English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/166323
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

Phenotyping and susceptibility of established porcine cells lines to African Swine Fever Virus infection and viral production

AuthorsSánchez, Elena G. ; Riera, Elena; Nogal, Marisa; Gallardo, Carmina; Fernández, Paloma; Bello-Morales, Raquel; López-Guerrero, José Antonio ; Chitko-Mckown, Carol G.; Richt, Jürgen A.; Revilla Novella, Yolanda
Issue Date4-Aug-2017
PublisherNature Publishing Group
CitationScientific Reports 7 (2017)
AbstractAfrican swine fever virus (ASFV) is a highly pathogenic, double-stranded DNA virus with a marked tropism for cells of the monocyte-macrophage lineage, affecting swine species and provoking severe economic losses and health threats. In the present study, four established porcine cell lines, IPAM-WT, IPAM-CD163, Câ2+ and WSL, were compared to porcine alveolar macrophage (PAM) in terms of surface marker phenotype, susceptibility to ASFV infection and virus production. The virulent ASFV Armenia/07, E70 or the naturally attenuated NHV/P68 strains were used as viral models. Cells expressed only low levels of specific receptors linked to the monocyte/macrophage lineage, with low levels of infection overall, with the exception of WSL, which showed more efficient production of strain NHV/P68 but not of strains E70 and Armenia/07.
URIhttp://hdl.handle.net/10261/166323
Identifiersdoi: 10.1038/s41598-017-09948-x
issn: 2045-2322
Appears in Collections:(CBM) Artículos
Files in This Item:
File Description SizeFormat 
RevillaY_PhenotypingAndSusceptibility.pdf2,33 MBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.