Pathogen Molecular Biology Department, London School of Hygiene and Tropical Medicine, London, United Kingdom.
Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, United Kingdom.
PLoS Genet. 2018 Jan 30;14(1):e1007172. doi: 10.1371/journal.pgen.1007172. eCollection 2018 Jan.
Significant selection pressure has been exerted on the genomes of human populations exposed to Plasmodium falciparum infection, resulting in the acquisition of mechanisms of resistance against severe malarial disease. Many host genetic factors, including sickle cell trait, have been associated with reduced risk of developing severe malaria, but do not account for all of the observed phenotypic variation. Identification of novel inherited risk factors relies upon high-resolution genome-wide association studies (GWAS). We present findings of a GWAS of severe malaria performed in a Tanzanian population (n = 914, 15.2 million SNPs). Beyond the expected association with the sickle cell HbS variant, we identify protective associations within two interleukin receptors (IL-23R and IL-12RBR2) and the kelch-like protein KLHL3 (all P<10-6), as well as near significant effects for Major Histocompatibility Complex (MHC) haplotypes. Complementary analyses, based on detecting extended haplotype homozygosity, identified SYNJ2BP, GCLC and MHC as potential loci under recent positive selection. Through whole genome sequencing of an independent Tanzanian cohort (parent-child trios n = 247), we confirm the allele frequencies of common polymorphisms underlying associations and selection, as well as the presence of multiple structural variants that could be in linkage with these SNPs. Imputation of structural variants in a region encompassing the glycophorin genes on chromosome 4, led to the characterisation of more than 50 rare variants, and individually no strong evidence of associations with severe malaria in our primary dataset (P>0.3). Our approach demonstrates the potential of a joint genotyping-sequencing strategy to identify as-yet unknown susceptibility loci in an African population with well-characterised malaria phenotypes. The regions encompassing these loci are potential targets for the design of much needed interventions for preventing or treating malarial disease.
在受到疟原虫感染的人群中,基因组受到了强烈的选择压力,导致对严重疟疾疾病产生了抗性机制。许多宿主遗传因素,包括镰状细胞特征,与降低发生严重疟疾的风险相关,但并不能解释所有观察到的表型变异。新型遗传风险因素的鉴定依赖于高分辨率全基因组关联研究(GWAS)。我们介绍了在坦桑尼亚人群中进行的严重疟疾 GWAS 的研究结果(n = 914,1520 万个 SNPs)。除了与镰状细胞 HbS 变体的预期关联外,我们还在两个白细胞介素受体(IL-23R 和 IL-12RBR2)和 Kelch 样蛋白 KLHL3 中发现了保护性关联(均 P<10-6),以及主要组织相容性复合物(MHC)单倍型的接近显著效应。基于检测扩展单倍型同质性的互补分析,确定了 SYNJ2BP、GCLC 和 MHC 为近期正选择的潜在基因座。通过对一个独立的坦桑尼亚队列(亲子三胞胎 n = 247)的全基因组测序,我们证实了常见多态性的等位基因频率与关联和选择有关,以及存在多个结构变异,这些变异可能与这些 SNP 连锁。在涵盖染色体 4 上糖蛋白基因的区域中对结构变异进行推断,导致鉴定出了 50 多个罕见变异,并且在我们的原始数据集(P>0.3)中没有与严重疟疾强烈关联的证据。我们的方法证明了联合基因分型-测序策略在具有特征性疟疾表型的非洲人群中识别未知易感性基因座的潜力。包含这些基因座的区域是设计预防或治疗疟疾疾病的急需干预措施的潜在目标。