enters into mammalian cells remains poorly described. METHODS: A combination of biochemical inhibition, dominant negative transfection of Eps15 and siRNA mediated gene silencing was used to explore the entry mechanism of dengue into HepG2 cells. RESULTS: Results were consistent with entry via multiple pathways, specifically via clathrin coated pit mediated endocytosis and macropinocytosis, with clathrin mediated endocytosis being the predominant pathway. CONCLUSION: We propose that entry of the dengue virus to mammalian cells can occur by multiple pathways, and this opens the possibility of the virus being directed to multiple cellular compartments. This would have significant implications in understanding the interaction of the dengue virus with the host cell machinery.
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spelling pubmed-26535182009-03-10 Characterization of dengue virus entry into HepG2 cells Suksanpaisan, Lukkana Susantad, Tharinee Smith, Duncan R J Biomed Sci Research BACKGROUND: Despite infections by the dengue virus being a significant problem in tropical and sub-tropical countries, the mechanism by which the dengue virus enters into mammalian cells remains poorly described. METHODS: A combination of biochemical inhibition, dominant negative transfection of Eps15 and siRNA mediated gene silencing was used to explore the entry mechanism of dengue into HepG2 cells. RESULTS: Results were consistent with entry via multiple pathways, specifically via clathrin coated pit mediated endocytosis and macropinocytosis, with clathrin mediated endocytosis being the predominant pathway. CONCLUSION: We propose that entry of the dengue virus to mammalian cells can occur by multiple pathways, and this opens the possibility of the virus being directed to multiple cellular compartments. This would have significant implications in understanding the interaction of the dengue virus with the host cell machinery. BioMed Central 2009-02-04 /pmc/articles/PMC2653518/ /pubmed/19272179 http://dx.doi.org/10.1186/1423-0127-16-17 Text en Copyright © 2009 Suksanpaisan et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Suksanpaisan, Lukkana
Susantad, Tharinee
Smith, Duncan R
Characterization of dengue virus entry into HepG2 cells
title Characterization of dengue virus entry into HepG2 cells
title_full Characterization of dengue virus entry into HepG2 cells
title_fullStr Characterization of dengue virus entry into HepG2 cells
title_full_unstemmed Characterization of dengue virus entry into HepG2 cells
title_short Characterization of dengue virus entry into HepG2 cells
title_sort characterization of dengue virus entry into hepg2 cells
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653518/
https://www.ncbi.nlm.nih.gov/pubmed/19272179
http://dx.doi.org/10.1186/1423-0127-16-17
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