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De Neve J.-W.,Harvard University | Fink G.,Center for Population and Development Studies | Subramanian S.V.,Center for Population and Development Studies | Moyo S.,Botswana Harvard AIDS Institute Partnership | Bor J.,Boston University
The Lancet Global Health | Year: 2015

Background: An estimated 2·1 million individuals are newly infected with HIV every year. Cross-sectional and longitudinal studies have reported conflicting evidence for the association between education and HIV risk, and no randomised trial has identified a causal effect for education on HIV incidence. We aimed to use a policy reform in secondary schooling in Botswana to identify the causal effect of length of schooling on new HIV infection. Methods: Data for HIV biomarkers and demographics were obtained from the nationally representative household 2004 and 2008 Botswana AIDS Impact Surveys (N=7018). In 1996, Botswana reformed the grade structure of secondary school, expanding access to grade ten and increasing educational attainment for affected cohorts. Using exposure to the policy reform as an instrumental variable, we used two-stage least squares to estimate the causal effect of years of schooling on the cumulative probability that an individual contracted HIV up to their age at the time of the survey. We also assessed the cost-effectiveness of secondary schooling as an HIV prevention intervention in comparison to other established interventions. Findings: Each additional year of secondary schooling caused by the policy change led to an absolute reduction in the cumulative risk of HIV infection of 8·1 percentage points (p=0·008), relative to a baseline prevalence of 25·5% in the pre-reform 1980 birth cohort. Effects were particularly large in women (11·6 percentage points, p=0·046). Results were robust to a wide array of sensitivity analyses. Secondary school was cost effective as an HIV prevention intervention by standard metrics (cost per HIV infection averted was US$27 753). Interpretation: Additional years of secondary schooling had a large protective effect against HIV risk in Botswana, particularly for women. Increasing progression through secondary school could be a cost-effective HIV prevention measure in HIV-endemic settings, in addition to yielding other societal benefits. Funding: Takemi Program in International Health at the Harvard T.H.Chan School of Public Health, Belgian American Educational Foundation, Fernand Lazard Foundation, Boston University, National Institutes of Health. © 2015 De Neve et al. Open access article distributed under the terms of CC BY.

Powis K.M.,Massachusetts General Hospital | Powis K.M.,Botswana Harvard AIDS Institute Partnership | Powis K.M.,Harvard University | Smeaton L.,Center for Biostatistics in Research | And 14 more authors.
Journal of Acquired Immune Deficiency Syndromes | Year: 2011

Background: The impact of in utero exposure to highly active antiretroviral therapy (HAART) on longitudinal growth of HIV-uninfected infants is unknown. Methods: The Mashi and Mma Bana PMTCT intervention trials enrolled HIV-infected pregnant women at four sites in Botswana. Breast-fed (BF), HIV-uninfected infants born at 37 weeks or greater were included in this analysis. Weight-for-age (WAZ), length-for-age (LAZ), and weight-for-length (WLZ) z-scores were calculated using World Health Organization Child Growth Standards. Mean z-scores were compared between in utero antiretroviral exposure groups using Student t test, response profiles analysis, and general linear mixed effects modeling. Results: Growth of 619 HAART-exposed and 440 zidovudine-exposed, HIV-uninfected infants was evaluated. Mean birth weights were 3.01 kg for HAART and 3.15 kg for zidovudine-exposed infants (P < 0.001) with lower mean birth WAZ, length-for-age (LAZ), and weight-for-length (WLZ) among HAART-exposed infants (all P < 0.001). HAART-exposed infants had greater improvement in WAZ and weight-for-length (WLZ) from birth through 2 months (P = 0.03, P < 0.001, respectively). The WAZ did not differ between groups from 3 through 6 months (P = 0.26). Length-for-age (LAZ) remained lower in HAART-exposed infants but the incidence of wasting or stunting did not differ between exposure groups. Conclusions: Lower weights in HAART-exposed uninfected infants at birth were rapidly corrected during the first 6 months of life. © 2011 Lippincott Williams & Wilkins.

Lockman S.,Brigham and Womens Hospital | Lockman S.,IID Inc | Lockman S.,Botswana Harvard AIDS Institute Partnership | Hughes M.D.,IID Inc | And 27 more authors.
New England Journal of Medicine | Year: 2010

Background: Peripartum administration of single-dose nevirapine reduces mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1) but selects for nevirapineresistant virus. Methods: In seven African countries, women infected with HIV-1 whose CD4+ T-cell counts were below 200 per cubic millimeter and who either had or had not taken singledose nevirapine at least 6 months before enrollment were randomly assigned to receive antiretroviral therapy with tenofovir - emtricitabine plus nevirapine or tenofovir- emtricitabine plus lopinavir boosted by a low dose of ritonavir. The primary end point was the time to confirmed virologic failure or death. Results: A total of 241 women who had been exposed to single-dose nevirapine began the study treatments (121 received nevirapine and 120 received ritonavir-boosted lopin avir). Significantly more women in the nevirapine group reached the primary end point than in the ritonavir-boosted lopinavir group (26% vs. 8%) (adjusted P = 0.001). Virologic failure occurred in 37 (28 in the nevirapine group and 9 in the ritonavir-boosted lopinavir group), and 5 died without prior virologic failure (4 in the nevirapine group and 1 in the ritonavir-boosted lopinavir group). The group differences appeared to decrease as the interval between single-dose nevirapine exposure and the start of antiretroviral therapy increased. Retrospective bulk sequencing of baseline plasma samples showed nevirapine resistance in 33 of 239 women tested (14%). Among 500 women without prior exposure to single-dose nevirapine, 34 of 249 in the nevirapine group (14%) and 36 of 251 in the ritonavir-boosted lopinavir group (14%) had virologic failure or died. Conclusions: In women with prior exposure to peripartum single-dose nevirapine (but not in those without prior exposure), ritonavir-boosted lopinavir plus tenofovir - emtricitabine was superior to nevirapine plus tenofovir - emtricitabine for initial antiretroviral therapy. Copyright © 2010 Massachusetts Medical Society.

