dc.creatorSilveira, Guilherme Ferreira
dc.creatorMeyer, Florencia
dc.creatorDelfraro, Adriana
dc.creatorMosimann, Ana Luiza Pamplona
dc.creatorColuchi, Norma
dc.creatorVasquez, Cyntia
dc.creatorProbst, Christian Macagnan
dc.creatorBáfica, André
dc.creatorBordignon, Juliano
dc.creatorSantos, Claudia Nunes Duarte dos
dc.date2018-09-19T16:45:53Z
dc.date2018-09-19T16:45:53Z
dc.date2011
dc.date.accessioned2023-09-26T23:17:49Z
dc.date.available2023-09-26T23:17:49Z
dc.identifierSILVEIRA, Guilherme F. et al. Dengue Virus Type 3 Isolated from a Fatal Case with Visceral Complications Induces Enhanced Proinflammatory Responses and Apoptosis of Human Dendritic Cells. Journal of Virology, v. 85, n. 11, p. 5374–5383, 2011.
dc.identifier0022-538X
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/28897
dc.identifier10.1128/JVI.01915-10
dc.identifier1098-5514
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8889000
dc.descriptionO artigo encontra-se disponível em acesso aberto no site do Editor.
dc.descriptionA recent (2007 to 2009) dengue outbreak caused by dengue virus (DENV) in Paraguay presented unusual severe clinical outcomes associated with 50% mortality rates. Although it has been reported that inflammatory responses influence the severity of dengue virus infection (T. Pang, M. J. Cardosa, and M. G. Guzman, Immunol. Cell Biol. 85:43-45, 2007), there remains a paucity of information on virus-innate immunity interactions influencing clinical outcome. Using human dendritic cells from a major innate immune cell population as an in vitro model, we have investigated signature cytokine responses as well as infectivity-replicative profiles of DENV clinical isolates from either a nonfatal case of classical dengue fever (strain DENV3/290; isolated in Brazil in 2002) or a fatal case of dengue fever with visceral complications isolated in Paraguay in 2007 (strain DENV3/5532). Strain DENV3/5532 was found to display significantly higher replicative ability than DENV3/290 in monocyte-derived dendritic cells (mdDCs). In addition, compared to DENV3/290 results, mdDCs exposed to DENV3/5532 showed increased production of proinflammatory cytokines associated with higher rates of programmed cell death, as shown by annexin V staining. The observed phenotype was due to viral replication, and tumor necrosis factor alpha (TNF-α) appears to exert a protective effect on virus-induced mdDC apoptosis. These results suggest that the DENV3/5532 strain isolated from the fatal case replicates within human dendritic cells, modulating cell survival and synthesis of inflammatory mediators.
dc.formatapplication/pdf
dc.languagepor
dc.publisherAmerican Society for Microbiology
dc.rightsopen access
dc.subjectDengue
dc.subjectDendritic Cells
dc.subjectCytokines
dc.subjectDengue Virus
dc.subjectPyroptosis
dc.subjectCélulas Dendríticas
dc.subjectCitocinas
dc.subjectVirus del Dengue
dc.subjectPiroptosis
dc.subjectCélulas Dendríticas
dc.subjectCitocinas
dc.subjectVírus da Dengue
dc.subjectPiroptose
dc.titleDengue virus type 3 isolated from a fatal case with visceral complications induces enhanced proinflammatory responses and apoptosis of human dendritic cells
dc.typeArticle


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