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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/56403
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dc.creatorÁtila Duque Rossipt_BR
dc.creatorAmilcar Tanuript_BR
dc.creatorMilton Ozório Moraespt_BR
dc.creatorRenato Santana de Aguiarpt_BR
dc.creatorConstantine Stratakispt_BR
dc.creatorCynthia Chester Cardosopt_BR
dc.creatorFabio Rueda Fauczpt_BR
dc.creatorAdriana Melopt_BR
dc.creatorGirlene Souza de Azevedopt_BR
dc.creatorPaula Pezzutopt_BR
dc.creatorOhanna Cavalcanti de Lima Bezerrapt_BR
dc.creatorFernanda Saloum de Neves Mantapt_BR
dc.creatorTamiris Azamorpt_BR
dc.creatorBruno Luiz Fonseca Schamber-Reispt_BR
dc.date.accessioned2023-07-17T17:41:44Z-
dc.date.available2023-07-17T17:41:44Z-
dc.date.issued2021-
dc.citation.volume13pt_BR
dc.citation.issue11pt_BR
dc.citation.spage1pt_BR
dc.citation.epage6pt_BR
dc.identifier.doihttps://doi.org/10.3390/v13112253pt_BR
dc.identifier.issn1999-4915pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56403-
dc.description.resumoAbstract: Congenital Zika syndrome (CZS) is characterized by a diverse group of congenital malformations induced by ZIKV infection during pregnancy. Type III interferons have been associated with placental immunity against ZIKV and restriction of vertical transmission in mice, and non-coding single-nucleotide polymorphisms (SNPs) on these genes are well known to influence susceptibility to other viral infections. However, their effect on ZIKV pathogenesis has not yet been explored. To investigate whether maternal non-coding SNPs at IFNL genes are associated with CZS, 52 women infected with ZIKV during pregnancy were enrolled in a case–control association study. A total of 28 women were classified as cases and 24 as controls based on the presence or absence of CZS in their infants, and seven Interferon-λ non-coding SNPs (rs12980275, rs8099917, rs4803217, rs4803219, rs8119886, rs368234815, rs12979860) were genotyped. The results of logistic regression analyses show an association between the G allele at rs8099917 and increased susceptibility to CZS under a log-additive model (adjustedOR = 2.80; 95%CI = 1.14–6.91; p = 0.02), after adjustment for trimester of infection and genetic ancestry. These results provide evidence of an association between Interferon-λ SNPs and CZS, suggesting rs8099917 as a promising candidate for further studies on larger cohorts.pt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICASpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofVirusespt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectZikapt_BR
dc.subjectType III interferonpt_BR
dc.subjectPolymorphismpt_BR
dc.subjectCongenital Zika syndromept_BR
dc.subjectGenetic susceptibilitypt_BR
dc.subject.otherVírus da Zikapt_BR
dc.subject.otherPolimorfismopt_BR
dc.titleAssociation between Maternal Non-Coding Interferon-λ Polymorphisms and Congenital Zika Syndrome in a Cohort from Brazilian Northeastpt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.mdpi.com/1999-4915/13/11/2253pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-6235-8807pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0570-750Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2653-0037pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5180-3717pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4058-5520pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7959-9842pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9570-8244pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0798-778Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4047-2091pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7640-1463pt_BR
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