BackgroundCharacterizing the parasite dynamics and population structure provides useful information to understand the dynamic of transmission and to better target control interventions. Despite considerable efforts for its control, vivax malaria remains a major health problem in Peru. In this study, we have explored the population genetics of Plasmodium vivax isolates from Iquitos, the main city in the Peruvian Amazon, and 25 neighbouring peri-urban as well as rural villages along the Iquitos-Nauta Road.Methodology/ ResultsFrom April to December 2008, 292 P. vivax isolates were collected and successfully genotyped using 14 neutral microsatellites. Analysis of the molecular data revealed a similar proportion of monoclonal and polyclonal infections in urban areas, while in rural areas monoclonal infections were predominant (p = 0.002). Multiplicity of infection was higher in urban (MOI = 1.5–2) compared to rural areas (MOI = 1) (p = 0.003). The level of genetic diversity was similar in all areas (He = 0.66–0.76, p = 0.32) though genetic differentiation between areas was substantial (PHIPT = 0.17, p<0.0001). Principal coordinate analysis showed a marked differentiation between parasites from urban and rural areas. Linkage disequilibrium was detected in all the areas ( = 0.08–0.49, for all p<0.0001). Gene flow among the areas was stablished through Bayesian analysis of migration models. Recent bottleneck events were detected in 4 areas and a recent parasite expansion in one of the isolated areas. In total, 87 unique haplotypes grouped in 2 or 3 genetic clusters described a sub-structured parasite population.Conclusion/SignificanceOur study shows a sub-structured parasite population with clonal propagation, with most of its components recently affected by bottleneck events. Iquitos city is the main source of parasite spreading for all the peripheral study areas. The routes of transmission and gene flow and the reduction of the parasite population described are important from the public health perspective as well for the formulation of future control policies.

Throughout the past few years, a lively debate emerged about the timing and magnitude of the human migrations between the Iberian Peninsula and the Maghreb. Several pieces of evidence, including archaeological, anthropological, historical, and genetic data, have pointed to a complex and intermingled evolutionary history in the western Mediterranean area. To study to what extent connections across the Strait of Gibraltar and surrounding areas have shaped the present-day genomic diversity of its populations, we have performed a screening of 2.5 million single-nucleotide polymorphisms in 142 samples from southern Spain, southern Portugal, and Morocco. We built comprehensive data sets of the studied area and we implemented multistep bioinformatic approaches to assess population structure, demographic histories, and admixture dynamics. Both local and global ancestry inference showed an internal substructure in the Iberian Peninsula, mainly linked to a differential African ancestry. Western Iberia, from southern Portugal to Galicia, constituted an independent cluster within Iberia characterized by an enriched African genomic input. Migration time modeling showed recent historic dates for the admixture events occurring both in Iberia and in the North of Africa. However, an integrative vision of both paleogenomic and modern DNA data allowed us to detect chronological transitions and population turnovers that could be the result of transcontinental migrations dating back from Neolithic times. The present contribution aimed to fill the gaps in the modern human genomic record of a key geographic area, where the Mediterranean and the Atlantic come together.

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Background: the aim of this study is to evaluate the effectiveness and coverage of a simplified protocol that is implemented in health centers (HCs) and health posts (HPs) for children who are suffering from severe acute malnutrition (SAM) in the humanitarian context of Diffa. Methods: We conducted a non-randomized community-controlled trial. The control group received outpatient treatment for SAM, without medical complications, at HCs and HPs with the standard protocol of community management of acute malnutrition (CMAM). Meanwhile, with respect to the intervention group, the children with SAM received treatment at the HCs and HPs through a simplified protocol wherein the mid-upper arm circumference (MUAC) and the presence of edema were used as the admission criteria, and the children with SAM were administered doses of fixed ready-to-use therapeutic food (RUTF). Results: A total of 508 children, who were all under 5 years and had SAM, were admitted into the study. The cured proportion was 87.4% in the control group versus 96.6% in the intervention group (p value = 0.001). There was no difference between the groups in the length of stay, which was 35 days, but the intervention group used a lower quantity of RUTF—70 sachets versus 90 sachets, per child cured. Coverage increases were observed in both groups. Discussion: the simplified protocol used at the HCs and HPs did not result in worse recovery and resulted in fewer discharge errors compared to the standard protocol.

Sickle cell disease (SCD), despite being a monogenic disease, presents a highly variable phenotype that essentially depends on the amount of fetal hemoglobin (HbF), constituting the main modulator of the disease. The variation of HbF levels between patients is genetically regulated. HbF determines both the phenotype of the disease and the response to treatment with the main drug used, hydroxyurea. Researchers’ efforts have focused on discovering the genetic factors responsible for its variation; mainly describing the haplotypes of the β cluster and SNPs in three different loci: BCL11A, HBS1L-MYB and the β-globin cluster. Objective: To determine, in a cohort of patients with SCD, the possible relationship between the number of SNPs and haplotypes with higher levels of HbF. A positive association could explain why certain haplotypes, such as Senegal or Arab-Indian, have higher levels. of HbF and less severe disease. Methods: To verify this hypothesis, the characterization of the haplotypes was carried out using the PCR-RFLP technique and the genotyping of three SNPs representative of the three loci with the greatest association with the variation of HbF: XmnI (rs7482144), BCL11A (rs4671393) and HBS1L-MYB (rs9376092). Results: A greater number of SNPs has been reported in the haplotypes related to higher HbF and a lower number in those with less HbF, although only the SNP XmnI (rs7482144) has shown a statistically significant association. Conclusions: A direct relationship between haplotypes and the number of SNPs has been found, reporting that haplotypes with higher levels of HbF and thus a less severe phenotype, had a greater number of SNPs. Thus, the Benín and Bantu haplotypes traditionally associated with poor prognosis are the ones that have shown a lower number of mutated SNPs.