An open dataset of Plasmodium falciparum genome variation in 7,000 worldwide samples.

MalariaGEN is a data-sharing network that enables groups around the world to work together on the genomic epidemiology of malaria. Here we describe a new release of curated genome variation data on 7,000 Plasmodium falciparum samples from MalariaGEN partner studies in 28 malaria-endemic countries. High-quality genotype calls on 3 million single nucleotide polymorphisms (SNPs) and short indels were produced using a standardised analysis pipeline. Copy number variants associated with drug resistance and structural variants that cause failure of rapid diagnostic tests were also analysed.  Almost all samples showed genetic evidence of resistance to at least one antimalarial drug, and some samples from Southeast Asia carried markers of resistance to six commonly-used drugs. Genes expressed during the mosquito stage of the parasite life-cycle are prominent among loci that show strong geographic differentiation. By continuing to enlarge this open data resource we aim to facilitate research into the evolutionary processes affecting malaria control and to accelerate development of the surveillance toolkit required for malaria elimination

Indigenous Knowledge Research in Kenya and South Africa: An Informetric Study

This article applies informetrics using descriptive bibliometrics to determine the state Indigenous Knowledge (IK) development in Kenya and South Africa. Data was analysed using the following variables: document type; growth of literature on the subject from 1990-2008; document source(s); document affiliation; subject domain; country of publication; and nature of authorship, among other attributes. International databases (OCLC – Online Computer Library Center, MEDLINE and AGRICOLA) and national databases – South Africa’s Southern African Bibliographic Information Network (SABINET databases, i.e. Current and Completed Research: CCR, Union Catalogue of Theses and Dissertations: UTD, and Index to South African Periodicals: ISAP) and Kenya’s Greenstone Database – were analysed using content analysis. Two keywords – indigenous knowledge and traditional knowledge – were used in all database searches. We found that IK was strongly represented in the SABINET and OCLC databases. The absence of a national (online) database showcasing Kenyan research output made it difficult to account for IK research in the country. Recommendations are provided for a follow up study and further research. The article could prove useful for decision support in IK management.Keywords: Knowledge management; indigenous knowledge; traditional knowledge; informetrics

Mechanistic Studies of the Negative Epistatic Malaria-protective Interaction Between Sickle Cell Trait and α+thalassemia

AbstractBackgroundIndividually, the red blood cell (RBC) polymorphisms sickle cell trait (HbAS) and α+thalassemia protect against severe Plasmodium falciparum malaria. It has been shown through epidemiological studies that the co-inheritance of both conditions results in a loss of the protection afforded by each, but the biological mechanisms remain unknown.MethodsWe used RBCs from >300 donors of various HbAS and α+thalassemia genotype combinations to study the individual and combinatorial effects of these polymorphisms on a range of putative P. falciparum virulence phenotypes in-vitro, using four well-characterized P. falciparum laboratory strains. We studied cytoadhesion of parasitized RBCs (pRBCs) to the endothelial receptors CD36 and ICAM1, rosetting of pRBCs with uninfected RBCs, and pRBC surface expression of the parasite-derived adhesion molecule P. falciparum erythrocyte membrane protein-1 (PfEMP1).FindingsWe confirmed previous reports that HbAS pRBCs show reduced cytoadhesion, rosetting and PfEMP1 expression levels compared to normal pRBC controls. Furthermore, we found that co-inheritance of HbAS with α+thalassemia consistently reversed these effects, such that pRBCs of mixed genotype showed levels of cytoadhesion, rosetting and PfEMP1 expression that were indistinguishable from those seen in normal pRBCs. However, pRBCs with α+thalassemia alone showed parasite strain-specific effects on adhesion, and no consistent reduction in PfEMP1 expression.InterpretationOur data support the hypothesis that the negative epistasis between HbAS and α+thalassemia observed in epidemiological studies might be explained by host genotype-specific changes in the pRBC-adhesion properties that contribute to parasite sequestration and disease pathogenesis in vivo. The mechanism by which α+thalassemia on its own protects against severe malaria remains unresolved

Erratum to “Mechanistic Studies of the Negative Epistatic Malaria-protective Interaction Between Sickle Cell Trait and α+thalassemia” [EBioMedicine 1 (2014) 29–36]

[This corrects the article DOI: 10.1016/j.ebiom.2014.10.006.]