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Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors
In human adenoviruses (HAdV), 240 copies of the 14.3-kDa minor capsid protein IX stabilize the capsid. Three N-terminal domains of protein IX form triskelions between hexon capsomers. The C-terminal domains of four protein IX monomers associate near the facet periphery. The precise biological role o...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Inc. Published by Elsevier Inc.
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111976/ https://www.ncbi.nlm.nih.gov/pubmed/21130482 http://dx.doi.org/10.1016/j.virol.2010.10.040 |
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author | de Vrij, Jeroen van den Hengel, Sanne K. Uil, Taco G. Koppers-Lalic, Danijela Dautzenberg, Iris J.C. Stassen, Oscar M.J.A. Bárcena, Montserrat Yamamoto, Masato de Ridder, Corrina M.A. Kraaij, Robert Kwappenberg, Kitty M. Schilham, Marco W. Hoeben, Rob C. |
author_facet | de Vrij, Jeroen van den Hengel, Sanne K. Uil, Taco G. Koppers-Lalic, Danijela Dautzenberg, Iris J.C. Stassen, Oscar M.J.A. Bárcena, Montserrat Yamamoto, Masato de Ridder, Corrina M.A. Kraaij, Robert Kwappenberg, Kitty M. Schilham, Marco W. Hoeben, Rob C. |
author_sort | de Vrij, Jeroen |
collection | PubMed |
description | In human adenoviruses (HAdV), 240 copies of the 14.3-kDa minor capsid protein IX stabilize the capsid. Three N-terminal domains of protein IX form triskelions between hexon capsomers. The C-terminal domains of four protein IX monomers associate near the facet periphery. The precise biological role of protein IX remains enigmatic. Here we show that deletion of the protein IX gene from a HAdV-5 vector enhanced the reporter gene delivery 5 to 25-fold, specifically to Coxsackie and Adenovirus Receptor (CAR)-negative cell lines. Deletion of the protein IX gene also resulted in enhanced activation of peripheral blood mononuclear cells. The mechanism for the enhanced transduction is obscure. No differences in fiber loading, integrin-dependency of transduction, or factor-X binding could be established between protein IX-containing and protein IX-deficient particles. Our data suggest that protein IX can affect the cell tropism of HAdV-5, and may function to dampen the innate immune responses against HAdV particles. |
format | Online Article Text |
id | pubmed-7111976 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Elsevier Inc. Published by Elsevier Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71119762020-04-02 Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors de Vrij, Jeroen van den Hengel, Sanne K. Uil, Taco G. Koppers-Lalic, Danijela Dautzenberg, Iris J.C. Stassen, Oscar M.J.A. Bárcena, Montserrat Yamamoto, Masato de Ridder, Corrina M.A. Kraaij, Robert Kwappenberg, Kitty M. Schilham, Marco W. Hoeben, Rob C. Virology Article In human adenoviruses (HAdV), 240 copies of the 14.3-kDa minor capsid protein IX stabilize the capsid. Three N-terminal domains of protein IX form triskelions between hexon capsomers. The C-terminal domains of four protein IX monomers associate near the facet periphery. The precise biological role of protein IX remains enigmatic. Here we show that deletion of the protein IX gene from a HAdV-5 vector enhanced the reporter gene delivery 5 to 25-fold, specifically to Coxsackie and Adenovirus Receptor (CAR)-negative cell lines. Deletion of the protein IX gene also resulted in enhanced activation of peripheral blood mononuclear cells. The mechanism for the enhanced transduction is obscure. No differences in fiber loading, integrin-dependency of transduction, or factor-X binding could be established between protein IX-containing and protein IX-deficient particles. Our data suggest that protein IX can affect the cell tropism of HAdV-5, and may function to dampen the innate immune responses against HAdV particles. Elsevier Inc. Published by Elsevier Inc. 2011-02-05 2010-12-04 /pmc/articles/PMC7111976/ /pubmed/21130482 http://dx.doi.org/10.1016/j.virol.2010.10.040 Text en Copyright © 2010 Elsevier Inc. Published by Elsevier Inc. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article de Vrij, Jeroen van den Hengel, Sanne K. Uil, Taco G. Koppers-Lalic, Danijela Dautzenberg, Iris J.C. Stassen, Oscar M.J.A. Bárcena, Montserrat Yamamoto, Masato de Ridder, Corrina M.A. Kraaij, Robert Kwappenberg, Kitty M. Schilham, Marco W. Hoeben, Rob C. Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title | Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title_full | Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title_fullStr | Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title_full_unstemmed | Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title_short | Enhanced transduction of CAR-negative cells by protein IX-gene deleted adenovirus 5 vectors |
title_sort | enhanced transduction of car-negative cells by protein ix-gene deleted adenovirus 5 vectors |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111976/ https://www.ncbi.nlm.nih.gov/pubmed/21130482 http://dx.doi.org/10.1016/j.virol.2010.10.040 |
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