| dc.contributor.author | Onyango Clinton O, Qiuying Cheng, Elly O Munde, Evans Raballah, Samuel B Anyona, Benjamin H McMahon, Christophe G Lambert, Patrick O Onyango, Kristan A Schneider, Douglas J Perkins, Collins Ouma | |
| dc.date.accessioned | 2023-03-10T13:51:15Z | |
| dc.date.available | 2023-03-10T13:51:15Z | |
| dc.date.issued | 2022 | |
| dc.identifier.uri | https://repository.maseno.ac.ke/handle/123456789/5644 | |
| dc.description | DOI: https://doi.org/10.21203/rs.3.rs-2207577/v1 | en_US |
| dc.description.abstract | Plasmodium falciparum malaria is a leading cause of pediatric morbidity and mortality in holoendemic
transmission areas. Severe malarial anemia [SMA, hemoglobin (Hb) < 5.0g/dL] 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.publisher | Research square | en_US |
| dc.subject | Plasmodium falciparum, malaria, severe malaria anemia (SMA), Natural cytotoxicity-triggering receptor 3 gene (NCR3), genotypes, and haplotypes | en_US |
| dc.title | Human NCR3 gene variants rs2736191 and rs11575837 influence susceptibility to the longitudinal development of pediatric severe malarial anemia | en_US |
| dc.type | Article | en_US |
