Background In Uganda, childhood anemia remains a health challenge and is associated with malaria infection as well as iron deficiency. Iron deficiency is intertwined with nutritional status, age and other comorbidities including helminths and Lead toxicity. Environmental Lead levels accounts for one’s blood Lead (BL) levels. Blood Lead competitively blocks iron absorption, inhibits hemoglobin (Hb) biosynthesis and elevates free erythrocyte protoporphyrin (FEP) levels. Lead toxicity’s contribution towards anemia pathogenesis, especially during malaria infection has not been studied. Concomitant exposure to both malaria infection and Lead pollution, exacerbates the anemia status. This study therefore aimed at expounding the anemia status of these Ugandan children aged under 5years who are exposed to both malaria infection and environmental Lead pollution. Methods Briefly, venous blood samples from 198 children were microscopically assayed for malaria parasite density (PD), and hemoglobin (Hb) concentrations using the cyanmethemoglobin method, while BL and FEP levels were determined by the standard atomic absorption spectrophotometric and fluorometric methods respectively. Results One hundred and fifty-one (76.3%) of the children analyzed had moderate anemia (Hb <10>5 g/dL) with Means of BLL=8.6 µg/dL, Hb =7.5 g/dL, FEP/Hb =8.3 µg/g and PD =3.21×103 parasites / µL, while eight (4%) were severely anemic (<5 g/dL). Regression analysis and statistical correlation between PD and Hb (r = -0.231, R2= 0.15 P-value < 0.001) was negative and weak as compared to that between FEP/Hb and Hb (r = -0.6, R2=0.572 P-value=0.001). Conclusion Based on the study’s findings, we conclude that BL significantly contributes to the pathogenesis of anemia and therefore its co-existence with malaria infection in the host exacerbates the anemia status.
Background Plasmodium falciparum is the most deadly and leading cause of morbidity and mortality in Africa. About 90% of all malaria deaths in the world today occur in Sub-Saharan Africa especially in children aged < 5 years. In 2018, it was reported that there were 228 million malaria cases that resulted in 405,000 deaths from 91 countries. Currently, a fully effective and long-lasting preventive malaria vaccine is still elusive therefore more effort is needed to identify better effective vaccine candidates. The aim of this study was to identify and characterize hypothetical proteins as vaccine candidates derived from Plasmodium falciparum 3D7 genome by reverse vaccinology. Results Of the 23 selected hypothetical proteins, 5 were predicted on the extracellular localization by WoLFPSORTv.2.0 program and all the 5 had less than 2 transmembrane regions that were predicted by TMHMMv2.0 and HMMTOP programs at default settings. Two out of the five proteins lacked secretory signal peptides as predicted by SignalP program. Among the 5 extracellular proteins, 3 were predicted to be antigenic by VaxiJen (score ≥ 0.5) and had negative GRAVY values ranging from − 1.156 to − 0.440. B cell epitope prediction by ABCpred and BCpred programs revealed a total of 15 antigenic epitopes. A total of 13 cytotoxic T cells were predicted from the 3 proteins using CTLPred online server. Only 2 out of the 13 CTL were antigenic, immunogenic, non-allergenic, and non-toxic using VaxiJen, IEDB, AllergenFp, and Toxinpred servers respectively in that order. Five HTL peptides from XP_001351030.1 protein are predicted inducers of all the three cytokines. STRING protein–protein network analysis of HPs revealed XP_001350955.1 closely interacts with nucleoside diphosphate kinase (PF13-0349) at 0.704, XP_001351030.1 interacts with male development protein1 (Mdv-1) at 0.645, and XP_001351047.1 with an uncharacterized protein (MAL8P1.53) at 0.400. Conclusion Reverse vaccinology is a promising strategy for the screening and identification of antigenic antigens with potential capacity to elicit cellular and humoral immune responses against P. falciparum infection. In this study, potential vaccine candidates of Plasmodium falciparum were identified and screened using standard bioinformatics tools. The vaccine candidates contained antigenic and immunogenic epitopes which could be considered for novel and effective vaccine targets. However, we strongly recommend in vivo and in vitro experiments to validate their immunogenicity and protective efficacy to completely decipher the vaccine targets against malaria.
BackgroundIn Uganda, childhood anemia remains a health challenge and is associated with malaria infection as well as iron deficiency. Iron deficiency is intertwined with nutritional status, age and other comorbidities including helminths and Lead toxicity. Environmental Lead levels accounts for one’s blood Lead (BL) levels. Blood Lead competitively blocks iron absorption, inhibits hemoglobin (Hb) biosynthesis and elevates free erythrocyte protoporphyrin (FEP) levels. Lead toxicity’s contribution towards anemia pathogenesis, especially during malaria infection has not been studied. Concomitant exposure to both malaria infection and Lead pollution, exacerbates the anemia status. This study therefore aimed at expounding the anemia status of these Ugandan children aged under 5years who are exposed to both malaria infection and environmental Lead pollution.MethodsBriefly, venous blood samples from 198 children were microscopically assayed for malaria parasite density (PD), and hemoglobin (Hb) concentrations using the cyanmethemoglobin method, while BL and FEP levels were determined by the standard atomic absorption spectrophotometric and fluorometric methods respectively.ResultsOne hundred and fifty-one (76.3%) of the children analyzed had moderate anemia (Hb <10>5 g/dL) with Means of BLL=8.6 µg/dL, Hb =7.5 g/dL, FEP/Hb =8.3 µg/g and PD =3.21×103 parasites / µL, while eight (4%) were severely anemic (<5 g/dL). Regression analysis and statistical correlation between PD and Hb (r = -0.231, R2= 0.15 P-value < 0.001) was negative and weak as compared to that between FEP/Hb and Hb (r = -0.6, R2=0.572 P-value=0.001).ConclusionBased on the study’s findings, we conclude that BL significantly contributes to the pathogenesis of anemia and therefore its co-existence with malaria infection in the host exacerbates the anemia status.Trial registration Not applicable
Background: Rapid industrialization, urbanization, and population explosion in sub-Saharan Africa escalate environmental lead levels and subsequently blood lead levels in children. Its levels in one’s environment account for their blood lead levels. One’s susceptibility to lead toxicity is governed by nutrition status, age and genetics. This study aimed at expounding susceptibility to lead toxicity by relating blood lead levels, delta-aminolevulinic acid dehydratase (ALAD) enzyme activity, and genetic variations of proteins that code for ALAD in urban children of Uganda. Methods: A total of 198 blood samples were spectrophotometrically analysed for blood lead levels (BLL), hemoglobin (Hb) levels, and ALAD enzyme activity before DNA extraction, polymerase chain reaction, and restriction fragment length digestion for ALAD polymorphism. Results: Up to 99.5% of the total samples analyzed coded for ALAD1 allele compared to 0.05% that coded for ALAD2. There was a significant relationship between BLL, Hb status and ALAD enzyme activity in the three isozymes (ALAD1-1, ALAD1-2 and ALAD2-2) in strength of ALAD1-1 (r = 0.42, p -value = 0.02) ˂ ALAD1-2 (r = 0.62, p -value = ˂ 0.001) ˂ ALAD2-2 (r = 0.67, p -value = ˂ 0.001). Conclusions: Majority of children in Uganda code for the ALAD1 allele, which is important for blood lead ions hoarding during lead toxicity. Hoarding of blood lead not only delays exposure effects but also accumulates its levels in deposit tissues and this poses adverse effects later in their lives
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