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A viral protein mediates superinfection exclusion at the whole organism level while is not required for exclusion at the cellular level

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A viral protein mediates superinfection exclusion at the whole organism level while is not required for exclusion at the cellular level

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dc.contributor.author Bergua, Maria es_ES
dc.contributor.author Zwart, Mark Peter es_ES
dc.contributor.author El-Mohtar, Choaa es_ES
dc.contributor.author Shilts, Turksen es_ES
dc.contributor.author Elena Fito, Santiago Fco es_ES
dc.contributor.author Folimonova, Svetlana Y. es_ES
dc.date.accessioned 2016-11-22T11:29:43Z
dc.date.available 2016-11-22T11:29:43Z
dc.date.issued 2014-10
dc.identifier.issn 0022-538X
dc.identifier.uri http://hdl.handle.net/10251/74497
dc.description Copyright © 2014, American Society for Microbiology. All Rights Reserved. es_ES
dc.description.abstract [EN] Superinfection exclusion (SIE), the ability of an established virus infection to interfere with a secondary infection by the same or a closely related virus, has been described for different viruses, including important pathogens of humans, animals, and plants. Citrus tristeza virus (CTV), a positive-sense RNA virus, represents a valuable model system for studying SIE due to the existence of several phylogenetically distinct strains. Furthermore, CTV allows SIE to be examined at the whole-organism level. Previously, we demonstrated that SIE by CTV is a virus-controlled function that requires the viral protein p33. In this study, we show that p33 mediates SIE at the whole-organism level, while it is not required for exclusion at the cellular level. Primary infection of a host with a fluorescent protein-tagged CTV variant lacking p33 did not interfere with the establishment of a secondary infection by the same virus labeled with a different fluorescent protein. However, cellular coinfection by both viruses was rare. The obtained observations, along with estimates of the cellular multiplicity of infection (MOI) and MOI model selection, suggested that low levels of cellular coinfection appear to be best explained by exclusion at the cellular level. Based on these results, we propose that SIE by CTV is operated at two levels-the cellular and the whole-organism levels-by two distinct mechanisms that could function independently. This novel aspect of viral SIE highlights the intriguing complexity of this phenomenon, further understanding of which may open up new avenues to manage virus diseases. IMPORTANCE Many viruses exhibit superinfection exclusion (SIE), the ability of an established virus infection to interfere with a secondary infection by related viruses. SIE plays an important role in the pathogenesis and evolution of virus populations. The observations described here suggest that SIE could be controlled independently at different levels of the host: the whole-organism level or the level of individual cells. The p33 protein of citrus tristeza virus (CTV), an RNA virus, was shown to mediate SIE at the whole-organism level, while it appeared not to be required for exclusion at the cellular level. SIE by CTV is, therefore, highly complex and appears to use mechanisms different from those proposed for other viruses. A better understanding of this phenomenon may lead to the development of new strategies for controlling viral diseases in human populations and agroecosystems. es_ES
dc.description.sponsorship This research was supported by the National Science Foundation under grant number 1050883 (to S. Y. Folimonova). Work in Valencia, Spain, was supported by grant BFU2012-30805 (to S. F. Elena) and by a Juan de la Cierva postdoctoral fellowship (JCI-2011-10379, to M. P. Zwart), both from the Spanish Ministerio de Economia y Competitividad.
dc.language Inglés es_ES
dc.publisher American Society for Microbiology es_ES
dc.relation NSF/1050883 es_ES
dc.relation MINECO/BFU2012-30805 es_ES
dc.relation MINECO/JCI-2011-10379
dc.relation.ispartof Journal of Virology es_ES
dc.rights Reserva de todos los derechos es_ES
dc.subject Citrus-tristeza-virus es_ES
dc.subject Hepatitis-C virus es_ES
dc.subject Avian Leukosis virus es_ES
dc.subject Borna-disease virus es_ES
dc.subject Rous sarcoma virus es_ES
dc.subject Nicotiana-Benthamiana es_ES
dc.subject Transient expression es_ES
dc.subject Antiviral Immunity es_ES
dc.subject Subgenomic RNAs es_ES
dc.subject Sindbis virus es_ES
dc.title A viral protein mediates superinfection exclusion at the whole organism level while is not required for exclusion at the cellular level es_ES
dc.type Artículo es_ES
dc.identifier.doi 10.1128/JVI.01612-14
dc.rights.accessRights Abierto es_ES
dc.contributor.affiliation Universitat Politècnica de València. Instituto Universitario Mixto de Biología Molecular y Celular de Plantas - Institut Universitari Mixt de Biologia Molecular i Cel·lular de Plantes es_ES
dc.description.bibliographicCitation Bergua, M.; Zwart, MP.; El-Mohtar, C.; Shilts, T.; Elena Fito, SF.; Folimonova, SY. (2014). A viral protein mediates superinfection exclusion at the whole organism level while is not required for exclusion at the cellular level. Journal of Virology. 88(19):11327-11338. doi:10.1128/JVI.01612-14 es_ES
dc.description.accrualMethod Senia es_ES
dc.relation.publisherversion https://dx.doi.org/10.1128/JVI.01612-14 es_ES
dc.description.upvformatpinicio 11327 es_ES
dc.description.upvformatpfin 11338 es_ES
dc.type.version info:eu-repo/semantics/publishedVersion es_ES
dc.description.volume 88 es_ES
dc.description.issue 19 es_ES
dc.relation.senia 280719 es_ES
dc.identifier.pmid 25031351
dc.identifier.pmcid PMC4178825 en_EN
dc.contributor.funder National Science Foundation, EEUU (NSF)
dc.contributor.funder Ministerio de Economía y Competitividad (MINECO)


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