The Mobile WACh RCT demonstrates that SMS improved practice of exclusive breastfeeding and early postpartum contraception.
Objective Cytomegalovirus (CMV) coinfection may influence HIV-1 disease progression during infancy. Our aim was to describe the incidence of CMV infection and the kinetics of viral replication in Kenyan HIV-infected and HIV-exposed uninfected infants. Methods HIV-1 and CMV plasma viral loads were serially measured in 20 HIV-exposed uninfected and 44 HIV-infected infants born to HIV-infected mothers. HIV-infected children were studied for the first 2 years of life, and HIV-exposed uninfected infants were studied for 1 year. Results CMV DNA was detected frequently during the first months of life; by 3 months of age, CMV DNA was detected in 90% of HIV-exposed uninfected infants and 93% of infants who had acquired HIV-1 in utero. CMV viral loads were highest in the 1–3 months following the first detection of virus and declined rapidly thereafter. CMV peak viral loads were significantly higher in the HIV-infected infants compared with the HIV-exposed uninfected infants (mean 3.2 versus 2.7 log10 CMV DNA copies/ml, respectively, P = 0.03). The detection of CMV DNA persisted to 7–9 months post-CMV infection in both the HIV-exposed uninfected (8/17, 47%) and HIV-infected (13/18, 72%, P = 0.2) children. Among HIV-infected children, CMV DNA was detected in three of the seven (43%) surviving infants tested between 19 and 21 months post-CMV infection. Finally, a strong correlation was found between peak CMV and HIV-1 viral loads (ρ = 0.40, P = 0.008). Conclusion Acute CMV coinfection is common in HIV-infected Kenyan infants. HIV-1 infection was associated with impaired containment of CMV replication.
BackgroundPreterm birth (PTB), low birth weight (LBW) and small for gestational age (SGA) contribute to neonatal mortality. Maternal HIV-1 infection has been associated with an increased risk of PTB, but mechanisms underlying this association are undefined. We describe correlates and outcomes of PTB, LBW, and SGA in HIV-exposed uninfected infants.MethodsThis was a retrospective analysis of cohort study. Between 1999–2002, pregnant, HIV-infected women were enrolled into an HIV-1 transmission study. Logistic regression was used to identify correlates of PTB, LBW and SGA in HIV-negative, spontaneous singleton deliveries. Associations between birth outcomes and mortality were measured using survival analyses.ResultsIn multivariable models, maternal plasma (OR = 2.1, 95% CI = 1.1-3.8) and cervical HIV-1 RNA levels (OR = 1.6, 95% CI = 1.1-2.4), and CD4 < 15% (OR = 2.4, 95% CI = 1.0-5.6) were associated with increased odds of PTB. Abnormal vaginal discharge and cervical polymorphonuclear leukocytes were also associated with PTB. Cervical HIV-1 RNA level (OR = 2.4, 95% CI = 1.5-6.7) was associated with an increased odds of LBW, while increasing parity (OR = 0.46, 95% CI = 0.24-0.88) was associated with reduced odds. Higher maternal body mass index (OR = 0.75, 95% CI = 0.61-0.92) was associated with a reduced odds of SGA, while bacterial vaginosis was associated with >3-fold increased odds (OR = 3.2, 95% CI = 1.4-7.4). PTB, LBW, and SGA were each associated with a >6-fold increased risk of neonatal death, and a >2-fold increased rate of infant mortality within the first year.ConclusionsMaternal plasma and cervical HIV-1 RNA load, and genital infections may be important risk factors for PTB in HIV-exposed uninfected infants. PTB, LBW, and SGA are associated with increased neonatal and infant mortality in HIV-exposed uninfected infants.
Human immunodeficiency virus type 1 (HIV-1) infection results in different patterns
Background Breast-feeding by infants exposed to human immunodeficiency virus type 1 (HIV-1) provides an opportunity to assess the role played by repeated HIV-1 exposure in eliciting HIV-1–specific immunity and in defining whether immune responses correlate with protection from infection. Methods Breast-feeding infants born to HIV-1–seropositive women were assessed for HLA-selected HIV-1 peptide–specific cytotoxic T lymphocyte interferon (IFN)–γ responses by means of enzyme-linked immunospot (ELISpot) assays at 1, 3, 6, 9, and 12 months of age. Responses were deemed to be positive when they reached ⩾50 HIV-1–specific sfu/1 × 106 peripheral blood mononuclear cells (PBMCs) and were at least twice those of negative controls. Results A total of 807 ELISpot assays were performed for 217 infants who remained uninfected with HIV-1 at ∼12 months of age; 101 infants (47%) had at least 1 positive ELISpot result (median, 78–170 sfu/1 × 106 PBMCs). The prevalence and magnitude of responses increased with age (P = .01 and P = .007, respectively); the median log10 value for HIV-1–specific IFN-γ responses increased by 1.0 sfu/1 × 106 PBMCs/month (P < .001) between 1 and 12 months of age. Of 141 HIV-1–uninfected infants with 1-month ELISpot results, 10 (7%) acquired HIV-1 infection (0/16 with positive vs. 10/125 [8%] with negative ELISpot results; P = .6). Higher values for log10 HIV-1–specific spot-forming units at 1 month of age were associated with a decreased risk of HIV-1 infection, adjusted for maternal HIV-1 RNA level (adjusted hazard ratio, 0.09 [95% confidence interval, 0.01–0.72]). Conclusions Breast-feeding HIV-1–exposed uninfected infants frequently had HIV-1–specific IFN-γ responses. Greater early HIV-1–specific IFN-γ responses were associated with decreased HIV-1 acquisition.
Background While traditional epidemiological approaches have supported significant reductions in malaria incidence across many countries, higher resolution information about local and regional malaria epidemiology will be needed to efficiently target interventions for elimination. The application of genetic epidemiological methods for the analysis of parasite genetics has, thus far, primarily been confined to research settings. To illustrate how these technical methods can be used to advance programmatic and operational needs of National Malaria Control Programmes (NMCPs), and accelerate global progress to eradication, this manuscript presents seven use cases for which genetic epidemiology approaches to parasite genetic data are informative to the decision-making of NMCPs. Methods The use cases were developed through a highly iterative process that included an extensive review of the literature and global guidance documents, including the 2017 World Health Organization’s Framework for Malaria Elimination, and collection of stakeholder input. Semi-structured interviews were conducted with programmatic and technical experts about the needs and opportunities for genetic epidemiology methods in malaria elimination. Results Seven use cases were developed: Detect resistance, Assess drug resistance gene flow, Assess transmission intensity, Identify foci, Determine connectivity of parasite populations, Identify imported cases, and Characterize local transmission chains. The method currently used to provide the information sought, population unit for implementation, the pre-conditions for using these approaches, and post-conditions intended as a product of the use case were identified for each use case. Discussion This framework of use cases will prioritize research and development of genetic epidemiology methods that best achieve the goals of NMCPs, and ultimately, inform the establishment of normative policy guidance for their uses. With significant engagement of stakeholders from malaria endemic countries and collaboration with local programme experts to ensure strategic implementation, genetic epidemiological approaches have tremendous potential to accelerate global malaria elimination efforts. Electronic supplementary material The online version of this article (10.1186/s12936-019-2784-0) contains supplementary material, which is available to authorized users.
Breast milk CMV levels and maternal CD4 count are major determinants of CMV transmission in the setting of maternal HIV-1. Maternal immune reconstitution or lowering breast milk CMV levels may reduce vertical CMV transmission.
EBV infection occurs early in infants born to HIV-infected women. HIV infection was associated with more frequent and higher quantity EBV DNA detection.
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