Predicted domain architecture of D. discoideum PPR proteins, PtcA-L.

<p>Blue boxes represent PPR motifs. The amino acid length of each protein is indicated at the C-terminus of each protein. Also displayed are the putative tRNA methyltransferase (yellow), MATH-like (green), and ubiquitin hydrolase-like (orange) domains of PtcE, PtcJ, and PtcK, respectively.</p

Amino acid sequence alignment of PtcK from D. discoideum (Dd) with ubiquitin hydrolases (UBHs) from other organisms.

<p>Sequences used in the alignment include UBHs from Homo sapiens (Hs, accession number NP_005993), Mus musculus(Mm, accession number AAF64193), Bos Taurus (Bt, accession number NP_001035631),Glomerella graminicola (Gg, accession number EFQ25707), Saccharomyces cerevisiae (Sc, accession number EDN63415), and WTF1, a PORR-containing protein from Zea mays(Zm, accession number ACI96105). Only the relevant portion of the alignment is shown. Boxed residues indicate conserved amino acids required for ubiquitin hydrolase activity while identical (*), conserved (:), and semiconserved (.) amino acids are also denoted.</p

Subcellular localisation of PtcB.

<p>Fluorescence microscopy of D. discoideum cells (a) expressing a PtcB:GFP fusion protein,(b) stained with Mitotracker, (c) indicating that the fusion protein and the mitochondria colocalise.</p

Plaque expansion rates of ptcB antisense transformants on Escherichia coli B2 lawns.

<p>Plaque expansion rates for ptcB antisense transformants are plotted against the copy number of the antisense construct present in each transformant, a reflection of the level of antisense inhibition. The number of copies of the antisense construct in each transformant was determined using qPCR. All transformants are shaded in grey while the wild type parental strain is in black.</p

Data repository analyses presented in Robinson et al. 2015 PLoS Medince

1) Albinama_Table1.dta: Baseline characteristics of cohort; 2) Albinama_Table2_Po: Survival analyses of risk of P. ovale infections; 3) Albinama_Table2_Pv_clin: Survival analyses of incidence risk of P. vivax clinical episodes; 4) Albinama_Table2_Pv_LM: survival analyses of incidence risk of light-microscopically positive P. vivax infections; 5) Albinama_Table2_Pv_PCR: survival analyses of incidence risk of PCR positive P. vivax infections; 6)Albinama_Table2_Pvg: survival analyses of incidence risk of gametocyte positive P. vivax infections; 7) Albinama_Table3_0-3mo: incidence of malaria endpoints for first 3 months of follow-up; 8) Albinama_Table3_4-8mo: incidence of malaria endpoints for months 4-8 of follow-up; 9) Albinama_Table3_0-8mo: incidence of malaria endpoints for entire 8 months follow-up; 10) Albinama_Table4_Pf_clin: Survival analyses of incidence risk of P. falciparum clinical episodes; 11) Albinama_Table4_Pf_LM: survival analyses of incidence risk of light-microscopically positive P. falciparum infections; 12) Albinama_Table4_Pf_PCR: survival analyses of incidence risk of PCR positive P. falciparum infections; 13)Albinama_Table4_Pm_PCR: survival analyses of incidence risk of PCR positive P. malariae infections

Time to first <i>Plasmodium</i> spp. infection and <i>P</i>. <i>vivax</i> clinical episode.

<p>Kaplan-Meier plots showing the time to first (or only) (A) <i>P</i>. <i>vivax</i> infection by qPCR, (B) <i>P</i>. <i>vivax</i> infection by LM, (C) <i>P</i>. <i>vivax</i> clinical episode, (D) <i>P</i>. <i>falciparum</i> infection by qPCR, (E) <i>P</i>. <i>malariae</i> infection by qPCR, and (F) <i>P</i>. <i>ovale</i> infection by qPCR, in the two treatment arms. Dashed lines represent the respective 95% confidence intervals.</p

Kaplan-Meier plots showing the time to first (or only) <i>P</i>. <i>vivax</i> infection by qPCR in the PL and PQ arms, stratified by <i>Plasmodium</i> infection status at enrolment.

<p>Dashed lines represent the respective 95% confidence intervals. PV, <i>P</i>. <i>vivax</i>.</p

Study design and follow-up schedule.

<p>After the drug treatment period, children were actively monitored for infection and illness every 2 wk for the first 12 wk. From week 14 to 32, children were actively monitored for illness every 2 wk and for infection every 4 wk.</p

Drug administration schedule.

<p>The drug regimen for the PQ and PL treatment arms was administered with direct observation on 20 d (Monday to Friday) over a 4-wk (26-d) period.</p

Mathematical-model-based predictions of impact of MDA and MSAT with either blood-stage drugs only or blood- plus liver-stage drugs on the population prevalence of <i>P</i>. <i>vivax</i> and <i>P</i>. <i>falciparum</i> infections.

<p>The effect of two rounds (6 mo apart) of MDA (A and B) or MSAT (C and D) with anti-malarial drugs at 80% coverage on <i>P</i>. <i>vivax</i> (A and C) and <i>P</i>. <i>falciparum</i> (B and D) blood-stage parasite prevalence, as predicted by a stochastic model in a human population of size 5,000. The lines represent the mean of 1,000 repeat simulations, and the shaded areas represent the envelopes containing 95% of stochastic simulations. The grey and green shaded bars denote the duration of prophylactic protection for DHA-PIP/CQ and tafenoquine, respectively, after each treatment round. DHA-PIP and CQ were assumed to be administered as part of a 3-d regimen, providing prophylaxis for 1 mo. PQ was assumed to be administered as part of a 14-d regimen, providing prophylaxis for 15 d. Tafenoquine was assumed to be administered via a single dose, providing prophylaxis for 2 mo.</p