Samuel Oyola is ILRI’s Specialist Scientist in Genomics and Molecular Biology. He holds a PhD in Molecular and Cellular Biology from the University of Cambridge. Before joining ILRI, he studied functional genomics of Leishmaniasis and host-parasite interaction as a postdoctoral fellow at the University of York. He then took a Scientist position at the Wellcome Trust Sanger Institute, Cambridge UK, where he worked on malaria; developing and applying high throughput genomic technologies to study natural genetic variations in malaria parasite populations. He developed novel molecular tools that enable application and translation of genomic technologies into basic healthcare and public health applications. At ILRI, Samuel is using his experience and expertise in modern genomics, biotechnology and molecular biology to study several aspects of animal and human health. Under epidemiology, Samuel is using modern genomic and bioinformatic tools to study epidemiology of rift valley fever virus (RVF), African swine fever virus (ASFV), Newcastle disease virus (NDV) and Peste des petits ruminants virus (PPRV). Under vaccine development, Samuel is employing his immunogenetics expertise to develop anti-east coast fever vaccine by profiling antibody immune (B-cell receptor repertoire) responses to candidate vaccine immunizations. Samuel is also actively involved in developing genomic capacity in Africa.
Gartner et al (2007). Mucosal prime-boost vaccination for tuberculosis based on TLR triggering OprI lipoprotein from Pseudomonas aeruginosa fused to mycolyl-transferase Ag85A. Immunol Lett. 111, 26-35Peacock et al., (2007). Comparative genomic analysis of three Leishmania species that cause diverse human disease. Nature genetics, 39, 839-847Oyola et al (2009). A kinetoplastid BRCA2 interacts with DNA replication protein CDC45. Int J Parasitol. 39, 59-69Oyola et al (2012). Functional Analysis of Leishmania Cyclopropane Fatty Acid Synthetase PLos One. 7(12):e513000Quail MA, Otto TD, Gu Y, Harris SR, Skelly TF, McQuillan JA, Swerdlow HP & Oyola SO. (2011). Optimal enzymes for amplifying sequencing libraries. Nature Methods. 9, 10-1Oyola et al (2012). Optimizing Illumina next-generation sequencing library preparation for extremely AT-biased genomes. BMC Genomics. 13, 1Manske et al (2012). Next-generation sequencing analysis of Plasmodium falciparum diversity within the host and across populations. Nature. 19, 375-9.Oyola et al (2013). Efficient depletion of host DNA contamination in malaria clinical sequencing. J Clin Microbiol. 51, 745-51Miotto et al (2013). Multiple populations of artemisinin-resistant Plasmodium falciparum in Cambodia. Nature genetics. 45(6):648-55 [doi: 10.1038/ng.2624]Feehery et al (2013). A Method for Selectively Enriching Microbial DNA from Contaminating Vertebrate Host DNA. Plos One. 8(10):e76096 [DOI: 10.1371/journal.pone.0076096]Wendler et al (2014). A genome wide association study of Plasmodium falciparum susceptibility to 22 antimalarial drugs in Kenya. Plos One 8;9(5):e96486 [doi: 10.1371/journal.pone.0096486]Oyola et al (2014) Optimized whole genome amplification strategies for NGS analysis. DNA Research 21(6):661-71 [doi: 10.1093/dnares/dsu028]Miotto et al (2015) Genetic architecture of artemisinin-resistant Plasmodium falciparum. Nature Genetics 47(3): 226-34Oyola et al (2016) Whole genome sequencing of Plasmodium falciparum from dried blood spots using selective whole genome amplification. Malar J 15: 597 [DOI 10.1186/s12936-016-1641-7]Böhme et al (2018) Complete avian malaria parasite genomes reveal features associated with lineage-specific evolution in birds and mammals. Genome Res. 28(4):547-560. [doi: 10.1101/gr.218123.116].Otto et al (2018) Genomes of all known members of a Plasmodium subgenus reveal paths to virulent human malaria. Nature Microbiology 3: 687-697 [doi:10.1038/s41564-018-0162-2].