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INTRODUCTION: This study aimed at estimating the incidence of pregnancy after antiretroviral therapy (ART) initiation in 8 West African countries over a 10-year period. METHODS: A retrospective analysis was conducted within the international database of the IeDEA West Africa Collaboration. All HIV-infected women aged

In sub-Saharan Africa, most HIV-infected patients receive antiretroviral therapy (ART) without virological monitoring. Longitudinal data on secondary resistance are rare.We conducted a prospective cohort study of HIV-1-infected adults initiating ART in 3 clinics using computerized monitoring systems. Patients had plasma HIV-1 RNA viral load (VL) tests at months 12 (M12) and 24 (M24) after ART initiation and HIV-1 resistance genotype tests if VL was detectable (≥300 copies/mL).Overall, 1573 patients initiated ART with stavudine/zidovudine plus lamivudine plus nevirapine/efavirenz. At M12 and M24, 944 and 844 patients, respectively, remained in active follow-up. Among them, 25% (M12) and 27% (M24) had detectable VLs and 12% (M12) and 19% (M24) had virus resistant to at least 1 antiretroviral drug, accounting for 54% (M12) and 75% (M24) of patients with detectable VLs. Among the resistant strains, 95% (M12) and 97% (M24) were resistant to lamivudine/emtricitabine, efavirenz, and/or nevirapine, the frequency of thymidine analog mutations increased from 8.1% (M12) to 14.7% (M24) and etravirine resistance increased from 13.5% (M12) to 24.5% (M24).Of the patients with detectable VLs at M24, 25% still did not harbor resistant virus. Preventing mutations from emerging with adherence reinforcement in patients with detectable VLs remains important beyond M24. Switching therapy early in patients with resistance to 3 TC/FTC and/or to nonnucleoside reverse transcriptase inhibitors to prevent extended resistance to nucleoside reverse transcriptase inhibitors and etravirine resistance from occurring is also a major challenge.

Background: In resource-limited countries, estimating CD4-specific incidence rates of mortality and morbidity among patients receiving antiretroviral therapy (ART) may help assess the effectiveness of care and treatment programmes, identify program weaknesses, and inform decisions. Methods: We pooled data from 13 research cohorts in 5 sub-Saharan African (Benin, Burkina Faso, Cameroon, Cote d'Ivoire, and Senegal) and 2 Asian (Cambodia and Laos) countries. HIV-infected adults (18 years and older) who received ART in 1998-2008 and had at least one CD4 count available were eligible. Changes in CD4 counts over time were estimated by a linear mixed regression. CD4-specific incidence rates were estimated as the number of first events occurring in a given CD4 stratum divided by the time spent within the stratum. Results: Overall 3917 adults (62% women) on ART were followed up during 10,154 person-years. In the

Background CD4-specific rates of mortality in sub-Saharan African adults with high CD4 counts have rarely been estimated. This estimation is useful to the when to start antiretroviral treatment (ART) debate. Methods We pooled data from National Agency for Research on AIDS and Viral Hepatitis (ANRS)-funded research cohorts or associated partners in West Africa. All HIV-infected adults (≥18 years) with available follow-up time off ART were eligible. We used a joint model to estimate CD4 count evolution. We estimated CD4-specific rates of mortality, loss-to-follow-up (LTFU) and ART initiation by dividing the number of first event by the follow-up time off ART within each CD4 category. Results Between 1996 and 2009, 2588 adults (80% women) from 5 cohorts in Cote d'Ivoire and Burkina Faso were followed off ART during 6862 person-years. In the 201-350, 351-500, 501-650, and >650 cells per cubic millimeter CD4 categories, mortality rates were: 3.0, 1.5, 0.4, 0.2 per 100 person-years; LTFU rates: 6.0, 4.6, 6.1, 6.0 per 100 person-years; and ART initiation rates: 18.1, 2.7, 0.5, 0.5 per 100 person-years, respectively. All estimates varied across cohorts; mortality rates were higher when rates of LFTU and ART initiation were lower; LTFU rates were 2-40 times higher than mortality rates. Conclusions Among untreated West African adults with high CD4 counts, mortality and LTFU rates were substantial. Even when data are collected under research conditions, informative censoring due to ART initiation and LTFU could lead to significantly underestimate mortality figures.