Powis K.M.,Massachusetts General Hospital | Powis K.M.,Harvard University | Powis K.M.,Botswana Harvard AIDS Institute Partnership | Smeaton L.,Harvard University | And 15 more authors.
AIDS | Year: 2016

Objective: To assess associations between in-utero triple antiretrovirals (cART) versus zidovudine (ZDV) monotherapy exposure and growth among HIV-uninfected children of HIV-infected women in Botswana. Design: Secondary retrospective data analysis from two randomized intervention trials of mother-to-child HIV transmission prevention. Methods: The Mashi and Mma Bana studies enrolled HIV-infected pregnant women, following their children through 24 months of age. This analysis includes singleton, fullterm, HIV-exposed uninfected children. Mothers received cART or ZDV at least 2 weeks predelivery, and breastfed up to 6 months. Weight-for-age (WAZ), length-for-age (LAZ) and weight-for-length (WLZ) z-scores were derived. Mean z-scores were compared by exposure group at 24 months (t-test, linear regression). Results: Of 819 children, 303 were ZDV-and 516 cART-exposed in utero. Maternal median enrolment CD4 was higher among ZDV versus cART-treated mothers (393 versus 324 cells/ml; P<0.0001). Median duration of antepartum antiretroviral use was shorter among ZDV-treated women (5.7 versus 12.0 weeks; P<0.0001). Median months breastfed were similar (5.9 and 6.0; P=0.43). At 24 months, mean LAZ and WAZwere significantly lower among cART-exposed children (LAZ-1.01 versus-0.74; P=0.003) (WAZ-0.53 versus-0.30; P=0.002) in unadjusted analyses. Adjusting for maternal CD4, viral load, enrolment site and maternal anthropometric measures, cART-exposed children had significantly lower LAZ and WAZ at 24 months (P=0.0004 for both). Conclusion: At 24 months, in-utero cART-exposed children had significantly lower LAZ and WAZ. Poor growth impacts childhood and adult mortality. These findings raise concerns for potential lasting health impacts among HIV-exposed uninfected children with in-utero cART exposure. © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Powis K.M.,Massachusetts General Hospital | Powis K.M.,Harvard University | Powis K.M.,Botswana Harvard AIDS Institute Partnership | McElrath T.F.,Brigham and Womens Hospital | And 17 more authors.
Journal of Acquired Immune Deficiency Syndromes | Year: 2013

Background: Risk factors associated with preeclampsia in HIVinfected women remain largely unknown. Systemic angiogenic imbalance contributes to preeclampsia in HIV-uninfected women, but changes in angiogenic markers after highly active antiretroviral therapy (HAART) initiation have not been studied. Methods: The Mma Bana study randomized 560 HIV-infected, HAART-naive pregnant women with CD4 counts $200 cells per cubic millimeter between 26 and 34 weeks gestation to lopinavir/ ritonavir/zidovudine/lamivudine or abacavir/zidovudine/lamivudine. Another 170 participants with CD4 counts less than 200 cells per cubic millimeter initiated nevirapine/zidovudine/lamivudine between 18 and 34 weeks gestation. Characteristics of 11 women who developed preeclampsia were compared with the remaining 722 Mma Bana participants who delivered using logistic regression. Plasma samples drawn at HAART initiation and 1 month later from 60 women without preeclampsia and at HAART initiation for all 11 preeclamptic women were assayed for placental growth factor (PlGF) and soluble FMS toll-like tyrosine kinase-1 (sFlt-1). Results: Pre-HAART viral load greater than 100,000 copies per milliliter was associated with preeclampsia (odds ratio: 5.8, 95% confidence interval: 1.8 to 19.4, P = 0.004).Median pre-HAART PlGF level was lower and sFlt-1 was higher in women who developed preeclampsia vs those who did not (130 vs 992 pg/mL, P = 0.001; 17.5 vs 9.4 pg/mL, P = 0.03, respectively). In multivariate analysis, PlGF and viral load remained significantly associated with preeclampsia. No significant changes in angiogenic factors were noted after 1 month of HAART treatment among non-preeclamptic women. Conclusions: Pre-HAART viral load greater than 100,000 copies per milliliter and PlGF predicted preeclampsia among women starting HAART in pregnancy. Among non-preeclamptic women, HAART treatment did not significantly alter levels of PlGF or sFlt-1 after 1 month of treatment. Copyright © 2012 by Lippincott Williams & Wilkins.

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