Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/27050
Title: Testing genotypic and phenotypic resistance in human immunodeficiency virus type 1 isolates of clade B and other clades from children failing antiretroviral therapy
Authors: Brindeiro, Patricia A.
Brindeiro, Rodrigo M.
Mortensen, Claudio
Hertogs, Kurt
De Vroey, Veronique
Rubini, Noema PM
Sion, Fernando S.
De Sa, Carlos AM
Machado, Deisy M. [UNIFESP]
Succi, Regina CM [UNIFESP]
Tanuri, Amilcar
Universidade Federal do Rio de Janeiro (UFRJ)
Universidade Federal de São Paulo (UNIFESP)
Gaffree & Guinle Univ Hosp
VIRCO NV
Issue Date: 1-Dec-2002
Publisher: Amer Soc Microbiology
Citation: Journal of Clinical Microbiology. Washington: Amer Soc Microbiology, v. 40, n. 12, p. 4512-4519, 2002.
Abstract: The 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.
URI: http://repositorio.unifesp.br/handle/11600/27050
ISSN: 0095-1137
Other Identifiers: http://dx.doi.org/10.1128/JCM.40.12.4512-4519.2002
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