Isaac Ssewanyana

The paper characterizes the population structure and drug resistance of Plasmodium falciparum in Uganda and neighboring countries using whole-genome data, identifying key resistance-associated haplotypes.

PfPHAST is a streamlined amplicon sequencing panel for malaria genomic surveillance, offering better quality control and cost efficiency than MAD4HatTeR without sacrificing performance on shared targets.

The paper characterizes malaria-specific Tfh and Tr1 cells in a longitudinal cohort, finding overlapping phenotypes and showing their decline after transmission interruption.

The paper identifies CXCR6⁺ CD127⁻ Tr1 cells as key regulators in Plasmodium falciparum infection, showing they balance immunity and parasite persistence.

This study investigates B cell and antibody responses to PfARMA, finding that IgM and IgG predominantly target the N-terminal IDR1 region, but these responses do not correlate with protection against malaria.

The paper examines how maternal malaria and early-life infections affect P. falciparum-specific antibody responses in infants, finding no protective association between maternal antibodies or early infections and clinical malaria.

The paper identifies a concurrent chickenpox outbreak during an Mpox outbreak in Uganda by analyzing metagenomic data from Mpox-negative samples.

The paper develops MAD4HatTeR, an amplicon sequencing panel and analysis pipeline for detecting Plasmodium falciparum diversity, resistance markers, and gene duplications/deletions, showing high sensitivity and reproducibility across settings.

The paper identifies two human monoclonal antibodies that broadly inhibit PfEMP1's binding to EPCR, a key process in severe malaria pathogenesis.

The paper expresses STEVOR and RIFIN recombinant proteins from Plasmodium falciparum and evaluates their seropositivity in Ugandan cohorts to assess their potential as infection markers.