Moses Robert Kamya

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 examines how exposure to P. falciparum and common cold viruses influences vaccine responses in Ugandan infants, finding positive associations between microbial exposure and antibody levels.

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 uses genomic data to analyze evolutionary dynamics of Anopheles gambiae under different insecticidal tools, revealing distinct resistance mechanisms and allele frequency shifts.

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 examines inhibitory NK receptors on γδ T cells in Ugandan children, finding that some enhance and others reduce antimalarial responses to repeated infections.

In Tororo, Uganda, An. funestus tolerated clothianidin-sprayed walls better than An. gambiae yet was killed on pirimiphos-methyl walls up to 7 months post-spray, implicating it in the malaria resurgence.

This paper uses genomic surveillance in a cluster randomized trial to detect insecticide resistance variants in Ugandan Anopheles funestus and An. gambiae s.l., showing differential population responses to pyrethroid and PBO interventions.

The paper compares methylation profiles of placentas with non-malarial and PM-associated FGR, finding distinct differentially methylated CpGs and a shared hypomethylated site in BMP4.