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Background Low vitamin D levels may increase the risk of tuberculosis disease; however, previous observational cohort studies showed variable results. We investigated the relationship between vitamin D levels in infancy and subsequent development of tuberculosis disease throughout childhood. Methods We enrolled pregnant women at 20–28 weeks' gestation attending antenatal care in a periurban South African setting in the Drakenstein Child Health Study. Serum 25(OH)D concentrations were measured in newborn infants aged 6–10 weeks. Children were followed prospectively for tuberculosis infection and disease using annual tuberculin skin testing, radiographic examinations, and microbiological diagnosis with GeneXpert, culture, and smear testing. Univariable and multivariable Cox regression was performed and HRs with 95% CIs were calculated. Results Children were followed for tuberculosis disease for a median of 7.2 years (IQR, 6.2–7.9). Among 744 children (<1% with human immunodeficiency virus (HIV), 21% HIV-exposed without HIV), those who were vitamin D deficient in early infancy were not at increased risk of developing tuberculosis disease (adjusted HR,.8; 95% CI,.4–1.6). Infants in the lowest vitamin D concentration tertile were at similar risk of tuberculosis as the highest tertile (adjusted HR,.7; 95% CI,.4–1.4). Vitamin D deficiency was associated with tuberculin conversion ≤2 years of age at a <30-nmol/L (adjusted OR, 1.9; 95% CI, 1.2–3.2), but not <50-nmol/L (adjusted OR, 1.5; 95% CI,.8–2.9), cutoff. Conclusions In a setting with hyperendemic rates of tuberculosis, vitamin D concentrations in infancy did not predict tuberculosis disease at any point in childhood. However, very low vitamin D levels were associated with tuberculin conversion in young children. [ABSTRACT FROM AUTHOR]

I copri i was previously reported to be significantly decreased but still present in the gut of children with AD compared to healthy controls in ASA.7 This species was further depleted and nearly absent in the majority of AA children with AD. Microbiome of the skin and gut in atopic dermatitis (AD): understanding the pathophysiology and finding novel management strategies. Keywords: atopic dermatitis; epidemiology; food allergy; omics- and systems biology; pediatrics EN atopic dermatitis epidemiology food allergy omics- and systems biology pediatrics 447 450 4 02/24/22 20220301 NES 220301 Key Messages African-heritage children with eczema from Chicago have lower microbiota diversity compared to children from South Africa. Atopic dermatitis, epidemiology, food allergy, omics- and systems biology, pediatrics. [Extracted from the article]

Background: Allergens can act as disease‐triggering factors in atopic dermatitis (AD) patients. The aim of the study was to elucidate the molecular IgE sensitization profile in children with and without AD living in urban and rural areas of South Africa. Methods: Specific IgE reactivity was assessed in 166 Black South African children aged 9‐38 months using a comprehensive panel of microarrayed allergens. According to clinical characterization children fell in four groups, urban AD cases (n = 32), urban controls (non‐AD, n = 40), rural cases (n = 49) and rural controls (non‐AD, n = 45). Results: IgE reactivity to at least one of the allergens was detected in 94% of urban and 86% of rural AD children. House dust mite (HDM; 81% urban, 74% rural AD) and animal‐derived allergens (50% urban, 31% rural AD) were the most frequently recognized respiratory allergens, whereas IgE to pollen allergens was almost absent. Urban AD children showed significantly higher frequency of IgE reactivity (50%) to mouse lipocalin, Mus m 1, than rural AD children (12%). The most frequently recognized food allergens were from egg (63% urban, 43% rural AD), peanut (31% vs 41%), and soybean (22% vs 27%), whereas milk sensitization was rare. α‐gal‐specific IgE almost exclusively occurred in rural children (AD: 14%, non‐AD: 49%). Conclusion: Molecular allergy diagnosis detects frequent IgE sensitization to HDM, animal but not pollen allergens and to egg, peanut, and soy, but not milk allergens in African AD children. Urban AD children reacted more often to Mus m 1, whereas α‐gal sensitization is more common in rural children likely due to parasite exposure. [ABSTRACT FROM AUTHOR]

Background: Conventional methods for modelling longitudinal growth data focus on the analysis of mean longitudinal trends or the identification of abnormal growth based on cross-sectional standardized z-scores. Latent Class Mixed Modelling (LCMM) considers the underlying heterogeneity in growth profiles and allows for the identification of groups of subjects that follow similar longitudinal trends., Methods: LCMM was used to identify underlying latent profiles of growth for univariate responses of standardized height, standardized weight, standardized body mass index and standardized weight-for-length/height measurements and multivariate response of joint standardized height and standardized weight measurements from birth to five years for a sample of 1143 children from a South African birth cohort, the Drakenstein Child Health Study (DCHS). Allocations across latent growth classes were compared to better understand the differences and similarities across the classes identified given different composite measures of height and weight as input., Results: Four classes of growth within standardized height (n 1 =516, n 2 =112, n 3 =187, n 4 =321) and standardized weight (n 1 =263, n 2 =150, n 3 =584, n 4 =142), three latent growth classes within Body Mass Index (BMI) (n 1 =481, n 2 =485, n 3 =149) and Weight for length/height (WFH) (n 1 =321, n 2 =710, n 3 =84) and five latent growth classes within the multivariate response of standardized height and standardized weight (n 1 =318, n 2 =205, n 3 =75, n 4 =296, n 5 =242) were identified, each with distinct trajectories over childhood. A strong association was found between various growth classes and abnormal growth features such as rapid weight gain, stunting, underweight and overweight., Conclusions: With the identification of these classes, a better understanding of distinct childhood growth trajectories and their predictors may be gained, informing interventions to promote optimal childhood growth., Competing Interests: Conflict of Interests: None declared.

