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Background:  We conducted a study to assess the virological effects and the frequency of genotypic resistance to antivirals (ARV) in Ivoirian children treated with highly active antiretrovival therapy (HAART) are not well understood.

Methods: Between October 2000 and September 2003, 269 HIV-1 infected children were included in the Agence Nationale de Recherche sur le SIDA (ANRS) 1278 Cohort: 115 (median age: 6.5 years [0.7 to15], 16% < 3 years) were treated with HAART for at least 6 months. Treatments consisted in 2 nucleoside reverse transcriptase inhibitors (NRTI) associated with nelfinavir (NFL) in 76% of cases or efavirenz (EFV) (24 %). Plasma HIV-RNA and CD4 cell count were carried out at baseline then every 6 months. Virological failure was defined as a viral load > 3 log copies/ml after at least 6 months of HAART. Genotypic resistance tests were performed in case of virological failure and interpretation of drug resistance patterns was done according to the 2003 French ANRS algorithm.

Results:  At HAART initiation, median HIV-RNA was 5.45 log [3.24 to 7.34] and median % CD4 cell count was 8.9 [0.1 to 22.7]. After a median of 10.2 months [6 to 20.9] of HAART, 65% (75 of 115) of children were in virological success (viral load below 3 log copies/mL), leaving 35% (40 in 115) in virological failure. Among them, 29 had available samples for the genotypic resistance tests. Baseline characteristics at HAART initiation (age, % CD4 cell count, viral load, type of treatment) were similar in children with virological success compared to those with failure. Twenty-three viruses presented with a resistance to at least one antiretroviral drug. Ten, 8, and 5 children had viruses with resistance to 1, 2, or 3 their treatment drugs, respectively. The resistant mutation 184V was detected in 14 of 15 patients (93%) treated with lamivudine (3TC). Five out of 6 (83%) treated with EFV had a NRTI-resistant mutation. The L90M, M46I, N88S, and I54V were also found in 11 (65%) of the 17 children who received NFL. Resistance mutations were detected in 2 out of the 3 children who used NRTI-bitherapy before HAART initiation.

Conclusion:  In this cohort, the efficacy of HAART (65%) was similar to what is generally observed in Europe and the United States in treated children. These encouraging results obtained with the drugs available in Abidjan support the concept that implementation of HAART is feasible for African children. However, an optimal clinical, biological, and close follow up is essential. The rate of resistant viruses was 22% (23 of 104) among treated children. Therefore, one could hypothesize that virologic success in African children could be improved with the use of regimens including boosted protease inhibitors.

Keywords: HAART; African children; Resistance