A5082598525- Trypanosoma species research and implications
- Complement system in diseases
- Vector-borne infectious diseases
- Toxin Mechanisms and Immunotoxins
- Malaria Research and Control
- Mosquito-borne diseases and control
Walter and Eliza Hall Institute of Medical Research
2022-2025
Abstract The most severe form of malaria is caused by Plasmodium falciparum . These parasites invade human erythrocytes, and an essential step in this process involves the ligand PfRh5, which forms a complex with cysteine-rich protective antigen (CyRPA) PfRh5-interacting protein (PfRipr) (RCR complex) binds basigin on host cell. We identified heteromeric disulfide-linked consisting P. thrombospondin-related apical merozoite (PfPTRAMP) small secreted (PfCSS) have shown that it RCR to...
Plasmodium vivax is emerging as the most prevalent species causing malaria outside Africa. Most P. infections are relapses due to reactivation of dormant liver stage parasites (hypnozoites). Hypnozoites a major reservoir for transmission but undetectable by commercial diagnostic tests. Antibodies against Reticulocyte Binding Protein 2b (PvRBP2b) among reliable serological biomarkers recent in prior nine months and act indirect risk relapse. We sought design stabilized variants PvRBP2b, under...
Invasion of erythrocytes by members the Plasmodium genus is an essential step parasite lifecycle, orchestrated numerous host-parasite interactions. In P. falciparum Rh5, with PfCyRPA, PfRipr, PfCSS, and PfPTRAMP, forms PCRCR complex which binds basigin on erythrocyte surface. Rh5 restricted to its close relatives; however, PTRAMP, CSS Ripr orthologs are present across genus. We investigated from three species elucidate common features complex. Like falciparum, PTRAMP form a disulfide-linked...
Anti-carbohydrate antibodies (Abs) play crucial roles in pathogen control, but their generation remains poorly understood. By studying responses to Streptococcus pyogenes humans, we reveal that the glycan-targeted response shifts from IgM towards IgG and IgA memory with age antigen exposure across blood, spleen, tonsils. Both natural colonization controlled human infection S. increased class-switched B cells, evidence of within-clone switching. Glycan-specific cells readily participated...