Nyctinomops laticaudatus bat-associated Rabies virus causes disease with a shorter clinical period and has lower pathogenic potential than strains isolated from wild canids

Full metadata record
DC FieldValueLanguage
dc.contributorLaboratório de Imunogenéticapt_BR
dc.contributor.authorFuoco, Natalia Langenfeldpt_BR
dc.contributor.authorFernandes, Elaine Ranieropt_BR
dc.contributor.authorGuedes, Fernandapt_BR
dc.contributor.authorSilva, Sandriana dos Ramospt_BR
dc.contributor.authorGuimarães, Leticia Patriciapt_BR
dc.contributor.authorSilva, Nayara Ugedapt_BR
dc.contributor.authorRibeiro, Orlando Garciapt_BR
dc.contributor.authorKatz, Iana Suly Santospt_BR
dc.date.accessioned2020-07-09T21:25:21Z-
dc.date.available2020-07-09T21:25:21Z-
dc.date.issued2019-
dc.identifier.citationFuoco NL, Fernandes ER, Guedes F, Silva SR, Guimarães LP, Silva NU, et al. Nyctinomops laticaudatus bat-associated Rabies virus causes disease with a shorter clinical period and has lower pathogenic potential than strains isolated from wild canids. Arch. virol.. 2019 Oct;164(10):2469–2477. doi:10.1007/s00705-019-04335-5.pt_BR
dc.identifier.issn0304-8608-
dc.identifier.issn1432-8798-
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2850-
dc.description.abstractRabies is a lethal viral disease that can affect a wide range of mammals. Currently, Rabies virus (RABV) in some European and American countries is maintained primarily in wild species. The regulation of viral replication is one of the critical mechanisms involved in RABV pathogenesis. However, the relationship between replication and the pathogenesis of RABV isolated from wild animals remains poorly understood. In the present study, we evaluated the pathogenicity of the street viruses Nyctinomops laticaudatus bat-associated RABV (NYBRV) and Cerdocyon thous canid-associated RABV (CECRV). Infection of mice with NYBRV led to 33% mortality with rapid disease evolution and marked histopathological changes in the CNS. In contrast, infection with CECRV led to 67% mortality and caused mild neuropathological lesions. The proportion of RABV antigen was significantly higher in the cytoplasm of neuronal cells of the cerebral cortex and in the meninges of mice infected with CECRV and NYBRV, respectively. Moreover, the replication rate of NYBRV was significantly higher (p < 0.001) than that of CECRV in neuroblastoma cells. However, CECRV replicated to a significantly higher titer in epithelial cells. Our results indicate that NYBRV infection results in rapid disease progression accompanied by frequent and intense histopathological alterations in the CNS in mice, and in a high replication rate in neuroblastoma cells. Although, CECRV is more pathogenic in mice, it caused milder histopathological changes in the CNS and replicated more efficiently in epithelial cells. Our data point to a correlation between clinical aspects of disease and the replication of RABV in different cell lines.pt_BR
dc.format.extent2469-2477pt_BR
dc.languageengpt_BR
dc.publisherSpringer-Verlagpt_BR
dc.relation.ispartofArchives of Virologypt_BR
dc.rightsOpen Accesspt_BR
dc.titleNyctinomops laticaudatus bat-associated Rabies virus causes disease with a shorter clinical period and has lower pathogenic potential than strains isolated from wild canidspt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1007/s00705-019-04335-5pt_BR
dc.identifier.urlhttps://doi.org/10.1007/s00705-019-04335-5pt_BR
dc.contributor.externalInstituto Pasteur¦¦Brasilpt_BR
dc.publisher.cityWienpt_BR
dc.identifier.citationvolume164pt_BR
dc.identifier.citationissue10pt_BR
dc.relation.ispartofabbreviatedArch. virol.pt_BR
dc.identifier.citationabntv. 164, n. 10, p. 2469–2477, oct. 2019pt_BR
dc.identifier.citationvancouver2019 Oct;164(10):2469–2477pt_BR
dc.publisher.countryAustriapt_BR
dc.contributor.butantanRibeiro, Orlando Garcia|:Pesquisador|:Laboratório de Imunogenética|:pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
item.openairetypeArticle-
item.fulltextCom Texto completo-
item.grantfulltextembargo_29990101-
crisitem.journal.journalissn#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.journal.journaleissn#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.dept#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.orcid#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
crisitem.author.parentorg#PLACEHOLDER_PARENT_METADATA_VALUE#-
Appears in Collections:Artigos de periódicos

Files in This Item:
File SizeFormat Existing users please Login
10.1007s00705-019-04335-5.pdf3.08 MBAdobe PDFEmbargoed until January 1, 2999    Request a copy
Show simple item record

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.