Testing genotypic and phenotypic resistance in human immunodeficiency virus type 1 isolates of clade B and other clades from children failing antiretroviral therapy

Testing genotypic and phenotypic resistance in human immunodeficiency virus type 1 isolates of clade B and other clades from children failing antiretroviral therapy

Author Brindeiro, Patricia A. Google Scholar
Brindeiro, Rodrigo M. Google Scholar
Mortensen, Claudio Google Scholar
Hertogs, Kurt Google Scholar
De Vroey, Veronique Google Scholar
Rubini, Noema PM Google Scholar
Sion, Fernando S. Google Scholar
De Sa, Carlos AM Google Scholar
Machado, Deisy M. Autor UNIFESP Google Scholar
Succi, Regina CM Autor UNIFESP Google Scholar
Tanuri, Amilcar Google Scholar
Institution Universidade Federal do Rio de Janeiro (UFRJ)
Universidade Federal de São Paulo (UNIFESP)
Gaffree & Guinle Univ Hosp
VIRCO NV
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.
Language English
Date 2002-12-01
Published in Journal of Clinical Microbiology. Washington: Amer Soc Microbiology, v. 40, n. 12, p. 4512-4519, 2002.
ISSN 0095-1137 (Sherpa/Romeo, impact factor)
Publisher Amer Soc Microbiology
Extent 4512-4519
Origin http://dx.doi.org/10.1128/JCM.40.12.4512-4519.2002
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000179631500018
URI http://repositorio.unifesp.br/handle/11600/27050

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