Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/3625
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dc.contributor.authorAngelis, Daniela Souza Araújo de
dc.contributor.authorFreire, Wilton Santos
dc.contributor.authorPannuti, Cláudio Sergio
dc.contributor.authorSucci, Regina Célia de Menezes [UNIFESP]
dc.contributor.authorMachado, Daisy Maria [UNIFESP]
dc.date.accessioned2015-06-14T13:36:49Z
dc.date.available2015-06-14T13:36:49Z
dc.date.issued2007-04-01
dc.identifierhttp://dx.doi.org/10.1590/S1413-86702007000200004
dc.identifier.citationBrazilian Journal of Infectious Diseases. Brazilian Society of Infectious Diseases, v. 11, n. 2, p. 196-198, 2007.
dc.identifier.issn1413-8670
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/3625
dc.description.abstractThe CCR5 molecule, a chemokine receptor, is the most important co-receptor for macrophage-tropic HIV-1. A 32-bp deletion in the gene encoding CCR5 (CCR5-del32) confers nearly complete resistance to HIV-1 infection in homozygotes, and slows the rate of progression to AIDS in heterozygous adults. The aim of this study was to describe the CCR5 genotypes and the characteristics of HIV disease progression in perinatally infected children. From a total of 51 children analyzed for the CCR5-del32 mutation, 18 (35%) were considered to be rapid progressors, 28 (55%) were moderate progressors and 5 (10%) were slow progressors. A portion of the CCR5 gene was amplified by PCR from genomic DNA followed by agarose gel electrophoresis. Forty-nine children (96%) carried the homozygous wild type genotype for CCR5 while 2 (4%) carried the heterozygous wt/del32 genotype. In the population studied, the CCR5 genotype was unable to account for the differences in pattern of the disease progression among the three groups (rapid, moderate and slow progressors), and the allele frequency of CCR5-del32 was too low to allow statistical comparisons with adequate resolving power. Studies on larger populations may help to further elucidate the role of this allele and other host factors in the regulation of HIV-1 pathogenesis in children.en
dc.format.extent196-198
dc.language.isoeng
dc.publisherBrazilian Society of Infectious Diseases
dc.relation.ispartofBrazilian Journal of Infectious Diseases
dc.rightsAcesso aberto
dc.subjectHIV-1en
dc.subjectCCR5 co-receptoren
dc.subjectHIV disease progressionen
dc.subjectperinatally infected childrenen
dc.titleCCR5 genotypes and progression to HIV disease in perinatally infected childrenen
dc.typeArtigo
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUSP HCFM Institute of Tropical Medicine of São Paulo
dc.description.affiliationUNIFESP Federal University of São Paulo
dc.description.affiliationUnifespUNIFESP, UNIFESP
dc.identifier.fileS1413-86702007000200004.pdf
dc.identifier.scieloS1413-86702007000200004
dc.identifier.doi10.1590/S1413-86702007000200004
dc.description.sourceSciELO
dc.identifier.wosWOS:000254388400004
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