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Low Rate of Resistance to Antiretroviral Drugs 6 Months after HAART Initiation in HIV-1-infected Sub-Saharan African: The ANRS 1269 TRIVACAN Trial
Marie-Laure Chaix*1, F Rouet2, T D Toni2, C Danel3, R Moh3, D Gabillard4, R Salamon4, E Bissagnene5, X Anglaret4, and C Rouzioux1
1Ctr Hosp Univ Necker, Paris, France; 2CeDReS, Ctr Hosp Univ de Treichville, Abidjan, Côte d'Ivoire; 3PACCI, Abidjan, Côte d'Ivoire; 4INSERM 593, Univ Victor Segalen Bordeaux 2, France; and 5Ctr Hosp Univ Treichville, Abidjan, Côte d'Ivoire
Background: Data on resistance to ART drugs in
sub-Saharan Africa are scarce. We studied the
6-month rate of resistance to ART drugs in HIV-1-infected adults who start
HAART in Cote d’Ivoire, West Africa, where CRF02 is the predominant HIV-1 strain.
Methods: HAART-naïve HIV-1-infected adults with a CD4
count at 150 to 350/mm3 were included in the pre-randomization phase
of a HAART structured treatment interruption trial in Abidjan (TRIVACAN ANRS 1269 trial). All
patients received a continuous HAART for at least 6 months. HIV-1 plasma viral
load was quantified at month 6 (real time polymerase chain reaction, threshold
300 copies/mL). In case of viral load >300 copies/mL, resistance genotypic test was performed.
Results: We started 824 HIV-1-infected adults (76%
women, median age 34 years, median baseline CD4 count 253/mm3) on zidovudine, lamivudine, and efavirenz (ZDV+3TC+EFV) (90%) or zidovudine,
lamivudine, and indinavir/ritonavir
(ZDV+3TC+IDV/r) (10%). At month 6, 10 patients were dead, 1 was lost to follow-up,
and 15 had missing data for viral loads. Among the 799 patients with available
viral load data, 682 (85%) had undetectable viral load and 117 (15%) detectable
viral load (median 5500 copies/mL, IQR 1300 to 33900). Strains of 5 patients were not amplified
(median viral load 1000 copies/mL). Of the 112
remaining patients, 79 (70%) had wild type viruses and 33 (30%) had at least 1
resistance mutation (patients on ZDV+3TC+EFV n = 28; patients on ZDV+3TC+IDV/r n = 5). The 6-months rate of resistance to at least 1 drug was
4.2% (33 of 794) overall, 3.9% (28 of
722) in patients receiving the non-nucleoside reverse transcriptase inhibitor
(NNRTI) -based regimen and 6.9% (5 of
72) in those receiving the protease inhibitor (PI) -based regimen. In
patients on ZDV+3TC+EFV, the 28 drug mutations were K103N alone (n = 17), K103N + M184V (n = 5), M184V alone (n = 5) and thymidine
analogue mutations (TAM) (n = 1). In
patients on ZDV+3TC+IDV/r, the 5 resistant virus had
M184V mutation. In women on ZDV+3TC+EFV, the 6-months rate of resistance to
NNRTI was 3.2% (17 of 529) overall, and:
20.4% (3 of 14), 0% (0 of 5), 0% (0 of 35), and 2.9% (14 of 475) in
women with a history of mother-to-child transmission with ZDV+NVP, ZDV+3TC+NVP,
ZDV alone, and no history of mother-to-child transmission, respectively.
Conclusions: In this large cohort of West African patients
starting HAART with low genetic barrier drugs, we observed, at 6 months, a high
rate of virological success (85%) and a low rate of
drug resistance (4.2%). Most patients (70%) with detectable viral load had no
resistant virus. Most of the resistant virus observed harbored NNRTI mutations
or 3TC mutation.
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