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http://hdl.handle.net/10261/8283
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Pariente, Nonia | - |
dc.contributor.author | Airaksinen, Antero | - |
dc.contributor.author | Domingo, Esteban | - |
dc.date.accessioned | 2008-11-06T15:08:18Z | - |
dc.date.available | 2008-11-06T15:08:18Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Journal of Virology, 2003, p. 7131-7138, Vol. 77, No. 12 | en_US |
dc.identifier.issn | 0022-538X | - |
dc.identifier.uri | http://hdl.handle.net/10261/8283 | - |
dc.description.abstract | RNA viruses replicate near the error threshold for maintenance of genetic information, and an increase in mutation frequency during replication may drive RNA viruses to extinction in a process termed lethal mutagenesis. This report addresses the efficiency of extinction (versus escape from extinction) of foot-and-mouth disease virus (FMDV) by combinations of the mutagenic base analog 5-fluorouracil (FU) and the antiviral inhibitors guanidine hydrochloride (G) and heparin (H). Selection of G- or H-resistant, extinction-escape mutants occurred with low-fitness virus only in the absence of FU and with high-fitness virus with some mutagen-inhibitor combinations tested. The combination of FU, G, and H prevented selection of extinction-escape mutants in all cases examined, and extinction of high-fitness FMDV could not be achieved by equivalent inhibitory activity exerted by the nonmutagenic agents. The G-resistant phenotype was mapped in nonstructural protein 2C by introducing the relevant mutations in infectious cDNA clones. Decreases in FMDV infectivity were accompanied by modest decreases in the intracellular and extracellular levels of FMDV RNA, maximal intracellular concentrations of FU triphosphate, and a decrease in the intracellular concentrations of UTP. In addition to indicating a key participation of mutagenesis in virus extinction, the results suggest that picornaviruses provide versatile experimental systems to approach the problem of extinction failure associated with inhibitor-escape mutants during treatments based on enhanced mutagenesis | en_US |
dc.description.sponsorship | Research was supported by grants BMC 2001-1823-C02-01 from MCyT, 08.2/0015/2001 from CAM, and an institutional grant from Fundación Ramón Areces. N.P. was supported by a predoctoral fellowship from MCyT (Spain), and A.A. was supported by a Marie Curie Fellowship of the European Community Quality of Life and Management of Living Resources program under contract umber QLK-CT-1999-51462 | en_US |
dc.format.extent | 294802 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | en_US |
dc.publisher | American Society for Microbiology | en_US |
dc.rights | openAccess | en_US |
dc.subject | Foot-and-mouth disease virus | en_US |
dc.title | Mutagenesis versus inhibition in the efficiency of extinction of foot-and-mouth disease virus | en_US |
dc.type | artículo | en_US |
dc.identifier.doi | 10.1128/JVI.77.12.7131-7138.2003 | - |
dc.description.peerreviewed | Peer reviewed | en_US |
dc.relation.publisherversion | http://dx.doi.org/10.1128/JVI.77.12.7131-7138.2003 | en_US |
dc.identifier.e-issn | 1098-5514 | - |
dc.contributor.funder | Ministerio de Ciencia y Tecnología (España) | - |
dc.contributor.funder | Comunidad de Madrid | - |
dc.contributor.funder | Fundación Ramón Areces | - |
dc.contributor.funder | European Commission | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100006280 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100008054 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100012818 | es_ES |
dc.identifier.pmid | 12768034 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | open | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.languageiso639-1 | en | - |
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