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Journal of Clinical Microbiology, December 2002, p. 4512-4519, Vol. 40, No. 12
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.12.4512-4519.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Testing Genotypic and Phenotypic Resistance in Human Immunodeficiency Virus Type 1 Isolates of Clade B and Other Clades from Children Failing Antiretroviral Therapy

Patrícia A. Brindeiro,1 Rodrigo M. Brindeiro,1 Cláudio Mortensen,2 Kurt Hertogs,3 Veronique De Vroey,3 Norma P. M. Rubini,4 Fernando S. Sion,4 Carlos A. M. De Sá,4 Deisy M. Machado,5 Regina C. M. Succi,5 and Amilcar Tanuri1*

Laboratory of Molecular Virology, Department of Genetics, Federal University of Rio de Janeiro,1 Gaffrée & Guinle University Hospital, Rio de Janeiro,4 Applied Biosystems,2 Federal University of São Paulo Medical School, São Paulo, Brazil,5 Tibotec-VIRCO NV, Mechelen, Belgium3

Received 7 June 2002/ Returned for modification 8 August 2002/ Accepted 17 September 2002

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 <= P <= 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 <= P <= 0.0704). Significant differences were found only in secondary resistance mutations and did not reflect significant phenotypic variation between clade B and non-B.

* Corresponding author. Mailing address: Universidade Federal do Rio de Janeiro, C.C.S., Instituto de Biologia, Depto. de Genética, bloco A, sala A2-121, 2° andar, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ, CEP: 21944-970, Brazil. Phone: (55 21) 2562-6384. FAX: (55 21) 2562-6384. E-mail: atanuri{at}biologia.ufrj.br.

Journal of Clinical Microbiology, December 2002, p. 4512-4519, Vol. 40, No. 12
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.12.4512-4519.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.





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