Fig. 4: Host genotype explains some variability in molFOI and malaria treatment incidence.
From: Marked heterogeneity in malaria infection rate in a Malian longitudinal cohort
a molFOI values from 2011, stratified by participant HBB genotype. molFOI is significantly different between some groups (Kruskal–Wallis test, χ2(2) = 23.53, p value = 7.8e−6, ε2 = 0.05. Dunn test with Holm adjustment, p values = 7.6e−6 (HbAA vs. HbAS), 9.1e−5 (HbAC vs. HbAS), 0.51 (HbAA vs. HbAC)). b Number of treatments for symptomatic disease in 2011, stratified by HBB genotype. Number of treatments is significantly different between some groups (Kruskal–Wallis test, χ2(2) = 6.55, p value = 0.038, ε2 = 0.014. Dunn test with Holm adjustment, p values = 0.032 (HbAA vs. HbAS), 0.12 (HbAC vs. HbAS), 0.93 (HbAA vs. HbAC)). c molFOI values from 2012 to 2016, stratified by participant HBB genotype. No significant differences between groups (Kruskal–Wallis test, χ2(2) = 0.96, p value = 0.62). d Number of treatments for symptomatic disease in 2012–2016 stratified by participant HBB genotype. Number of treatments is significantly different between some groups (Kruskal–Wallis test, χ2(2) = 12.58, p value = 0.0019, ε2 = 0.11. Dunn test with Holm adjustment, p values = 0.0016 (HbAA vs. HbAS), 0.36 (HbAC vs. HbAS), 0.53 (HbAA vs. HbAC)). In all panels, horizontal lines represent significant differences between groups, and colors represent the same categories as the x-axis. Violin plots represent the density of the distribution, with horizontal lines representing the 25th, 50th, and 75th percentiles. HBB hemoglobin subunit beta locus, molFOI molecular force of infection.
