Background: Iron deficiency (ID) is a major public health burden in African children and accurate prevalence estimates are important for effective nutritional interventions. However, ID may be incorrectly estimated in Africa because most measures of iron status are altered by inflammation and infections such as malaria. Through the current study, we have assessed different approaches to the prediction of iron status and estimated the burden of ID in African children. Methods:We assayed iron and inflammatory biomarkers in 4853 children aged 0-8 years from Kenya, Uganda, Burkina Faso, South Africa, and The Gambia. We described iron status and its relationship with age, sex, inflammation, and malaria parasitemia. We defined ID using the WHO guideline (ferritin < 12 μg/L or < 30 μg/L in the presence of inflammation in children < 5 years old or < 15 μg/L in children ≥ 5 years old). We compared this with a recently proposed gold standard, which uses regression-correction for ferritin levels based on the relationship between ferritin levels, inflammatory markers, and malaria. We further investigated the utility of other iron biomarkers in predicting ID using the inflammation and malaria regression-corrected estimate as a gold standard. Results: The prevalence of ID was highest at 1 year of age and in male infants. Inflammation and malaria parasitemia were associated with all iron biomarkers, although transferrin saturation was least affected. Overall prevalence of WHOdefined ID was 34% compared to 52% using the inflammation and malaria regression-corrected estimate. This unidentified burden of ID increased with age and was highest in countries with high prevalence of inflammation and malaria, where up to a quarter of iron-deficient children were misclassified as iron replete. Transferrin saturation < 11% most closely predicted the prevalence of ID according to the regression-correction gold standard. Conclusions: The prevalence of ID is underestimated in African children when defined using the WHO guidelines, especially in malaria-endemic populations, and the use of transferrin saturation may provide a more accurate approach. Further research is needed to identify the most accurate measures for determining the prevalence of ID in sub-Saharan Africa.
Background: Limited data are available on the incidence and factors associated with viral rebound following viral suppression among HIV-infected individuals taking antiretroviral therapy (ART) in Kenya. Furthermore, the durability of viral suppression among HIV individuals taking ART is unknown. Information on incidence rates and factors associated with HIV viral load rebound and the durability of viral suppression (undetectable HIV copies in plasma) among HIV-infected individuals taking ART, will help improve the long-term management of HIV-infected individuals and explore approaches to longterm HIV remission or complete cure. Objectives: The objectives of this study were to investigate the incidence rates of viral rebound following viral suppression, factors associated with viral rebound, and the durability of viral suppression among HIV-infected individuals on ART from Kilifi, Meru, and Nakuru counties in Kenya. Methods: This was a retrospective study involving 600 HIV-infected individuals taking combination ART (cART) and enrolled in comprehensive care centers (CCCs) at Malindi Sub-county Hospital, Nakuru Level 5 Hospital, and Meru Level 5 Hospital in Kenya. The medical files were inspected and medical history records abstracted for the selected participants. Participant laboratory data including HIV viral loads, types and history of ART, and treatment history of any opportunistic infections were abstracted using an abstraction checklist. Participants were grouped into those who achieved HIV viral suppression, with viral loads lower than the detection limit (LDL) (viral suppression), and those who experienced one or more detectable viral load measurements >40 copies/ml following the initial LDL (viral rebound). Durable viral suppression was defined as all viral load values at LDL over the 2-year period (2017)(2018)(2019). Univariate and multivariate Poisson regression analyses were performed to assess the rates of viral rebound, as well as to investigate factors associated with it. Results: Out of 549 HIV-positive patients, 324/549 (59%) achieved HIV viral suppression (Meru 159/ 194 (82%), Nakuru 21/178 (12%), and Malindi 144/177 (81%)). The overall viral rebound rate was 41%, with site-specific viral rebound of 88.2%, 18.6%, and 18.0% in Nakuru, Malindi, and Meru, respectively. There was an overall rate of first viral rebound of 3.9 (95% confidence interval (CI) 6.9-14.4), 0.7 (95% CI 0.5-1.0), and 0.89 (95% CI 0.64-1.24) per 100 person-months in Nakuru, Malindi, and Meru, respectively. Good ART adherence (p = 0.0002), widow status (p = 0.0062), and World Health Organization (WHO) stage I (p = 0.0002) were associated with viral suppression, while poor ART adherence (p < 0.0001), WHO stage II (p = 0.0024), and duration on ART of 36 months (p = 0.0350) were associated with viral rebound. Conclusions: The rate of viral suppression in patients on cART in the CCCs fell short of the WHO target. However, the study provides proof of evidence of undetectable viral load levels for more than 2 years, a sign that the Un...
Summary Rift Valley fever (RVF) is a viral hemorrhagic disease first discovered in Kenya in 1930. Numerous animal studies have demonstrated that protective immunity is acquired following RVF virus (RVFV) infection and that this correlates with acquisition of virus-neutralizing antibodies (nAbs) that target the viral envelope glycoproteins. However, naturally acquired immunity to RVF in humans is poorly described. Here, we characterized the immune response to the viral envelope glycoproteins, Gn and Gc, in RVFV-exposed Kenyan adults. Long-lived IgG (dominated by IgG1 subclass) and T cell responses were detected against both Gn and Gc. However, antigen-specific antibody depletion experiments showed that Gn-specific antibodies dominate the RVFV nAb response. IgG avidity against Gn, but not Gc, correlated with nAb titers. These data are consistent with the greater level of immune accessibility of Gn on the viral envelope surface and confirm the importance of Gn as an integral component for RVF vaccine development.
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ID appears to protect against malaria infection in African children when defined using ferritin and transferrin saturation, but not when defined by hepcidin, sTfR or hemoglobin. Further research is required to determine causality.
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