Adherence is a strong determinant of viral suppression with antiretroviral therapy (ART) but measuring it is challenging. Medication delivery can be measured accurately in settings with computerized prescription databases. We studied the association between medication possession ratio (MPR), virologic suppression, and resistance to ART in Côte d'Ivoire.We conducted a prospective cohort study of HIV-1-infected adults initiating ART in 3 clinics using computerized monitoring systems. Patients had viral load (VL) tests at month 6 (M6) and month 12 (M12) after ART initiation and genotype tests if VL was detectable (≥300 copies/mL). MPR was defined as the number of daily doses of antiretroviral drug actually provided divided by the total number of follow-up days since ART initiation.Overall, 1573 patients started ART with stavudine/zidovudine plus lamivudine plus nevirapine/efavirenz. At M6 and M12, 996 and 942 patients were in active follow-up; 20% (M6) and 25% (M12) of patients had detectable VL, including 7% (M6) and 11% (M12) with ≥1 resistance mutation. Among patients with MPR of ≥95%, 80%-94%, 65%-79%, 50%-64%, and50% at M12, the proportion with detectable VL [resistance] was 9% [4%], 17% [7%], 45% [24%], 67% [31%], and 85% [37%]. Among patients with ≥1 mutation at M12, 86% were resistant to lamivudine/emtricitabine and/or nevirapine/efavirenz but not to other drugs.MPR was strongly associated with virologic outcomes. Half of those with detectable VL at M12 had no resistance mutations. MPR should be used at M6 to identify patients who might benefit from early interventions to reinforce adherence.

International audience; OBJECTIVE: We compared CD4+ decline among untreated HIV-1-infected seroconverters living in Côte d'Ivoire (CI) and in France. METHODS: HIV-1-infected adults were enrolled in the ANRS1220 PRIMO-CI (CI, 1997-2006) and ANRSCO2 SEROCO (France, 1988-1995) cohorts. CD4+ count and percentage declines were estimated from enrollment until 24 months of seroconversion by linear random-effect models adjusted for time since seroconversion, age, gender, cell-associated HIV DNA, HIV RNA, and country. RESULTS: Overall 521 seroconverters (CI 148, 62% men; France 373, 77% men) were enrolled after a median of 7.6 months since seroconversion. Median follow-up duration was 12.7 months. Median age was 28 years. Median baseline CD4+ count was 472 and 560 cells per cubic millimeter, respectively. Median baseline HIV RNA was 4.4 and 4.0 log10 copies per milliliter and median HIV DNA was 3.0 and 2.8 log10 copies per 10(6) peripheral blood mononuclear cells, respectively. In adjusted models, CD4+ count and percentage at baseline were lower in CI than in France (P < 0.01), and the difference did not vary during follow-up (P = 0.55). Low HIV RNA and low HIV DNA at baseline were associated with higher CD4+ count at baseline. CONCLUSIONS: CD4+ count and percentage were lower in CI than in France. These differences were already observed during early infection and remained similar after adjustment.

The aim of this study was to evaluate the heat-dissociated p24 antigen (HD p24 Ag) assay as an alternative low-cost tool for diagnosis of HIV-I infection and quantitation of HIV-1 RNA levels in African adults mainly infected with HIV-1 CRF02―AG strains. One hundred seventeen plasma specimens were obtained from HIV-1-seropositive subjects enrolled in the ANRS 1220 PRIMO-CI cohort (Abidjan, Cote d'lvoire, West Africa). Results of the HD p24 Ag assay were comparable with those of HIV-1 RNA levels quantified in the same antibody-positive plasma samples by the Amplicor HIV-1 Monitor assay (1.5 version; Roche Diagnostics, Indianapolis, IN): sensitivity, 95.7% versus 96.6%, respectively; specificity (evaluated with samples from 75 seronegative subjects), 94.7% versus 100%, respectively. HD p24 Ag and HIV-1 RNA assays were weakly correlated (Spearman coefficient correlation, r 0.33; P < 0.001) except for HIV-1 RNA levels of ≥5 log 10 copies/mL (r = 0.62; P < 0.001). Quantitation of HD p24 antigenemia in 76 plasma specimens from 14 patients treated with highly active antiretroviral therapy demonstrated weaker changes during treatment than those observed with the HIV-I RNA assay. Follow-up of infected patients using both markers showed different results. The reliability of the HD p24 Ag assay is questionable for clinical and biologic management as a surrogate tool for measurement of HIV-1 RNA levels in Africa.