A5024468348- Malaria Research and Control
- Signaling Pathways in Disease
- Trypanosoma species research and implications
- Complement system in diseases
- HIV Research and Treatment
- Mosquito-borne diseases and control
- RNA and protein synthesis mechanisms
- Drug Transport and Resistance Mechanisms
- HIV/AIDS drug development and treatment
- Insect Resistance and Genetics
- Biochemical and Molecular Research
- Aquaculture disease management and microbiota
- vaccines and immunoinformatics approaches
- Probiotics and Fermented Foods
- Protein Degradation and Inhibitors
- MicroRNA in disease regulation
- Genomics and Phylogenetic Studies
- Iron Metabolism and Disorders
- Insect symbiosis and bacterial influences
- Bacteriophages and microbial interactions
- Adolescent and Pediatric Healthcare
- Vector-borne infectious diseases
- Plant Pathogenic Bacteria Studies
- Bat Biology and Ecology Studies
- Clostridium difficile and Clostridium perfringens research
Harvard University
2013-2025
Swiss Tropical and Public Health Institute
2022-2024
University of Basel
2023-2024
University of Bern
2019
Bernhard Nocht Institute for Tropical Medicine
2008-2013
Transmission represents a population bottleneck in the Plasmodium life cycle and key intervention target of ongoing efforts to eradicate malaria. Sexual differentiation is essential for this process, as only sexual parasites, called gametocytes, are infective mosquito vector. Gametocyte production rates vary depending on environmental conditions, but external stimuli remain obscure. Here, we show that host-derived lipid lysophosphatidylcholine (LysoPC) controls P. falciparum cell fate by...
Malaria remains one of the greatest public health challenges worldwide, particularly in sub-Saharan Africa. The clinical outcome individuals infected with Plasmodium falciparum parasites depends on many factors including host systemic inflammatory responses, parasite sequestration tissues and vascular dysfunction. Production pro-inflammatory cytokines chemokines promotes endothelial activation as well recruitment infiltration cells, which turn triggers further cell sequestration....
Malaria blood stage parasites export a large number of proteins into their host erythrocyte to change it from container predominantly hemoglobin optimized for the transport oxygen niche parasite propagation. To understand this process, is crucial know which are exported cell. This has been aided by PEXEL/HT sequence, five-residue motif found in many proteins, leading prediction exportome. However, several negative (PNEPs) indicate that exportome incomplete and remains unknown if how further...
Measures to combat the parasites that cause malaria have become compromised because of reliance on a small arsenal drugs and emerging drug resistance. We conducted transposon mutagenesis screen in primate parasite Plasmodium knowlesi , producing most complete classification gene essentiality any spp. date, with resolution define truncatable genes. found conservation druggable genome between divergences mitochondrial metabolism. Perturbation analyses frontline antimalarial artemisinin...
A short motif termed Plasmodium export element (PEXEL) or vacuolar targeting signal (VTS) characterizes proteins exported into the host cell. These mediate cell modifications essential for parasite survival and virulence. However, several PEXEL-negative indicate that currently predicted malaria exportome is not complete it unknown whether how these relate to PEXEL-positive export. Here we show N-terminal 10 amino acids of protein REX2 (ring-exported 2) are necessary its a single-point...
Significance During malaria infections, Plasmodium falciparum parasites invade RBCs. Identification of host factors for parasite invasion guides the development vaccines and host-targeted therapeutics. Here we describe an in vitro culture system functional analysis RBC determinants using immortal erythroleukemia cell line JK-1. JK-1 cells can be induced to differentiate synchronously, support invasion, are amenable genetic manipulation. Using this system, validated two factors, basigin CD44,...
Abstract Malaria pathogenesis is caused by the replication of Plasmodium parasites within red blood cells (RBCs) vertebrate host. This selective pressure has favored evolution protective polymorphisms in erythrocyte proteins, a subset which serve as cognate receptors for parasite invasion ligands. Recently, generation RBCs from immortalized hematopoietic stem (HSCs) offered more tractable system genetic manipulation and long‐term vitro culture, enabling elucidation functional determinants...
Plasmodium falciparum is a human-adapted apicomplexan parasite that causes the most dangerous form of malaria. P. cysteine-rich protective antigen (PfCyRPA) an invasion complex protein essential for erythrocyte invasion. The precise role PfCyRPA in this process has not been resolved. Here, we show lectin targeting glycans terminating with α2-6-linked N-acetylneuraminic acid (Neu5Ac). >50-fold binding preference human, Neu5Ac over non-human, N-glycolylneuraminic acid. sites were predicted by...
Plasmodium vivax has 2 invasion ligand/host receptor pathways (P. Duffy-binding protein/Duffy antigen for chemokines [DARC] and P. reticulocyte binding protein 2b/transferrin [TfR1]) that are promising targets therapeutic intervention. We optimized assays with isogenic cultured reticulocytes. Using a blockade approach multiple isolates, we found all strains utilized both DARC TfR1, but significant variation in usage. This suggests vivax, like falciparum, uses alternative pathways,...
Plasmodium falciparum, the parasite that causes deadliest form of malaria, has evolved multiple proteins known as invasion ligands bind to specific erythrocyte receptors facilitate human erythrocytes. The EBA-175/glycophorin A (GPA) and Rh5/basigin ligand-receptor interactions, referred pathways, have been subject intense study. In this study, we focused on less-characterized sialic acid-containing glycophorin B (GPB) C (GPC). Through bioinformatic analysis, identified extensive variation in...
Plasmodium falciparum accounts for the majority of over 600,000 malaria-associated deaths annually. Parasites resistant to nearly all antimalarials have emerged and need drugs with alternative modes action is thus undoubted. The FK506-binding protein Pf FKBP35 has gained attention as a promising drug target due its high affinity macrolide compound FK506 (tacrolimus). Whilst there considerable interest in targeting small molecules, genetic validation this factor missing function parasite...
Plasmodium falciparum accounts for the majority of over 600’000 malaria-associated deaths annually. Parasites resistant to nearly all antimalarials have emerged and need drugs with alternative modes action is thus undoubted. The FK506-binding protein Pf FKBP35 has gained attention as a promising drug target due its high affinity macrolide compound FK506 (tacrolimus). Whilst there considerable interest in targeting small molecules, genetic validation this factor missing function parasite...
Plasmodium falciparum accounts for the majority of over 600,000 malaria-associated deaths annually. Parasites resistant to nearly all antimalarials have emerged and need drugs with alternative modes action is thus undoubted. The FK506-binding protein Pf FKBP35 has gained attention as a promising drug target due its high affinity macrolide compound FK506 (tacrolimus). Whilst there considerable interest in targeting small molecules, genetic validation this factor missing function parasite...
Plasmodium falciparum accounts for the majority of over 600’000 malaria-associated deaths annually. Parasites resistant to nearly all antimalarials have emerged and need drugs with alternative modes action is thus undoubted. The FK506-binding protein Pf FKBP35 has gained attention as a promising drug target due its high affinity macrolide compound FK506 (tacrolimus). Whilst there considerable interest in targeting small molecules, genetic validation this factor missing function parasite...
Abstract Plasmodium falciparum accounts for the majority of over 600’000 malaria-associated deaths annually. Parasites resistant to nearly all antimalarials have emerged and need drugs with alternative modes action is thus undoubted. The FK506-binding protein Pf FKBP35 has gained attention as a promising drug target due its high affinity macrolide compound FK506 (tacrolimus). Whilst there considerable interest in targeting small molecules, genetic validation this factor missing function...