SARS-CoV-2 infection in children typically results in asymptomatic or mild disease. There is a paucity of studies on antiviral immunity in African children. We investigated SARS-CoV-2-specific T cell responses in 71 unvaccinated asymptomatic South African children who were seropositive or seronegative for SARS-CoV-2. SARS-CoV-2-specific CD4+ T cell responses were detectable in 83% of seropositive and 60% of seronegative children. Although the magnitude of the CD4+ T cell response did not differ significantly between the two groups, their functional profiles were distinct, with SARS-CoV-2 seropositive children exhibiting a higher proportion of polyfunctional T cells compared to their seronegative counterparts. The frequency of SARS-CoV-2-specific CD4+ T cells in seronegative children was associated with the endemic human coronavirus (HCoV) HKU1 IgG response. Overall, the presence of SARS-CoV-2-responding T cells in seronegative children may result from cross-reactivity to endemic coronaviruses and could contribute to the relative protection from disease observed in SARS-CoV-2-infected children., Competing Interests: DECLARATION OF INTERESTS The authors have no competing interests.

Background: The risk of tuberculosis disease after recent exposure is greatest before age 5 years; however, the mechanisms explaining this increased risk are not well elucidated. Acquisition of viral infections, such as cytomegalovirus, in early life might modulate the immune system. We aimed to evaluate the acquisition of cytomegalovirus infection in infancy and the development of tuberculosis disease in children., Methods: In this prospective, birth cohort study we enrolled pregnant women who were between 20 and 28 weeks of gestation attending antenatal care in Paarl, a periurban setting outside of Cape Town, South Africa. Participants were recruited from two clinics (TC Newman and Mbekweni). Infants were given Bacillus Calmette-Guérin vaccination at birth as per national policy. Nasopharyngeal swabs for cytomegalovirus detection using qPCR were done for infants at birth, age 3 and 6 weeks, and age 3, 6, 12, and 24 months. Children were prospectively followed up for tuberculosis disease until age 9 years using tuberculin skin testing, radiographic examinations, GeneXpert, and sputum testing. Tuberculin skin tests were done at the 6-month visit and then at age 12, 24, 36, 48, and 60 months, and at the time of lower respiratory tract infection. We compared tuberculosis disease incidence after age 1 year or after age 6 months in children with and without cytomegalovirus infection using Cox regression and hazard ratios (HRs) with 95% CIs., Findings: Between March 5, 2012, and March 31, 2015, 1225 pregnant women were recruited and enrolled in the birth cohort. 88 (7%) women were excluded because of loss to antenatal follow-up or pregnancy losses. Of 1143 livebirths, 68 (6%) mother-infant pairs were excluded. In total, 963 children were serially tested for cytomegalovirus (7186 cytomegalovirus measurements taken; median six tests per child, IQR 2-11). The prevalence of congenital cytomegalovirus at age younger than 3 weeks was 2% (18 of 816). Cytomegalovirus positivity increased continuously with age from 3% (27 of 825) by age 6 weeks to 21% (183 of 882) by 3 months, 35% (315 of 909) by 6 months, and 42% (390 of 933) by 12 months. Mother-infant pairs were followed up for a median of 6·9 years (IQR 6·0-7·8). The risk of tuberculosis disease in children after age 1 year was higher in those with cytomegalovirus infection by age 6 weeks (adjusted HR 4·1, 95% CI 1·2-13·8; p=0·022), 3 months (2·8, 1·4-5·8; p=0·0040), 6 months (3·6, 1·7-7·3; p<0·0001), 12 months (3·2, 1·6-6·4; p=0·0010), and 24 months (4·2, 2·0-8·8; p<0·0001). The risk of microbiologically confirmed tuberculosis disease was also higher among children acquiring cytomegalovirus infection before age 3 months (adjusted HR 3·2, 95% CI 1·0-10·6; p=0·048), 6 months (3·9, 1·2-13·0; p=0·027), 12 months (4·4, 1·2-16·3; p=0·027), and 24 months (6·1, 1·3-27·9; p=0·020). In children older than 1 year, the risk of tuberculosis disease was consistently greater in those with high cytomegalovirus loads than in those with low cytomegalovirus loads that were acquired before age 3 months (adjusted HR 2·0 vs 3·7; p trend =0·0020; both groups compared with cytomegalovirus negative reference) and before age 12 months (2·7 vs 3·7; p trend =0·0009)., Interpretation: Infants that acquire cytomegalovirus in the first year of life are at high risk of subsequently developing tuberculosis disease. Efforts to prevent tuberculosis in early childhood in high-burden countries might need to deter or delay acquisition of cytomegalovirus perinatally or in the first months of life., Funding: Bill & Melinda Gates Foundation, MRC South Africa, National Research Foundation South Africa, and Wellcome Trust., Competing Interests: Declaration of interests HJZ reports grants from the Bill & Melinda Gates Foundation, the South African Medical Research Council, the South African National Research Foundation, and the National Institutes of Health. All other authors declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)