Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/204227
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dc.contributor.authorMorales, Lucía-
dc.contributor.authorOliveros, Juan C.-
dc.contributor.authorFernandez-Delgado, Raúl-
dc.contributor.authortenOever, Benjamin Robert-
dc.contributor.authorEnjuanes Sánchez, Luis-
dc.contributor.authorSolá Gurpegui, Isabel-
dc.date.accessioned2020-03-17T13:25:46Z-
dc.date.available2020-03-17T13:25:46Z-
dc.date.issued2017-03-08-
dc.identifierdoi: 10.1016/j.chom.2017.01.015-
dc.identifiere-issn: 1934-6069-
dc.identifierpmid: 28216251-
dc.identifier.citationCell Host and Microbe 21(3): 344-355 (2017)-
dc.identifier.urihttp://hdl.handle.net/10261/204227-
dc.description.abstractSevere acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, which is characterized by exacerbated inflammatory response and extensive lung pathology. To address the relevance of small non-coding RNAs in SARS-CoV pathology, we deep sequenced RNAs from the lungs of infected mice and discovered three 18–22 nt small viral RNAs (svRNAs). The three svRNAs were derived from the nsp3 (svRNA-nsp3.1 and -nsp3.2) and N (svRNA-N) genomic regions of SARS-CoV. Biogenesis of CoV svRNAs was RNase III, cell type, and host species independent, but it was dependent on the extent of viral replication. Antagomir-mediated inhibition of svRNA-N significantly reduced in vivo lung pathology and pro-inflammatory cytokine expression. Taken together, these data indicate that svRNAs contribute to SARS-CoV pathogenesis and highlight the potential of svRNA-N antagomirs as antivirals.-
dc.description.sponsorshipThis work was supported by grants from the Ministry of Science and Innovation of Spain ( BIO2010-16705 , BIO2013-42869-R , and BIO2016-75549-R AEI/FEDER, UE ), the European Zoonoses anticipation and preparedness initiative ZAPI ( IMI_JU_115760 ), and U.S. National Institutes of Health ( NIH ) ( 2P01AI060699 and 0258-3413/HHSN266200700010C ). L.M. received a fellowship from the Ministry of Science an Innovation of Spain ( BIO2010-16705 ) and a contract from ZAPI. R.F.-D received contracts from NIH and ZAPI.-
dc.languageeng-
dc.publisherCell Press-
dc.relationMINECO/ICTI2013-2016/BIO2013-42869-R-
dc.relationMINECO/ICTI2013-2016/BIO2016-75549-R-
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/115760-
dc.rightsopenAccess-
dc.subjectCoronavirus-
dc.subjectSARS-CoV-
dc.subjectSmall viral RNAs-
dc.subjectVirus-host interaction-
dc.subjectLung inflammatory pathology-
dc.subjectAntagomirs-
dc.subjectDeep sequencing-
dc.subjectNon-coding RNAs-
dc.subjectInnate immune response-
dc.subjectAntiviral-
dc.titleSARS-CoV-Encoded Small RNAs Contribute to Infection-Associated Lung Pathology-
dc.typeartículo-
dc.identifier.doi10.1016/j.chom.2017.01.015-
dc.relation.publisherversionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662013/-
dc.date.updated2020-03-17T13:25:47Z-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderEuropean Commission-
dc.contributor.funderInnovative Medicines Initiative-
dc.contributor.funderNational Institutes of Health (US)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/100000002es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100010767es_ES
dc.identifier.pmid28216251-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeartículo-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
Appears in Collections:(CNB) Artículos
(VICYT) Colección Especial COVID-19
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