English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/34093
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:

An interfering activity against lymphocytic choriomeningitis virus replication associated with enhanced mutagenesis

AuthorsMartín, Verónica; Abia, David ; Domingo, Esteban ; Grande-Pérez, Ana
Keywordslymphocytic choriomeningitis virus (LCMV)
Issue DateApr-2010
PublisherSociety for General Microbiology
CitationJournal of General Virology 91(Pt 4): 990-1003 (2010)
AbstractPrevious studies have documented that, in the presence of the mutagenic base analogue 5-fluorouracil (FU), lymphocytic choriomeningitis virus (LCMV) that persisted in BHK-21 cells decreased its infectivity to a larger extent than intracellular viral RNA levels, prior to virus extinction. This observation, together with in silico simulations, led to the proposal of the lethal defection model of virus extinction. This model suggests the participation of defective-interfering genomes in the loss of infectivity by increased mutagenesis. Since LCMV naturally produces defective-interfering particles, it was important to show that a capacity to interfere is produced in association with FU treatment. Here, we document that BHK-21 cells persistently infected with LCMV grown in the presence of FU, but not in its absence, generated an interfering activity that suppressed LCMV infectivity. Interference was specific for LCMV and was sensitive to UV irradiation and its activity was dose- and time-dependent. The interfering preparations produced positive LCMV immunofluorescence and viral particles seen by electron microscopy when used to infect cells, despite some preparations being devoid of detectable infectivity. Interference did not involve significant increases of mutant spectrum complexity, as predicted by the lethal defection model. The results provide support for a specific interference associated with LCMV when the virus replicates in the presence of FU. The excess of interference relative to that observed in the absence of FU is necessary for LCMV extinction.
Publisher version (URL)http://dx.doi.org/10.1099/vir.0.017053-0
Appears in Collections:(CBM) Artículos
Files in This Item:
File Description SizeFormat 
EDomingo_JGenVir_990.pdf2,31 MBAdobe PDFThumbnail
Show full item record

Related articles:

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