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dc.contributor.authorOnyango, Clinton O
dc.contributor.authorCheng, Qiuying
dc.contributor.authorMunde, Elly O
dc.contributor.authorRaballah, Evans
dc.contributor.authorAnyona, Samuel B
dc.contributor.authorMcMahon, Benjamin H
dc.contributor.authorLambert, Christophe G
dc.contributor.authorOnyango, Patrick O
dc.contributor.authorSchneider, Kristan A
dc.contributor.authorPerkins, Douglas J
dc.contributor.authorOuma, Collins
dc.date.accessioned2023-09-18T15:15:40Z
dc.date.available2023-09-18T15:15:40Z
dc.date.issued2023-09-13
dc.identifier.urihttps://repository.maseno.ac.ke/handle/123456789/5783
dc.descriptionhttps://doi.org/10.1186/s12864-023-09565-1en_US
dc.description.abstractPlasmodium falciparum malaria is a leading cause of pediatric morbidity and mortality in holoendemic transmission areas. Severe malarial anemia [SMA, hemoglobin (Hb) < 5.0 g/dL in children] is the most common clinical manifestation of severe malaria in such regions. Although innate immune response genes are known to influence the development of SMA, the role of natural killer (NK) cells in malaria pathogenesis remains largely undefined. As such, we examined the impact of genetic variation in the gene encoding a primary NK cell receptor, natural cytotoxicity-triggering receptor 3 (NCR3), on the occurrence of malaria and SMA episodes over time.en_US
dc.publisherBioMed Centralen_US
dc.titleHuman NCR3 gene variants rs2736191 and rs11575837 alter longitudinal risk for development of pediatric malaria episodes and severe malarial anemiaen_US
dc.typeArticleen_US


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