Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/27050
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dc.contributor.authorBrindeiro, Patricia A.
dc.contributor.authorBrindeiro, Rodrigo M.
dc.contributor.authorMortensen, Claudio
dc.contributor.authorHertogs, Kurt
dc.contributor.authorDe Vroey, Veronique
dc.contributor.authorRubini, Noema PM
dc.contributor.authorSion, Fernando S.
dc.contributor.authorDe Sa, Carlos AM
dc.contributor.authorMachado, Deisy M. [UNIFESP]
dc.contributor.authorSucci, Regina CM [UNIFESP]
dc.contributor.authorTanuri, Amilcar
dc.date.accessioned2016-01-24T12:33:36Z-
dc.date.available2016-01-24T12:33:36Z-
dc.date.issued2002-12-01
dc.identifierhttp://dx.doi.org/10.1128/JCM.40.12.4512-4519.2002
dc.identifier.citationJournal of Clinical Microbiology. Washington: Amer Soc Microbiology, v. 40, n. 12, p. 4512-4519, 2002.
dc.identifier.issn0095-1137
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/27050-
dc.description.abstractThe emergence of resistance to antiretroviral drugs is a major obstacle to the successful treatment of human immunodeficiency virus type 1 (HIV-1) -infected patients. in this work, we correlate clinical and virological trends such as viral load (VL) and CD4 counts to genotypic and phenotypic antiretroviral (ARV) resistance profiles of HIV-1 isolates from the B and non-B subtypes found in vertically infected children failing ARV therapy. Plasma samples were collected from 52 vertically HIV-1-infected children failing different ARV therapies. Samples underwent HIV-1 pol sequencing and phenotyping and were clustered into subtypes by phylogenetic analysis. Clinical data from each patient were analyzed together with the resistance (genotypic and phenotypic) data obtained. Thirty-five samples were from subtype B, 10 samples were non-B (subtypes A, C, and F), and 7 were mosaic samples. There was no significant difference concerning treatment data between B and non-B clades. Prevalence of known drug resistance mutations revealed slightly significant differences among B and non-B subtypes: L10I, 21 and 64%, K20R, 13 and 43%, M36I, 34 and 100%, L63P, 76 and 36%, A71V/T, 24 and 0%, and V77I, 32 and 0%, respectively, in the protease (0.0001 less than or equal to P less than or equal to 0.0886), and D67N, 38 and 8%, K70R, 33 and 0%, R211K, 49 and 85%, and K219Q/E, 31 and 0%, respectively, in the reverse transcriptase (0.0256 less than or equal to P less than or equal to 0.0704). Significant differences were found only in secondary resistance mutations and did not reflect significant phenotypic variation between clade B and non-B.en
dc.format.extent4512-4519
dc.language.isoeng
dc.publisherAmer Soc Microbiology
dc.relation.ispartofJournal of Clinical Microbiology
dc.rightsAcesso aberto
dc.titleTesting genotypic and phenotypic resistance in human immunodeficiency virus type 1 isolates of clade B and other clades from children failing antiretroviral therapyen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal do Rio de Janeiro (UFRJ)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionGaffree & Guinle Univ Hosp
dc.contributor.institutionVIRCO NV
dc.description.affiliationUniv Fed Rio de Janeiro, CCS, Inst Biol, Dept Genet,Lab Mol Virol, BR-21944970 Rio de Janeiro, RJ, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Sch Med, São Paulo, Brazil
dc.description.affiliationGaffree & Guinle Univ Hosp, Rio de Janeiro, Brazil
dc.description.affiliationVIRCO NV, Tibotec, Mechelen, Belgium
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Sch Med, São Paulo, Brazil
dc.identifier.fileWOS000179631500018.pdf
dc.identifier.doi10.1128/JCM.40.12.4512-4519.2002
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000179631500018
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