Fig. 1. DHA kills wild-type T. gondii efficiently and its effect is influenced by mutation of K13.

a Treatment with increasing concentrations of dihydroartemisinin (DHA) or pyrimethamine (Pyr) over 24 h resulted in a reduction in parasite viability, measured as the number of vacuoles with two or more parasites normalized to untreated wells. Results are mean ± SEM for n = 4 independent experiments. b Viability was similarly assessed for extracellular parasites treated with 1 or 10 µM DHA for varying periods of time, then washed and allowed to invade host cells. Viable vacuoles were normalized to untreated parasites kept extracellular for equal periods of time. Results are mean ± SEM for n = 3 independent experiments, each performed in technical triplicate. c Quantification of host monolayer lysis after treatment with 1 or 10 μM DHA for the indicated time, normalized to uninfected monolayers. Results are mean ± SEM for n = 4 independent experiments. d Alignment of the mutated region of K13 in P. falciparum and T. gondii displaying the chromatogram for the K13^C627Y T. gondii line. e Extracellular dose–response curve for parental or K13^C627Y parasites treated with DHA for 5 h. Results are mean ± SEM for n = 7 or 5 independent experiments with parental or K13^C627Y parasites, respectively. f Monolayer lysis following infection with parental or K13^C627Y parasites for 1 h, prior to a 5 h treatment with varying concentrations of DHA. Results are mean ± SEM for n = 4 independent experiments. g Monolayer lysis following infection with parental or K13^C627Y parasites for 24 h, prior to 5 h treatment with varying concentrations of DHA. Results are mean ± SEM for n = 4 or 3 independent experiments with parental or K13^C627Y parasites, respectively. h Graph summarizing the fold change in DHA EC₅₀ between parental and K13^C627Y parasites, treated 1 or 24 h after invasion. Results are mean ± SD for n = 4 or 3 independent experiments, p-value calculated from two-tailed unpaired t-test.